Online repository of biological information which aims to create a knowledge base for students by the provision of animations and lectures.Its one largest database of biological videos(more than 1200 Videos)
Synovial joints (or diarthroses, or diarthroidal joints) are the most common and most movable type of joints in the human body. As with most other joints, synovial joints achieve movement at the point of contact of the articulating bones.
Structural and functional differences distinguish synovial joints from cartilaginous joints (synchondroses and symphyses) and fibrous joints (sutures, gomphoses, and syndesmoses). The main structural differences between synovial and fibrous joints is the existence of capsules surrounding the articulating surfaces of a synovial joint and the presence of lubricating synovial fluid within that capsule (synovial cavity).
Structure
Articular capsule: The fibrous capsule is continuous with the periosteum of bone. It is also highly innervated but avascular (lacking blood and lymph vessels)
Articular cartilage: lines the epiphyses of joint end of bone. Provides the loading and unloading mechanism to resist load and shock
Synovial membrane: the inner layer of the fibrous articular capsule. The synovial membrane covers the lining of the synovial cavity where articular cartilage is absent.
Sequential activation of members of the cyclin-dependent protein kinase (CDK) family promotes the correct timing and ordering of events required for cell growth and cell division . In addition to driving progress through the cell cycle, CDKs are also the downstream targets of checkpoint pathways. These checkpoints act to ensure that critical cell cycle events have been successfully completed before the cell progresses into the next cell cycle stage. They are composed of a surveillance system that detects when a particular cell cycle event has not been correctly executed and a signal transduction pathway whose ultimate target can be a CDK. Monomeric CDKs are inactive and require both association with a positive regulatory subunit, called a cyclin, and phosphorylation on a conserved threonine residue that lies within the activation loop for full activity. Both the CDK and cyclin families have multiple members, but only CDKs 1, 2, 4 and 6, when bound to their cognate cyclins, appear to have major roles in controlling cell cycle progression. These CDK/cyclin complexes are then additionally controlled by mechanisms that include inhibitory phosphorylation, protein association, subcellular localisation and targeted destruction of regulatory proteins.
Long-term potentiation (LTP) is the long-lasting improvement in communication between two neurons that results from stimulating them simultaneously. Since neurons communicate via chemical synapses, and because memories are believed to be stored within these synapses, LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.
LTP shares many features with long-term memory that make it an attractive candidate for a cellular mechanism of learning. For example, LTP and long-term memory are triggered rapidly, each depends upon the synthesis of new proteins, each has properties of associativity, and each can potentially last for many months. LTP may account for many types of learning, from the relatively simple classical conditioning present in all animals, to the more complex, higher-level cognition observed in humans.
By enhancing synaptic transmission, LTP improves the ability of two neurons, one presynaptic and the other postsynaptic, to communicate with one another across a synapse. The precise mechanisms for this enhancement of transmission have not been fully established, in part because LTP is governed by multiple mechanisms that vary by such things as brain region, animal age, and species. Yet in the most well understood form of LTP, enhanced communication is predominantly carried out by improving the postsynaptic cell's sensitivity to signals received from the presynaptic cell. These signals, in the form of neurotransmitter molecules, are received by neurotransmitter receptors present on the surface of the postsynaptic cell. LTP improves the postsynaptic cell's sensitivity to neurotransmitter in large part by increasing the activity of existing receptors and by increasing the number of receptors on the postsynaptic cell surface.
LTP was discovered in the rabbit hippocampus by Terje Lømo in 1966 and has remained a popular subject of research since. Most modern LTP studies seek to better understand its basic biology, while others aim to draw a causal link between LTP and behavioral learning. Still others try to develop methods, pharmacologic or otherwise, of enhancing LTP to improve learning and memory. LTP is also a subject of clinical research, for example, in the areas of Alzheimer's disease and addiction medicine.
Mechanism
Long-term potentiation occurs through a variety of mechanisms throughout the nervous system; no single mechanism unites all of LTP's many types. However, for the purposes of study, LTP is commonly divided into three phases that occur sequentially: short-term potentiation, early LTP, and late LTP. Little is known about the mechanisms of short-term potentiation,
Each phase of LTP is governed by a set of mediators, small molecules that dictate the events of that phase. These molecules include protein receptors that respond to events outside of the cell, enzymes that carry out chemical reactions within the cell, and signaling molecules that allow the progression from one phase to the next. In addition to these mediators, there are also modulator molecules, described later, that interact with mediators to finely alter the LTP ultimately generated.
The early (E-LTP) and late (L-LTP) phases of LTP are each characterized by a series of three events: induction, maintenance, and expression. Induction is the process by which a short-lived signal triggers that phase of LTP to begin. Maintenance corresponds to the persistent biochemical changes that occur in response to the induction of that phase. Expression entails the long-lasting cellular changes that result from activation of the maintenance signal. Thus the mechanisms of LTP can be discussed in terms of the mediators that underlie the induction, maintenance, and expression of E-LTP and L-LTP.
Jim Lockhart speaks with Anuradha Mittal of The Oakland Institute and Mark Des Marets of Northwest Resistance Against Genetic Engineering. Northwest Resistance Against Genetic Engineering www.nwrage.org From the webite SPEAKOUT! www.speakoutnow.org : Anuradha Mittal, a native of India, is an internationally renowned expert on trade, development, human rights, democracy, and agriculture issues. She is the founder and director of a policy think tank, The Oakland Institute, that works to ensure public participation and democratic debate on the most crucial economic and social policy issues that affect peoples' lives through nonpartisan research, analysis, and advocacy. Building on the identification of human rights as the foundation of global democracy, the Oakland Institute uses the rights-based approach to reframe the public debate and build an agenda for common action.
ERIC KANDEL 2000 Nobel Laureate in Physiology or Medicine. Professor of Physiology &; Cellular Biophysics, Biochemistry & Molecular Biophysics, and Psychiatry, Columbia University "Mice, Men and Mental Illness: Animal Models of Human Mental Disorders" 5th May, 2007 lecture by Eric R. Kandel (2007 Arnold Pfeffer Prize) at the Arnold Pfeffer Centre for Neuropsychoanalysis, New York Psychoanalytical Society. In the last two decades molecular genetics has transformed neurology. Diagnoses of neurological disorders are no longer based only on signs and symptoms, but also on tests for the dysfunction of specific genes, proteins, and nerve cell components as well as brain scans for disturbances of neural systems. Molecular genetics also has led to the discovery of 1) several newly defined molecular diseases caused by mutations in specific genes, such as the channelopathies and 2) new mechanisms of pathogensis such as the trinucleotide-repeat and the prion disorders. To date, however, molecular biology has had only a modest impact on psychiatry. I propose to address this issue by illustrating that whereas neurology has long been based on the location of disease in the brain, there is not a comparable strong neuropathology of mental illness. In addition, tracing the genetic causes of mental illness is a much more difficult task than finding the gene for Huntington’s disease. There is no single gene for schizophrenia, or most other mental illnesses. Most psychiatric disorders have a combined multigenic and environmental basis. As a result of these limitations, psychiatry has not been *years things will change dramatically. The field is beginning to identify some genes involved in the major mental illnesses. We also are beginning to know something about the neural circuits affected by these diseases. As a result, we can now develop satisfactory animal models of components of these disorders. I will devote most of the lecture to describe attempts to develop mouse models of the cognitive deficits present in two major mental disorders: 1) anxiety disorders that have a component of learned fear and 2) schizophrenia, focusing on the cognitive symptoms reflected in working memory deficit.
Raloxifene is an oral selective estrogen receptor modulator (SERM) that has estrogenic actions on bone and anti-estrogenic actions on the uterus and breast. It is used in the prevention of osteoporosis in postmenopausal women. It was announced on April 17, 2006, that raloxifene is as effective as tamoxifen in reducing the incidence of breast cancer in certain high risk groups of females, though with a reduced risk of thromboembolic events and cataracts in patients taking raloxifene versus those taking tamoxifen. On September 14, 2007, the U.S. Food and Drug Administration announced approval of raloxifene for reducing the risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer.
There has been criticism in the mainstream oncology press of the way that information about the drug was released.There has been some confusion in the lay media about the meaning of the trial results. There is no specific clinical evidence for the use of raloxifene in the adjuvant treatment of breast cancer over established drugs such as tamoxifen or anastrozole.
The word "laparoscopy" means to look inside the abdomen with a special camera or scope. Surgery performed with the aid of these cameras is known as "keyhole," "porthole," or "minimally invasive" surgery.
Traditional surgery requires a long incision (cut) down the center of the abdomen and a lengthy recovery period. Laparoscopic surgery eliminates the need for this large incision. As a result, you may experience less pain and scarring after surgery, more rapid recovery, and less risk of infection.
For laparoscopic prostate surgery, this technique requires five small (5-10 millimeters) incisions (or "portholes") -- one just below the belly button and two each on both sides of the lower abdomen. Carbon dioxide is passed into the abdominal cavity through a small tube placed into the incision below the belly button. This gas lifts the abdominal wall to give the surgeon a better view of the abdominal cavity once the laparoscope is in place. The surgeon is then guided by the laparoscope, which transmits a picture of the prostate onto a video monitor.
Laparoscopy is a relatively new technique for prostate removal, but it looks promising. Men who undergo this technique have less blood loss, less need for pain medicine, shorter hospital stays, quicker return to regular diet and activities, early removal of urethral catheters (tubes inserted through the penis to drain urine from the bladder), and a quicker recovery. Laparoscopy also appears to treat the cancer as well as conventional "open" procedures that are performed with a large incision.
What are the advantages of laparoscopy?
As is the case with other minimally invasive procedures, laparoscopic prostate removal has significant advantages over traditional "open" surgery:
Laparoscopy can shorten your hospital stay to one or two days. About 50 percent of men are discharged one day after surgery. (The length of stay depends on how quickly you recover and the extent of the surgery.)
There is significantly less bleeding during the operation.
You are less likely to need prescription painkillers after you leave the hospital. Patients generally need nothing more than Tylenol.
At your follow-up appointment one week after surgery, the tube — or catheter — draining your bladder will be removed if there are no signs of other problems. Occasionally, the catheter must remain in place for another week, as is routinely the case following conventional "open" surgery.
About 90 percent of patients can return to work or resume full activity in only two to three weeks.
Am I eligible for this surgery?
You are eligible if you have cancer that has not spread outside the prostate and is not very aggressive, as well as a PSA blood test less than 10. You are not eligible if you have had previous open or laparoscopic pelvic surgery, even for another reason, or a history of hormone treatment called LH-RH agonist (luteinizing hormone-releasing hormone), which reduces the size of the prostate tumor.
What are the side effects?
Medical research so far has shown the frequency of incontinence and impotence to be similar between minimally invasive surgery and open surgery -- with men usually returning to normal urinary function within three months for both types of surgeries. Both types of surgeries also have similar rates of incontinence.
Because this technique is nerve-sparing, postoperative sexual potency rate should be comparable to that of conventional open surgery. However, it is important to note that minimally invasive prostate surgery has not been in use long enough to truly assess whether or not it leads to higher rates of potency. But early results are promising.
How do I prepare for surgery?
Your surgeon will meet with you to answer any questions you might have. You will be asked questions about your health history, and a general physical examination will be performed. If your intestine requires cleaning, you will be given a prescription for a laxative medicine to take the evening before the surgery.
All patients are generally asked to provide a blood sample. Depending on your age and general health, you might also have an EKG (electrocardiogram), a chest X-ray, lung function tests, or other tests.
Finally, you will meet with an anesthesiologist who will discuss the type of anesthesia you will be given for surgery. You will also learn about pain control after the operation, which might include a PCA (patient controlled analgesia) pump.
