Golden Raisin Tofutti Cake with Grand Marnier


Easy, Quick and Delicious! ©Joyce Hays, Target Health Inc.






7 eggs

7 Tablespoons Splenda

5 Tablespoons Canola oil

4 containers of Tofutti (8 oz each)

3 drops vanilla extract (use the best)

2 teaspoons fresh lemon juice

1-2 teaspoons baking powder

3/4 cup golden raisins

Grand Marnier (optional)




All ingredients in one place ©Joyce Hays, Target Health Inc.





1. Preheat oven to 335 degrees

2. Oil a springform pan

3. In the bowl of an electric mixer, add the Splenda and the eggs and mix well until everything becomes white.




The orange reflection on the beater is me taking the photo ©Joyce Hays, Target Health Inc.


4. Continue mixing with the electric beaters, and add the Canola oil and the vanilla extract until well mixed. Continue beating and add the lemon juice.

5. Make the last ingredient you beat in, the baking powder.

6. Finally, add the golden raisins, but fold them in mixing by hand.

7. Now, with a spatula, pour and scrape the cheese cake mixture into the springform pan and bake for 60 minutes.

8. When done, allow the cake to cool, before you remove from the pan. Finally, before removing, run a knife around the pan just to free up anything sticking to the pan, and unlock the pan, around the cheese cake. Place on a plate and serve, still slightly warm.

9. Splash of Grand Marnier to your taste (optional).


This is the less fattening adaptation of a “cheesecake.“ I did NOT have the nerve to let you see the cholesterol laden version, because it’s packed with such a large amount of cream cheese and butter not to mention sugar, that anyone watching calories and general health, could only have eaten a nano thimble-full, so what’s the point?


We started this dinner with a crunchy endive salad and chilled Sauvignon Blanc from New Zealand (Cloudy Bay). Then, pasta cooked in chicken stock and olive oil was served with a new recipe I’m trying out, of baked halibut with carrot-ginger sauce, topped with toasted maple cashews. Jules gave this new fish recipe 5 stars, so I’ll share it in the future. Finally, for dessert we had the tofutti cake with golden raisins and Grand Marnier. Jules also added some blueberries and strawberries that had been soaked in Grand Marnier.  I just splashed on the Grand Marnier.



Made from a blend of fine French Cognac and wild bitter oranges from the tropics. Its secret recipe was created in 1871 and has been closely guarded ever since.


We saw comedian/writer, (now playwright), Larry David’s new venture on Broadway, called, Fish in the Dark. If you liked Larry David in TV sit-coms, you would love this play. However, if you were expecting more, which we were, you might be let down. On the other hand, Jules and I both liked the ending, a lot. We won’t say more than that, in case you plan to see this show. Wouldn’t want to be spoilers.


Weather in the Big Apple is quite cold, but it’s great weather for sleeping soundly, and now, 5 pm is no longer dark, so Spring must be around the corner.




Cloudy Bay Sauvignon Blanc, an old standby of ours – ©Joyce Hays, Target Health Inc.



From Our Table to Yours!


Bon Appetit!


February 18, 2015


National Institute of Environmental Health Sciences (NIEHS)


Much like mapping the human genome laid the foundations for understanding the genetic basis of human health, new maps of the human epigenome may further unravel the complex links between DNA and disease. The epigenome is part of the machinery that helps direct how genes are turned off and on in different types of cells.



An epigenomic signature can be made on the genome in two ways, both of which play a role in turning genes off or on. The first occurs when chemical tags called methyl groups are attached to a DNA molecule directly (DNA methylation). The second occurs when a variety of chemical tags attach to the tails of histone proteins that package DNA (histone modifications).
Credit: Image courtesy of John Stamatoyannopoulos and Rae Senarighi



Much like mapping the human genome laid the foundations for understanding the genetic basis of human health, new maps of the human epigenome may further unravel the complex links between DNA and disease. The epigenome is part of the machinery that helps direct how genes are turned off and on in different types of cells.

Researchers supported by the National Institutes of Health Common Fund’s Roadmap Epigenomics Program have mapped the epigenomes of more than 100 types of cells and tissues, providing new insight into which parts of the genome are used to make a particular type of cell. The data, available to the biomedical research community, can be found at the National Center for Biotechnology Information website.

“This represents a major advance in the ongoing effort to understand how the 3 billion letters of an individual’s DNA instruction book are able to instruct vastly different molecular activities, depending on the cellular context,” said NIH Director Francis Collins, M.D., Ph.D. “This outpouring of data-rich publications, produced by a remarkable team of creative scientists, provides powerful momentum for the rapidly growing field of epigenomics.”

Researchers from the NIH Common Fund’s Roadmap Epigenomics Program published a description of the epigenome maps in the journal Nature. More than 20 additional papers, published in Nature and Nature-associated journals, show how these maps can be used to study human biology.

“What the Roadmap Epigenomics Program has delivered is a way to look at the human genome in its living, breathing nature from cell type to cell type,” said Manolis Kellis, Ph.D., professor of computer science at the Massachusetts Institute of Technology, Cambridge, and senior author of the paper.

Understanding epigenomics

Almost all human cells have identical genomes that contain instructions on how to make the many different cells and tissues in the body. During the development of different types of cells, regulatory proteins turn genes on and off and, in doing so, establish a layer of chemical signatures that make up the epigenome of each cell. In the Roadmap Epigenomics Program, researchers compared these epigenomic signatures and established their differences across a variety of cell types. The resulting information can help us understand how changes to the genome and epigenome can lead to conditions such as Alzheimer’s disease, cancer, asthma, and fetal growth abnormalities.

