Date:
June 28, 2017

Source:
BMJ

Summary:
Higher intelligence (IQ) in childhood is associated with a lower lifetime risk of major causes of death, including heart disease, stroke, smoking related cancers, respiratory disease and dementia, finds a new study.

 

Smart kids can look forward to a long life, study suggests.
Credit: © Mikkel Bigandt / Fotolia

 

 

Higher intelligence (IQ) in childhood is associated with a lower lifetime risk of major causes of death, including heart disease, stroke, smoking related cancers, respiratory disease and dementia, finds a study published by The BMJ today.

It is the largest study to date reporting causes of death in men and women across the life course, and the findings suggest that lifestyle, especially tobacco smoking, is an important component in the effect of intelligence on differences in mortality.

Previous studies have shown that, on average, individuals with higher IQs tend to live a little longer than those with lower IQs, but these are largely based on data from male conscripts followed up only to middle adulthood.

So a team of researchers from the University of Edinburgh set out to examine the association between intelligence test scores measured at age 11 and leading causes of death in men and women up to age 79.

Their findings are based on data from 33,536 men and 32,229 women born in Scotland in 1936, who took a validated childhood intelligence test at age 11, and who could be linked to cause of death data up to December 2015.

Cause of death included coronary heart disease, stroke, specific cancers, respiratory disease, digestive disease, external causes (including suicide and death from injury), and dementia.

After taking account of several factors (confounders) that could have influenced the results, such as age, sex and socioeconomic status, the researchers found that higher childhood intelligence was associated with a lower risk of death until age 79.

For example, a higher test score was associated with a 28% reduced risk of death from respiratory disease, a 25% reduced risk of death from coronary heart disease, and a 24% reduced risk of death from stroke.

Other notable associations were seen for deaths from injury, smoking related cancers (particularly lung and stomach), digestive disease, and dementia. There was no evident association between childhood intelligence and death from cancers not related to smoking.

The authors outline some study limitations which could have introduced bias. However, key strengths include the whole population sample, 68-year follow up, and ability to adjust for important confounders.

They also point out that significant associations remained after further adjustment for smoking and socioeconomic status, suggesting that these factors did not fully account for mortality differences. And they say future studies “would benefit from measures of the cumulative load of such risk factors over the life course.”

This study is the largest to date reporting causes of death across the life course, and it provides us with interesting results, say researchers based in Sweden, in a linked editorial.

“Importantly, it shows that childhood IQ is strongly associated with causes of death that are, to a great extent, dependent on already known risk factors,” they write. And they suggest that “tobacco smoking and its distribution along the socioeconomic spectrum could be of particular importance here.”

In conclusion, they say: “It remains to be seen if this is the full story or if IQ signals something deeper, and possibly genetic, in its relation to longevity.”


Story Source:

Materials provided by BMJNote: Content may be edited for style and length.


Journal References:

  1. Daniel Falkstedt, Anton C J Lager. Higher IQ in childhood is linked to a longer lifeBMJ, 2017; j2932 DOI: 10.1136/bmj.j2932
  2. Catherine M Calvin, G David Batty, Geoff Der, Caroline E Brett, Adele Taylor, Alison Pattie, Iva Čukić, Ian J Deary. Childhood intelligence in relation to major causes of death in 68 year follow-up: prospective population studyBMJ, 2017; j2708 DOI: 10.1136/bmj.j2708

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Hardest-hit areas are big solar investors: China, India, Arabian peninsula

Date:
June 26, 2017

Source:
Duke University

Summary:
Global solar energy production is taking a major hit due to air pollution and dust. The first study of its kind shows airborne particles and their accumulation on solar cells is cutting energy output by more than 25 percent in certain parts of the world. The regions hardest hit are also those investing the most in solar energy installations — China, India and the Arabian Peninsula.

 

Duke engineering professor Michael Bergin (left) stands with Indian Institute of Technology-Gandhinagar colleague Chinmay Ghoroi (right) next to that university’s extremely dusty solar panel array.
Credit: Michael Bergin, Duke University

 

 

Global solar energy production is taking a major hit due to air pollution and dust.