What happens during surgery?
Your surgeon will place a small needle just below your belly button and insert the needle into your abdominal cavity. The needle is connected to a small tube, and carbon dioxide is passed into the abdominal cavity. This gas lifts the abdominal wall to give the surgeon a better view of the abdominal cavity once the laparoscope is in place. The surgeon is then guided by the laparoscope, which transmits a picture of the prostate onto a video monitor.
Next, a small incision will be made near your belly button. The laparoscope is placed through this incision and is connected to a video camera. The image your surgeon sees in the laparoscope is projected onto video monitors placed near the operating table.
Before starting the surgery, the surgeon will take a thorough look at your abdominal cavity to make sure the laparoscopy procedure will be safe for you. If the surgeon determines that the procedure will not be safe for you because of the presence of scar tissue, infection ,or abdominal disease, the procedure will not be continued.
If the surgeon decides the surgery can be safely performed, additional small incisions will be made, giving your surgeon access to the abdominal cavity. If necessary, one of these small incisions might be enlarged to remove the pelvic lymph nodes.
What happens after surgery?
You can expect to follow a liquid diet and you gradually will be able to eat solid foods. When you go home, you will follow a soft diet, which generally means no raw fruits or vegetables. A dietitian can provide more specific dietary guidelines.
Nausea and vomiting are common and occur because the intestines are temporarily disabled during anesthesia and surgery. Your doctor can prescribe medicines to relieve these symptoms, which will improve a few days after surgery.
You will be encouraged to get out of bed and walk as much as possible, starting the first day after surgery. You should steadily increase your activity after you go home. For six weeks after surgery, you should not lift or push anything over 30 pounds, and do not do abdominal exercises such as sit-ups.
Lecture was delivered by Dr. Siddhartha Sankar Ghosh during CORRAL Special talk, for the students' of IIT Guwahati. In this he explains the nobel prize work of Mario R. Capecchi, Ph.D., distinguished professor of human genetics and biology at the University of Utah's Eccles Institute of Human Genetics and a Howard Hughes Medical Institute investigator
Roger David Kornberg (born April 24, 1947) is an American biochemist and professor of structural biology at Stanford University School of Medicine.
Kornberg was awarded the Nobel Prize in Chemistry in 2006 for his studies of the process by which genetic information from DNA is copied to RNA, "the molecular basis of eukaryotic transcription." His father, Arthur Kornberg, who was also a professor at Stanford University, was awarded the Nobel Prize in Physiology or Medicine in 1959.
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Scientific Discoveries and Nobel Prize
All organisms are controlled by their genes, which are coded by DNA, which is copied to RNA, which creates proteins, which are sequences of amino acids. DNA resides in the nucleus. When a cell expresses a gene, it copies (transcribes) that gene's DNA sequence onto a messenger RNA (mRNA) sequence. mRNA is transported out of the nucleus to ribosomes. The ribosomes read the mRNA and translate the code into the right amino acid sequence to make that gene's protein.
The DNA is transcribed to mRNA by an enzyme, RNA polymerase II, with the help of many other proteins. Using yeast, Kornberg identified the role of RNA polymerase II and other proteins in transcribing DNA, and he created three-dimensional images of the protein cluster using X-ray crystallography. Polymerase II is used by all organisms with nuclei, including humans, to transcribe DNA.
Kornberg and his research group have made several fundamental discoveries concerning the mechanisms and regulation of eukaryotic transcription. While a postdoctoral fellow working with Aaron Klug and Francis Crick at the MRC in the 1970s, Kornberg discovered the nucleosome as the basic protein complex packaging chromosomal DNA in the nucleus of eukaryotic cells (chromosomal DNA is often termed "Chromatin" when it is bound to proteins in this manner, reflecting Walther Flemming's discovery that certain structures within the cell nucleus would absorb dyes and become visible under a microscope).Within the nucleosome, Kornberg found that roughly 200 bp of DNA are wrapped around an octamer of histone proteins.
Kornberg's research group at Stanford later succeeded in the development of a faithful transcription system from baker's yeast, a simple unicellular eukaryote, which they then used to isolate in a purified form all of the several dozen proteins required for the transcription process. Through the work of Kornberg and others, it has become clear that these protein components are remarkably conserved across the full spectrum of eukaryotes, from yeast to human cells.
Using this system, Kornberg made the major discovery that transmission of gene regulatory signals to the RNA polymerase machinery is accomplished by an additional protein complex that they dubbed Mediator. As noted by the Nobel Prize committee, "the great complexity of eukaryotic organisms is actually enabled by the fine interplay between tissue-specific substances, enhancers in the DNA and Mediator. The discovery of Mediator is therefore a true milestone in the understanding of the transcription process."
At the same as Kornberg was pursuing these biochemical studies of the transcription process, he devoted two decades to the development of methods to visualize the atomic structure of RNA polymerase and its associated protein components. Initially, Kornberg took advantage of expertise with lipid membranes gained from his graduate studies to devise a technique for the formation of two-dimensional protein crystals on lipid bilayers. These 2D crystals could then be analyzed using electron microscopy to derive low-resolution images of the protein's structure. Eventually, Kornberg was able to use X-ray crystallography to solve the 3-dimensional structure of RNA polymerase at atomic resolution. The structure of RNA polymerase obtained by Kornberg is the most complex protein structure solved to date. He has recently extended these studies to obtain structural images of RNA polymerase associated with accessory proteins.[8]Through these studies, Kornberg has created an actual picture of how transcription works at a molecular level. According to the Nobel Prize committee, "the truly revolutionary aspect of the picture Kornberg has created is that it captures the process of transcription in full flow. What we see is an RNA-strand being constructed, and hence the exact positions of the DNA, polymerase and RNA during this process."
In 1959, Roger Kornberg's father, Arthur Kornberg, received the Nobel Prize in Physiology or Medicine for studies of how genetic information is transferred from one DNA molecule to another in a process called DNA replication. Specifically, Arthur Kornberg isolated the first enzyme capable of synthesizing DNA, bacterial DNA polymerase I, which was then the first known enzyme to take its instructions from a template, thus ensuring the conservation of genetic information during cellular growth and division. Roger Kornberg's younger brother, Thomas Bill Kornberg, discovered DNA polymerases II and III in 1970 and is now a geneticist at the University of California, San Francisco. All three Kornbergs have thus worked to understand how genetic information is put to use in cells. Roger and Arthur Kornberg are the sixth father-son pair to win Nobel Prizes.
Dr.Cameron Mello was awarded the 2006 Nobel prize for Medicine , along with colleague Dr. Andrew Z. Fire, for the discovery of RNA interference. In this video, he discusses his research and his experiences as a scientist and recent Nobel Prize
Craig Cameron Mello (born October 18, 1960) is an American biologist and Professor of Molecular Medicine at the University of Massachusetts Medical School in Worcester, Massachusetts. He was awarded the 2006 Nobel Prize for Physiology or Medicine, along with Andrew Z. Fire, for the discovery of RNA interference. This research was conducted at the University of Massachusetts Medical School and published in 1998. Mello has been a Howard Hughes Medical Institute investigator since 2000.
About Speaker
Mello and Fire received the Nobel Prize for work that began in 1998, when Mello and Fire along with their colleagues (SiQun Xu, Mary Montgomery, Stephen Kostas, and Sam Driver) published a paper [3] in the journal Nature detailing how tiny snippets of RNA fool the cell into destroying the gene's messenger RNA (mRNA) before it can produce a protein - effectively shutting specific genes down.
In this Prof.Harald zur Hausen answers question from Students about HPV.Harald zur Hausen (born March 11, 1936) is a German virologist and professor emeritus. He has done research on cancer of the cervix, where he discovered the role of papilloma viruses, for which he received the Nobel Prize in Physiology or Medicine 2008.
Scientific merits
Zur Hausen's specific field of research is the study of oncoviruses. In 1976, he published the hypothesis that human papilloma virus plays an important role in the cause of cervical cancer. Together with his collaborators, he then identified HPV16 and HPV18 in cervical cancers in 1983-4. This research directly made possible the development of a vaccine which was introduced in 2006. See also HPV vaccine. He is also credited with discovery of the virus causing genital warts (HPV 6) and a monkey lymphotropic polyomavirus that is a close relative to a recently discovered human Merkel cell polyomavirus, as well as techniques to immortalize cells with Epstein-Barr virus and to induce replication of the virus using phorbol esters. His work on papillomaviruses and cervical cancer received a great deal of scientific criticism on initial unveiling but subsequently was confirmed and extended to other high-risk papillomaviruses.
He received the Gairdner Foundation International Award in 2008 for his contributions to medical science.He also shared the 2008 Nobel Prize in Medicine with Luc Montagnier and Françoise Barré-Sinoussi, who discovered the human immunodeficiency virus.
Nobel prize for medicine 2008 was Shared between Harald zur Hausen "for his discovery of human papilloma viruses causing cervical cancer" and to Françoise Barré-Sinoussi and Luc Montagnier for their discovery of human immunodeficiency virus.
Harald zur Hausen (born March 11, 1936) is a German virologist and professor emeritus. He has done research on cancer of the cervix, where he discovered the role of papilloma viruses,
Discovery of human papilloma virus causing cervical cancer
Against the prevailing view during the 1970s, Harald zur Hausen postulated a role for human papilloma virus (HPV) in cervical cancer. He assumed that the tumour cells, if they contained an oncogenic virus, should harbour viral DNA integrated into their genomes. The HPV genes promoting cell proliferation should therefore be detectable by specifically searching tumour cells for such viral DNA. Harald zur Hausen pursued this idea for over 10 years by searching for different HPV types, a search made difficult by the fact that only parts of the viral DNA were integrated into the host genome. He found novel HPV-DNA in cervix cancer biopsies, and thus discovered the new, tumourigenic HPV16 type in 1983. In 1984, he cloned HPV16 and 18 from patients with cervical cancer. The HPV types 16 and 18 were consistently found in about 70% of cervical cancer biopsies throughout the world.
Françoise Barré-Sinoussi
Françoise Barré-Sinoussi (born 30 July 1947) is a French virologist and director of the Unité de Régulation des Infections Rétrovirales at the Institut Pasteur in Paris, France. Born in Paris, France, Barré-Sinoussi performed some of the fundamental work in the identification of the human immunodeficiency virus (HIV) as the cause of AIDS
Luc Montagnier (born August 18, 1932) is a French virologist and joint recipient with Françoise Barré-Sinoussi and Harald zur Hausen of the 2008 Nobel Prize in Physiology or Medicine.
Discovery of HIV
Following medical reports of a novel immunodeficiency syndrome in 1981, the search for a causative agent was on. Françoise Barré-Sinoussi and Luc Montagnier isolated and cultured lymph node cells from patients that had swollen lymph nodes characteristic of the early stage of acquired immune deficiency. They detected activity of the retroviral enzyme reverse transcriptase, a direct sign of retrovirus replication. They also found retroviral particles budding from the infected cells. Isolated virus infected and killed lymphocytes from both diseased and healthy donors, and reacted with antibodies from infected patients. In contrast to previously characterized human oncogenic retroviruses, the novel retrovirus they had discovered, now known as human immunodeficiency virus (HIV), did not induce uncontrolled cell growth. Instead, the virus required cell activation for replication and mediated cell fusion of T lymphocytes. This partly explained how HIV impairs the immune system since the T cells are essential for immune defence. By 1984, Barré-Sinoussi and Montagnier had obtained several isolates of the novel human retrovirus, which they identified as a lentivirus, from sexually infected individuals, haemophiliacs, mother to infant transmissions and transfused patients. The significance of their achievements should be viewed in the context of a global ubiquitous epidemic affecting close to 1% of the population.
