Discover all the latest about our products, technology, and Target Health culture on our official blog.
December 10, 2018Target Healthy Eating
Making this spinach pie, created such wonderful aromas emanating from our kitchen. The flavor is spectacular! If I do say so myself, this delicious recipe was a great success. I'm planning to make it again over the holidays when people come for dinner. ©Joyce Hays, Target Health Inc.
2.5 pounds fresh spinach, chopped (you can substitute frozen, thawed well and squeezed dry with paper towels)
1/4 cup olive oil
4 large onions, diced
2 bunches scallions (use white and (tender only) green part
1/2 cup parsley, chopped
1/2 cup fresh dill, chopped
1/4 teaspoon ground nutmeg; buy the whole nutmeg and freshly grate it. I ended up using already ground nutmeg
Pinch black pepper or to taste
Pinch chili flakes
1/2 pound feta cheese, crumbled
4 eggs, lightly beaten
1/2 pound ricotta
Into a medium size bowl add all the ingredients, below and mix together. Set aside, until it's time to add the topping to the spinach pie.
4 eggs beaten
1 1/4 cups plain Greek yogurt
Pinch black pepper
Pinch paprika or chili flakes
1/2 to 1 cup freshly grated kashkaval cheese (or kefalotyri). I got the kashkaval cheese at FreshDirect, but Amazon probably carries it also
Preheat oven to 350 degrees
Make the topping first and set aside, until the spinach part has baked.
Wash and drain the chopped spinach at least 3 times, to be sure you get all of the sand and grit out. Nothing ruins a spinach recipe more, than biting down on sand. The last time this happened, I had to throw the whole baked dish, out, after serving it. (so-o embarrassing). If using frozen spinach, thaw completely and squeeze out excess water. Spinach should be dry. I cannot emphasize enough, the important of getting the spinach as dry as you can, in this recipe. Otherwise, later, your spinach pie will be too juicy.
Heat the olive oil in a large pan. Saute the onions and scallions (or chives, or shallots) until tender.
Add the spinach, parsley, and dill and cook for 5 to 10 minutes until the spinach is wilted and heated through. Add the nutmeg and season with salt and pepper.
If using frozen spinach, you will want to cook until excess moisture evaporates. Spinach mixture should be on the dry side.
Remove from heat and set the spinach aside to cool.
In a large mixing bowl, combine the feta cheese, eggs, and ricotta cheese. Add to the cooled spinach mixture and mix until combined.
Oil a deep baking dish, with 1 teaspoon of olive oil, and pour the spinach mixture in. Use a spatula to scrape all the spinach out of the mixing bowl.
Bake in a preheated 350 degree oven for approximately 20 to 25 minutes of cooking time. You're going to bake the pie first, without the topping. One reason is to be sure the spinach is well cooked and dry. You don't want it to ooze all over the baking dish
When you take the spinach pie out of the oven, let it sit on a counter to set. Wait about 1/2 hour before you pour the topping over the pie. Put it back into the oven at 350 degrees and bake for 10 to 15 to 20 minutes, with your eye on the oven, so the topping doesn't burn. You want it to turn a golden brown color, so when that happens, take it out of the oven right away. Let the color of the topping guide you, as to when to remove pie from oven.
Now, bake the topping for approximately 10 to 20 minutes of cooking time, depending on your oven (keep your eye on it, so it doesn't burn).
Serve nice and warm. You could warm up some pita bread for the last 5 minutes, along with the spinach pie; the two would go well together. Dip the warm pita in some olive oil.
From Our Table to Yours
Have a Great Week Everyone!
December 10, 2018Regulatory
According to the Centers for Disease Control and Prevention (CDC), more than half of adults by age 40 have been infected with cytomegalovirus (CMV). However, most people infected with CMV show no signs or symptoms of infection. However, CMV infection can cause serious health problems for people with weakened immune systems and for some newborns. Congenital CMV occurs when a baby is infected with CMV during pregnancy. Although most babies with CMV will not have any signs or symptoms of infection, some babies can develop hearing problems or other long-term health problems.
The FDA cleared for marketing a new diagnostic test to aid in detecting CMV in newborns less than 21 days of age. The Alethia CMV Assay Test System is to be used as an aid in the diagnosis of congenital CMV infection by detecting CMV deoxyribonucleic acid (DNA) from a saliva swab. However, test results should be used only in conjunction with the results of other diagnostic tests and clinical information. For the approval, FDA evaluated the analytical and clinical performance of the device. Data from a prospective clinical study showed that 1,472 saliva samples out of 1,475 samples collected from newborns were correctly identified by the device as negative for the presence of CMV DNA. Three samples were incorrectly identified as positive when they were negative. Five collected saliva specimens were correctly identified as positive for the presence of CMV DNA. The FDA also reviewed data from a testing of 34 samples of archived specimens from babies known to be infected with CMV in which all the archived specimens were correctly identified by the device as positive for presence of CMV DNA.