The value of epigenomic data

Researchers can now take data from different cell types and directly compare them. “Today, sequencing the human genome can be done rapidly and cheaply, but interpreting the genome remains a challenge,” said Bing Ren, Ph.D., professor of cellular and molecular medicine at the University of California, San Diego, and co-author of the Nature paper and several of the associated papers. “These 111 reference epigenome maps are essentially a vocabulary book that helps us decipher each DNA segment in distinct cell and tissue types. These maps are like snapshots of the human genome in action.”

“This is the most comprehensive catalog of epigenomic data from primary human cells and tissues to date,” said Lisa Helbling Chadwick, Ph.D., project team leader and a program director at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. “This coordinated effort, along with uniform data processing, makes it much easier for researchers to make direct comparisons across the entire data set.”

“Researchers from the 88 projects supported by the program, including those from this recent series of papers, have propelled the development of new epigenomic technologies,” said John Satterlee, Ph.D., co-coordinator of the Roadmap Epigenomics Program, and program director at the National Institute on Drug Abuse (NIDA), part of NIH. Satterlee added that the work of this program has served as a foundation for continued exploration of the human epigenome through the International Human Epigenome Consortium.

“With this increased understanding of the full epigenome, and the datasets available to the entire scientific community, the NIH Common Fund is striving to catalyze future research, to aid the understanding of how epigenomics plays a role in human diseases, with the expectation that further studies will identify early indications of disease and targets for therapeutics,” said James Anderson, M.D., Ph.D., director of NIH Division of Program Coordination, Planning, and Strategic Initiatives that oversees the NIH Common Fund.

NIDA, NIEHS, and the National Institute on Deafness and Other Communication Disorders are co-administrators of the NIH Common Fund’s Epigenomics Program.

Story Source:

The above story is based on materials provided by National Institute of Environmental Health Sciences (NIEHS). Note: Materials may be edited for content and length.

Journal Reference:

  1. Roadmap Epigenomics Consortium et al. Integrative analysis of 111 reference human epigenomes. Nature, 2015; 518 (7539): 317 DOI: 10.1038/nature14248



National Institute of Environmental Health Sciences (NIEHS). “Epigenome of more than 100 tissue and cell types mapped.” ScienceDaily. ScienceDaily, 18 February 2015. <>.

February 18, 2015


University of California – San Diego


Mutations that cause autism in children are connected to a pathway that regulates brain development, scientists have found. The researchers studied a set of well-known autism mutations called copy number variants or CNVs. They investigated when and where the genes were expressed during brain development.



Autism mutations may influence brain size through RhoA pathway during fetal brain development.
Credit: UC San Diego School of Medicine



Scientists at the University of California, San Diego School of Medicine have found that mutations that cause autism in children are connected to a pathway that regulates brain development. The research, led by Lilia Iakoucheva, PhD, assistant professor in the Department of Psychiatry, is published in the February 18 issue of Neuron.

The researchers studied a set of well-known autism mutations called copy number variants or CNVs. They investigated when and where the genes were expressed during brain development. “One surprising thing that we immediately observed was that different CNVs seemed to be turned on in different developmental periods,” said Iakoucheva.

Specifically, the scientists noted that one CNV located in a region of the genome known as 16p11.2, contained genes active during the late mid-fetal period. Ultimately, they identified a network of genes that showed a similar pattern of activation including KCTD13 within 16p11.2 and CUL3, a gene from a different chromosome that is also mutated in children with autism.

“The most exciting moment for us was when we realized that the proteins encoded by these genes form a complex that regulates the levels of a third protein, RhoA,” said Iakoucheva. Rho proteins play critical roles in neuronal migration and brain morphogenesis at early stages of brain development. “Suddenly, everything came together and made sense.”

Further experiments confirmed that CUL3 mutations disrupt interaction with KCTD13, suggesting that 16p11.2 CNV and CUL3 may act via the same RhoA pathway. RhoA levels influence head and body size in zebrafish, a model organism used by geneticists to investigate gene functions. Children with 16p11.2 CNV also have enlarged or decreased head sizes and suffer from obesity or are underweight. “Our model fits perfectly with what we observe in the patients,” said Guan Ning Lin, PhD, a fellow in Iakoucheva’s laboratory and co-first author with Roser Corominas, PhD.

Interestingly, the RhoA pathway has recently been implicated in a rare form of autism called Timothy syndrome, which is caused by the mutation in a completely different gene. “The fact that three different types of mutations may act via the same pathway is remarkable,” said Iakoucheva. “My hope is that we would be able to target it therapeutically.”

Iakoucheva and colleagues are planning to test RhoA pathway inhibitors using a stem cell model of autism. “If we can discover the precise mechanism and develop targeted treatments for a handful of children, or even for a single child with autism, I would be happy,” she said.

Story Source:

The above story is based on materials provided by University of California – San Diego. Note: Materials may be edited for content and length.

Journal Reference:

  1. Guan Ning Lin, Roser Corominas, Irma Lemmens, Xinping Yang, Jan Tavernier, David E. Hill, Marc Vidal, Jonathan Sebat, Lilia M. Iakoucheva. Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases.Neuron, 2015; 85 (4): 742 DOI: 10.1016/j.neuron.2015.01.010


University of California – San Diego. “Autism genes activate during fetal brain development.” ScienceDaily. ScienceDaily, 18 February 2015. <>.

