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October 21, 2019Target Healthy Eating
3 cups fresh blueberries
1 teaspoon your best vanilla extract
2 Tablespoons white sugar
1 1/4 cups organic almond flour
1/2 cup white sugar
1/2 cup organic almond meal or wheat flour
2 teaspoons baking powder
2 pinches salt
pinch of cinnamon
1 cup almond milk
Amaretto liqueur, added just before cutting
Fresh mint leaves, for tiny garnish
6 Tablespoons hot melted butter poured into bottom or baking dish (FYI, there are 8 Tablespoons in one stick of butter)
1. Take out your baking dish. I used a rectangular one, about 9 x 12 inches.
2. Wash blueberries, drain well, pick and throw away, any leaves and stems; pat dry with paper towel
3. In a medium bowl, add blueberries, sugar and vanilla extract and mix well. Allow to sit for several hours before using.
4. Melt butter in small pan over very low heat. When melted remove from heat and pour into the bottom of the baking dish. Set aside.
5. Pour your 1 cup of almond milk into a measuring cup and set aside.
6. Toast the chopped almonds.
7. In larger bowl, add all the dry ingredients and mix well.
8. Add milk to dry ingredients and mix everything very well for the cake batter.
9. HERE'S THE ONLY TRICK IN THIS RECIPE: Pour the batter on top of the melted butter, but don't mix them together. Instead of mixing, take a spatula and gently pull the batter almost to the edges of the baking pan. Do not cover the butter with the batter. Look at the photo below, at the melted butter, to see what we did.
10. Pour the sweetened berries over the batter.
11. Bake the Blueberry Betty at 350 degrees for 45 to 50 minutes. Keep your eye on the cake after 40 minutes to be sure it doesn't burn. See photo below.
12. Finally, add the almonds you toasted earlier
13. Just before serving, add as much Amaretto as you like, let it sink in for five minutes, before you cut the Blueberry Betty. Over top of each piece, add a dollop of vanilla ice cream (perfection) or whipped cream or cool whip, then a tiny mint leaf.
Editor's (Jules) note: This dessert is FANTASTIC
From Our Table to Yours
Have a Great Week Everyone!
October 21, 2019Regulatory
According to the Centers for Disease Control and Prevention, 38,739 people received an HIV diagnosis in the U.S. in 2017. To confront this epidemic, an initiative entitled, Ending the HIV Epidemic: A Plan for America, was launched on February 5, 2019. This opportunity to eliminate new HIV infections in our nation seeks to provide our hardest-hit communities with additional expertise, technology and resources required to address the HIV epidemic. The aim is to reduce new infections by 75% in the next five years and by 90% in the next ten years, averting more than 250,000 HIV infections in that span.
The FDA has approved Descovy (emtricitabine 200 mg and tenofovir alafenamide 25 mg) in at-risk adults and adolescents weighing at least 35kg for HIV-1 pre-exposure prophylaxis (PrEP) to reduce the risk of HIV-1 infection.
PrEP is an HIV prevention method in which people who do not have HIV take medicine on a daily basis to reduce their risk of getting HIV if they are exposed to the virus. Descovy for PrEP should be used as part of a comprehensive strategy, including adherence to daily administration and safer behavior practices, to reduce the risk of sexually acquired infections.
The safety and efficacy of Descovy for PrEP were evaluated in a randomized, double-blind multinational trial in 5,387 HIV-negative men and transgender women who were at risk of HIV-1 infection. The trial compared once daily Descovy to Truvada (emtricitabine, tenofovir disoproxil fumarate, 200 mg/300 mg), a daily fixed dose combination of two drugs approved in 2012 to prevent the sexual acquisition of HIV; participants were followed for 48 to 96 weeks. The primary endpoint was the rate of HIV-1 infection in each group. The trial showed that Descovy was similar to Truvada in reducing the risk of acquiring HIV-1 infection. The most common adverse reaction in individuals without HIV who were taking Descovy for PrEP was diarrhea.
There is a boxed warning for individuals who take Descovy who also have hepatitis B virus (HBV) to be aware of the risk of exacerbations of HBV in those who discontinue products with emtricitabine or tenofovir disproxil fumarate, and which may occur in individuals who discontinue Descovy. Descovy for HIV-1 PrEP is contraindicated in individuals with unknown or positive HIV-1 status and should only be prescribed to individuals confirmed to be HIV-negative immediately prior to initiating and at least every three months during use.