The FDA reviewed the Alethia CMV Assay Test System through the de novo premarket review pathway, a regulatory pathway for novel, low-to-moderate-risk devices of a new type. Along with this authorization, the FDA is establishing criteria, called special controls, which determines the requirements for demonstrating accuracy, reliability and effectiveness of tests intended to be used as an aid in the diagnosis of congenital CMV infection. These special controls, when met along with general controls, provide a reasonable assurance of safety and effectiveness for tests of this type. This action also creates a new regulatory classification, which means that subsequent devices of the same type with the same intended use may go through the FDA's 510(k) process, whereby devices can obtain marketing authorization by demonstrating substantial equivalence to a predicate device.
The FDA granted marketing authorization of the Alethia CMV Assay Test System to Meridian Bioscience, Inc.
December 10, 2018Extra-Terrestrial Research
When traveling in space, astronauts experience physiological changes normally associated with aging, such as bone loss, muscle deterioration and altered immune systems. When the astronauts return to Earth, the changes often reverse. To better understand the relevance of the astronauts' experience to human health - both on the ground and beyond - NIH's National Center for Advancing Translational Sciences (NCATS) partnered with the International Space Station U.S. National Laboratory (ISS National Lab) to send tissue chips, a research technology that reflects the human body, into space. The ISS National Lab and NASA partnered to use the U.S. portion of the space station for research initiatives leveraging the unique microgravity environment in space.
This month, a set of tissue chips that model aspects of the human immune system were launched on SpaceX's 16th commercial resupply mission (awarded by NASA) from Cape Canaveral, Florida, to the ISS National Lab. The chip set is the first of several supported by the NIH that will travel to the ISS National Lab over the next few months. Led by NCATS through its Tissue Chips in Space initiative, researchers at the University of California, San Francisco (UCSF), developed the immune system chip to explore the relationship between aging and immune responses and to look for possible ways to slow the aging process.
According to the NIH, research on the ISS National Lab is creating unprecedented opportunities for scientists to study microgravity-induced changes in human physiology relevant to diseases on Earth, as well as to accelerate the development of translational technologies for earthly applications. NIH added that this research will not only contribute valuable knowledge on the aging process, but also may reveal new approaches to ameliorating the effects of aging.
Designed to work like human organs, tissue chips mimic living human tissues and cells. Each immune system chip includes three types of cells: a specific type of immune cell; cells from bone marrow, which make immune cells; and cells from the lining of blood vessels, where immune cells encounter infection. A few dozen of the immune system chips are now traveling to the space station, where they will stay in an incubator. After two weeks, the chips will be frozen and preserved. Later, they will be transported back to Earth for analysis.
It was concluded that this research will give scientists new insights into the molecular basis for many human conditions, which in this particular project relates to how microgravity induces aging of the immune system that may lead to the development of novel therapies here on Earth.
Another launch, currently planned for March 2019, also from Cape Canaveral, will send kidney chips, bone and cartilage chips, and chips modeling the blood-brain barrier, which is a protective mesh of blood vessels and tissue that can stymie therapies from reaching the brain, to the ISS-NL. A planned April 2019 launch from Wallops Island, Virginia, will include a lung chip connected to a bone marrow chip, for studying infections. View the launch schedule for the most up-to-date information.
The ISS National Lab, NCATS and NIH's National Institute of Biomedical Imaging and Bioengineering announced awards for additional Tissue Chips in Space research projects in October 2018 for future travel to the ISS National Lab.
December 10, 2018Public Health
Editor's Note: We were just at a Multi-Regional Clinical Trial (MRCT) meeting at Harvard where we were told that life expectancy in the low income, rural areas of Arkansas, was 10 years less than in the more educated urban areas.
The presence of systemic cotinine indicates that a child/person was exposed to second- or third-hand smoke. Second-hand smoke comes from a lit tobacco product, an electronic smoking device or the smoker. Third-hand smoke is an invisible residue from smoke that settles onto floors, furniture and clothing.