February 17, 2015


Asociación RUVID


Bacteria may be able to jump between host species far easier than was previously thought, a new study suggests. Researchers discovered that a single genetic mutation in a strain of bacteria infectious to humans enables it jump species to also become infectious to rabbits. The discovery has major implications for how we assess the risk of bacterial diseases that can pass between humans and animals. It is well known that relatively few mutations are required to support the transmission of viruses — such as influenza — from one species to another. Until now it was thought that the process was likely to be far more complicated for bacteria.



This is the research team.
Credit: Image courtesy of Asociación RUVID



A new study suggests that bacteria may be able to jump between host species far easier than was previously thought. Researchers discovered that a single genetic mutation in a strain of bacteria infectious to humans enables it jump species to also become infectious to rabbits. The discovery has major implications for how we assess the risk of bacterial diseases that can pass between humans and animals. It is well known that relatively few mutations are required to support the transmission of viruses — such as influenza — from one species to another. Until now it was thought that the process was likely to be far more complicated for bacteria.

Scientists at the universities of CEU Cardenal Herrera (Spain) and Glasgow and Edinburgh (UK) studied a strain of bacteria called Staphylococcus aureusST121, which is responsible for widespread epidemics of disease in the global rabbit farming industry. The team looked at the genetic make-up of ST121 to work out where the strain originated and the changes that occurred that enabled it to infect rabbits. They found that ST121 most likely evolved through a host jump from humans to rabbits around 40 years ago with a genetic mutation at a single site in the bacterial DNA code the cause for this.

The discovery transforms our understanding of the minimal genetic changes that are required for bacteria to infect different species. ST121 is found in the respiratory tract and on the skin of some people. While it is usually harmless, the bacteria can cause a variety of conditions from minor skin infections to meningitis and sepsis. In rabbits, the bacteria can cause serious skin infections.

Professors David Viana, of CEU-UCH Veterinary Faculty, and Jose Penades, of theInstitute of Infection, Immunity and Inflammation at the University of Glasgow, who co-led the study, said: “The ability for pathogens to switch host-species and lead to an epidemic in a new host population is of major concern to veterinary and public health professionals. Our results represent a paradigm shift in understanding of the minimal adaptions required for a bacterium to overcome species barriers and establish in new host populations.”

Professor Ross Fitzgerald, from the University of Edinburgh’s Roslin Institute, who co-led the study, said: “Domestication of animals, industrialisation of agriculture and globalisation have provided new opportunities for the transmission of bacteria between humans and animals. This latest research has important public and veterinary health implications which will require a re-examination of the future threat posed by bacterial host switching events.”

Story Source:

The above story is based on materials provided by Asociación RUVID. Note: Materials may be edited for content and length.

Journal Reference:

  1. David Viana, María Comos, Paul R McAdam, Melissa J Ward, Laura Selva, Caitriona M Guinane, Beatriz M González-Muñoz, Anne Tristan, Simon J Foster, J Ross Fitzgerald, José R Penadés. A single natural nucleotide mutation alters bacterial pathogen host tropism. Nature Genetics, 2015; DOI: 10.1038/ng.3219


Asociación RUVID. “Bacteria jump between species more easily than previously thought.” ScienceDaily. ScienceDaily, 17 February 2015. <>.

February 16, 2015


Baylor University


Using a relatively new scientific dating technique, geologists were able to document — for the first time — a drastic climate change 4,200 years ago in northern China that affected vegetation and led to mass migration from the area.



China’s Hunshandake Sandy Lands.
Credit: Courtesy of Steve Forman



Using a relatively new scientific dating technique, a Baylor University geologist and a team of international researchers were able to document — for the first time — a drastic climate change 4,200 years ago in northern China that affected vegetation and led to mass migration from the area.

Steve Forman, Ph.D., professor of geology in the College of Arts & Sciences, and researchers — using a dating technique called Optically Stimulated Luminescence — uncovered the first evidence of a severe decrease in precipitation on the freshwater lake system in China’s Hunshandake Sandy Lands. The impact of this extreme climate change led to desertification — or drying of the region — and the mass migration of northern China’s Neolithic cultures.

Their research findings appeared in a recent issue of the Proceedings of the National Academy of Sciences.

“With our unique scientific capabilities, we are able to assert with confidence that a quick change in climate drastically changed precipitation in this area, although, further study needs to be conducted to understand why this change occurred,” Forman said.

Between 2001 and 2014, the researchers investigated sediment sections throughout the Hunshandake and were able to determine that a sudden and irreversible shift in the monsoon system led to the abrupt drying of the Hunshandake resulting in complications for the population.

“This disruption of the water flow significantly impacted human activities in the region and limited water availability. The consequences of a rapid climatic shift on the Hunshandake herding and agricultural cultures were likely catastrophic,” Forman said.

He said these climatic changes and drying of the Hunshandake continue to adversely impact the current population today. The Hunshandake remains arid and even with massive rehabilitation efforts will unlikely regrow dense vegetation.

“This study has far-reaching implications for understanding how populations respond and adapt to drastic climate change,” Forman said.

Forman is the director of the Geoluminescence Dating Research Lab in the department of geology.

Story Source:

The above story is based on materials provided by Baylor University. Note: Materials may be edited for content and length.

Journal Reference:

  1. Xiaoping Yang, Louis A. Scuderi, Xulong Wang, Louis J. Scuderi, Deguo Zhang, Hongwei Li, Steven Forman, Qinghai Xu, Ruichang Wang, Weiwen Huang, Shixia Yang. Groundwater sapping as the cause of irreversible desertification of Hunshandake Sandy Lands, Inner Mongolia, northern China. Proceedings of the National Academy of Sciences, 2015; 112 (3): 702 DOI:10.1073/pnas.1418090112


Baylor University. “First-ever evidence of drastic climate change of Northern China region 4,200 years ago.” ScienceDaily. ScienceDaily, 16 February 2015. <>.