According to a new study, airborne particles and their accumulation on solar cells are cutting energy output by more than 25 percent in certain parts of the world. The regions hardest hit are also those investing the most in solar energy installations: China, India and the Arabian Peninsula.

The study appears online June 23 in Environmental Science & Technology Letters.

“My colleagues in India were showing off some of their rooftop solar installations, and I was blown away by how dirty the panels were,” said Michael Bergin, professor of civil and environmental engineering at Duke University and lead author of the study. “I thought the dirt had to affect their efficiencies, but there weren’t any studies out there estimating the losses. So we put together a comprehensive model to do just that.”

With colleagues at the Indian Institute of Technology-Gandhinagar and the University of Wisconsin at Madison, Bergin measured the decrease in solar energy gathered by the IITGN’s solar panels as they became dirtier over time. The data showed a 50-percent jump in efficiency each time the panels were cleaned after being left alone for several weeks.

The researchers also sampled the grime to analyze its composition, revealing that 92 percent was dust while the remaining fraction was composed of carbon and ion pollutants from human activity. While this may sound like a small amount, light is blocked more efficiently by smaller humanmade particles than by natural dust. As a result, the human contributions to energy loss are much greater than those from dust, making the two sources roughly equal antagonists in this case.

“The humanmade particles are also small and sticky, making them much more difficult to clean off,” said Bergin. “You might think you could just clean the solar panels more often, but the more you clean them, the higher your risk of damaging them.”

Having previously analyzed pollutants discoloring India’s Taj Mahal, Bergin already had a good idea of how these different particles react to sunlight. Using his earlier work as a base, he created an equation that accurately estimates the amount of sunlight blocked by different compositions of solar panel dust and pollution buildup.

But grimy buildup on solar panels isn’t the only thing blocking sunlight — the ambient particles in the air also have a screening effect.

For that half of the sun-blocking equation, Bergin turned to Drew Shindell, professor of climate sciences at Duke and an expert in using the NASA GISS Global Climate Model.

Because the climate model already accounts for the amount of the sun’s energy blocked by different types of airborne particles, it was not a stretch to estimate the particles’ effects on solar energy. The NASA model also estimates the amount of particulate matter deposited on surfaces worldwide, providing a basis for Bergin’s equation to calculate how much sunlight would be blocked by accumulated dust and pollution.

The resulting calculations estimate the total loss of solar energy production in every part of the world. While the United States has relatively little migratory dust, more arid regions such as the Arabian Peninsula, Northern India and Eastern China are looking at heavy losses — 17 to 25 percent or more, assuming monthly cleanings. If cleanings take place every two months, those numbers jump to 25 or 35 percent.

There are, of course, multiple variables that affect solar power production both on a local and regional level. For example, a large construction zone can cause a swift buildup of dust on a nearby solar array.

The Arabian Peninsula loses much more solar power to dust than it does humanmade pollutants, Bergin said. But the reverse is true for regions of China, and regions of India are not far behind.

“China is already looking at tens of billions of dollars being lost each year, with more than 80 percent of that coming from losses due to pollution,” said Bergin. “With the explosion of renewables taking place in China and their recent commitment to expanding their solar power capacity, that number is only going to go up.”

“We always knew these pollutants were bad for human health and climate change, but now we’ve shown how bad they are for solar energy as well,” continued Bergin. “It’s yet another reason for policymakers worldwide to adopt emissions controls.”

This work was supported by the US Agency for International Development and the Office of the Vice Provost for Research at Duke University.


Story Source:

Materials provided by Duke University. Original written by Ken Kingery. Note: Content may be edited for style and length.


Journal Reference:

  1. Mike H. Bergin, Chinmay Ghoroi, Deepa Dixit, James Jay Schauer, Drew Shindell. Large reductions in solar energy production due to dust and particulate air pollutionEnvironmental Science & Technology Letters, 2017; DOI: 10.1021/acs.estlett.7b00197

 

Source: Duke University. “Air pollution casts shadow over solar energy production: Hardest-hit areas are big solar investors: China, India, Arabian peninsula.” ScienceDaily. ScienceDaily, 26 June 2017. <www.sciencedaily.com/releases/2017/06/170626135724.htm>.