According to an article published in Nicotine & Tobacco Research (6 December 2018), infants and toddlers in low-income, rural areas may be at higher risk for second- and third-hand smoke than previously reported. The study analyzed data from the Family Life Project, a long-term study of rural poverty in North Carolina and Pennsylvania. For the study, saliva samples were collected from 1,218 children at age 6 months, 15 months, 2 years and 4 years, and tested it for cotinine. Results showed that approximately 15% of children in the study tested positive for cotinine, at levels comparable to those of adult smokers. About 63% of children in the study had detectable levels of cotinine, suggesting widespread exposure to smoke.
The researchers classified the children into three groups based on their cotinine levels. Fifteen percent of the children were in the high exposure group, with cotinine levels comparable to active adult smokers (12ng/mL or higher), 48% were in the moderate exposure group (0.46 to 12ng/mL) and 37% were in the low exposure group (less than or equal to 0.46ng/mL). These values are higher than those seen in data previously reported in the National Health and Nutrition Examination Survey, which found that only one-third to one-half of children's blood samples had detectable cotinine. According to the authors, it was found that infants had higher cotinine levels compared to toddlers, most likely because infants often put objects into their mouths and crawl on floors, thus more more likely to ingest smoke residue or get it on their skin, compared to older children.
The study team evaluated independent factors that may influence a child's probability of being in one of the three exposure groups. They found that lower income, less education, frequent residential moves and fluctuations in the number of adults within the home were associated with high smoke exposure, whereas time spent at a center-based daycare was associated with lower smoke exposure.
Factors influencing cotinine levels included the following:
1. When a caregiver had at least a high school degree, a child was 85% less likely to be in the high exposure group, compared to the other two groups.
2. Each residential move increased a child's odds of being in the high exposure group, compared to the low exposure group, by 43%.
3. Each adult moving into or out of the home increased this risk by 11%.
4. A child who spent time in a center-based daycare was 81% less likely to be in the high exposure group, compared to the low exposure group.
December 10, 2018History of Medicine
Ralph Marvin Steinman (January 14, 1943 - September 30, 2011) was a Canadian physician and medical researcher at Rockefeller University, who in 1973 discovered and named dendritic cells while working as a postdoctoral fellow in the laboratory of Zanvil A. Cohn, also at the Rockefeller University. Steinman was one of the recipients of the 2011 Nobel Prize in Physiology or Medicine.
Ralph Steinman was born into an Ashkenazi Jewish family in Montreal, one of four children of Irving Steinman (d. 1995), a haberdasher, and Nettie Steinman (nee Takefman, 1917-2016). The family moved to Sherbrooke, where the father opened and ran a small clothing store called, Mozart's.
After graduating from Sherbrooke High School, Steinman moved back to Montreal where he stayed with his maternal grandparents Nathan and Eva Takefman. He received a Bachelor of Science degree from McGill University and received his M.D. (magna cum laude) in 1968 from Harvard Medical School. He completed his internship and residency at Massachusetts General Hospital.
On October 3, 2011, the Nobel Committee for Physiology or Medicine announced that he had received one-half of the Nobel Prize in Physiology or Medicine, for his discovery of the dendritic cell and its role in adaptive immunity. The other half went to Bruce Beutler and Jules A. Hoffmann, for their discoveries concerning the activation of innate immunity. However, the committee was not aware that he had died three days earlier, on September 30, from pancreatic cancer. This created a complication, since the statutes of the Nobel Foundation stipulate that the prize is not to be awarded posthumously. After deliberation, the committee decided that as the decision to award the prize was made in good faith, it would remain unchanged. Steinman's daughter said that he had joked the previous week with his family about staying alive until the prize announcement. Steinman said: I know I have got to hold out for that. They don't give it to you if you have passed away. I got to hold out for that.
The term dendritic cells was coined in 1973 by Ralph M. Steinman and Zanvil A. Cohn. In 1973, along with his mentor, Zanvil Cohn, Steinman published the discovery of a new class of cell in the immune system - the dendritic cell. Like many new discoveries, his faced a deeply skeptical reception. The experiments couldn't be immediately reproduced, but Steinman was convinced of his discovery. He fought for a decade before immunologists began to broadly recognize the central importance of those cells to their field. Dendritic cells are antigen-presenting cells (also known as accessory cells) of the mammalian immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems. Dendritic cells are present in those tissues that are in contact with the external environment, such as the skin (where there is a specialized dendritic cell type called the Langerhans cell) and the inner lining of the nose, lungs, stomach and intestines. They can also be found in an immature state in the blood. Once activated, they migrate to the lymph nodes where they interact with T cells and B cells to initiate and shape the adaptive immune response. At certain development stages they grow branched projections, like branches of a tree. The word dendrites are from dendron, which is Greek for tree. While similar in appearance, these are structures distinct from the dendrites of neurons. Immature dendritic cells are also called veiled cells, as they possess large cytoplasmic ?veils' rather than dendrites.