Clinical Trials Transformation Initiative (CTTI)

The Clinical Trials Transformation Initiative (CTTI) is a public-private partnership to identify and promote practices that will increase the quality and efficiency of clinical trials. CTTI now comprises more than 60 organizations from across the clinical trial enterprise. Members include representatives of government agencies (the FDA, Centers for Medicare and Medicaid Services, Office of Human Research Protections, National Institutes of Health, and other national and international governmental bodies), industry representatives (pharmaceutical, biotech, device, and clinical research organizations), patient advocacy groups, professional societies, investigator groups, academic institutions, and other interested parties.


Target Health Inc. became a member of CTTI after our friend and colleague, Duke University Professor, Dr. Judith Kramer said Target Health would “be an extremely valuable participant at the table.“ Now, 7 years later, we’re honored that Dr. Jules T. Mitchel, has been re-elected Steering Committee (SC) liaison to the Executive Committee (EC).


Twilight Casts Puple Glow Over Manhattan – View From the 24th Floor Offices of Target Health Inc.



Evening Clouds From the 24th Floor Offices of Target Health, 2015 ©Target Health Inc.


ON TARGET is the newsletter of Target Health Inc., a NYC-based, full-service, contract research organization (eCRO), providing strategic planning, regulatory affairs, clinical research, data management, biostatistics, medical writing and software services to the pharmaceutical and device industries, including the paperless clinical trial.


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 104). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website.


Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor



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A mask, painted by a Marine who attends art therapy to relieve post-traumatic stress disorder symptoms, is displayed at an art expo May 3, 2012. The expo provided a way to raise awareness about PTSD and the benefits of art therapy. During therapy sessions, participants use a variety of art supplies, including paints, clay, markers, charcoal and images for collages, to express their thoughts, feelings and memories. (Official U.S. Marine Corps photo by Cpl. Andrew Johnston)


Part of the Chris Kyle narrative, (American Sniper) as presented in the recent Clint Eastwood movie, is the story of Kyle’s death, not in the Middle East, but tragically, right here in the U.S. where he was shot and killed by another war vet apparently suffering from a PTSD psychotic episode . . . a double tragedy of war. As one of the Middle East war vets advising on this movie said, this week, “There’s real evil in this world and someone has to deal with it.“


PTSD described by Shakespeare before1597 (Henry IV, Part 1):


“Tell me, sweet lord, what is’t that takes from thee 

Thy stomach, pleasure and thy golden sleep?

Why dost thou bend thine eyes upon the earth, 

And start so often when thou sit’st alone? 

Why hast thou lost the fresh blood in thy cheeks; 

And given my treasures and my rights of thee 

To thick-eyed musing and cursed melancholy?

In thy faint slumbers I by thee have watch’d, 

And heard thee murmur tales of iron wars; 

Speak terms of manage to thy bounding steed; 

Cry ‘Courage! to the field!’ And thou hast talk’d 

Of sallies and retires, of trenches, tents,

Of palisadoes, frontiers, parapets, 

Of basilisks, of cannon, culverin, 

Of prisoners’ ransom and of soldiers slain, 

And all the currents of a heady fight. 

Thy spirit within thee hath been so at war

And thus hath so bestirr’d thee in thy sleep, 

That beads of sweat have stood upon thy brow 

Like bubbles in a late-disturbed stream;

And in thy face strange motions have appear’d, 

Such as we see when men restrain their breath

On some great sudden hest. O, what portents are these? 

Some heavy business hath my lord in hand,

And I must know it, else he loves me not.




Regions of the brain associated with stress and posttraumatic stress disorder


Post traumatic stress disorder (PTSD) may develop after a person is exposed to one or more traumatic events, such as an assault, warfare, serious injury, or threats of imminent 1) ___. The diagnosis may be given when a group of symptoms, such as disturbing recurring flashbacks, avoidance or numbing of memories of the event, and hyperarousal, continue for more than a month after the occurrence of a traumatic event. Most people having experienced a traumatizing event will not develop PTSD. People who experience assault-based trauma are more likely to develop PTSD, as opposed to people who experience non-assault based trauma such as witnessing trauma, accidents, and fire events. War veterans are commonly at risk for PTSD.


Post-traumatic stress 2) ___ is classified as an anxiety disorder in the DSM IV; the characteristic symptoms are not present before exposure to the violently traumatic event. In the typical case, the individual with PTSD persistently avoids all thoughts and emotions, and discussion of the stressor event and may experience amnesia for it. However, the event is commonly relived by the individual through intrusive, recurrent recollections, flashbacks, and nightmares. The characteristic symptoms are considered acute if lasting less than three months, and chronic if persisting three months or more, and with delayed onset if the symptoms first occur after six months or some years later. PTSD is distinct from the briefer acute stress disorder, and can cause clinical impairment in significant areas of functioning.


Persons considered at risk include, for example, combat military personnel, victims of natural disasters, concentration camp survivors, and victims of violent crime. Individuals frequently experience “survivor’s guilt“ for remaining alive while others died. Causes of the symptoms of PTSD are the experiencing or witnessing of a stressor event involving death, serious injury or such threat to the self or others in a situation in which the individual felt intense fear, horror, or powerlessness. Persons employed in occupations that expose them to violence (such as soldiers) or disasters (such as emergency service workers) are also at 3) ___.  Children or adults may develop PTSD symptoms by experiencing bullying.


Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and a smaller hippocampal volume have been identified as biomarkers for the risk of developing PTSD. Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing 4) ___. There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twin’s having PTSD compared to twins that were 5) ___ (non-identical twins). There is evidence that those with a genetically smaller hippocampus are more likely to develop PTSD following a traumatic event. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities. Studies have demonstrated a relationship between intrusive thoughts and intentional control responses such that suppression increases the frequency of unwanted intrusive thoughts. These results suggest that 6) ___ of intrusive thoughts may be important in the development and maintenance of PTSD. The physical trauma soldiers may face when serving in combat increases the risk of developing PTSD. Protective effects include social support and social support also helps with recovery if it develops. Early intervention appears to be a critical preventive measure


PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the 7) ___. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations. During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD. Low cortisol levels may predispose individuals to PTSD: Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol, experience a poorly contained – that is, longer and more distressing – response, setting the stage for PTSD. Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity. Serotonin also contributes to the stabilization of glucocorticoid production. Dopamine levels in patients with PTSD can help contribute to the symptoms associated. Low levels of dopamine can contribute to anhedonia, apathy, impaired attention, and motor deficits. Increased levels of dopamine can cause psychosis, agitation, and restlessness. Hyper responsiveness in the norepinephrine system can be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with PTSD. A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing, so that the experience, and emotions the person is experiencing during a 8) ___ are not associated with the current environment.


However, there is considerable controversy within the medical community regarding the neurobiology of PTSD. A review of existing studies on this subject showed no clear relationship between cortisol levels and PTSD. However, the majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone. In human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuro-imaging studies in humans have revealed both morphological and functional aspects of PTSD. However, during high stress times the hippocampus, which is associated with the ability to place memories in the correct context of space and time, and with the ability to recall the memory, is suppressed. This suppression is hypothesized to be the cause of the flashbacks that often plague PTSD patients. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the actual terrifying event was never properly recorded in the patients 9) ___. The amygdalo-centric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus in particular during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition. The maintenance of the fear involved with PTSD has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. The HPA axis that coordinates the hormonal response to stress, which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma. This over-consolidation increases the likelihood of one’s developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a 10) ___.


The beta blocker, propranolol, is currently being investigated as a potential treatment for post-traumatic stress disorder. Propranolol works to inhibit the actions of norepinephrine (noradrenaline), a neurotransmitter that enhances memory consolidation. Individuals given propranolol immediately after a traumatic experience show less severe symptoms of PTSD compared to their respective control groups who did not receive the drug. Propranolol reduces the effects of nightmare-related cardiac activity by keeping sinus rhythm low during nightmares, as a higher pulse and increased adrenaline are associated with severe nightmares. However, results remain inconclusive as to the success of propranolol in treatment of PTSD, including nightmares experienced by those with PTSD.


The United States Department of Veterans Affairs has diagnosed >200,000 American veterans with PTSD since 2001. A March 2011 Congressional report estimated spending related to the terror wars, through fiscal year 2011 at $1.2 trillion, and that spending through 2021 assuming a reduction to 45,000 troops would be $1.8 trillion. A June 2011 academic report covering additional areas of spending related to the terror wars, estimated it through 2011 at $2.7 trillion, and long term spending at $5.4 trillion including interest. In 2014 The United States military announced plans to treat and monitor psychiatric disorders including Post Traumatic Stress Disorder (PTSD) with high-tech devices implanted into patients’ brains. The five-year, $70 million program was launched by Defense Advanced Research Projects Agency (DARPA). The program aims to help military personnel suffering from psychiatric disorders such as PTSD, depression, and anxiety. DARPA announced it would take advantage of President Obama’s initiative to explore the human brain. The program’s funding will develop the electronic devices in order to monitor and electrically stimulate specific brain circuits. Simple versions of the future brain implants are already being used to help patients with Parkinson’s. The team, led by researchers at the University of California San Francisco in conjunction with Massachusetts General Hospital, and the United States Veterans Administration, plan to begin with volunteers who already have probes in their brains because of Parkinson’s or epilepsy. The UCSF team expects to receive $26 million to fund their research and MGH researchers are expected to get $30 million to fund their part of the project. Researchers say that because many epileptic patients and people with Parkinson’s Disease also suffer from the psychiatric disorders they are hoping to treat, these patients will help them understand how specific brain circuitry works in these disorders in real time.


According to the Department of Veteran Affairs, 11 to 20% of veterans who served in the Iraq and Afghanistan operations (Operations Iraqi and Enduring Freedom) are believed to suffer from PTSD and 30% of Vietnam veterans are believed to have suffered from or are still being treated for symptoms of PTSD. DARPA hopes that the research involving the brain implants will significantly improve our understanding of mental disorders like anxiety and PTSD.