Importance of the HIV discovery
Soon after the discovery of the virus, several groups contributed to the definitive demonstration of HIV as the cause of acquired human immunodeficiency syndrome (AIDS). Barré-Sinoussi and Montagnier's discovery made rapid cloning of the HIV-1 genome possible. This has allowed identification of important details in its replication cycle and how the virus interacts with its host. Furthermore, it led to development of methods to diagnose infected patients and to screen blood products, which has limited the spread of the pandemic. The unprecedented development of several classes of new antiviral drugs is also a result of knowledge of the details of the viral replication cycle. The combination of prevention and treatment has substantially decreased spread of the disease and dramatically increased life expectancy among treated patients. The cloning of HIV enabled studies of its origin and evolution. The virus was probably passed to humans from chimpanzees in West Africa early in the 20th century, but it is still unclear why the epidemic spread so dramatically from 1970 and onwards.
Identification of virus−host interactions has provided information on how HIV evades the host’s immune system by impairing lymphocyte function, by constantly changing and by hiding its genome in the host lymphocyte DNA, making its eradication in the infected host difficult even after long-term antiviral treatment. Extensive knowledge about these unique viral host interactions has, however, generated results that can provide ideas for future vaccine development as well as for therapeutic approaches targeting viral latency.
HIV has generated a novel pandemic. Never before has science and medicine been so quick to discover, identify the origin and provide treatment for a new disease entity. Successful anti-retroviral therapy results in life expectancies for persons with HIV infection now reaching levels similar to those of uninfected people
Dr. Lam graduated as Valedictorian from Cistercian Preparatory School and completed his undergraduate degree at Princeton University and his medical degree at Baylor College of Medicine, both with honors. He trained for six years in head and neck surgery at Columbia University College of Physicians & Surgeons in New York City and then completed a prestigious fellowship in facial plastic and reconstructive surgery in which he refined his technique for hair restoration. Dr. Lam has written over 100 scientific articles and book chapters as well as three major medical textbooks. He has written numerous scientific articles on hair restoration in distinguished journals like Dermatologic Surgery as well as a textbook on hair transplantation
Ovulation is the process in the menstrual cycle by which a mature ovarian follicle ruptures and discharges an ovum (also known as an oocyte, female gamete, or casually, an egg) that participates in reproduction. Ovulation also occurs in the estrous cycle of other female mammals, which differs in many fundamental ways from the menstrual cycle.
Overview
The process of ovulation is controlled by the hypothalamus of the brain and through the release of hormones secreted in the anterior lobe of the pituitary gland, (Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH)). In the follicular (pre-ovulatory) phase of the menstrual cycle, the ovarian follicle will undergo a series of transformations called cumulus expansion, this is stimulated by the secretion of FSH. After this is done, a hole called the stigma will form in the follicle, and the ovum will leave the follicle through this hole. Ovulation is triggered by a spike in the amount of FSH and LH released from the pituitary gland. During the luteal (post-ovulatory) phase, the ovum will travel through the fallopian tubes toward the uterus. If fertilized by a sperm, it may perform implantation there 6-12 days later.
In humans, the few days near ovulation constitute the fertile phase. The average time of ovulation is the fourteenth day of an average length (twenty-eight day) menstrual cycle. It is normal for the day of ovulation to vary from the average, with ovulation anywhere between the tenth and nineteenth day being common.
Cycle length alone is not a reliable indicator of the day of ovulation. While in general an earlier ovulation will result in a shorter menstrual cycle, and vice versa, the luteal (post-ovulatory) phase of the menstrual cycle may vary by up to a week between women.
Osteoarthritis , is a group of diseases and mechanical abnormalities entailing painful degradation of joints, including cartilage and the subchondral bone next to it. Clinical symptoms of OA may include joint pain, tenderness, stiffness, inflammation, and creaking of joints. In OA, a variety of potential forces -- hereditary, developmental, metabolic, and mechanical -- may initiate processes leading to loss of cartilage -- a strong protein matrix that lubricates and cushions the joints. As the body struggles to contain ongoing damage, immune and regrowth process can accelerate damage. When bone surfaces become less well protected by cartilage, subchondral bone may be exposed and damaged, with regrowth leading to a proliferation of ivory-like, dense, reactive bone in central areas of cartilage loss, a process called eburnation. The patient increasingly experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax. OA is the most common form of arthritis
Method and System for Treatment of Blood and/or Other Body Fluids and/or Synthetic Fluids using Combined Filter Elements and Electric Field Forces
In 1990, an astounding discovery was reported at Albert Einstein College of Medicine in NYC by Drs. Kaali and Wyman, resulting in Patent No. 5,188,738 being issued in 1993 entitled "Alternating Current Supplied Electrically Conductive Method and System for Treatment of Blood and/or Other Body Fluids and/or Synthetic Fluids with Electric Forces.". Their research work involved an in vitro & in vivo human Blood Electrification process, which electronically sterilizes the blood, resulting in all known pathogens, including bacteria, viruses, parasites, and fungus, being completely eliminated! Their research had been anticipated 24 years earlier in 1973 with the research involved in Patent No. 3,753,886. Not surprisingly though, due to the stranglehold, that the Pharmaceutical Cartel has in the U.S., this revolutionary clinical data was almost totally suppressed. Other than a few News Articles such as the Science News: Mar. 30, `91 pg. 207, Longevity: Dec. `92/pg. 14, and Houston Post: Mar. 20, '91 /Sect. A-10, plus the Patent No. 5,188,738,
Abstract ~ A method and system for the treatment of blood and/or other body fluids (such as amniotic fluids) as well as synthetic fluids such as tissue culture medium whereby a fluid to be treated is mechanically filtered for elimination of particles contained therein which exceed 0.2 microns in size (or some other minutely small size) and in addition subjecting the fluid being treated to electric field forces in the microwatt/milliwatt region induced by relatively low voltage of a few volts and low current density which does not exceed values which could impair the biological usefulness and characteristics of the blood or other fluid being treated.
If you’re worried about getting cancer, do yourself a favor: steer clear of red meat and rich foods, and avoid cigarettes. In this lecture, Robert Weinberg provides the scientific basis for this commonplace advice, as well as a layman’s look at the genetic, biochemical and environmental factors that make good cells go bad.
Normal cells are civic-minded, lining up together in a precise architecture that gives structure to body tissue. When the cell’s genes are damaged, they send out faulty instructions, turning orderly structure into a chaotic mess. This kind of injury to cells likely comes from the outside – as many as 90% of human cancers are due to bad diets and smoking. Weinberg wants to understand the specific pathways by which the cells’ enemies invade and do their damage, in hopes of then being able to halt the process and freeze a cancer’s growth. But, cautions Weinberg, better to count on prevention than a cure in the fight against cancer.
About the Speaker
Robert A. Weinberg '64, PhD '69
Founding Member, MIT Center for Cancer Research
Member, Whitehead Institute Daniel K. Ludwig and American Cancer Society Professor for Cancer Research
Department of Biology
Robert A. Weinberg has earned some of the top honors in his field. Most recently, he won the 2006 Landon-AACR Prize for Basic and Translational Cancer Research. He is also a 1997 National Medal of Science awardee.
Weinberg's laboratory discovered the first human oncogene and the first tumor suppressor gene. Today, much of his research focuses on new models of breast cancer development including the stages of tumor invasiveness and metastasis.
He earned his Ph.D. in biology from MIT in 1969, and was one of the Founding Members of the MIT Center for Cancer Research in 1973. He was appointed a professor at MIT in 1982, the same year he joined the Whitehead Institute. Weinberg was named American Cancer Society Research Professor in 1985 and received the Daniel K. Ludwig Professorship for Cancer Research in 1997. He is a member of the National Academy of Sciences and the Institute of Medicine.
There's been much controversy concerning embryonic stem cell research in recent years. However, a new study finds some patients are benefitting from ADULT stem cell therapy right now, and doctors hope we are one step closer to some major breakthroughs... Dr. Sean Kenniff reports... Donald Reid is hoping adult stem cells will give him more time. (Donald Reid/Heart Patient) THERE'S NOT MANY OPTIONS LEFT FOR ME. The 57-year-old has clogged arteries and heart disease so bad he's not a candidate for surgery. Instead he's joined an experimental study that involves this machine. It's taking his blood and pulling out stem cells. We're not talking about stem cells from an embryo. These are Donald's own adult stem cells. In the coming days doctors will inject them directly into Donald's heart… with the hope it will regenerate and revitalize the damaged organ. (Dr. Sean Kenniff/CBS NEWS) Adult stem cells have become standard therapy for treating several types of cancers like lukemia and lymphoma. But according to new research this treatment is now starting to show real promise in treating other diseases. A review of hundreds of trials found in some patients adult stem cells have stopped auto-immune diseases like rheumatoid arthritis and multiple sclerosis. Some heart patients like Donald have also seen improvement. Weill Cornell's Michael Schuster is excited by the results but warns it's still early. (Dr. Michael Schuster/NY Pres., Weill Cornell Med. Ctr.) WE DON'T KNOW YET WHAT THE BEST TECHNIQUE IS, WE DON'T REALLY KNOW HOW MUCH OF A BENEFIT THE PATIENTS WILL HAVE. And when it comes to diseases like Diabetes, Alzheimer's and Parkison's. (Dr. Michael Schuster/NY Pres., Weill Cornell Med. Ctr.) I THINK WE'RE STILL A FEW YEARS AWAY FROM KNOWING WHETHER STEM CELLS REALLY TURN OUT TO BE THE ANSWER. Donald should have an answer much sooner. His wish….. (Donald Reid/Heart Patient) TO BE LIKE EVERYONE ELSE AND NOT HAVE TO WORRY ABOUT THAT MY HEART MIGHT GIVE OUT. In the coming weeks he'll know if that wish came true
A Healthy Brain The healthy brain is made up of millions of interconnecting nerve cells, called neurons. Neurons constantly communicate with each other by sending signals through tentacle-like connections called axons and dendrites. How Alzheimer's Disease Affects the Brain The brain of a patient with Alzheimer's disease is much different. The orderly, organized arrangement of nerve cells found in a healthy brain become entangled, full of senile plaques and neurofibrillary tangles. The plaques and tangles interfere with the normal activity between neurons in the area of the brain responsible for intellectual thought. Symptoms of Alzheimer's Disease Alzheimer's disease affects people in different ways. The disease is slowly progressive from onset. Memory loss, confusion, disorientation, and poor judgment are a few of the symptoms of Alzheimer's disease.
Since innovation is “not necessarily always predictable,” Daniel Vasella declines to discuss it in a systematic way, and instead, focuses on a case study of one of his company’s flagship pharmaceuticals, Gleevec. The discovery, development and marketing of this drug, which fights the rare chronic myeloid leukemia (CML), may point to some of the things Novartis does right, suggests Vasella.
Many significant drugs result from years of basic research that takes place outside of industry. Pathbreaking work that occurred decades ago uncovered chromosome damage in patients with CML, and revealed an abnormal protein secreted due to this mutation. In the early 1990s, Novartis began the creative work of trying to block the signal of this cancer-causing protein.
After testing numerous compounds, Gleevec was synthesized in 1992, and “then the problems started,” says Vasella. When the drug was delivered intravenously, there were toxic effects, and they couldn’t reproduce results from cell cultures. With 100 researchers laboring on the problem, recounts Vasella, “marketing said, ‘stop this damn thing.’”