Steinman had received numerous other awards and recognitions for his lifelong work on dendritic cells, such as the Albert Lasker Award For Basic Medical Research (2007), the Gairdner Foundation International Award (2003), and the Cancer Research Institute William B. Coley Award (1998). In addition, he was made a member of Institute of Medicine (U.S.A.; elected 2002) and the National Academy of Sciences (U.S.A.; elected 2001).
Immunology tries to understand resistance to infection. Infections are first resisted by innate immunity, followed by adaptive immunity which has memory and so can prevent reinfection. Two questions that Immunologists ask: 1) by what mechanism do innate and adaptive resistance come about? 2) how do these mechanisms contribute to other fields of medicine such as cancer, allergy, autoimmunity etc.? In the 20th century, Dr. Steinman came up with two theories: 1) macrophages mediate innate resistance through phagocytosis and intracellular killing 2) Ab mediate adaptive resistance by neutralizing microbial toxins. Steinman discovered that dendritic cells link innate to adaptive immunity, including adaptive Tcell-mediated immunity. Steinman studied the initiation of antibody responses in tissue culture in the laboratory. He found out that antigens, lymphocytes and accessory cells together create immune responses. Accessory cells contain a new cell type with probing cell process or dendrites. These cells proved to be the missing link between innate and adaptive immunity. Steinman together with Dr. John Leonora demonstrated that dental decay originates as a disruption of the endocrine system that impacts the dentinal fluid and allows bacteria to gain a foothold. This theory challenges traditional theories concerning both oral hygiene and fluoride use.
Several features were used to identify and purify dendritic cells from mouse spleen. Because dendritic cells were discovered amongst adherent accessory cells (i.e. those that attach to tissue culture surfaces), they had to be distinguished from macrophages, whose hallmarks were persistent phagocytosis and adherence to tissue culture surfaces. However, Steinman found that dendritic cells (blue) had different morphology and expressed different molecules from macrophages. For example, they did not express FcR- receptors but did express major components of the Major Histocompatibility Complex II and did not adhere to surfaces or exploit phagocytosis. Macrophages on the other hand showed the opposite characteristics. The study was carried out in collaboration with Zanvil A. Cohn, who studied resistance to infectious diseases especially the biology of macrophages. Some general features of T cell responses that are initiated by dendritic cells: - adaptive immunity develops in two stages: Dendritic cells present antigens and initiate the afferent limb, while the other APC mediate the effectors to eliminate the antigen or infection - in tissue cultures, immunity develops in clusters of Dendritic cells and lymphocytes. You can actually observe the onset of adaptive immunity in vitro. Dendritic cells were therefore considered nature's adjuvants for T cell immunity, meaning they helped induce T cells. Dendritic cells can produce protective substances like cytokines, interferons, chemokines, anti-microbial peptides Dendritic cells can mobilize innate lymphocytes such as natural killer cells (which in turn produce cytokines or kill target cells upon recognition) However, unlike macrophages, Dendritic cells do not phagocytose or kill microbes. Dendritic cells capture, process and present antigens: - some receptors such as FcR death receptor can activate/inhibit Dendritic cells function - Antigen processing and presentation of proteins and lipids seems efficient and can include cross presentation on MHC I and CD1 - Uptake and processing are regulated by environmental stimuli - In vivo, dendritic cells process antigens to form peptide-MHC complexes in the steady state, especially in lymphoid organs - Most Dendritic cells in vivo in the steady state are immature, able to take up and present antigens, but unable to adaptive T cell immunity - Environmental stimuli, e.g., microbial products, alter or mature Dendritic cells and/or act together with Dendritic cells to control the formation of different types of helper, cytotoxic and regulatory types of T cells. Maturing dendritic cells also carry out innate responses, particularly the formation of cytokines and chemokines - Maturation links innate to adaptive immunity; it controls the quality of the response that develops in Dendritic cells and in lymphocytes that recognize presented antigens - subset refers to distinct DC with different receptor for antigen uptake and maturation, and distinct functions in innate and adaptive immunity. they reside in the peripheral organs and induce different forms of antigen-specific peripheral tolerance. Antigens from the periphery are captured by Dendritic cells in lymphoid tissues, even in steady (not matured) state. In steady state, Dendritic cells induce tolerance so that Dendritic cell maturation can lead to immunity to microbial antigen - However, maturing Dendritic cells capture microbial as well as self, dying cells, thus resulting in autoreactivity and chronic inflammation.