“When will they ever learn,

When will they ever learn.“

                          Pete Seeger


ANSWERS: 1) death; 2) disorder; 3) risk; 4) trauma; 5) dizygotic; 6) suppression; 7) brain; 8) flashback; 9) memory; 10) threat




Department of Veterans Affairs (VA)


Flag of the Department of Veterans Affairs


The United States has the most comprehensive system of assistance for Veterans of any nation in the world, with roots that can be traced back to 1636, when the Pilgrims of Plymouth Colony were at war with the Pequot Indians. The Pilgrims passed a law that stated that disabled soldiers would be supported by the colony. Later, the Continental Congress of 1776 encouraged enlistments during the Revolutionary War, providing pensions to disabled soldiers. In the early days of the Republic, individual states and communities provided direct medical and hospital care to Veterans. In 1811, the federal government authorized the first domiciliary and medical facility for Veterans. Also in the 19th century, the nation’s Veterans assistance program was expanded to include benefits and pensions not only for Veterans, but for their widows and dependents. Following the Civil War, many state Veterans homes were established. Since domiciliary care was available at all state Veterans homes, incidental medical and hospital treatment was provided for all injuries and diseases, whether or not of service origin. Indigent and disabled Veterans of the Civil War, Indian Wars, Spanish-American War, and Mexican Border period, as well as the discharged regular members of the Armed Forces, received care at these homes. As the U.S. entered World War I in 1917, Congress established a new system of Veterans benefits, including programs for disability compensation, insurance for service personnel and Veterans, and vocational rehabilitation for the disabled. By the 1920s, three different federal agencies administered the various benefits: the Veterans Bureau, the Bureau of Pensions of the Interior Department, and the National Home for Disabled Volunteer Soldiers.


The first consolidation of federal Veterans programs took place August 9, 1921, when Congress combined all World War I Veterans programs to create the Veterans Bureau. Public Health Service Veterans’ hospitals were transferred to the bureau, and an ambitious hospital construction program for World War I Veterans commenced. World War I was the first fully mechanized war, and as a result, soldiers who were exposed to mustard gas, other chemicals and fumes required specialized care after the war. Tuberculosis and neuro-psychiatric hospitals opened to accommodate Veterans with respiratory or mental health problems. A majority of existing VA hospitals and medical centers began as National Home, Public Health Service, or Veterans Bureau hospitals. In 1924, Veterans benefits were liberalized to cover disabilities that were not service-related. In 1928, admission to the National Homes was extended to women, National Guard and militia Veterans.


The second consolidation of federal Veterans programs took place July 21, 1930, when President Herbert Hoover signed Executive Order 5398 and elevated the Veterans Bureau to a federal administration – creating the Veterans Administration – to “consolidate and coordinate Government activities affecting war veterans.“ At that time, the National Homes and Pension Bureau also joined the VA. The three component agencies became bureaus within the Veterans Administration. Brig. Gen. Frank T. Hines, who had directed the Veterans Bureau for seven years, was named the first Administrator of Veterans Affairs, a job he held until 1945. Dr. Charles Griffith, VA’s second Medical Director, came from the Public Health Service and Veterans Bureau. Both he and Hines were the longest serving executives in VA’s history.


Following World War II, there was a vast increase in the Veteran population, and Congress enacted large numbers of new benefits for war Veterans – the most significant of which was the World War II GI Bill, signed into law June 22, 1944. It is said the GI Bill had more impact on the American way of life than any law since the Homestead Act of 1862.



President Roosevelt signs the GI Bill


The GI Bill placed VA second to the War and Navy Departments in funding and personnel priorities. Modernizing the VA for a new generation of Veterans was crucial, and replacement of the “Old Guard“ World War I leadership became a necessity.


Veterans Benefits Administration (VBA)

The VA Home Loan Guaranty Program is the only provision of the original GI Bill that is still in force. Between the end of World War II and 1966, one-fifth of all single-family residences built were financed by the GI Bill for either World War II or Korean War Veterans. From 1944 through December 1993, VA guaranteed 13.9 million home loans valued at more than $433.1 billion. Eligible loan guaranty users are now able to negotiate loan terms, including the interest rate, which helps VA loan participants to compete better in the housing market. The loan guaranty program no longer has a terminating date and can be used by any Veteran who served after Sept. 16, 1940, as well as men and women on active duty, surviving spouses and reservists.


To assist the Veteran between discharge and reemployment, the 1944 GI Bill also provided unemployment benefits of $20 per week, for a maximum of 52 weeks. It was a lesser amount than the unemployment benefits available to non-veterans. This assistance avoided a repetition of the World War I demobilization, when unemployed Veterans were reduced to relying on charities for food and shelter.

Critics dubbed the benefit the “52-20 Club“ and predicted most Veterans would avoid jobs for the 52 weeks that the checks were available. But only a portion of Veterans were paid the maximum amount available. Less than one-fifth of the potential benefits were claimed, and only one out of 19 Veterans exhausted the full 52 weeks of checks.


In 1945, General Omar Bradley took the reins at VA and steered its transformation into a modern organization. In 1946, Public Law 293 established the Department of Medicine and Surgery within VA, along with numerous other programs like the VA Voluntary Service. The law enabled VA to recruit and retain top medical personnel by modifying the civil service system. When Bradley left in 1948, there were 125 VA hospitals. The VA was elevated to a cabinet-level executive department by President Ronald Reagan in October 1988. The change took effect March 15, 1989, and administrative changes occurred at all levels. President George H. W. Bush hailed the creation of the new Department, saying, “There is only one place for the Veterans of America, in the Cabinet Room, at the table with the President of the United States of America.“ The Veterans Administration was then renamed the Department of Veterans Affairs, and continued to be known as VA.




VA Medical Center in Manhattan, New York City


VA’s Department of Medicine and Surgery, established in 1946, was re-designated as the Veterans Health Services and Research Administration at that time, though on May 7, 1991, the name was changed to the Veterans Health Administration (VHA).