Despite the setbacks, “We persisted,” says Vasella. Indeed, the first clinical human trials, on 31 patients, were so spectacular -- 100% remission rates -- that Vasella didn’t believe the data. The company moved into frenetic pitch to complete the additional clinical trials necessary for FDA approval, and then on to production. Employees volunteered to work in 24-hour shifts, seven days a week. Vasella faced another issue: “We had to come up with a way we’d make money,” since CML affected a relative handful of patients globally. And the fewer the patients, the higher the price of the drug, potentially keeping it out of the hands of those who most needed it. The company decided to subsidize the cost of Gleevec for patients of little means. In spite of this, Gleevec “has surpassed all expectations.” Sales this year alone will exceed $2.4 billion.
What elements might have led to this triumph and Novartis’ more recent successes? Vasella cites “intrinsic motivation” in each Novartis staff member, high standards, savvy risk-taking and persistence in both research and marketing, and a company culture that brings out the best in everyone.
About the Speaker
Daniel Vasella
Chairman and CEO, Novartis
Daniel Vasella, M.D., was appointed Chairman in April 1999, having served as CEO and Head of the Group Executive Committee since the merger that created Novartis in 1996. Previously, Dr. Vasella was CEO of Sandoz Pharma Ltd. and a member of the Sandoz Group Executive Committee.
As CEO, Vasella created the Novartis Institute for BioMedical Research and moved the company’s research headquarters to Cambridge, Massachusetts, to be closer to top scientific talent as well as patient and hospital networks. He also established The Genomics Institute of the Novartis Research Foundation, which is focused on developing therapeutics from the data generated from the mapping of the human genome.
Vasella has implemented pioneering initiatives to ensure access to medicines, which include the founding of the Novartis Institute for Tropical Diseases for research on neglected diseases of the developing world, and the International Patient Assistance Program for the breakthrough cancer drug Gleevec®/Glivec™, an agreement to supply the novel malaria treatment Coartem® at cost to the World Health Organization and a pledge to donate the drug therapy needed to eradicate leprosy worldwide.
In 2003, Vasella was awarded The CancerCare Human Services Award and also the Harvard Business School’s Alumni Achievement Award. He holds the rank of Chevalier in the Ordre National de la Légion d’Honneur (France). Vasella is a member of the Board of Directors of PepsiCo, Inc., United States. In addition, he is a member of the Board of Dean’s Advisors at the Harvard Business School. He is also President of the International Federation of Pharmaceutical Manufacturers Associations.
About the Speaker
Daniel Vasella
Chairman and CEO, Novartis
Daniel Vasella, M.D., was appointed Chairman in April 1999, having served as CEO and Head of the Group Executive Committee since the merger that created Novartis in 1996. Previously, Dr. Vasella was CEO of Sandoz Pharma Ltd. and a member of the Sandoz Group Executive Committee.
As CEO, Vasella created the Novartis Institute for BioMedical Research and moved the company’s research headquarters to Cambridge, Massachusetts, to be closer to top scientific talent as well as patient and hospital networks. He also established The Genomics Institute of the Novartis Research Foundation, which is focused on developing therapeutics from the data generated from the mapping of the human genome.
Vasella has implemented pioneering initiatives to ensure access to medicines, which include the founding of the Novartis Institute for Tropical Diseases for research on neglected diseases of the developing world, and the International Patient Assistance Program for the breakthrough cancer drug Gleevec®/Glivec™, an agreement to supply the novel malaria treatment Coartem® at cost to the World Health Organization and a pledge to donate the drug therapy needed to eradicate leprosy worldwide.
In 2003, Vasella was awarded The CancerCare Human Services Award and also the Harvard Business School’s Alumni Achievement Award. He holds the rank of Chevalier in the Ordre National de la Légion d’Honneur (France). Vasella is a member of the Board of Directors of PepsiCo, Inc., United States. In addition, he is a member of the Board of Dean’s Advisors at the Harvard Business School. He is also President of the International Federation of Pharmaceutical Manufacturers Associations.
When Fiona Murray visited research centers in China recently, scientists greeted her quizzically: “People were baffled about what a business school professor was doing in stem cell and gene sequencing labs,” Murray says.
As it turns out, Murray’s tour was integral to her own MIT Sloan research exploring how science serves as a source of competitive advantage. As China and India and other developing countries produce scientists and engineers at a quickening pace, Murray hopes to find out if their capacity to capitalize on scientific ideas is expanding in a comparable way.
One challenge to this kind of research, says Murray, is that the market for scientific ideas “is poorly functioning.” Traditional markets, say for pork bellies, oil or diamonds have well-defined products, well-established metrics,” but how do you measure the quality of scientific ideas?
Murray’s solution is to visit key scientific and engineering institutes in other countries to observe both scientific infrastructure -- the physical state of laboratories -- and how researchers collaborate and generate useful knowledge. She also scans the scientific literature to see how many papers a particular country publishes, in what subdisciplines, and how many citations scientists receive.
Murray’s work may aid commercial enterprises intent on taking advantage of growing global scientific and engineering expertise. Some initial insights: places like China and India hold tremendous potential for firms, whether through their permissive regulatory climates or unique natural resources. But, she advises, don’t enter one of these countries expecting to hire scientists at bargain basement prices, since “the real costs of scientific labor are hidden.” Also, expect poor lab facilities, enormous bureaucracies and a crazy quilt of intellectual property and licensing rules.
Counsels Murray, “Start by collaborating on R&D with research institutes and labs. That allows you to understand their expertise, social rules of engagement and to potentially shape the rules.”
Synthetic biology is a new area of biological research that combines science and engineering in order to design and build ("synthesize") novel biological functions and systems
There’s no mistaking Drew Endy’s profession: “I like to make things -- that’s what I do.” From his engineer’s perspective, the slow and painful methods of bioengineering demand a solution. Endy hopes to refine the tools necessary to move the field forward. “We’re going from looking at the living world as only coming from nature, to a subset of the living world being produced by engineers who design and build hopefully useful living artifacts according to our specifications,” says Endy.
Thirty years ago, scientists figured out how to use enzymes to cut and paste genetic material, leading to recombinant DNA technology. But the techniques involved are painfully slow, requiring very specific physical materials and “know-how via the guild-like structure of biology.” Endy points to methods coming on line that will make it easier to design and build biological systems.
One is DNA synthesis, in which a machine fed information and sugars generates a physical piece of DNA. It reminds Endy of the “matter compilers” seen on Star Trek, where “food materializes from a cubby in the wall.” This technique will allow the economical production of long sequences of DNA. Another key ingredient in bioengineering will be the development of standards for making and measuring DNA, in the same way that machining hardware came to be governed by common standards in the 19th century. Endy also suggests that biotechnology will be increasingly informed by useful abstraction, so that scientists will manipulate raw materials less and refined and repackaged materials more, in order to make new things simply and more reliably. These advances will also enable bioengineers to “be experts in our own domains without having to be masters of everything.”
But as bioengineering becomes easier, and “people start to engineer biology,” we’ll need to worry about new issues, says Endy: Will people synthesize pathogens from scratch? Will groups pool knowledge legally? Will there be accreditation and oversight of those who create biological systems?
About the Speaker
Andrew Endy
Cabot Assistant Professor of Biological Engineering
Drew Endy earned degrees in civil, environmental, and biochemical engineering at Lehigh and Dartmouth. He studied genetics & microbiology as a postdoc at U.T. Austin and U.W. Madison. From 1998 through 2001 he helped to start the Molecular Sciences Institute, an independent not-for-profit biological research lab in Berkeley, CA.
In 2002, Endy started a group as a fellow in the Department of Biology and the Biological Engineering Division at MIT. He joined the MIT faculty in 2004. Endy co-founded the MIT Synthetic Biology working group and the Registry of Standard Biological Parts, and organized the First International Conference on Synthetic Biology. With colleagues he taught the 2003 and 2004 MIT Synthetic Biology labs that led to the organization of iGEM, the international Genetically Engineered Machine competiton.
In 2004 Endy co-founded Codon Devices, Inc., a venture-funded startup that is working to develop next-generation DNA synthesis technology. In 2005 Endy co-founded the BioBricks Foundation, a not-for-profit organization that is working to develop legal and economic strategies needed to support open biotechnology.
How do we distinguish our friends from foes? How does dementia destroy memory? And how can past experience invade the present with destructive force? Scientists are closing in on the biochemical roots of these neurological puzzles.
Thomas Insel describes the profound impact of a small group of neuropeptides on social behavior in animals, from worms to humans. Oxytocin, the hormone which turns on maternal behavior and cognition, turns out to play a large role in determining social memories. Mice whose genes for producing oxytocin are knocked out can’t seem to remember animals they’ve met 30 minutes earlier – what Insel describes as “dense social amnesia.” An area of the brain’s amygdala is particularly rich in oxytocin receptors, and when the peptide is injected into a nearby ventricle, the animals’ social interactions revert more closely to normal behavior. Oxytocin is a useful tool for interrogating the circuitry that enables humans to determine “who’s important to me, who I’d die for, who I’m pair-bonded with, who will take care of me,” says Insel.
Alzheimer’s Disease (AD), which afflicts 20 million people worldwide, begins by literally clogging and tangling the hippocampus, the part of the brain essential for learning and memory. Li-Huei Tsai and other researchers have found “compelling evidence” that a small protein may be critically important in activating AD’s awful atrophy of memory. By manipulating specific enzymes, Tsai has managed to model in animals “all the pathological hallmarks of Alzheimer’s Disease,” and zero in on the source of the plaques and tangles seen in human Alzheimer’s patients. Tsai foresees drug interventions that inhibit these enzymes. But, she says, a big task remains “even after we’re successful in halting a deleterious process--how can we restore learning and retrieve lost memory in AD patients?”
Why is it that only some people exposed to a shocking event develop post-traumatic stress disorder (PTSD)? Kerry Ressler’s research posits that some kind of learning must take place in the brain’s amygdala -- its fear response center—that cannot readily be extinguished. Researchers have tracked down a molecular factor that increases “after learning of fear or extinction of fear.” He believes that if this molecule is somehow blocked from doing its job, then someone suffering from PTSD cannot extinguish fear. In a fortuitous medical convergence, the drug D-cycloserine, which has been approved for years to treat tuberculosis, proves very effective in enhancing the effects of the molecule, and reducing fear of all kinds. One example: When people with fear of heights were given D-cycloserine as they took rides in elevators, they reported a significant, long-lasting reduction in their phobias.
Dr. Langer received the 2002 Charles Stark Draper Prize for inventing medical drug delivery technologies that prolong lives and ease suffering for millions every year.
Robert Langer has more than 500 issued or pending patents worldwide. In 2005, Langer received the $500,000 Albany Medical Center Prize in Medicine and Biomedical Research, America's top prize in medicine. In 2002, he received the Charles Stark Draper Prize, considered the equivalent of the Nobel Prize for engineers, from the National Academy of Engineering. Among numerous other awards Langer has received are the Heinz Award for Technology, Economy and Employment (2003), the John Fritz Award (2003) (given previously to inventors such as Thomas Edison and Orville Wright) and the General Motors Kettering Award for Cancer Research (2004). Langer is one of very few people ever elected to all three U.S. National Academies and the youngest in history (age 43) ever to receive this distinction.
He received his Bachelor’s Degree from Cornell University in 1970 and his Sc.D. from the Massachusetts Institute of Technology in 1974, both in Chemical Engineering.