When Ralph Steinman learned he had pancreatic cancer, the dogged immunologist put his life's work to the test. He launched a life-and-death experiment in the most personal of personalized medicine. By unlucky coincidence, he had been diagnosed with a disease that might benefit from the therapies he had spent his life researching. Usually, medical research proceeds at a glacial, thorough pace: cell studies lead to studies in small animals which lead to studies in larger animals, which eventually lead to small, highly-selective clinical trials in humans. But Steinman didn't have that kind of time. He did, however, have access to world class facilities, cutting-edge technology, and some of the world's most brilliant medical minds, thanks to his position as a researcher at Rockefeller University. So, Steinman decided to make his own body the ultimate experiment. He had removed a piece of the tumor that would eventually kill him. He then trained his immune cells to track down any hint of the tumor that might have escaped the surgery, like putting hounds on a scent. The made-for-Hollywood story of the renegade scientist who fights the establishment to prove his discovery, and then uses it to cure himself, was powerful enough to compel hope. On a Friday, four-and-a-half years after he was diagnosed with a disease that kills the vast majority of its victims in less than one, that experiment came to an end. Steinman died at the end of a week in which he continued his work in the lab. It was a testament to the undying optimism of the scientific enterprise, to the unrelenting man, and to the limits of both. His experiment was an open secret on campus, registered with the hospital and aided by a long-time friend and staff physician. The sense of hope was palpable, bound up in respect for the man but also something broader.
Steinman bet that if he could train his dendritic cells to recognize and tag his cancer, they would be able to convince the T and B cells to do the rest. There was no good reason to expect that Steinman could fashion a cure for one of the world's most vicious cancers in time to save his own life. But it was easy to think it was at least possible. Unfortunately, the dendritic cell-based treatments didn't work - at least not well enough.
One dendritic-cell based vaccine - Provenge - is available now for advanced prostate cancer, leading the way to commercialization for drug makers. Other vaccines are under development
December 10, 2018Quiz
By OpenStax College - Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013., CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=30148457
Pancreatic cancer is the fourth leading cause of cancer 1) ___ in the United States. Approximately 32,?000 individuals in the USA and over 200,?000 individuals worldwide die from the disease each year. The incidence approximates the mortality rate, which reflects the poor prognosis of pancreatic cancer. Although there have been many advances in pancreatic cancer research, the 5-year survival rate for affected patients remains under 5%.
The aggressiveness that characterizes pancreatic cancer arises from multiple heterogeneous genetic changes that occur before the onset of clinical symptoms. Studies performed over the past decade have shed some light on the molecular and histological events that are associated with pancreatic carcinogenesis. Future progress in this area will hopefully lead to improved diagnostic tests, early detection, and new treatments for patients who suffer from this devastating disease. The accumulation of multiple nonrandom genetic changes over time is a hallmark of pancreatic cancer. Genetic abnormalities include alterations in chromosome or 2) ____ copy number, microsatellite instability, epigenetic silencing, intragenic point mutations, and gene overexpression secondary to increased transcription.
Pancreatic cancer arises when cells in the pancreas, a glandular organ behind the 3) ___, begin to multiply out of control and form a mass. These cancerous cells have the ability to invade other parts of the body. There are a number of types of pancreatic cancer. The most common, pancreatic adenocarcinoma, accounts for about 85% of cases, and the term pancreatic cancer is sometimes used to refer only to that type. These adenocarcinomas start within the part of the pancreas which makes digestive enzymes. Several other types of cancer, which collectively represent the majority of the non-adenocarcinomas, can also arise from these cells. One to two percent of cases of pancreatic cancer are neuroendocrine tumors, which arise from the hormone-producing 4) ___ of the pancreas. These are generally less aggressive than pancreatic adenocarcinoma. Signs and symptoms of the most common form of pancreatic cancer may include yellow skin, abdominal or back pain, unexplained 5)___ loss, light-colored stools, dark urine and loss of appetite. There are usually no symptoms in the disease's early stages, and symptoms that are specific enough to suggest pancreatic cancer typically do not develop until the disease has reached an advanced stage. By the time of diagnosis, pancreatic cancer has often spread to other parts of the body.