Veterans Health Administration (VHA)

VHA evolved from the first federal soldiers’ facility established for Civil War Veterans of the Union Army. On March 3, 1865 – a month before the Civil War ended and the day before his second inauguration – President Abraham Lincoln signed a law to establish a national soldiers and sailors asylum. Renamed as the National Home for Disabled Volunteer Soldiers in 1873, it was the first-ever government institution created specifically for honorably discharged volunteer soldiers. The first national home opened November 1, 1866, near Augusta, Maine. The national homes were often called “soldiers’ homes“ or “military homes,“ and only soldiers who fought for the Union Army – including U.S. African American Troops – were eligible for admittance. These sprawling campuses became the template for succeeding generations of federal Veterans’ hospitals. By 1929, the federal system of national homes had grown to 11 institutions that spanned the country and accepted Veterans of all American wars.


But it was World War I that brought about the establishment of the second largest system of Veterans’ hospitals. In 1918, Congress tasked two Treasury agencies — the Bureau of War Risk Insurance and Public Health Service –with operating hospitals specifically for returning World War I Veterans. They leased hundreds of private hospitals and hotels for the rush of returning injured war Veterans and began a program of building new hospitals.


Today’s VHA–the largest of the three administrations that comprise VA–continues to meet Veterans’ changing medical, surgical and quality-of-life needs. New programs provide treatment for traumatic brain injuries, post-traumatic stress, suicide prevention, women Veterans and more. VA has opened outpatient clinics, and established telemedicine and other services to accommodate a diverse Veteran population, and continues to cultivate ongoing medical research and innovation to improve the lives of America’s patriots. VHA operates one of the largest health care systems in the world and provides training for a majority of America’s medical, nursing and allied health professionals. Roughly 60 percent of all medical residents obtain a portion of their training at VA hospitals; and VA medical research programs benefit society at-large. The VA health care system has grown from 54 hospitals in 1930, to include 152 hospitals, 800 community-based outpatient clinics, 126 nursing home care units and 35 domiciliaries. The VA manages specialized hospitals like major burn centers, in San Antonio, Texas, and major trauma, wound care and rehab centers like Walter Reed Hospital


National Cemetery Administration (NCA)

On July 17, 1862, Congress enacted legislation that authorized the president to purchase “cemetery grounds“ to be used as national cemeteries “for soldiers who shall have died in the service of the country.“ That first year, 14 cemeteries were established, including one in the sleepy Maryland town of Sharpsburg, where 4,476 Union soldiers were laid to rest following the bloody Battle of Antietam. By 1870, the remains of nearly 300,000 Union dead from the Civil War had been buried in 73 national cemeteries. Most of the cemeteries were located in the Southeast, near the battlefields and campgrounds of the Civil War. After the war, Army crews scoured the countryside to locate the remains of soldiers who had died in battle. They were buried with honor in the new national cemeteries. However, the identities are unknown for nearly half of those who died in service to the Union and are buried in national cemeteries. The national cemetery system has evolved slowly since the initial period of great challenge associated with the Civil War. All honorably discharged Veterans became eligible for burial in 1873.




Grave marker for Private Dennis O’Leary, Santa Fe National Cemetery. Courtesy of the Department of Veterans Affairs, National Cemetery Administration, History Program.


In the 1930s, new national cemeteries were established to serve Veterans living in major metropolitan areas such as New York, Baltimore, Minneapolis, San Diego, San Francisco and San Antonio. Several of them, closely associated with battlefields such as Gettysburg, were transferred to the National Park Service because of the value of their use in interpreting the historical significance of the battles. In 1973, Public Law 93-43 authorized the transfer of 82 national cemeteries from the Department of the Army to the Veterans Administration, now the Department of Veterans Affairs. Joining with 21 VA Veterans cemeteries located at hospitals and nursing homes, the National Cemetery System comprised 103 cemeteries after the transfer. On November 11, 1998, the President signed the Veterans Programs Enhancement Act of 1998, changing the name of the National Cemetery System to the National Cemetery Administration (NCA). Today, there are 147 national cemeteries in all, with new cemeteries in development. Through NCA, VA administers 131 of them. Two national cemeteries – Arlington and the United States Soldiers’ and Airmen’s Home National Cemetery – are still maintained by the Department of the Army. Fourteen national cemeteries are maintained by the Department of the Interior. More than 3.7 million people, including Veterans of every war and conflict – from the Revolutionary War to the wars in Iraq and Afghanistan – are honored by burial in VA’s national cemeteries. Today there are more than 22 million living Veterans who have earned the honor of burial in a national cemetery, including the more than 350 Medal of Honor recipients buried in VA’s national cemeteries. More than 19,000 acres of land are devoted to the memorialization of those who served this nation.


Walter Reed National Military Medical Center


Walter Reed National Military Medical Center serves more than 150,000 active and retired personnel from all branches of the military, admitting 16,000 patients a year. As a provider of tertiary (specialized) care and a referral center for the North Atlantic Regional Medical Command, Walter Reed offers a broad range of clinical, educational, and research opportunities. For instance, on an average day, over 6,000 radiographic, MRI and CAT procedures are performed, and over 4,000 meals are served.