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Date:
June 26, 2017

Source:
CAGE – Center for Arctic Gas Hydrate, Climate and Environment

Summary:
Scientists have reconstructed in detail the collapse of the Eurasian ice sheet at the end of the last ice age. The big melt wreaked havoc across the European continent, driving home the original Brexit 10,000 years ago.

 

The Eurasian ice sheet was an enormous conveyor of ice that covered most of northern Europe some 23,000 years ago. Its extent was such that one could have skied 4,500 km continuously across it — from the far southwestern isles in Britain to Franz Josef Land in the Siberian Arctic. Suffice to say its existence had a massive and extremely hostile impact on Europe at the time.

 

 

This ice sheet alone lowered global sea-level by over 20 meters. As it melted and collapsed, it caused severe flooding across the continent, led to dramatic sea-level rise, and diverted mega-rivers that raged on the continent. A new model, investigating the retreat of this ice sheet and its many impacts has just been published in Quaternary Science Reviews.

Ten times the melt of Greenland and Antarctica today

“Our model experiments show that from 15000 to 13000 years ago, the Eurasian ice sheet lost 750 cubic kilometres of ice a year. For short periods, it peaked at ice loss rates of over 3000 cubic kilometres per year.” says first author Henry Patton, researcher at CAGE Centre for Arctic Gas Hydrate, Environment and Climate at UiT The Arctic University of Norway.

A cubic kilometre of ice is difficult to imagine, but think of a cube that is 1km long on each side: It will contain 1,000,000,000 tonnes of water. Now multiply that by 3000.

“There is an event in this deglaciation story called Meltwater Pulse 1A. This was a period of very rapid sea level rise that lasted some 400-500 years when global temperatures were rising very quickly. During this period, we estimate that the Eurasian Ice Sheet contributed around 2.5 metres to global sea level rise” states Patton.

“To place it in context,” says professor Alun Hubbard, the paper’s second author and a leading glaciologist, “this is almost ten times the current rates of ice being lost from Greenland and Antarctica today. What’s fascinating is that not all Eurasian ice retreat was from surface melting alone. Its northern and western sectors across the Barents Sea, Norway and Britain terminated directly into the sea. They underwent rapid collapse through calving of vast armadas of icebergs and undercutting of the ice margin by warm ocean currents.”

“This is a harbinger of what’s starting to happen to the Greenland ice sheet” warns Hubbard.

All rivers in Europe unite

The influence of the Eurasian ice sheet extended far beyond what was directly covered by ice. One of the most dramatic impacts was the formation of the enormous Fleuve Manche. This was a mega-river network that drained the present-day Vistula, Elbe, Rhine and Thames rivers, and the meltwater from the ice sheet itself, through the Seine Estuary and into the North Atlantic.

“Some speculate that at some points during the European deglaciation this river system had a discharge twice that of the Amazon today. Based on our latest reconstruction of this system, we have calculated that its catchment area was similar to that of the Mississippi. It was certainly the largest river system to have ever drained the Eurasian continent,” says Patton.

The original Brexit is a fact

The vast reach of this catchment meant that this mega-river had the capacity to contribute enormous volumes of cold freshwater directly into the North Atlantic, enough to have severely modified the Gulf Stream — a major climate influencer.

Also, the sea level rise and the colossal amounts of meltwater discharged from the collapsing ice sheet meant that areas that previously were land eventually became seabed.

“Britain and Ireland, which had been joined to Europe throughout the last ice age, finally separated with the flooding of the English Channel around 10,000 years ago. It was the original Brexit, so to speak” says Alun Hubbard.

The ice retreats, the humans advance

The ice reconstruction in this study provides a fascinating image of a changing Europe during the time prehistoric humans came to populate the continent. The environmental challenges they met must have been spectacular.

“One thing that we show pretty well in this study is that our simulation is relevant to a range of different research disciplines, not only glaciology. It can even be useful for archaeologists who look at human migration routes, and are interested to see how the European environment developed over the last 20 000 years.” says Patton.