Pancreatic cancer rarely occurs before the age of 40, and more than half of cases of pancreatic adenocarcinoma occur in those over 70. Risk factors for pancreatic cancer include tobacco smoking, obesity, diabetes, and certain rare genetic conditions. About 25% of cases are linked to smoking, and 5-10% are linked to inherited genes. Pancreatic cancer is usually diagnosed by a combination of medical imaging techniques such as ultrasound or computed tomography, blood tests, and examination of tissue samples (biopsy). The disease is divided into stages, from early (stage I) to late (stage IV). Screening the general population has not been found to be effective. The risk of developing pancreatic cancer is lower among non-smokers, and people who maintain a healthy weight and limit their consumption of red or processed meat. A smoker's chance of developing the disease decreases if they stop 6) ___, and almost returns to that of the rest of the population after 20 years.
Pancreatic cancer can be treated with surgery, radiotherapy, chemotherapy, palliative care, or a combination of these. Treatment options are partly based on the cancer stage. Surgery is the only treatment that can cure pancreatic adenocarcinoma, and may also be done to improve quality of life without the potential for cure. Pain management and medications to improve digestion are sometimes needed. Early palliative care is recommended even for those receiving treatment that aims for a cure. The disease occurs most often in the 7) ___ world, where about 70% of the new cases in 2012 originated. Pancreatic adenocarcinoma typically has a very poor prognosis: after diagnosis, 25% of people survive one year and 5% live for five years. For cancers diagnosed early, the five-year survival rate rises to about 20%. Neuroendocrine cancers have better outcomes; at five years from diagnosis, 65% of those diagnosed are living, though survival varies considerably depending on the type of tumor.
The pancreas has multiple functions, served by the endocrine cells in the islets of Langerhans and the exocrine acinar cells. Pancreatic cancer may arise from any of these and disrupt any of their functions. The many types of pancreatic 8) ___ can be divided into two general groups. The vast majority of cases (about 95%) occur in the part of the pancreas which produces digestive enzymes, known as the exocrine component. There are several sub-types of exocrine pancreatic cancers, but their diagnosis and treatment have much in common. The small minority of cancers that arise in the hormone-producing (endocrine) tissue of the pancreas have different clinical characteristics and are called pancreatic neuroendocrine tumors, sometimes abbreviated as PanNETs. Both groups occur mainly (but not exclusively) in people over 40, and are slightly more common in men, but some rare sub-types mainly occur in women or children.
Pancreatic cancer can be difficult to diagnose. That's partly because the pancreas is located deep in the belly and is difficult to feel or examine, and partly because symptoms may develop gradually. A single standard diagnostic test for pancreatic cancer does not yet exist. So, if a person has symptoms that suggest pancreatic cancer, his or her doctor may use a variety of tests to make the diagnosis and to stage the cancer. The tests may include a number of different imaging tests (MRI, CT, PET, and ultrasound) as well as blood chemistry studies, biopsies, and more. The diagnostic tests the doctor orders may differ depending on whether he or she suspects an exocrine tumor or a pancreatic neuroendocrine tumor (PNET). While it is virtually impossible to tell what caused a specific person to develop pancreatic cancer, there are some important principles of cancer biology that can help us understand why pancreatic cancer develops, and large population-based studies help us understand the many risk factors for this disease.
Pancreatic cancer is fundamentally a disease caused by damage to the DNA. This damage is often referred to as mutations. These 9) ___ can be inherited from either parent, or they can be acquired as we age. With inherited mutations, there are two copies of each gene - one copy we inherit from our mother, the other copy we inherit from our father. Most individuals with an inherited cancer syndrome inherit one mutant copy (let us say from dad) and one intact (normal) copy (let us say from mom) of a cancer associated gene. As these individuals with an inherited cancer syndrome age, some of will sustain damage the good copy of the gene (the copy they got from mom) in a cell in their pancreas. That cell will then have two damaged copies of the gene (one inherited and one acquired during life), and, as a result, that cell in the pancreas will begin to grow abnormally and will eventually form a cancer. From this understanding it should be clear that not everyone with an inherited predisposition will get cancer. Instead, since individuals with an inherited cancer syndrome are born with only one good copy of the cancer associated gene, they are more likely to get cancer. The second way we can damage our DNA is with our behavior. For example, the carcinogens (cancer causing chemicals) in cigarette smoke can damage our DNA. If the carcinogens damage a key cancer-associated gene in a cell in the pancreas, then that cell may grow into a cancer. Simply put, don't smoke! The third way our DNA gets damaged is by chance. This is probably the least satisfying explanation, but it is true. Every cell in our body (and there are trillions of them!) contains two copies of each of the 23 chromosomes and these 46 chromosomes contain billions of base-pairs (letters) of DNA. Every time a cell divides it has to copy all of that DNA (so that it can make daughter cells with a full complement of DNA). The DNA copying machinery in cells is good, but is not perfect. Occasionally mistakes are made copying DNA. On one hand, this is good from the perspective of a population or species, because these mistakes allow for evolution to occur (if we copied our DNA perfectly we would not evolve!). On the other hand, if one of these chance mistakes in copying (DNA mutations) damages a key cancer-associated gene in a cell in the pancreas, then that cell may grow into a cancer.