Tyler Jacks introduces the key research areas and scientists who will speak in the succeeding sessions. He offers a thumbnail sketch of cancer as a molecular genetic progression involving sequential alterations in, and the proliferation of, abnormal cells. “Think of a cancer cell like an integrated circuit: the same kinds of complexities in electronic networks also exist within cells,” notes Jacks. Because of work on the human genome, and advances in scientists’ ability to untangle these complex molecular interactions, “We now have the first generation of anti-cancer drugs targeted against molecular alterations in cancer,” says Jacks. Two highly successful drugs have already been derived from MIT research.
In addition, says Jacks, collaboration among biologists, engineers and mathematicians are yielding “a tremendous collection of tools and technologies.” These include tiny probes that enable diagnosis of cancers at earlier stages, nanoparticles that deliver a therapeutic payload directly to cancer cells, and devices that can be implanted in the body.
In Doug Lauffenburger’s view, MIT’s new bioengineering degree program is not merely justified, it is essential. Revolutionary changes in biological sciences—specifically, in molecular biology and genomics—have given scientists the means to understand and control both the building blocks and larger systems of living things. Now, says Lauffenburger, the “operation of biological functions needs to be understood in terms of biomolecular machines.” But the hard part, he says, is “predicting what happens when you manipulate them. It’s almost trial and error. That’s where engineering comes in.”
Linda Griffith provides one paradigm for such research. She is designing a scaffold on which to grow human cells for use in tissue implants. Using a “computer controlled process that builds complex 3D objects up from scratch,” Griffith creates a device that mimics the complex structures of joints and other body parts – suited for joint repair, or bone regeneration. Her research might someday produce organs for transplant. But Griffith’s grander goal involves “putting surgeons out of business,” by eliminating transplants altogether. She’s building a “liver on a chip” – growing liver cells on a tiny wafer with the architecture and molecular properties of actual liver cells. This biomechanical product can be used to test drug toxicity and gene therapies, and perhaps someday to model and block the growth of cancers.
Angela Belcher models her bioengineered devices on some of nature’s most ingenious products, such as the incredibly strong and exquisitely structured abalone shell. She designs on a nanoscale, getting viruses and antibodies to work with inorganic materials. “How far can you push organisms?” Belcher wonders. To date, she’s taught a nontoxic virus to recognize a specific metal used in a semiconductor wafer. Someday viruses could detect atomic defects in electronics. Belcher also describes virus scaffolds for growing semiconductor wires, and for generating lightweight batteries woven into soldier’s uniforms. She’s even looking into ways of spinning viruses, as spiders spin silk, for generating optical materials.
Rudolf Jaenisch quietly insists, and instead look closely at the biology involved. First, note that there are two different kinds of cloning: reproductive cloning, the attempt to create an exact replica of a human being, which Jaenisch believes to be both biologically flawed and morally questionable; and therapeutic cloning, which offers potential cures to some of mankind’s most devastating diseases, and from Jaenisch’s point of view, sidesteps ethical pitfalls. Both involve transferring the genetic material from a somatic cell (from the skin, for instance) into an individual egg cell. The fertilized cell gives rise to embryonic stem cells, which have the near miraculous capacity to differentiate into every kind of tissue found in the body. Jaenisch says human embryonic stem cell research could help reveal the mechanisms behind biological growth, and enable a customized approach to treating such diseases as diabetes and Parkinson’s. Once scientists create these ES cells, they can grow them in vitro.
Ethical problems emerge, Jaenisch believes, when a cloned embryo is implanted in a uterus with the intent of creating a full-term clone, or with the intent of harvesting stem cells from an aborted fetus. These involve the “destruction of potential life.” The creation of cloned ES cells for research purposes, however, is the “propagation of existing life,” says Jaenisch.
Stephen Marks delineates the various human rights arguments around cloning: Are we at risk “of turning people into products?” Can “we pursue genetic health and enhancements” while maintaining the individual’s dignity? He describes the U.S. administration’s current opposition to any form of cloning and in particular, its attempt to throttle international treaties that might eventually permit therapeutic cloning.
About the Speakers
Rudolf Jaenisch
Professor of Biology, MIT Founding Member, Whitehead Institute for Biomedical Research
Jaenisch is one of the founders of transgenic science (gene transfer to create mouse models of human disease). His lab has produced mouse models leading to new understanding of cancers and various neurological diseases.
He received his doctorate in medicine from the University of Munich in 1967. He came to the Whitehead from the University of Hamburg in Germany, where he was head of the Department of Tumor Virology at the Heinrich Pette Institute.
Jaenisch received the 2002 Robert Koch Prize for Excellence in Scientific Achievement. In 2003, he was awarded the Charles Rodolphe Brupbacher Prize for basic research in oncology and was elected a member of the National Academy of Sciences.
Jaenisch is a fellow of the American Academy of Arts and Sciences and the American Academy of Microbiology, and a member of the American Association for the Advancement of Science.
Stephen P. Marks
François-Xavier Bagnoud Professor of Health and Human Rights Department of Population and International Health
Harvard School of Public Health
Stephen Marks' current interests include integrating human rights into sustainable human development. He has been a consultant to the United Nations Development Program on this topic and is principal investigator for a major grant by the Government of the Netherlands on the right to development. Another current research interest is international efforts to limit human genetic manipulation, focusing on human reproductive cloning and germline gene therapy. This study explores the human rights implications of these techniques and the assumptions of opposing attitudes on this question. Among his many degrees, he holds a Doctor of Laws (Docteur d’Etat en droit), with high honors, Institute of the Law of Peace and Development, Faculty of Law and Economics, University of Nice, 1979; an advanced degree (Diplôme d’études appliqués avancées, DEAA) in administrative litigation and human rights, Faculty of Law, Economics and Political Science of the University of Besançon, 1977; and a Certificate of European Studies, Institute of Advanced European Studies of the University of Legal, Political and Social Sciences of Strasbourg, 1972.
If the future once lay in plastics, as the film “The Graduate” claimed, today the watchword may be “feedstocks.” This term includes corn, wheat, soy, sunflower, rapeseed (canola)—the array of carbohydrates and proteins growing in fields across the planet. The news, as Douglas Cameron makes clear, is that these crops no longer serve just as staples for animal and human diets, but as the basis for a “revolution in the chemical industry.” Cameron’s company, Cargill, is exploring a host of biotech applications for carbohydrates, fats and proteins found in common crops. For instance, they’re attempting to convert a plastic derivative of lactic acid (derived from fermented starch) into inexpensive polymers for medical implants. Another application: polylactide fibers that not only give comfort to clothing but provide high wicking power. Cameron also sees soy and vegetable oils as a promising industrial “platform.” Cargill envisions transforming them for use in engines, as lubricants, hydraulic and transformer fluids, replacing environmentally unfriendly chemicals. If industry can find effective conversion methods, grains and legumes may emerge as primary sources of fuel, key ingredients in drugs and diet supplements, clothing and paper products, and as heightened versions of themselves—more nutritious food for people and animals.
Douglas C. Cameron PhD '87
Director of Biotechnology Biotechnology Development Center Cargill, Inc.
Douglas C. Cameron leads molecular biology and metabolic engineering research and development at Cargill. From 1986-1998, Cameron was a professor in the Department of Chemical Engineering and an affiliate in the Molecular Biology Program at the University of Wisconsin-Madison. In 1996 he was a guest professor in the Institute for Biotechnology at the ETH in Zurich, Switzerland. From 1979-1981 Cameron held the position of Biochemical Engineer at Advanced Harvesting Systems, a plant biotechnology company funded by International Harvester. Cameron is a Fellow of the American Institute of Medical and Biological Engineering (AIMBE). He is on the editorial boards of Metabolic Engineering and Biomacromolecules. Cameron serves on the Minnesota Governor's Bioscience Council and the board of directors of Minnesota Biotechnology Industry Organization. He is a member of the MIT Biological Engineering visiting committee and on the managing board of the newly formed Society for Biological Engineering. Cameron is also a Consulting Professor in the Department of Chemical Engineering at Stanford University. He has a B.S.E. in biomedical engineering in 1979 from Duke University, and a Ph.D. in biochemical engineering in 1986 from MIT
The very first tablet or drop of a new medicine comes at a dear price-- $800 million – according to recent studies of R&D in pharmaceutical industries. But manufacturing subsequent pills costs literally pennies. What’s a fair way to price life-improving, or life-saving medicine? The two speakers in this part of the forum vigorously defend charging different prices for medicines in different parts of the world. Judy Lewent argues that differential pricing ensures global access. She says, “There would be little sense selling drugs at prices people can’t afford.” It also generates the revenues necessary to generate new cures. “When we price for access, it’s a reflection of our belief in the power of free markets to advance the social good. We can meet the world’s health needs and also make a profit and continue to prevent, treat and cure disease.” Mark McClellan sees on the horizon a new order of drug treatments, such as tailoring molecules to the needs of an individual patient. But, he says, we won’t reap the benefits of these potential cures if current trends continue: nations that band together to lower drug costs for their citizens, and the reimportation of brand name innovator drug products. McClellan says if we don’t “provide financial rewards that reflect the value of innovation, we may not continue to get improvements that biotech makes possible.” Both speakers endorse more affordable medicines, but through insurance coverage rather than price controls.
Mark McClellan PhD '93
Administrator, Centers for Medicare & Medicaid Services (CMS)
McClellan previously served as Commissioner of the Food and Drug Administration beginning in November 2002. During 2001 and 2002, Dr. McClellan served in the White House as a Member of the President's Council of Economic Advisers and was a senior policy director for health care and related economic issues. From 1998-99, he was Deputy Assistant Secretary of the Treasury for Economic Policy, where he supervised economic analysis and policy development on a wide range of domestic policy issues. McClellan is on leave from Stanford University , where he was Associate Professor of Economics and Associate Professor of Medicine at Stanford Medical School. He was also a Research Associate of the National Bureau of Economic Research and a Visiting Scholar at the American Enterprise Institute. Additionally, he was a Member of the National Cancer Policy Board of the National Academy of Sciences, Associate Editor of the Journal of Health Economics, and co-Principal Investigator of the Health and Retirement Study (HRS), a longitudinal study of the health and economic well-being of older Americans. McClellan is a Member of the Institute of Medicine . He earned his M.D. from the Harvard-MIT Division of Health Sciences and Technology and his Ph.D. in Economics from MIT.
Judy C. Lewent SM '72
Executive VP, CFO, President, Human Health Asia, Merck & Co., Inc.
Lewent is responsible for worldwide financial, corporate development, and corporate licensing matters, as well as for the Merck human health business in Asia North and Asia South, and for the Merck current joint venture relationships with Johnson & Johnson and Aventis. She is Chairman as well as a Board member of Merck Capital Ventures. Lewent also serves as a member of Merck's Management Committee, a senior management group which makes strategic decisions for the Company. Lewent is a member of the Board of Directors of Dell Inc., Motorola, the National Bureau of Economic Research, and Penn Medicine (University of Pennsylvania Health System); a trustee of the Rockefeller Family Trust; a life member of the MIT Corporation; and a member of the American Academy of Arts & Sciences. Lewent earned a B.S. in Economics from Goucher College in 1970 and an M.S. in Management from MIT's Sloan School of Management in 1972.
No diagnosis of cancer is welcome, but some scenarios are more dreaded than others. Richard Hynes discusses what happens “when cells in the primary tumor lose their sense of address and wander off to places they’re not supposed to go.” His talk lays out the process of invasion, by which the cancer spreads into tissues adjacent to the tumor, and that of metastasis, where the cancer disseminates to distant sites.