Descovy was FDA approved in 2016 in combination with other antiretoviral drugs to treat HIV-1 infection in adults and pediatric patients. The FDA granted the approval of Descovy to Gilead Sciences Inc.
October 21, 2019Gene Therapy
Sickle cell disease affects about 100,000 people in the United States and millions worldwide. Sickle cell disease is an inherited blood disorder caused by a mutation, or misspelling, in the beta-globin gene (or ?-globin gene). This mutation causes hemoglobin, the main ingredient of blood cells, to produce sickle-shaped cells that can stick to the walls of blood vessels, causing blockage, pain, anemia, organ damage, and early death. With gene therapy, doctors modify the patient's bone marrow hematopoietic (blood-producing) stem cells in the lab by adding a normal copy of the beta-globin gene through the use of a viral vector. They then reinfuse the modified stem cells into the patient to produce normal, disc-shaped red blood cells.
According to an article published in Nature Communications (2 October 2019), a new and improved viral vector -- a virus-based vehicle that delivers therapeutic genes - has been developed for use in gene therapy for sickle cell disease. In advanced lab tests using animal models, the new vector was up to 10 times more efficient at incorporating corrective genes into bone marrow stem cells than the conventional vectors currently used, and it had a carrying capacity of up to six times higher. The development of the vector could make gene therapy for sickle cell disease much more effective and pave the way for wider use of it as a curative approach for the painful, life-threatening blood disorder.
For the past 30 years, researchers have been designing these beta-globin vectors in a reverse structural orientation, meaning the therapeutic genes incorporated into the virus are translated, or read, from right to left by the viral vector-making machinery-much like reading an English sentence backwards. The reason for the reverse orientation is the sensitive expression of a key molecular component of the vector called intron 2. This segment is required for high-level beta-globin gene expression but gets clipped out during the normal vector preparation process if it is left in the natural, forward direction. Gene therapy trials using reverse-oriented vectors for sickle cell disease and beta-thalassemia have largely been encouraging, but this complicated gene translation process has made vector preparation and gene-transfer efficiency more difficult.
About 10 years ago, the authors searched for an improved delivery vehicle -- like designing a better car -- and decided to undertake a radical redesign of the beta-globin vector. They came up with a unique work-around design that left intron 2 intact and created the new forward-oriented beta-globin vector. In contrast to the old vector, the gene sequence, or message, of the new beta-globin vector is read from left to right -- like reading a normal sentence -- making the gene translation approach less complicated. The authors then tested the new vectors in mice and monkeys and compared the results to reverse-oriented vectors. Results showed that the new vectors could transfer a much higher viral load -- up to six times more therapeutic beta-globin genes than the conventional vectors -- and had four to 10 times higher transduction efficiency, a measure of the ability to incorporate corrective genes into repopulating bone marrow cells. The new vectors also showed a capacity for longevity, remaining in place four years after transplantation. The authors also found that they could be produced in much higher amounts than the conventional vectors, potentially saving time and lowering costs associated with large-scale vector production.
The new vector, for which the NIH holds the patent, still needs to undergo clinical testing in humans. Already an estimated 27 people with sickle cell disease have undergone experimental gene therapy using conventional vectors. Through its Cure Sickle Cell Initiative, NIH is working to accelerate the development of these and other new genetic therapies, including gene editing, with the goal of finding a cure for the disease. The initiative is part of NIH's larger multi-pronged approach to reducing the burden of blood disorders. People with sickle cell disease can find a clinical trial that is actively enrolling.
October 21, 2019Pediatrics
According to an article published in JAMA Network Open (3 October 2019), children born to women who have high blood levels of lead are more likely be overweight or obese, compared to those whose mothers have low levels of lead in their blood.