The 345-bed medical center has a full range of intensive and specialty and subspecialty medical services, including specialized facilities for military personnel. It’s the U.S. military’s premier hospital for casualty and beneficiary care, it provides postgraduate education and other training, and serves as a critical medical research center. The present day center opened May 1, 1909, and was named in honor of Maj. Walter Reed, best known for his etiology and epidemiology research. From its onset, the center focused on integrated patient care, teaching and research. Before WWI the hospital’s capacity was 80 patient beds. But during the war it grew to 2,500 in a matter of months. Through World War II, Korea, and Vietnam the facility treated hundreds of thousands of Soldiers. Today, surgical teams at WRAMC perform approximately 700 operations in 16 operating rooms annually. These operations range from open-heart surgeries to organ transplants. The hospital has a support staff of more than 600 staff physicians, 535 military and civilian registered nurses, more than 600 licensed professional nurses and other paraprofessionals in its department of nursing. As a leader in clinical research, WRAMC generates the largest number of ongoing clinical research studies within the Department of Defense and is often referred to as the flagship of DoD clinical research. The Walter Reed Army Institute of Research is the largest and most diverse biomedical research laboratory in DoD. Its resources include a laboratory in Maryland, a specialized detachment in Texas and Illinois, plus laboratory and clinical facilities in Asia, Africa and Europe. Also located on the campus is the internationally known Armed Forces Institute of Pathology. Today this tri-service organization employs more than 800 people, including 250 pathologists, to help diagnose unusual or difficult cases.




Iron Supplementation After Blood Donation Shortens Hemoglobin Recovery Time


Blood donors are allowed to give one pint of blood every eight weeks. A major concern is that about 25-35% of regular donors develop iron deficiency. Since iron is needed for red blood cell production, low iron can cause fatigue and anemia — a condition in which the blood has a lower than normal number of red blood cells — and can lead to temporary ineligibility for future donations. It can take months to recover the lost iron. According to a study published online in the Journal of the American Medical Association (10 February 2015), found that iron supplementation significantly reduced the time to recovery of post-donation lost iron and hemoglobin. Hemoglobin is an iron-rich protein that carries oxygen in red blood cells throughout the body.


The goal of this randomized study was to determine the effect of oral iron supplementation on hemoglobin recovery time (days to recovery of 80% of hemoglobin removed) and recovery of iron stores in iron-depleted (“low ferritin,“ <26 ng/mL) and iron-replete (“higher ferritin,“ >26 ng/mL) blood donors. The trial ran from April 2012 to December 2012 at four blood centers in the United States and included 215 blood donors aged 18 and older. The study was conducted by the NHLBI-supported Recipient Epidemiology and Donor Evaluation Study-III (REDS-III), a large, multicenter research program that seeks to optimize health outcomes in donors and transfusion recipients and to help ensure the safety and availability of transfused blood products in the United States and internationally. The study measured the effect of low dose daily iron supplementation on the time to recovery of lost hemoglobin and iron after donating a unit of blood. Participants included 136 females (63%) and 79 males (37%); 52 donors (24%) were 60 years or older. Although all were blood donors, none had donated blood in the last four months.


For the study, blood donors were randomized into two groups based on their iron levels: a lower iron and a higher iron group. Half of each group was randomized to take one tablet of ferrous gluconate (38 mg of low dose iron) daily for 24 weeks following their blood donation. Hemoglobin and iron levels were measured seven times during the study. Results showed that compared to donors who did not take iron, the donors taking iron supplements returned to pre-donation hemoglobin levels faster in both the lower iron (five weeks versus 23 weeks) and higher iron groups (four weeks versus 11 weeks). Similarly, donors taking iron supplements recovered lost iron more rapidly than those not receiving supplements (11 weeks versus more than 24 weeks). Without iron supplementation, two thirds of the donors did not recover the iron lost from donating blood after 24 weeks.


According to the authors, among blood donors with normal hemoglobin levels, low-dose iron supplementation, compared with no supplementation, reduced time to 80% recovery of the post-donation decrease in hemoglobin concentration in donors with low ferritin (<26 ng/mL) or higher ferritin (>26 ng/mL



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Safety of Measles-Containing Vaccines in 1-Year-Old Children


All measles-containing vaccines are associated with several types of adverse events, including seizure, fever, and immune thrombocytopenia purpura (ITP). However this risk vs. benefit is very low, whereas the benefit is very high.


Because the measles-mumps-rubella-varicella (MMRV) vaccine compared with the separate measles-mumps-rubella (MMR) and varicella (MMR + V) vaccine increases a toddler’s risk for febrile seizures, a study published in Pediatrics (2015; 135:2 e321-e329) investigated whether MMRV is riskier than MMR + V and whether either vaccine elevates the risk for additional safety outcomes.


The study evaluated 123,200 MMRV and 584,987 MMR + V doses in children aged 12 to 23 months who participated in the Vaccine Safety Datalink from 2000 to 2012. Nine study outcomes were investigated: 7 main outcomes (anaphylaxis, ITP, ataxia, arthritis, meningitis/encephalitis, acute disseminated encephalomyelitis, and Kawasaki disease), seizure, and fever. Comparing MMRV with MMR + V, relative risk was estimated by using stratified exact binomial tests. Secondary analyses examined post-MMRV or MMR + V risk versus comparison intervals; risk and comparison intervals were then contrasted for MMRV versus MMR+V.


Results showed no significantly differences when comparing MMRV with MMR + V, risks for the 7 main outcomes, with several outcomes having few or zero post-vaccination events. Comparing risk versus comparison intervals, ITP risk was higher after MMRV (odds ratio [OR]: 11.3) and MMR + V (OR: 10) and ataxia risk was lower after both vaccines. Compared with MMR + V, MMRV increased risk of seizure and fever 7 to 10 days after vaccination.


According to the authors, the study did not identify any new safety concerns comparing MMRV with MMR + V or after either the MMRV or the MMR + V vaccine, and provides reassurance that these outcomes are unlikely after either vaccine.


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