Hynes describes the transitions a cancer undergoes as it spreads. He explains how tissue in our bodies is made of sheets of epithelial cells that are carefully arranged on a “basement membrane” by a series of adhesion receptors. These receptors, if functioning properly, don’t usually allow the cells to go anywhere. When a cell becomes tumorigenic, it loses some adhesion, and then if it becomes more damaged “wanders off into the underlying tissue.” This is called invasion. Hynes and other researchers are looking at the molecules responsible for cells’ adhesive qualities, and at the mutations in genes that trigger a loss of adhesion. Some of these processes are part of normal development, but occasionally, a “switch gets thrown in cells that should have stayed epithelial” and they become migratory instead.
Once on the move, cancer cells “need plumbing to grow,” says Hynes. Tumors recruit blood vessels to feed them and remove waste, and they can also exploit the body’s white blood cells and platelets to promote their own growth. Hynes describes “cross talk between tumor cells and cells in bone,” where the “two cells get together in evil combination to damage the bone and enhance the growth of metastases.” Scientists have discovered “a lot of different mechanisms by which metastatic cells learn new tricks and suborn the mechanism of the host to get them where they’re going.” Hynes finds such insidious workings an “appealing thing, since these alterations offer opportunities for therapies.” Researchers can tinker with circuits between cells, restore growth suppression and interfere with blood vessel recruitment. It’s “a complex problem,” says Hynes, but there are “lots of ways to get at this.”
About the Speaker
Richard O. Hynes PhD
Daniel K. Ludwig Professor for Cancer Research, Department of Biology Investigator, Howard Hughes Medical Institute
Richard Hynes received his B.A. in biochemistry from the University of Cambridge, U.K., and his Ph.D. in biology from MIT. After postdoctoral work at the Imperial Cancer Research Fund in London, where he initiated his work on cell adhesion, he returned to MIT as a faculty member.
Hynes is a fellow of the Royal Society of London, the American Academy of Arts and Sciences, and the American Association for the Advancement of Science, and a member of the National Academy of Sciences and the Institute of Medicine. He has received the Gairdner Foundation International Award for achievement in medical science and recently served as president of the American Society for Cell Biology.
A microscopic roundworm has come to play a dominant role in some of the most pivotal medical research of our time. In the labs of Robert Horvitz and his colleagues, C. elegans has helped reveal cell death as a normal part of biological development.
In this talk, Horvitz painstakingly delineates the series of discoveries based on C. elegans that identified the genetics behind programmed cell death (apoptosis), the disorders that emerge if this normal process stalls, and human counterparts to these disorders, which suggest potential targets for therapy.
Because the mature roundworm consists of just 959 cells, it was possible for scientists to track the organism’s entire lineage of cell divisions, and to characterize what genetic accidents created mutant worms.
Scientists figured out genetic pathways that were essential to normal development in the worm, and which, if disrupted, led to harmful mutations. For instance, the immature roundworm contains 131 cells that are not found in the adult, because they are genetically programmed to die. Every animal, Horwitz says, undergoes apoptosis as a “normal aspect of development.” Tadpoles lose their tails to become frogs; lots of animals have webbing “sculpted out by the process of programmed cell death.” Over years, Horvitz and his colleagues determined the precise genes responsible for programmed cell death in C. elegans, as well as the genes that protect cells from dying, and the way these genes interact. Horvitz’s teams also found likely human equivalents to these critical genes and pathways. If these genes go awry, says Horvitz, “then something is going to lead to disease.”
Cancer, autoimmune diseases and viral infections result from too little programmed cell death. That’s because cell division goes unchecked. There are also human diseases that occur because cells die when they should not: neurodegenerative disorders, retinal degeneration, liver disease, and heart attacks. As a result of Horvitz’s work, many new targets have emerged for these diseases, some of which Horvitz himself is pursuing. Horvitz is now aiming his sights at different genetic regulators that tell certain types of cells to live or die, leading to novel therapies for some of our most formidable diseases.
About the Speaker
H. Robert Horvitz
David H. Koch Professor of Cancer Biology at MIT
H. Robert Horvitz won the 2002 Nobel Prize in Physiology or Medicine (with Sydney Brenner and John Sulston), for his work on programmed cell death (apoptosis), and for his studies concerning organ development in C. elegans. His apoptosis studies may also improve the understanding of neurological disorders such as amyotrophic lateral sclerosis (ALS), a disease that killed Horvitz's father in 1989. In collaboration with others, Horvitz identified a gene involved in the inherited form of ALS, and he is also pursuing other genes involved in the disease. "My hope is that my discoveries will one day lead to advances in medicine that alleviate human suffering and contribute to the world in ways that will benefit mankind," Horvitz has said.
He is also an investigator for the Howard Hughes Medical Institute and a member of the McGovern Institute for Brain Research at MIT, and a member of the MIT Center for Cancer Research. He holds appointments at the Massachusetts General Hospital in neurology and in medicine.
Horvitz received bachelor's degrees in mathematics and economics from MIT (1968) and an M.A. and Ph.D. (1974) in biology from Harvard University. He was a postdoctoral researcher at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England. He joined the faculty of MIT in 1978 and became professor of biology in 1986 and an investigator of the Howard Hughes Medical Institute in 1988.
Cancer is a conniving enemy. Try to kill it off through surgery or chemotherapy, and it finds a way to sneak back in. Jacqueline Lees tells an engaged Soap Box audience what insights and tools research now offers in the longstanding battle against this relentless disease.
Big gains have come from molecular study of tumors at different stages, Lees says. It often takes many years for a cancerous cell to develop into a dangerous tumor, one that can yield metastases. There might be six phases of development over 15 years in a cancer’s evolution, and scientists have formed a good understanding of what these different lesions look like in various cancers, and how they behave. Lees calls this process “actually a beautiful example of evolution,” since the cell that mutates and begins to divide uncontrollably evolves to become more successful relative to other cells in the tissue.
Other research focuses on the genetic basis of cancers. Two “flavors” of genes appear responsible for provoking cancerous changes in cells: oncogenes and tumor suppressor genes. It may be possible to intervene along the genetic pathways underlying cancer growth, says Lees. Her own work, involving mutant mice and zebrafish, hopes to identify the mechanisms involved in specific kinds of tumors, and to figure out ways of inhibiting cancer cell growth. Understanding the nature of specific cancers might help prevent treating people with chemical agents that don’t work for their kind of cancer, and that actually increase their tumor’s growth.
With the advent of fast and inexpensive genetic screens, it may soon be possible to determine whether each of us carries genes that predispose us toward certain kinds of cancers. But Lees questions the universal adoption of DNA testing, not just because of privacy concerns, but because there may very well be no known cure if a predisposition to disease is found. “If we sequenced every baby, and said you’re highly predisposed to a cancer, and there’s nothing we can do, would that be information people want to have?” Lees wonders. “If we could find a rapid way to sequence small subsets of genome, identify people with high risk and we could treat them if we knew they had those diseases, there’d be an argument for that, much as we do testing for diseases where we know can intervene if find children carrying them,” says Lees.
About the Speaker
Jacqueline Lees SM '86, PhD '90
Associate Director
MIT Center for Cancer Research;
Professor of Biology
Jacqueline Lees' research is focused on identifying the proteins and pathways that play a key role in tumorigenicity and establishing the mechanism of their action in both normal and tumor cells. Her lab uses a combination of molecular and cellular analyses, mutant mouse models and genetic screens in zebrafish.
Lees received her Ph.D. in 1990 from the University of London.
When a Nobel Prize-winning pioneer of molecular biology embraces a new area of research as revolutionary, attention must be paid. Phillip A. Sharp’s own discoveries involving gene expression opened up new territory in the search for the genetic causes of cancer and other diseases. He now has great hopes for similar breakthroughs with the process of gene silencing.
This latest advance in understanding gene regulation is quite recent. In 1998, Andrew Fire and Craig Mello discovered the process of RNA interference in the worm C. elegans. When they introduced short, double strands of synthesized RNA into a cell, the RNA silenced a gene in the cell and turned off a specific protein. (Fire and Mello were awarded the 2006 Nobel for this work.) Previously, scientists had viewed RNA as simply “the slave molecule between DNA and protein,” as Sharp puts it, or in spliced form, capable of generating a great number of diverse proteins. But revelation of the mechanism of interfering RNA has made the field “a lot more interesting,” says Sharp.
In just a few years, researchers have learned that small RNA “taps into a pathway that’s present in every cell,” says Sharp. “At minimum, one in four or one in five of our genes is controlled by small RNAs.” Researchers also suspect RNA pathways may occupy a central role in establishing controls in the “human germ line” to prevent redundant pieces of DNA from being expressed in a destructive way. This offers researchers more than a powerful, new investigative tool. Says Sharp, “This is MIT. If you’ve got something in the lab that’s new and you know people need it outside of the lab, you’re under an obligation to try to translate it into therapy.” One big question is whether small RNA can be used to treat cancers.
There’s evidence that small RNAs injected directly into the eyeball can potentially silence interconnecting genes responsible for cancers in the back of the eye. The same technique might also work for cancers in the brain and lung, says Sharp. One challenge involves getting the highly water soluble RNA across the cell membrane. Nanoparticle packaging may help prevent the RNAs from being absorbed before they’re delivered to the target area. Sharp also mentions experiments that suggest misregulation of small RNAs can cause cancer. “We as a field are now struggling with the issue of just what role short RNAs play in general in control of our genes and our normal physiological processes. It’s getting really interesting.”
Phillip A. Sharp
Institute Professor
Founding Director McGovern Institute for Brain Research
Nobel Laureate in Medicine 1993
Phillip A. Sharp received the 1993 Nobel Prize in Physiology or Medicine for the discovery that genes in eukaryotes are not contiguous strings but contain introns, and that the splicing of messenger RNA to delete those introns can occur in different ways, yielding different proteins from the same DNA sequence Much of Sharp’s scientific work has been conducted at MIT’s Center for Cancer Research, which he joined in 1974 and directed from 1985 to 1991. He subsequently led the Department of Biology from 1991 to 1999. Sharp is co-founder of Biogen, Inc and also co-founder of Alnylam Pharmaceuticals.
He earned a B.A. from Union College, KY, and a Ph.D. in chemistry from the University of Illinois, Champaign-Urbana in 1969.
Sharp has authored more than 300 scientific papers and is a member of the National Academy of Sciences, the Institute of Medicine, the American Academy of Arts and Sciences, and the American Philosophical Society. In 2006, he received the National Medal of Science.
Early on in his lecture, Michael Yaffe serves up an amazing fact: If the distance between each DNA base pair were one foot apart, then each time a cell divided, it would have to copy 568 thousand miles of DNA. This, says Yaffe, is enough to go around the circumference of the earth more than 22 times. What’s more, the cell has to copy its DNA with no errors. “I don’t know (if) civil engineers ... could make 10 miles of road without making single error,” says Yaffe.
In the 12 hours a cell takes to copy its DNA to create two daughter cells, “it goes to great pains to make sure everything is done correctly. It initiates checkpoints, like border crossings.” Because everyday life exposes DNA to all kinds of damage, cells have evolved “an elaborate surveillance mechanism” to “blow the whistle, signal repair, and recruit repair machinery,” or if damage is too great, essentially commit suicide. If something goes wrong with this mechanism at crucial times during cell division, cancer frequently results.
Yaffe’s in the business of exploring and mathematically mapping the elaborate signal pathways inside cells that sense broken DNA and coordinate damage response. While studying one such process, cell death in the colon, Yaffe found that the traditional biochemistry approach -- picking one molecule, one stimulus and one readout-- doesn’t work. “It’s like the blind man feeling the elephant’s tail, and saying it’s a long, thin animal.” Yaffe learned that one signal may activate a series of proteins, triggering an amplification loop. A slight change might yield a “whopping response.”