This model reconstruction has already proven a vital constraint for understanding complex systems beyond the ice sheet realm. For example, data from this study has been used to examine the evolution of gas hydrate stability within the Eurasian Arctic over glacial timescales, exploring the development of massive mounds and methane blow-out craters that have been recently discovered on the Arctic seafloor.


Story Source:

Materials provided by CAGE – Center for Arctic Gas Hydrate, Climate and EnvironmentNote: Content may be edited for style and length.


Journal Reference:

  1. Henry Patton, Alun Hubbard, Karin Andreassen, Amandine Auriac, Pippa L. Whitehouse, Arjen P. Stroeven, Calvin Shackleton, Monica Winsborrow, Jakob Heyman, Adrian M. Hall. Deglaciation of the Eurasian ice sheet complexQuaternary Science Reviews, 2017; 169: 148 DOI: 10.1016/j.quascirev.2017.05.019

 

Source: CAGE – Center for Arctic Gas Hydrate, Climate and Environment. “Collapse of European ice sheet caused chaos in past.” ScienceDaily. ScienceDaily, 26 June 2017. <www.sciencedaily.com/releases/2017/06/170626180557.htm>.

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DIA 2017 and James Farley Photograph

 

We are back from the annual DIA meeting in Chicago, and it was quite a success. Our presentation on How eSource Solutions are Impacting Clinical Research Sites, Patients, Regulators and Drug and Device Companieswith Jonathan Helfgott and Mitchell Efros, was well-attended and quite stimulating.

 

Two-Striped Grasshopper – James Farley Photographer Par Excellence

Two-Striped Grasshopper – ©JFarley Photography.

 

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. Please visit the Target Health Website.

 

Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor

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Two Brains Are Better Than One

Graphic source: National Cancer Institute; Public Domain, Wikipedia Commons

 

 

Technically known as the enteric nervous system, the second brain consists of sheaths of neurons embedded in the walls of the long tube of our gut, or alimentary 1) ___, which measures about nine meters end to end from the esophagus to the anus. The enteric nervous system is one of the main divisions of the nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system; it has been described as a “second brain“ for several reasons. The enteric nervous system can operate autonomously. It normally communicates with the central nervous system (CNS) through the parasympathetic (e.g., via the vagus nerve) and sympathetic (e.g., via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the Vegas 2) ___ is severed, the enteric nervous system continues to function.

 

In vertebrates, the enteric nervous system includes efferent neurons, afferent neurons, and interneurons, all of which make the enteric nervous system capable of carrying reflexes in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the 3) ___ neurons control peristalsis and churning of intestinal contents. Other neurons control the secretion of enzymes. The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. More than 90% of the body’s 4) ___ lies in the gut, as well as about 50% of the body’s dopamine and the dual function of these neurotransmitters is an active part of gut-brain research. Researchers found noticeable improvements in the ability of rats to cope with stressful activity (such as swimming) when diets are supplemented by specific gut microbiota.

 

The gut-brain axis, a bidirectional neurohumoral communication system, is important for maintaining homeostasis and is regulated through the central and ENS 5) ___ ___ ___ and the neural, endocrine, immune, and metabolic pathways, and especially including the hypothalamic-pituitary-adrenal axis (HPA axis). That term has been expanded to include the role of the gut flora as part of the “microbiome-gut-brain axis“, a linkage of functions including the gut flora. Interest in the field was sparked by a 2004 study showing that germ-free mice (genetically homogeneous laboratory mice, birthed and raised in an antiseptic environment) showed an exaggerated HPA axis response to 6) ___ compared to non-GF laboratory mice. The gut flora can produce a range of neuroactive molecules, such as acetylcholine, catecholamines, ?-aminobutyric acid, histamine, melatonin, and serotonin, which is essential for regulating peristalsis and sensation in the gut. Changes in the composition of the gut flora due to diet, drugs, or disease correlate with changes in levels of circulating cytokines, some of which can affect brain function. The gut flora also releases molecules that can directly activate the vagus nerve which transmits information about the state of the intestines to the brain. Likewise, chronic or acutely stressful situations activate the hypothalamic-pituitary-adrenal axis, causing changes in the gut flora and intestinal epithelium, and possibly having systemic effects. Additionally, the cholinergic anti-inflammatory pathway, signaling through the vagus nerve, affects the gut epithelium and flora. Hunger and satiety are integrated in the brain, and the presence or absence of food in the gut and types of food present, also affect the composition and activity of gut 7) ___.