For the study, the authors analyzed data on 1,442 mother-child pairs from the Boston Birth Cohort, a large observational study that aims to determine the causes of preterm birth. Mothers' blood samples were analyzed for lead exposure 24 to 72 hours after they gave birth. Children had their weight assessed periodically throughout childhood. At an average age of 8.1 years, children born to mothers with high lead levels were more than four times as likely to be overweight or obese than children born to mothers with low lead levels. Among women who had high lead levels, the risk of their children being obese or overweight decreased if the women had adequate levels of folate 24 to 72 hours after giving birth. The U.S. Preventive Services Task Force recommends that all women of reproductive age consume 400 micrograms of folic acid (the synthetic form of folate) each day to help prevent neural tube defects, a class of birth defects affecting the brain and spine. Women in the study had earlier responded to a questionnaire indicating whether they had taken a supplement containing folic acid in the second and third trimesters of pregnancy. The authors noted that if their results are confirmed, testing pregnant women for lead exposure and then offering folic acid to those who have high levels could potentially reduce their children's risk of being overweight or obese.
Lead exposure during pregnancy also may have harmful effects on mother and baby. The U.S. Centers for Disease Control and Prevention offers advice on how pregnant women can reduce their exposure to lead.
October 21, 2019History of Medicine
George Huntington (April 9, 1850 - March 3, 1916) was an American physician who contributed a classic clinical description of the disease that bears his name - Huntington's disease. Huntington described this condition in the first of only two scientific papers he ever wrote. He wrote this paper when he was 22, a year after receiving his medical degree from Columbia University in New York. He first read the paper before the Meigs and Mason Academy of Medicine in Middleport, Ohio on February 15, 1872 and then published it in the Medical and Surgical Reporter of Philadelphia on April 13, 1872. In a 1908 review, the eminent physician William Osler said of this paper: In the history of medicine, there are few instances in which a disease has been more accurately, more graphically or more briefly described.
Huntington's father and grandfather, George Lee Huntington (1811-1881) and Abel Huntington (1778-1858), were also physicians in the same family practice. Their longitudinal observations combined with his own were invaluable in precisely describing this hereditary disease in multiple generations of a family in East Hampton on Long Island.
In 1874 George Huntington returned to Dutchess County, New York to practice medicine. He joined a number of medical associations and started working for the Matteawan General Hospital. In 1908 the scientific journal Neurograph dedicated him a special edition.
Probably the most famous person to suffer from Huntington's was Woody Guthrie, the prolific folk singer who died in 1967 at age 55. Woodrow Wilson Guthrie, better known as Woody Guthrie, he was born in Okemah, Oklahoma, on July 14, 1912. The folk singer, activist and songwriter recorded album after album of beloved and socially important songs, including This Land is Your Land. Guthrie was brought up by middle-class parents in Okemah, Oklahoma, until he was 14, when his mother Mary was hospitalized as a consequence of Huntington's disease, a fatal hereditary neurological disorder. His father moved to Pampa, Texas, to repay debts from unsuccessful real estate deals. During his early teens, Guthrie learned folk and blues songs from his parents' friends. He married at 19, but with the advent of the dust storms that marked the Dust Bowl period, he left his wife and three children to join the thousands of Okies who were migrating to California looking for employment. He worked at Los Angeles radio station KFVD, achieving some fame from playing hillbilly music; made friends with Will Geer and John Steinbeck. Guthrie also wrote a wonderful series of songs he called The Dust Bowl Ballads, which included Do Re Mi, (a song about experiences of the Dust Bowl migrants, often known as Okies, with the famous refrain, Oh if you ain't got the do re mi, folks, you ain't got the do re mi?), Tom Joad (inspired by the main character in Steinbeck's The Grapes of Wrath), and Pretty Boy Floyd, (a song celebrating the famous gangster and some of his criminal exploits in Oklahoma).
Steinbeck and Guthrie knew each other well; Guthrie named one of his sons Joady, after the novelist's protagonist. In 1943, Guthrie even penned a partially fictionalized, semi-autobiography called Bound for Glory, which many have compared in power to Steinbeck's The Grapes of Wrath. (It was later made into a film in 1976 starring Keith Carradine.)
By almost everyone's measure, including his own, Guthrie suffered from active alcoholism for most of his adult life. But he was dealt an extra blow - inheriting Huntington's disease (HD), from his mother, Nora Belle Guthrie. HD is primarily an autosomal dominant genetic disorder, meaning a child has a 50-percent chance of inheriting the dominant trait and, hence, the disease from the affected parent. In rare cases, HD may be due to a new mutation. Most Huntington's patients do not develop obvious symptoms until between the ages of 30 and 50. HD sets in motion the production of an abnormal protein that destroys brain cells, leading to serious mood disorders, followed by uncoordinated and involuntary body movements (known as chorea), balance problems, psychotic breaks, dementia and death, roughly 15 to 20 years after the diagnosis is first made.