To summarize, pancreatic cancer is caused by DNA mutations, and there are three ways that we can damage our DNA. We can be born with a DNA mutation inherited from our mother or father, we can do something, like smoking, that damages our DNA, or finally our DNA can be damaged by chance. The second way to answer the question about what causes pancreatic cancer is to ask what are the risk factors for pancreatic cancer? Some of the risk factors include: Cigarette smoking doubles the risk of pancreatic cancer. In fact, some scientists have estimated that one in four, or one in five cases of pancreatic cancer are caused by smoking cigarettes. Smoking is also associated with early age at diagnosis. Very importantly, the risk of pancreatic cancer drops close to normal in people who quit smoking. Simply put, 10) ___ smoking is the leading preventable cause of pancreatic cancer.
Sources: http://www.mcancer.org/news/archive/what-makes-pancreatic-cancer-so-aggressive-new-study-sheds-light; http://pathology.jhu.edu/pc/BasicCauses.php?area=ba; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2020752/;
ANSWERS: 1) death; 2) gene; 3) stomach; 4) cells; 5) weight; 6) smoking; 7) developed; 8) cancer; 9) mutations; 10) cigarette
December 10, 2018What's New
To our colleagues and friends, Happy Holidays to all from all of us at Target Health and a Healthy and Happy New Year to you and your families.
For more information about Target Health, contact Warren Pearlson (212-681-2100 ext. 165). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel. The Target Health software tools are designed to partner with both CROs and Sponsors.
Joyce Hays, Founder and Editor in Chief of On Target
Jules Mitchel, Editor
December 3, 2018Target Healthy Eating
2 Cooked leftover turkey breasts or chicken breast, cut into bite-size cubes
Ground 4 fresh Garlic clove using a mortar & pestle
1 teaspoon curry powder
Pinch black pepper
Pinch chili flakes
2 scallions, chopped up to half the white part
2 Fuji apples sliced very thin, then cut in half, (leave red skin on)
1 endive, leaves separated, cut lengthwise
1 cup Red seedless grapes cut in half
1 cup green seedless grapes, cut in half
1.5 cups chopped (candied) walnuts
2 cups Blue cheese dressing (see below)
1. Do all your cutting, chopping, slicing
2. Get out the salad serving bowl you plan to use and put the bite-size leftover turkey into the bowl and add the garlic, spices and seasoning. Mix these ingredients so they're well combined.
3. Add the scallions, endive pieces and the fruit and toss lightly.
4. Add half of the candied or glazed walnuts. If you can't find these particular nuts, substitute candied or glazed pecan, or cashews. Toss lightly simple to distribute the nuts.
5. Make the blue cheese dressing.
6. Just before you plan to serve the salad, pour the dressing over it and toss lightly until the dressing covers everything.
7. Finally, sprinkle the remaining candied walnuts over the top of the salad.
8. Enjoy with your favorite chilled white wine, warm French bread and unsalted Irish (or French) butter.
Blue Cheese Dressing
Combine all of the ingredients into a mixing bowl and mix well.
1/4 cup Kraft mayonnaise
1/4 cup almond milk
1/4 cup sour cream
1/3 cup blue cheese
1 teaspoon ground curry
1 pinch black pepper
1 pinch chili flakes
4 garlic cloves, ground in mortar & pestle
We saw the B'way play, American Son; an extremely relevant story with a punch in the gut ending.
From Our Table to Yours
Have a Great Week Everyone!
December 3, 2018Regulatory
The FDA has approved Firdapse (amifampridine) tablets for the treatment of LEMS in adults. This is the first FDA approval of a treatment for Lambert-Eaton myasthenic syndrome (LEMS).
In people with LEMS, the body's own immune system attacks the neuromuscular junction (the connection between nerves and muscles) and disrupts the ability of nerve cells to send signals to muscle cells. LEMS may be associated with other autoimmune diseases, but more commonly occurs in patients with cancer such as small cell lung cancer, where its onset precedes or coincides with the diagnosis of cancer. The prevalence of LEMS is estimated to be three per million individuals worldwide.