Just as engineers test integrated circuits at a variety of points, Yaffe came up with a method of testing cell signaling with a variety of proteins. His team came up with 7,000 signaling measurements in 760 dimensions, and 1,400 signal responses. But this data-heavy model for predicting which molecules lead to cell death didn’t satisfy Yaffe. With additional mathematical sleight of hand, Yaffe’s group boiled down the cell signaling measurements to what Yaffe calls two “canonical super axes”: “a global measure of cell stress and death, and another of survival signaling.” He hopes to use this slimmed-down model to think about drugs targeting cancer and inflammation.
About the Speaker
Michael Yaffe
Howard S. and Linda B. Stern Associate Professor of Biology, Department of Biology and the Center for Cancer Research
Michael Yaffe received his Ph.D. in Biophysical Chemistry in 1987, and an M.D. in 1989, both from Case Western Reserve University. Before MIT, he served as a surgeon in teaching hospitals in Cleveland and the Boston area, including the Harvard Medical School.
He received multiple teaching awards from University Hospitals of Cleveland, and earned the 1998 Howard Hughes Physician Scientist Award, and the 1999 Burroughs Wellcome Career Development Award.
Eric Lander likens the current age of biological discovery to the days of great ocean-going exploration. After the world was mapped, no one could imagine what it was like to live “before you knew what would happen if you sailed west.” Following the current revolution in biology, we “won’t be able to imagine what science was like...” This transformation, claims Lander, will be complete in the next decade or so. “MIT students in 2020 will look back with a mixture of amusement and horror at the late 20th century and say, ‘Imagine, people spent years looking for the gene for something.’”
Lander views biology as a vast library that will soon contain information not just about the DNA sequences of species, but ‘volumes’ on individuals, tissues, and cells. With great effort, researchers deciphered the secrets of chromosomes, the double helix, and more recently, the human genome and that of other species. But progress in such discoveries is now moving at a much faster clip due to high-speed computing and the Internet. MIT currently sequences ¼ million pieces of DNA per day, says Lander. He projects this pace will quicken by 20 fold in the next several years.
Fortified by this progress, Lander has compiled an ambitious ‘to-do list:’ identifying “everything that matters” in the human genome, from proteins to the things that control genes; knowing all human genetic variation in the population; knowing how to recognize when a cell “is thinking of one thing or another” based on how genes are turned on or off; knowing all the mechanisms that cause cancer and how to modulate all the genes.
Astonishingly, he says, “This is not the to-do list of the next century, but the next decade.” Lander is confident that researchers will in the not-distant future generate a catalog of the unique genetic signatures associated with “different flavors” of a type of cancer. Scientists will find patterns in diseases, genes and drug responses, and eventually assemble a list of all the genetic variants in the human genome that put individuals at risk for different diseases. These various gene databases will serve “as foundational information for biology for centuries to come,” concludes Lander.
About Speaker
Eric Lander was a world leader of the international Human Genome Project, the effort to map the blueprint for a human being. Today, Lander is using the knowledge of the human genome to tackle the fundamental issue of medicine: to find the causes of disease.
Lander received his Ph.D. in mathematics from Oxford in 1981, as a Rhodes Scholar. He joined Whitehead Institute in 1986 and founded the Whitehead Institute/MIT Center for Genome Research in 1990. Lander became the founding director of the newly created Broad Institute in 2003.
Lander is a member of the U.S. National Academy of Sciences, and U.S. Institute of Medicine. He was a MacArthur Fellow (1987-1992), and earned the Woodrow Wilson Prize from Princeton University(1998); the Baker Memorial Award for Undergraduate Teaching at MIT (1992); the City of Medicine Prize (2001); and the Gairdner International Prize (2002).
Robert Weinberg plots the 200-year course of cancer research, finding neglected byways, wrong turns, and astonishing advances. He starts with Percival Pott, a London surgeon who noticed that chimney sweeps often developed a rare kind of cancer. In Europe, where people bathed more often, this cancer was much less evident, leading to “the first indication in public literature that there was a close correlation between one’s experience in life and the incidence of rare cancer,” says Weinberg. In 1910, Japanese scientist Katsusaburo Yamigiwa, painted coal tars onto the ears of rabbits and produced tumors, which “led to the realization that one can experimentally provoke cancer rather than wait for it to arise spontaneously.” He was “overlooked by Nobel,” Weinberg notes. Other similarly unrecognized scientists discovered that transferring leukemic tissue into healthy tissue could induce cancer, and that cancer could be caused by infectious disease. But there were major missteps, says Weinberg. In one notorious episode, a Danish Nobel Prize winner’s cancer research was discovered to be in error. And when Howard M. Temin suggested that cancer originated through an atypical genetic process called reverse transcription, he “was shunned as a pariah.”
In 1970, Temin was vindicated as he and David Baltimore separately discovered an enzyme central to such a process. Next came the Nixon Administration’s ‘war on cancer,’ which was attacked as a fraudulent waste of taxpayers’ money when seven years of searching for viruses in human tumors produced no results. Yet this dead end suddenly yielded scientific pay dirt in the 80s, when researchers found viral ‘oncogenes’ in the DNA of normal cells, which caused malignancies. Scientists then demonstrated that by altering normal genes, they too could create cancerous cells. Advances in biochemistry have led to “a rapidly evolving conceptualization of how cancer occurs,” says Weinberg. “We’re beginning to talk about cancer as aberrations of an integrated signaling circuit, which if we could only understand its design….would lead us to be able to restore normalcy to a cancer cell or preferentially, kill it.”
About Speaker
Robert A. Weinberg '64, PhD '69
Founding Member, MIT Center for Cancer Research
Member, Whitehead Institute Daniel K. Ludwig and American Cancer Society Professor for Cancer Research
Department of Biology
Robert A. Weinberg has earned some of the top honors in his field. Most recently, he won the 2006 Landon-AACR Prize for Basic and Translational Cancer Research. He is also a 1997 National Medal of Science awardee.
Weinberg's laboratory discovered the first human oncogene and the first tumor suppressor gene. Today, much of his research focuses on new models of breast cancer development including the stages of tumor invasiveness and metastasis.
He earned his Ph.D. in biology from MIT in 1969, and was one of the Founding Members of the MIT Center for Cancer Research in 1973. He was appointed a professor at MIT in 1982, the same year he joined the Whitehead Institute. Weinberg was named American Cancer Society Research Professor in 1985 and received the Daniel K. Ludwig Professorship for Cancer Research in 1997. He is a member of the National Academy of Sciences and the Institute of Medicine.
Subra Suresh fleshes out the promise of nanotechnology, at least in regard to our understanding of disease. His talk, which focuses on malaria and its impact on red blood cells, demonstrates how the fields of engineering, biology and medicine are converging.
To function properly, he explains, a red blood cell -- eight micrometers in diameter or 1/10th the thickness of a human hair -- must be able to squeeze through three micrometer openings in blood vessels. Working with a “laser tweezer” and two tiny (nano-sized) glass beads, Suresh can apply pressure to stretch single cells so that they become thin enough to fit through small openings. He uses a computer to simulate in three dimensions how red blood cells might fold and lengthen under normal conditions in the human body.
With malaria, infected red blood cells lose their ability to stretch, and Suresh can measure precisely the degree of deformation. The parasite changes the molecular structure of the cell, which “becomes stiff and sticky,” unable to move through small blood vessels. So the spleen, which normally clears impurities from the body, can’t do its job, and the disease progresses.
With a global group of collaborators, Suresh is working on genetic manipulation of the malaria parasite to see how knocking out individual proteins might impact the structure of the infected cell. This kind of biomolecular measurement and manipulation may some day lead to new therapies for a disease that infects more than 400 million people per year.
Suresh is also applying nanotech approaches to other diseases. He is looking into how cancer cells “become less stiff, move more easily, leading to metastatic invasions.” This may ultimately prove useful in studying breast cancer, he says.
About the Speaker
Subra Suresh ScD '81
Dean, MIT School of Engineering
Ford Professor of Engineering;
Professor of Biological Engineering
Subra Suresh received his Sc.D. from MIT in 1983. Prior to joining the MIT faculty in 1993 as the R. P. Simmons Professor, he was Professor of Engineering at Brown University. His current research focuses on experimental and computational studies of the mechanical responses of single biological cells and molecules and their implications for human health and diseases.
Professor Suresh is a member of the National Academy of Engineering, serving presently as the Vice Chair of its Materials Section Peer Committee, and a Foreign Fellow of the Indian National Academy of Engineering. His recent honors include the Gordon Moore Distinguished Scholar award from CalTech, the Brahm Prakash Visiting Professorship from the Indian Institute of Science, selection by the Institute for Scientific Information as one of the most highly cited researchers in Materials Science, the Clark B. Millikan Visiting Professorship at CalTech, the TFR Swedish National Chair in Engineering from the Royal Instiute of Technology, Stockholm and the Distinguished Alumnus Award from Indian Institute of Technology, Madras.
Suresh has been elected a fellow of The Minerals, Metals and Materials Society, the American Society of Mechanical Engineers, the American Ceramic Society, and the American Society for Materials International, and an Honorary Member of the Materials Research Society of India.
Out of a world population of 6 billion, 57 million people die each year. And while we have gained 20 years in life expectancy since World War 2, diseases like HIV have taken a toll on morbidity in many developing nations. But according to Rick Young, “the global disease burden is much larger than the number of deaths.” Countless millions suffer from cardiopulmonary diseases, cancer, and malaria, to name but a few, at a nearly incalculable cost to their families and society. Young’s mission is to attack the problem of global disease at the genetic level: he’s hunting for specific proteins that can turn the genetic machinery of diseases on, or off. These “gene regulators” can be knocked out of whack by a virus like HIV or by a mutation that results in a disease like mature onset diabetes. Young’s group has developed a DNA microarray technology that helps them link gene regulators to their corresponding genes. They’ve worked out the connections in yeast, and they’re targeting the human genome next. Young’s ultimate goal: “By continuing to focus on your 2000 gene regulators, we could eventually develop great insights into how organ systems work… (And) in all instances where disease is associated with misregulation, we could develop new strategies for drug development based on that.”
About the Speaker
Richard A. Young Member, Whitehead Institute Professor of Biology, MIT
Richard A. Young is a pioneer in gene transcription, the process by which cells read and interpret the genetic instructions embedded in DNA. His lab’s achievements include novel AIDS vaccine candidates and new approaches to drug-resistant tuberculosis.
Young received his Ph.D. in molecular biophysics and biochemistry from Yale University in 1979. He has been director of the National Cooperative Vaccine Development Group for AIDS at the Whitehead Institute and has served on several international committees for the World Health Organization. He received the Burroughs Wellcome Scholar Award in 1987 and the Chiron Corporation Biotechnology Research Award from the American Society for Microbiology in 1994. Young was elected a fellow of the American Academy of Microbiology in 1994, and a charter fellow of the Molecular Medicine Society in 1995.
Inspired by the vast potential of bioengineering, ordinary people are seeking their inner Frankenstein -- doctor, not monster. Two speakers who know their way around Petri dish and beaker discuss the possibilities and pitfalls of do-it-yourself biology with an MIT Museum crowd.
Showing ads from a 1980 Omni magazine, Natalie Kuldell reflects on the vast changes in computer engineering in the past few decades – from 20-lb PCs to laptops and handhelds. In contrast, she laments, genetic engineering today still resembles in large part its 1980 antecedents -- inserting bits of DNA into organisms like E. coli. She avers that computer engineering made such leaps because its technology was widely available to amateurs, who helped drive many advances. Biotech hasn’t moved as fast, and won’t, believes a nascent do-it-yourself (DIY) community, until basic components of biology become accessible to a larger population.