This terrible malady was first described in a paper entitled On Chorea, which appeared in the April 13, 1872, issue of the Philadelphia Medical and Surgical Reporter. It was written by George Huntington, the American physician who was practicing in Ohio at the time he presented his paper to the Meigs and Mason Academy of Medicine located in Middleport, Ohio. A brief quote from his remarkable essay is merited:
The hereditary chorea, as I shall call it, is confined to certain and fortunately a few families, and has been transmitted to them, an heirloom from generations away back in the dim past. It is spoken of by those in whose veins the seeds of the disease are known to exist, with a kind of horror, and not at all alluded to except through dire necessity, when it is mentioned as that disorder. It is attended generally by all the symptoms of common chorea, only in an aggravated degree, hardly ever manifesting itself until adult or middle life, and then coming on gradually but surely, increasing by degrees, and often occupying years in its development, until the hapless sufferer is but a quivering wreck of his former self. There are three marked peculiarities in this disease: 1) Its hereditary nature. 2) A tendency to insanity and suicide. 3) Its manifesting itself as a grave disease only in adult life.
In 1908, the great Johns Hopkins physician William Osler applauded Huntington's paper with a glowing review: In the history of medicine, there are few instances in which a disease has been more accurately, more graphically or more briefly described.
Chronic alcoholism, itself, can cause a host of neurologic and cognition problems and can add much fuel to the fire that is HD. As a result, when Guthrie was beginning to show classic symptoms of HD in the late 1940s, he and his doctors blamed his health issues on booze. Adding to the confusion was that fact that back in the mid-20th century HD was a rare and difficult-to-diagnose disease. Chorea keeps me just as dizzy [as whiskey] and [was] a good bit cheaper.
In 1952, Woody was committed to the Brooklyn State Hospital and his doctors told his wife Marjorie to divorce him and take custody of his children because of Woody's raging paranoia and occasional violent acts against family members. Despite the divorce, she remained close to Woody for the rest of his life and supervised all of his complex health needs. When he was discharged in September of 1952, Woody wrote his friend Pete Seeger that he was suffering from the mental disease my mother had, Huntington's Chorea and that the chorea keeps me just as dizzy as whiskey and was a good bit cheaper. I feel a thousand million times better now that I'm an old dry drunk AA Alcoholic's Anonymous man. By 1965, Guthrie was unable to talk and could only communicate to Marjorie by flailing his arm at flash cards she made saying No and Yes. All too soon, he could not even do that, but appeared to blink his eyes purposefully when Marjorie entered the room.
Woody died at age 55 on Oct. 3, 1967 at the Creedmoor State Hospital in Queens, New York. That same year, Marjorie founded the Committee to Combat Huntington Disease (CCHD), which offered care and information to afflicted families and raised funds for discovering research and medical treatments. For years, she lobbied state legislatures and the U.S. Congress to allocate more money for research on this terrible disease. Only a few months after Marjorie's death, in 1983, scientists discovered the gene that causes HD, known as HTT, on the short arm of chromosome 4. HD caused by the abnormal and multiple (36 or more) repeats of an unstable Cytosine-Adenosine-Guanine sequence in the HTT gene coding for a cytoplasmic protein known as huntingtin. Thanks to his remarkable body of work, the splendid songs and searching prose, Woody Guthrie's legacy remains vibrant and continues to grow. His musical influence inspired numerous songsmiths of our era, including his son, Arlo Guthrie, Bruce Springsteen and, perhaps most famously, Nobel laureate Bob Dylan. Long after he sang his anthems for the everyman, Woody's legacy is also alive in the organization founded in his honor, now called Huntington's Disease Society of America, that continues its important work in this land, and by similar groups around the world
Sources: Wikipedia; PBS.org
October 21, 2019Quiz
Huntington's disease (HD), also known as Huntington's chorea, is an inherited disorder that results in the death of brain 1) ___. HD affects about 4 to 15 in 100,000 people of European descent. It is rare among Japanese, while the occurrence rate in Africa is unknown. The disease affects men and women equally. Complications such as pneumonia, heart disease, and physical injury from falls reduce life expectancy. Suicide is the cause of death in about 9% of cases. Death typically occurs fifteen to twenty years from when the disease was first detected.