The efficacy of Firdapse was studied in two clinical trials that together included 64 adult patients who received Firdapse or placebo. The studies measured the Quantitative Myasthenia Gravis score (a 13-item physician-rated categorical scale assessing muscle weakness) and the Subject Global Impression (a seven-point scale on which patients rated their overall impression of the effects of the study treatment on their physical well-being). For both measures, the patients receiving Firdapse experienced a greater benefit than those on placebo. The most common side effects experienced by patients in the clinical trials were burning or prickling sensation (paresthesia), upper respiratory tract infection, abdominal pain, nausea, diarrhea, headache, elevated liver enzymes, back pain, hypertension and muscle spasms. Seizures were observed in patients without a history of seizures.
The FDA granted this application Priority Review and Breakthrough Therapy designations. Firdapse also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases.
The FDA granted the approval of Firdapse to Catalyst Pharmaceuticals, Inc.
December 3, 2018Infectious Disease
Although most people experience a mild illness or no symptoms when infected with Zika virus, babies born to women infected with Zika virus during pregnancy may have birth defects and/or develop health problems in their early years. Zika virus is primarily transmitted to humans by the bite of an infected mosquito. As a result, the Centers for Disease Control and Prevention (CDC) advises that pregnant women should not travel to areas with risk of Zika. CDC also recommends that partners of pregnant women and couples considering pregnancy should know pregnancy risks and take certain precautions. The U.S. Zika Pregnancy and Infant Registry has recorded the number of pregnant women with laboratory evidence of possible Zika virus infection since 2015. As of July 17, 2018, the registry had recorded 2,474 pregnancies in states and the District of Columbia and 4,900 pregnancies in U.S. territories and freely associated states.
Vaccinations have begun in a first-in-human trial of an experimental live, attenuated Zika virus vaccine developed by scientists at the National Institute of Allergy and Infectious Diseases (NIAID). The trial is enrolling a total of 28 healthy, non-pregnant adults ages 18 to 50 at the Johns Hopkins Bloomberg School of Public Health Center for Immunization Research in Baltimore, Maryland, and at the Vaccine Testing Center at the Larner College of Medicine at the University of Vermont in Burlington.
NIAID's Laboratory of Viral Diseases, led the efforts to develop the experimental vaccine, known as rZIKV/D4?30-713. The laboratory used genetic engineering techniques to create a chimeric virus, made by combining genes from multiple viruses. The chimeric virus consists of a dengue virus type 4 backbone (dengue is caused by any of four related viruses, termed serotypes) that expresses Zika virus surface proteins. The chimeric virus is live but attenuated, or weakened, so it cannot cause disease in recipients. When injected into the body, the weakened virus should prompt an immune response. The Phase 1 clinical trial will analyze this response in participants and assess the safety of the experimental vaccine, which showed promise in earlier tests in rhesus macaques (monkeys). Charles River Laboratories, in Malvern Pennsylvania, manufactured the vaccine candidate for the Phase 1 clinical trial.
The research team also has developed a live, attenuated dengue vaccine candidate called TV003 designed to elicit antibodies against all four dengue virus serotypes. The experimental vaccine is currently under evaluation in a Phase 3 clinical trial conducted in Brazil by the Butantan Institute. The goal is to develop a single vaccine that would protect against both Zika and dengue viruses. According to the CDC, dengue is endemic in at least 100 countries in Asia, the Pacific, the Americas, Africa and the Caribbean. Zika virus has been found to circulate in many of these same areas. Once the Zika vaccine candidate proves safe in Phase 1 clinical testing, the plan is to add the Zika component to the tetravalent dengue vaccine candidate and evaluate the new pentavalent candidate in a Phase 1 clinical trial.
Study participants who test positive for a prior flavivirus infection (such as Zika, dengue, or yellow fever) will be excluded from the trial to ensure that any antibodies detected in blood samples are related to the experimental vaccine alone. All participants will be randomly assigned to receive a single subcutaneous dose of the experimental vaccine (20 participants) or a placebo (eight participants). Neither the participants nor the investigators will know who is receiving the experimental vaccine. After the vaccination, participants will receive a diary card to record their temperature at home at certain timepoints. During the following 6 months, they will return to the clinic periodically for physical examinations and to provide blood and other samples. Investigators will test the blood samples to see if participants are developing antibodies in response to the experimental vaccine.