 

Scientists have made an important step in understanding the organization of nerve cells embedded within the gut that control its function — a discovery that could give insight into the origin of common gastrointestinal diseases, including irritable bowel syndrome and chronic constipation and much more. The findings, published in Science, reveal how the enteric nervous system — a chaotic network of half a billion nerve cells and many more supporting cells inside the gut wall — is formed during mouse development. The research was led by the Francis Crick Institute, in collaboration with the University of Leuven, Stanford University, the Hubrecht Institute and the Quadram Institute Bioscience. The work was funded by the Francis Crick Institute, the Medical Research Council and the UK Biotechnology and Biological Sciences Research Council. Often known as the ‘second brain’ for its vast number of 8) ___ and complex connectivity, the enteric nervous system has a crucial role in maintaining a healthy gut. Therefore, understanding how this neural mosaic is organized could help scientists find treatments for common gastrointestinal disorders. During development, a unique and dynamic population of cells known as progenitor cells divide to produce copies of themselves, which can then generate many other types of cells. Using genetic tools, the study labelled individual progenitor cells of the enteric nervous system with unique colors and followed their descendants — also marked with the same color — through development and into the adult animal. By examining the type of cells produced by single progenitors, they could understand their properties. Results showed that some progenitors only produced nerve cells, others only produced nerve-supporting cells called glia, and some produced both. Neurons and 9) ___ originating from the same parent stayed close to each other, forming relatively tight groups of cells. Cell groups that descended from different but neighboring parent cells overlapped like a Venn diagram that could be viewed on the gut surface. Interestingly, this close relationship was maintained by the descendants of single progenitors down through all layers of the gut wall thereby forming overlapping columns of cells. The team explored whether this intricate structure of the enteric nervous system also contributes to nerve cell activity in the gut. According to the authors, a subtle electrical stimulation to the enteric nervous system showed that nerve cells generated by the same parent cell responded in synchrony, and that this suggested that developmental relationships between cells of the enteric nervous system of mammals are fundamental for the neural regulation of gut function. The authors added that now that there is a better understanding of how the enteric nervous system is built and works, it is possible to start looking at what happens when things go wrong particularly during the critical stages of embryo development or early life. Perhaps mistakes in the blueprint used to build the neural networks of the gut are the basis of common gastrointestinal problems. Recent research indicates a possible connection between early gut flora and 10) ___.

 

Sources: The Francis Crick Institute: Researchers: Reena Lasrado, Werend Boesmans, Jens Kleinjung, Carmen Pin, Donald Bell, Leena Bhaw, Sarah McCallum, Hui Zong, Liqun Luo, Hans Clevers, Pieter Vanden Berghe, Vassilis Pachnis. Lineage-dependent spatial and functional organization of the mammalian enteric nervous system. Science, 2017; 356 (6339): 722; ScienceDaily.com; Wikipedia

 

ANSWERS: 1) canal; 2) nerve; 3) motor; 4) serotonin; 5) enteric nervous systems; 6) stress; 7) flora; 8) neurons; 9) glia; 10) autism

 

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Michael D. Gershon, MD

Michael Gershon MD: “Serotonin is a sword and a shield of the bowel: serotonin plays offense and defense.“ Photo credit: Columbia University Medical School, MD/PhD Program

 

Michael D. Gershon, is Professor of Pathology and Cell Biology, at Columbia University Medical School and Center. Gershon has been called the “father of neurogastroenterology“ because, in addition to his seminal work on neuronal control of gastrointestinal (GI) behavior and development of the enteric nervous system (ENS), his classic trade book, The Second Brain, has made physicians, scientists, and the lay public aware of the significance of the unique ability of the ENS to regulate GI activity in the absence of input from the brain and spinal cord. Gershon’s demonstration that serotonin is an enteric neurotransmitter was the first indication that the ENS is more than a collection of cholinergic relay neurons transmitting signals from the brain to the bowel. He was the first to identify intrinsic primary afferent neurons that initiate peristaltic and secretory reflexes and he demonstrated that these cells are activated by the mucosal release of serotonin. Dr. Gershon has published almost 400 peer-reviewed papers including major contributions relative to disorders of GI motility, including irritable bowel syndrome, identification of serotonin as a GI neurotransmitter and the initial observation in the gut of intrinsic sensory nerve cells that trigger propulsive motor activity. Dr. Gershon also discovered that the serotonin transporter (SERT) is expressed by enterocytes (cells that line the lumen of the gut) as well as by enteric neurons and is critical in the termination of serotonin-mediated effects.