The earliest symptoms are often subtle problems with mood or mental abilities. A general lack of coordination and an unsteady gait often follow. As the disease advances, uncoordinated, jerky body movements become more apparent. Physical abilities gradually worsen until coordinated movement becomes difficult and the person is unable to talk. Mental abilities generally decline into dementia. The specific symptoms vary somewhat between people. Symptoms usually begin between 30 and 50 years of age, but can start at any 2) ___. The disease may develop earlier in life in each successive generation. About eight percent of cases start before the age of 20 years and typically present with symptoms more similar to Parkinson's disease. People with HD often underestimate the degree of their problems.
HD is typically inherited, although up to 10% of cases are due to a new mutation. The disease is caused by an autosomal dominant mutation in either of an individual's two copies of a 3) ___ called Huntingtin. This means a child of an affected person typically has a 50% chance of inheriting the disease. The Huntingtin gene provides the genetic information for a protein that is also called huntingtin. Expansion of CAG (cytosine-adenine-guanine) triplet repeats in the gene coding for the Huntingtin protein results in an abnormal protein, which gradually damages cells in the 4) ___, through mechanisms that are not fully understood. Diagnosis is by genetic testing, which can be carried out at any time, regardless of whether or not symptoms are present. This fact raises several ethical debates: the age at which an individual is considered mature enough to choose testing; whether parents have the right to have their children tested; and managing confidentiality and disclosure of test results. There is no cure for 5) ___. Full-time care is required in the later stages of the disease. Treatments can relieve some symptoms and in some improve quality of life. The best evidence for treatment of the movement problems is with tetrabenazine.
The first likely description of the disease was in 1841 by Charles Oscar Waters. The condition was described in further detail in 1872 by the physician George Huntington. The genetic basis was discovered in 1993 by an international collaborative effort led by the Hereditary Disease Foundation. Research and support organizations began forming in the late 1960s to increase public awareness, to provide support for individuals and their families, and to promote research. Current research directions include determining the exact mechanism of the 6) ___, improving animal models to aid with research, testing of medications to treat symptoms or slow the progression of the disease, and studying procedures such as stem cell therapy with the goal of repairing damage caused by the disease. Embryos produced using in vitro 7) ___ may be genetically tested for HD using preimplantation genetic diagnosis (PGD). This technique, where one or two cells are extracted from a typically 4- to 8-cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos affected with HD genes are not implanted, and therefore any offspring will not inherit the disease. Some forms of preimplantation genetic diagnosis - non-disclosure or exclusion testing - allow at-risk people to have HD-free offspring without revealing their own parental genotype, giving no information about whether they themselves are destined to develop HD. In exclusion testing, the embryos' DNA is compared with that of the parents and grandparents to avoid inheritance of the chromosomal region containing the HD gene from the affected grandparent. In non-disclosure testing, only disease-free embryos are replaced in the uterus while the parental genotype and hence parental risk for HD are never disclosed. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the 8) ___, using fetal genetic material acquired through chorionic villus sampling. An amniocentesis can be performed if the pregnancy is further along, within 14-18 weeks. This procedure looks at the amniotic fluid surrounding the baby for indicators of the HD mutation. This, too, can be paired with exclusion testing to avoid disclosure of parental genotype. Prenatal testing can be done when a parent has been diagnosed with HD, when they have had genetic testing showing the expansion of the HTT gene, or when they have a 50% chance of inheriting the disease. The parents can be counseled on their options, which include termination of pregnancy, and on the difficulties of a child with the identified gene. In addition, in at-risk pregnancies due to an affected male partner, non-invasive prenatal diagnosis can be performed by analyzing cell-free fetal DNA in a blood sample taken from the mother (via venipuncture) between six and twelve weeks of pregnancy. It has no procedure-related risk of miscarriage (excepting via needle contamination).
Huntington's disease, particularly the application of the genetic test for the disease, has raised several ethical issues. The issues for genetic 9) ___ include defining how mature an individual should be before being considered eligible for testing, ensuring the confidentiality of results, and whether companies should be allowed to use test results for decisions on employment, life insurance or other financial matters. The development of an accurate diagnostic test for Huntington's disease has caused social, legal, and ethical concerns over access to and use of a person's results. Many guidelines and testing procedures have strict procedures for disclosure and confidentiality to allow individuals to decide when and how to receive their results and also to whom the results are made available. Financial institutions and businesses are faced with the question of whether to use genetic test results when assessing an individual, such as for life 10) ___ or employment.