Synthetic biology aims to make new biological forms easier to engineer. Kuldell complains that “much of my time is spent doing things to do the experiments I need to do. It would be terrific not to have to build things in advance.” But building biological components and streamlining processes is difficult in biology, because biosystems are complex, and unpredictable. Can amateurs working with “Tupperware, thermometers and genetic engineering in the kitchen” discover “something remarkable doing their biology at home?”
Reshma Shetty thinks engineered organisms can do more than sense toxic metals in the environment or determine whether seawater is contaminated. She can “imagine a DIY bioengineer…doing something more fantastical, ambitious…. What about growing your own house?” Shetty describes a home experiment that can make bacteria smell like bananas. This is a small feat, but to achieve something significant, a real contribution to science, Shetty says DIY biologists need bio-engineered friendly organisms that will serve as common models, safe, easy to grow “and fun to use.” Candidates include moss, an easy to grow bacterium called Acinetobacter, and the salt-loving Halobacterium. By giving people the right tools, “they can build something fun and creative others can appreciate.”
Professor Hector F. DeLuca's laboratory has been devoted to the understanding of metabolism and mechanism of action of vitamins A and D. Sponsored by Wisconsin Academy of Sciences, Arts and Letters in partnership with the Wisconsin Alumni Research Foundation, Dr. DeLuca discusses the fascinating history of the discovery and applications of Vitamin D. Also touched upon is the creation of the Wisconsin Alumni Research Foundation, whose mission is to transform university research into real products that benefit the society at large.
Stem cells do not just come from human embryo, but also found in most body and extra embryonic tissues and membranes. What separates stem cells from other cells is its ability to self renew or make more of them without ageing. Normally when cell divides the DNA loses its end tips known as the telomeres,and this thought to be what makes cell age, these things doesn't happen in stem cells, but still retain the same length. this is one thing that no other body cell can do.
The circulatory system can be viewed as two circuits - the pulmonary circuit and systemic circuit.
Pulmonary circulation involves the transport of blood to and from the lungs. Deoxygenated blood returns to the right side of the heart. This blood is then pumped by the right ventricle into the pulmonary artery (deoxygenated blood) and into the capillaries of the lungs. In the capillaries of the alveoli, oxygen enters the blood and binds to hemoglobin in red blood cells as carbon dioxide diffuses out of the blood into the lungs for removal. The oxygenated blood then travels in the pulmonary vein back to the left atrium of the heart where it joins the systemic circuit.
Systemic circulation involves the transport of blood to and from all the tissues of the body. This circuit is much larger than the pulmonary circuit and so the walls of the left ventricle of the heart are much larger than on the right side. This thicker muscle generates the force required to pump blood all around the systemic circuit. Oxygenated blood is pumped by the left ventricle into the aorta. The aorta then branches into many smaller arteries that carry blood to all areas of the body. In the capillaries, oxygen is delivered to cells and carbon dioxide is picked up for removal. The deoxygenated blood then returns to the anterior vena cava from the upper body and the posterior vena cava from the lower body. Both vessels enter the right atrium of the heart and blood is returned back to the pulmonary circuit for oxygenation.
Threonine (abbreviated as Thr or T) is an α-amino acid with the chemical formula HO2CCH(NH2)CH(OH)CH3. Its codons are ACU, ACA, ACC, and ACG. This essential amino acid is classified as polar. Together with serine and tyrosine, threonine is one of three proteinogenic amino acids bearing an alcohol group.
The threonine residue is susceptible to numerous posttranslational modifications. The hydroxy side chain can undergo O-linked glycosylation. In addition, threonine residues undergo phosphorylation through the action of a threonine kinase. In its phosphorylated form, it can be referred to as phosphothreonine.
Allo-threonine
With two chiral centers, threonine can exist in four possible stereoisomers, or two possible diastereomers of L-threonine. However, the name L-threonine is used for one single enantiomer, (2S,3R)-2-amino-3-hydroxybutanoic acid. The second diastereomer (2S,3S), which is rarely present in nature, is called L-allo-threonine.
Biosynthesis
As an essential amino acid, threonine is not synthesized in humans, hence we must ingest threonine in the form of threonine-containing proteins. In plants and microorganisms, threonine is synthesized from aspartic acid via α-aspartyl-semialdehyde and homoserine. Homoserine undergoes O-phosphorylation; this phosphate ester undergoes hydrolysis concomitant with relocation of the OH group.[2] Enzymes involved in a typical biosynthesis of threonine include:
It is converted to pyruvate via threonine dehydrogenase. An intermediate in this pathway can undergo thiolysis with CoA to produce Acetyl-CoA and glycine.
In humans, it is converted to alpha-ketobutyrate in a less common pathway via the enzyme serine dehydratase, and thereby enters the pathway leading to succinyl-CoA.
Sources
Foods high in threonine include cottage cheese, poultry, fish, meat, lentils, and sesame seeds.[citation needed]
Racemic threonine can be prepared from crotonic acid by alpha-functionalization using mercury(II) acetate.
Threonine. (2009, February 13). In Wikipedia, The Free Encyclopedia. Retrieved 08:47, February 17, 2009, from http://en.wikipedia.org/w/index.php?title=Threonine&oldid=270547548
Dietary selenium prevents chemically induced carcinogenesis in many rodent studies. It has been proposed that Selenium may help prevent cancer by acting as an antioxidant or by enhancing immune activity.
SELECT stands for the Selenium and Vitamin ECancer Prevention Trial, a clinical trial to see if one or both of these substances can help prevent prostate cancer when taken as dietary supplements. The trial is funded primarily by the National Cancer Institute (NCI) and is being coordinated by the Southwest Oncology Group (SWOG), an international network of research institutions that receives NCI funding. Enrollment for the trial began in 2001 and ended in 2004. More than 400 sites in the United States, Puerto Rico, and Canada are taking part in the study. Over 35,000 men are participating in SELECT.
Rotator cuff tears are tears of one, or more, of the four tendons of the rotator cuff muscles.Rotator cuff tears are among the most common conditions affecting the shoulder.
The tendons of the rotator cuff, not the muscles, are most commonly torn. Of the four tendons, the supraspinatus is most frequently torn; the tear usually occurs at its point of insertion onto the humeral head at the greater tuberosity.
Anatomy
The rotator cuff muscles, a group of four muscles that surround the shoulder, are the: supraspinatus, infraspinatus, teres minor and subscapularis. The four rotator cuff muscle tendons combine to form a broad, conjoined tendon, called the rotator cuff tendon, and insert onto the bone of the humeral head in the shoulder. The humeral head is the ball side of the “ball and socket” shoulder joint; the socket is called the glenoid fossa.
Symptoms associated with rotator cuff tears:
The most reliable symptom for determining a rotator cuff tear is probably the least common and is found when there is a complete rupture with detachment of the rotator cuff leading to the complaint of complete loss of function, such as, loss of the ability to actively move the arm away from the side of the body (loss of abduction). Fortunately this finding is rare and when tears are symptomatic, most tears present as pain with limitation of function, a non-specific complaint that cannot distinguish between tendinitis, bursitis or arthritis. The clinical picture of a completely detached tear is more clear-cut, while the more common shoulder problems greatly overlap in their clinical presentation.
Pain in the anterolateral aspect of the shoulder can be due to many causes, [4] symptoms may reflect pathology outside of the shoulder which cause referred pain to the shoulder from sites such as the neck, heart or gut.
Patient history will often include pain or ache over the front and outer aspect of the shoulder, pain aggravated by leaning on the elbow and pushing upwards on the shoulder (such as leaning on the armrest of a reclining chair), intolerance to overhead activity, pain at night when lying directly on the affected shoulder, pain when reaching forward (e.g. unable to lift a gallon of milk from the refrigerator). Weakness may be reported, but is often masked by pain and is usually found only through examination. With longer standing pain, the shoulder is favored and gradually loss of motion and weakness may develop which, due to pain and guarding are often missed by the patient and are only brought out during the examination.
Primary shoulder problems may cause pain over the deltoid muscle that is made worse by abduction against resistance, called the impingement sign. Impingement reflects pain arising from the rotator cuff but cannot distinguish between inflammation, strain, or tear. Patients may report their experience with the impingement sign when they report that they are unable to reach upwards to brush their hair or to reach in front to lift a can of beans up from an overhead shelf.
Bursitis is the inflammation of one or more bursae (small sacs) of synovial fluid in the body. The bursae rest at the points where internal functionaries, such as muscles and tendons, slide across bone. Healthy bursae create a smooth, almost frictionless functional gliding surface making normal movement painless. When bursitis occurs, however, movement relying upon the inflamed bursa becomes difficult and painful. Moreover, movement of tendons and muscles over the inflamed bursa aggravates its inflammation, perpetuating the problem.
Causes
Bursitis is commonly caused by repetitive movement and excessive pressure. Elbows and knees are the most commonly affected. Inflammation of the bursae might also cause other inflammatory conditions such as rheumatoid arthritis. Although infrequent, scoliosis might cause bursitis of the shoulders; however, shoulder bursitis is more commonly caused by overuse of the shoulder joint and related muscles.
Traumatic injury is another cause of bursitis. The inflammation irritates because the bursa no longer fits in the original small area between the bone and the functionary muscle or tendon. When the bone increases pressure upon the bursa, bursitis results.
Lumbar disk disease is a frequent source of low back pain. Sciatica is defined as neuralgia along the course of the sciatic nerve.The intervertebral disks act as shock absorbers and are found between the bodies of the vertebrae. They have a central area composed of a colloidal gel, called the nucleus pulposus, which is surrounded by a fibrous capsule, the annulus fibrosis. This structure is held together by the anterior longitudinal ligament, which is anterior to the vertebral bodies, and the posterior longitudinal ligament, which is posterior to the vertebral bodies and anterior to the spinal cord. The muscles of the trunk provide additional support.
Colonoscopy is the endoscopic examination of the large colon and the distal part of the small bowel with a CCD camera or a fiber optic camera on a flexible tube passed through the anus. It may provide a visual diagnosis (e.g. ulceration, polyps) and grants the opportunity for biopsy or removal of suspected lesions. Virtual colonoscopy, which uses 2D and 3D imagery reconstructed from computed tomography (CT) scans or from nuclear magnetic resonance (MR) scans, is also possible, as a totally non-invasive medical test, although it is not standard and still under investigation regarding its diagnostic abilities. Furthermore, virtual colonoscopy does not allow for therapeutic maneuvers such as polyp/tumor removal or biopsy nor visualization of lesions smaller than 5 millimeters.
If a growth or polyp is detected using CT colonography, a standard colonoscopy would still need to be performed. Colonoscopy can remove polyps as small as one millimeter or less. Once polyps are removed, they can be studied with the aid of a microscope to determine if they are precancerous or not. Colonoscopy is similar to but not the same as sigmoidoscopy. The difference between colonoscopy and sigmoidoscopy is related to which parts of the colon each can examine. Sigmoidoscopy allows doctors to view only the final two feet of the colon, while colonoscopy allows an examination of the entire colon, which measures four to five feet in length. Often a sigmoidoscopy is used as a screening procedure for a full colonoscopy. In many instances a sigmoidoscopy is performed in conjunction with a fecal occult blood test (FOBT), which can detect the formation of cancerous cells throughout the colon. Other times, a sigmoidoscopy is preferred to a full colonoscopy in patients having an active flare of ulcerative colitis or Crohn's disease to avoid perforation of the colon. Additionally, surgeons have lately been using the term pouchoscopy to refer to a colonoscopy of the ileo-anal pouch.