 

Dr. Gershon has identified roles in GI physiology that specific subtypes of serotonin receptor play and he has provided evidence that serotonin is not only a neurotransmitter and a paracrine factor that initiates motile and secretory reflexes, but also as a hormone that affects bone resorption and inflammation. He has called serotonin “a sword and shield of the bowel“ because it is simultaneously proinflammatory and neuroprotective. Mucosal serotonin triggers inflammatory responses that oppose microbial invasion, while neuronal serotonin protects the ENS from the damage that inflammation would otherwise cause. Neuron-derived serotonin also mobilizes precursor cells, which are present in the adult gut, to initiate the genesis of new neurons, an adult function that reflects a similar essential activity of early-born serotonergic neurons in late fetal and early neonatal life to promote development of late-born sets of enteric neurons.

 

Dr. Gershon has made many additional contributions to ENS development, including the identification of necessary guidance molecules, adhesion proteins, growth and transcription factors; his observations suggest that defects that occur late in ENS development lead to subtle changes in GI physiology that may contribute to the pathogenesis of functional bowel disorders. More recently, Drs. Michael and Anne Gershon have demonstrated that varicella zoster virus (VZV) infects, becomes latent, and reactivates in enteric neurons, including those of humans. They have demonstrated that “enteric zoster (shingles)“ occurs and may thus be an unexpected cause of a variety of gastrointestinal disorders, the pathogenesis of which is currently unknown.

 

Born in New York City in 1938, Dr. Michael D. Gershon received his B.A. degree in 1958 “with distinction from Cornell University and his M.D. in 1963, again from Cornell. Gershon received postdoctoral training with Edith Bulbring in Pharmacology at Oxford University before returning to Cornell as an Assistant Professor of Anatomy in 1967. He was promoted to Professor before leaving Cornell to Chair the Department of Anatomy & Cell Biology at Columbia University’s College of P&S from 1975-2005. Gershon is now a Professor of Pathology & Cell Biology at Columbia.

 

Gershon’s contributions to the identification, location, and functional characterization of enteric serotonin receptors have been important in the design of drugs to treat irritable bowel syndrome, chronic constipation, and chemotherapy-associated nausea. Gershon’s discovery that the serotonin transporter (SERT), which terminates serotonergic signaling, is expressed in the bowel both by enterocytes and neurons opened new paths for research into the pathophysiology of irritable bowel syndrome and inflammatory bowel disease. He has linked mucosal serotonin to inflammation and neuronal serotonin to neuroprotection and the generation of new neurons from adult stem cells. These discoveries have led to the new idea that the function of serotonin is not limited to paracrine signaling and neurotransmission in the service of motility and secretion, but is also a sword and a shield of the gut.

 

Gershon has teamed with his wife, Anne Gershon, to show that the mannose 6-phosphate receptor plays critical roles in the entry and exit of varicella zoster virus (VZV). The Gershons have also developed the first animal model of VZV disease, which enables lytic and latent infection as well as reactivation to be studied in isolated enteric neurons. The Gershons have also shown that following varicella, VZV establishes latency in the human ENS. Finally, Gershon has made major contributions to understanding the roles played by a number of critical transcription and growth factors in enabling emigres from the neural crest to colonize the bowel, undergo regulated proliferation, find their appropriate destinations in the gut wall, and terminally differentiate into the most phenotypcially diverse component of the peripheral nervous system.