The death of Woody Guthrie led to the foundation of the Committee to Combat Huntington's Disease. In 1968, after experiencing HD in his wife's family, Dr. Milton Wexler was inspired to start the Hereditary Disease Foundation (HDF), with the aim of curing genetic illnesses by coordinating and supporting research. At roughly the same time as the HDF formed, Marjorie Guthrie helped to found the Committee to Combat Huntington's Disease (now the Huntington's Disease Society of America), after her husband Woody Guthrie died from complications of HD. Sources: Wikipedia; ScienceDaily.com
ANSWERS: 1) cells; 2) age; 3) gene; 4) brain; 5) HD; 6) disease; 7) fertilization; 8) womb; 9) testing; 10) insurance
October 21, 2019What's New
One of the features in ON TARGET this week is Huntington's disease (HD), a rare and devastating disease. Target Health received feedback from FDA on a program in HD and we all look forward to a successful outcome. Target Health is currently very active in the rare and orphan disease space with 2 new orphan disease designations granted by FDA this month. In addition, a meeting was held last week with FDA to discuss a novel approach for a rare disease and another meeting with FDA for a very rare disease will take place next month. A phase 1 study is also underway which will support the phase 2 program in a rare neurological disease.
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. Also visit the Target Health Eating Website to see all of the fantastic recipes since 2012.
Joyce Hays, Founder and Editor in Chief of On Target
Dr. Jules T. Mitchel, Editor
September 23, 2019Target Healthy Eating
Extra virgin olive oil for frying
Handful of fresh garlic cloves, for cooking
1 large eggplant, sliced thin on a mandolin
salt for sprinkling over eggplant
1 pound fresh buffalo or burrata mozzarella (thinly sliced)
basil leaves, rinsed, then dried with paper towels
2 extra large or jumbo eggs, beaten
1/2 cup chickpea flour
Panko Mixture Ingredients
1 teaspoon garlic powder
1 teaspoon turmeric
Zest of 1 lemon
1 cup Panko
1/2 cup freshly grated parmesan
1. Make the Panko mixture now, then set aside. If you have some leftover, save it for another recipe.
2. Slice the eggplant on a mandolin
7. Make circular sandwiches out of 2 slices of eggplant with a slice of mozzarella and a basil leaf in between the eggplant.
My Version Marinara Sauce
Feel free to add or subtract from my recipe, so you have a sauce that's totally to your own taste
1/4 cup extra virgin olive oil (some people swear by butter, but I prefer OO. You decide)
1 onion, finely chopped
3 anchovy fillets ground in mortar & pestle with 3 garlic cloves
12 more fresh garlic cloves, thinly sliced
2 sprigs fresh basil, or several leaves
1 Tablespoon fresh oregano, chopped
1 heaping teaspoon dried oregano
1 pinch black pepper (or more to your taste)
2 pinches chili flakes (or more to your taste)
1 28-ounce can CENTO whole San Marzano tomatoes
1 small can CENTO tomato paste
1. Use a large skillet and add the olive oil, over a medium flame. Add the onion, the anchovy/garlic paste, the rest of the garlic.
2. When garlic gets soft, but NOT BROWN, CENTO tomatoes and paste. Swirl water in both cans to get every last bit of the tomato liquid out of the cans and add to skillet. Crush the tomatoes with a fork or masher, right in the pan.
3. To the skillet, add the chili flakes, black pepper, oregano. Stir.
4. Add the fresh basil and watch it wilt on the surface of the sauce, then stir it into the sauce.
5. Lower your heat to a simmer and cook the sauce until it thickens, which should be about 15 minutes.
6. Turn off heat until ready to serve. Just before serving, with a slotted spoon, remove the basil leaves.
Note: You will probably have some sauce leftover, so save it in the fridge and use it for pasta during the week or as a sauce for meatballs or meatloaf or chicken or fish.
From Our Table to Yours
Have a Great Week Everyone!
September 23, 2019Regulatory
This article is fully compatible with what we observed in the DPharm Disruptive Innovations meeting in Boston last week.