 

Dr. Michael Gershon has devoted his career to understanding the human bowel (the stomach, esophagus, small intestine, and colon). His thirty years of research have led to an extraordinary rediscovery: nerve cells in the gut that act as a brain. This “second brain“ can control our gut all by itself. Our two brains — the one in our head and the one in our bowel — must cooperate. If they do not, then there is chaos in the gut and misery in the head — everything from “butterflies“ to cramps, from diarrhea to constipation.

 

Gershon’s groundbreaking book, The Second Brain represents a quantum leap in medical knowledge and is already benefiting patients whose symptoms were previously dismissed as neurotic or “it’s all in your head.“ Dr. Gershon’s research, clearly demonstrates that the human gut actually has a brain of its own. This remarkable scientific breakthrough offers fascinating proof that “gut instinct“ is biological, a function of the second brain. An alarming number of people suffer from heartburn, nausea, abdominal pain, cramps, diarrhea, constipation, or related problems. Often thought to be caused by a “weakness“ of the mind, these conditions may actually be a reflection of a disorder in the second brain. The second brain, located in the bowel, normally works smoothly with the brain in the head, enabling the head-brain to concentrate on the finer pursuits of life while the gut-brain attends to the messy business of digestion. A breakdown in communication between the two brains can lead to stomach and intestinal trouble, causing sufferers great abdominal grief and too often labeling them as neurotic complainers. Dr. Gershon’s research into the second brain provides understanding for those who suffer from gut-related ailments and offers new insight into the origin, extent, and management. The culmination of his work is an extraordinary contribution to the understanding of gastrointestinal illnesses, as well as a fascinating glimpse into how our gut really works.

 

A light touch: The irreplaceable, indomitable, Stephen Colbert interviews the great Michael Gershon MD about the Second Brain, in the gut

 

Michael Gershon clearly explains some of his research. This is video one out of seven. You can find the other six

videos on YouTube.

 

Very short student note regarding Dr Gershon

 

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Predicting Cognitive Deficits in People with Parkinson’s Disease

 

Currently available Parkinson’s disease (PD) medications are only effective in improving motor deficits caused by the disease. However, the loss of cognitive abilities severely affects the individual’s quality of life and independence. One barrier to developing treatments for the cognitive effects of PD is the considerable variability among patients. As a result, a study must enroll several hundred patients when designing clinical trials to test treatments. Although PD is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25% of patients also experience deficits in cognition that impair function.

 

According to an article published online in Lancet Neurology (16 June 2017), a newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The study combined data from 3,200 people with PD, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, a computer-based risk calculator was built that may predict the chance that an individual with PD will develop cognitive deficits. Interestingly, a patient’s education appeared to have a powerful impact on the risk of memory loss. The more years of formal education patients in the study had, the greater was their protection against cognitive decline.

 

Moving forward, the authors plan to further improve the cognitive risk score calculator. The team is scanning the genome of patients to hunt for new progression genes. Ultimately, it is their hope that the tool can be used in the clinic in addition to helping with clinical trial design. However, considerable research remains to be done before that will be possible. One complication for the use of this calculator in the clinic is the lack of available treatments for PD-related cognitive deficits. Clinicians face ethical issues concerning whether patients should be informed of their risk when there is little available to help them. It is hoped that by improving clinical trial design, the risk calculator can first aid in the discovery of new treatments and determine which patients would benefit most from the new treatments.

 

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Genetic Gains and Losses in Tourette Syndrome

 

NRXN1 and CNTN6 are important during brain development and produce molecules that help brain cells form connections with one another. In addition, the two genes are turned on in areas that are part of the cortico-striatal-thalamo-cortical circuit, a loop of brain cells connecting the cortex to specific regions involved in processing emotions and movement. While copy number variants in NRXN1 have been implicated in other neurological disorders including epilepsy and autism, this is the first time that scientists have linked copy number variants in CNTN6 to a specific disease, Tourette syndrome.

 

According to an article published online in Neuron(21 June 2017), structural changes have been identified in two genes that increase the risk of developing Tourette syndrome, a neurological disorder characterized by involuntary motor and vocal tics. Although involuntary tics are very common in children, they persist and worsen over time in people with Tourette syndrome. Tics associated with Tourette syndrome appear in children, peak during the early teenage years and often disappear in adulthood. Many people with Tourette syndrome experience other brain disorders including attention deficit disorder and obsessive-compulsive disorder.