Recent scientific and biomedical advances - from genomic sequencing to development of cell and gene therapies and nanotechnologies - have brought the promise of significant improvements to the health of many millions of Americans. To date, however, most have seen little of this promise in our day-to-day lives because a large and persistent gap separates important scientific advances and the technologies needed to translate those advances into new therapies for patients and new ways to protect the public health. The FDA's FDA's Technology Modernization Action Plan, described in this document, is an important step FDA is taking to address and close this gap. It describes important near-term actions that FDA is taking to modernize use of technology - computer hardware, software, data, and analytics - to advance FDA's public health mission.
TMAP has three elements:
1. modernization of FDA's technical infrastructure;
2. enhancing FDA's capabilities to develop technology products to support its regulatory mission; and
3. communication and collaboration with stakeholders to drive technological progress that is interoperable across the system and delivers value to consumers and patients.
The TMAP provides a sturdy technological foundation for development of FDA's ongoing strategy around data itself - a strategy for the stewardship, security, quality control, analysis, and real-time use of data - that will accelerate the path to better therapeutic and diagnostic options for patients and clinical care providers, and better tools to enhance and promote public health.
September 23, 2019Neurology
Rapid eye movement, or REM, is one of several sleep stages the body cycles through every night. It first occurs about 90 minutes after falling asleep and is characterized by darting eyes, raised heart rates, paralyzed limbs, awakened brain waves and dreaming. For more than a century, scientists have explored the role of sleep in storing memories. While many have shown that sleep helps the brain store new memories, others, including Francis Crick, the co-discoverer of the DNA double helix, have raised the possibility that sleep - in particular REM sleep - may be a time when the brain actively eliminates or forgets excess information. Moreover, recent studies in mice have shown that during sleep - including REM sleep - the brain selectively prunes synaptic connections made between neurons involved in certain types of learning. However, until this study was published, no one had shown how this might happen.
REM sleep is a fascinating period when most of our dreams are made. Now, in a study of mice, it has been shown that it may also be a time when the brain actively forgets. The study results, published in Science (19 September 2019), suggest that forgetting during sleep may be controlled by neurons found deep inside the brain that were previously known for making an appetite stimulating hormone. The authors, have spent years examining the role of a hormone called hypocretin/orexin in controlling sleep and narcolepsy. Narcolepsy is a disorder that makes people feel excessively sleepy during the day and sometimes experience changes reminiscent of REM sleep, like loss of muscle tone in the limbs and hallucinations. The authors and others have helped to show how narcolepsy may be linked to the loss of hypocretin/orexin-making neurons in the hypothalamus, a peanut-sized area found deep inside the brain. For the study, the authors looked at neighboring cells that produce melanin concentrating hormone (MCH), a molecule known to be involved in the control of both sleep and appetite. In agreement with previous studies, the authors found that a majority (52.8%) of hypothalamic MCH cells fired when mice underwent REM sleep whereas about 35% fired only when the mice were awake and about 12% fired at both times. The authors also uncovered clues suggesting that these cells may play a role in learning and memory. Electrical recordings and tracing experiments showed that many of the hypothalamic MCH cells sent inhibitory messages, via long stringy axons, to the hippocampus, the brain's memory center.
To test this idea, the authors used a variety of genetic tools to turn on and off MCH neurons in mice during memory tests. Specifically, the authors examined the role that MCH cells played in retention, the period after learning something new but before the new knowledge is stored, or consolidated, into long term memory. The authors used several memory tests including one that assessed the ability of mice to distinguish between new and familiar objects. Unexpectedly, it was found found that turning on MCH cells during retention worsened memory whereas turning the cells off improved memories. For instance, activating the cells reduced the time mice spent sniffing around new objects compared to familiar ones, but turning the cells off had the opposite effect. Further experiments suggested that MCH neurons exclusively played this role during REM sleep. Mice performed better on memory tests when MCH neurons were turned off during REM sleep. In contrast, turning off the neurons while the mice were awake or in other sleep states had no effect on memory.
According to the authors, the results suggest that MCH neurons help the brain actively forget new, possibly, unimportant information. The authors added that since dreams are thought to primarily occur during REM sleep, the sleep stage when the MCH cells turn on, activation of these cells may prevent the content of a dream from being stored in the hippocampus - consequently, the dream is quickly forgotten.
In the future, the authors plan to explore whether this new circuit plays a role in sleep and memory disorders.