 

For the study, genetic analyses were conducted on 2,434 individuals with Tourette syndrome and compared them to 4,093 controls, focusing on copy number variants, changes in the genetic code resulting in deletions or duplications in sections of genes. The results determined that deletions in the NRXN1 gene or duplications in the CNTN6 gene were each associated with an increased risk of Tourette syndrome. In the study, approximately 1 in 100 people with Tourette syndrome carried one of those genetic variants.

 

The authors are planning to take a closer look at the mutations using animal and cellular models, and more  research is needed to learn about ways in which the genes contribute to development of Tourette syndrome and whether they may be potential therapeutic targets.

 

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First Subcutaneous C1 Esterase Inhibitor to Treat Hereditary Angioedema (HAE)

 

Hereditary Angioedema (HAE), which is caused by having insufficient amounts of a plasma protein called C1-esterase inhibitor (or C1-INH), affects approximately 6,000 to 10,000 people in the U.S. People with HAE can develop rapid swelling of the hands, feet, limbs, face, intestinal tract or airway. These attacks of swelling can occur spontaneously, or can be triggered by stress, surgery or infection.

 

The FDA has approved Haegarda, the first C1 Esterase Inhibitor (Human) for subcutaneous (under the skin) administration to prevent HAE attacks in adolescent and adult patients. The subcutaneous route of administration allows for easier at-home self-injection by the patient or caregiver, once proper training is received.

 

Haegarda is a human plasma-derived, purified, pasteurized, lyophilized (freeze-dried) concentrate prepared from large pools of human plasma from U.S. donors. Haegarda is indicated for routine prophylaxis to prevent HAE attacks, but is not indicated for treatment of acute HAE attacks. The efficacy of Haegarda was demonstrated in a multicenter controlled clinical trial. The study included 90 subjects ranging in age from 12 to 72 years old with symptomatic HAE. Subjects were randomized to receive twice per week subcutaneous doses of either 40 IU/kg or 60 IU/kg, and the treatment effect was compared to a placebo treatment period. During the 16 week treatment period, patients in both treatment groups experienced a significantly reduced number of HAE attacks compared to their placebo treatment period.

 

The most common side effects included injection site reactions, hypersensitivity (allergic) reactions, nasopharyngitis (swelling of the nasal passages and throat) and dizziness. Haegarda should not be used in individuals who have experienced life-threatening hypersensitivity reactions, including anaphylaxis, to a C1-INH preparation or its inactive ingredients.

 

Haegarda received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs to treat rare diseases or conditions.

 

The FDA granted approval of Haegarda to CSL Behring LLC.

 

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Avocado Toast Manhattan Style (move over California)

Born in California. Nuanced in New York. Healthy, easy, beyond tasty, and attractive to serve, especially in the summer. Here and there, I began seeing “avocado toast“ popping up. It seemed too easy to make a big deal out of, but here, there and everywhere, this homage to avocados was ubiquitous. Maybe all the exposure was a subtle marketing tool, but who cares; avocados are on everyone’s top ten list of healthiest foods. Finally, I decided to take a toast challenge, into our kitchen, add my own touches and share the results with our wonderfully responsive readers. ©Joyce Hays, Target Health Inc.

 

The basic recipe is one slice of whole wheat or whole grain bread, toasted. Then, cut a ripe avocado in half and pit it. With a spoon, scoop the avocado out of its skin, leaving as little of the flesh as you can. Next, slice it, arrange the slices on the toast. (optional) drizzle a little extra virgin olive oil over the avocado, add seasoning, if you wish. Cut toast in half, in quarters or leave uncut, and eat. Here you see the basic ingredients for avocado toast. Below, are ingredients I have added, to enable you to mix and match, so that this healthy and easy dish stays fresh and new, all summer, indoors or out. Brunch, lunch, beach, backyard, snack or supper. Good with icy beer, chilled white or rose wine, flavored or plain ice water?..just plain delicious with everything, anywhere.

Ingredients

Whole wheat or whole grain bread, toasted

Ripe avocado, cut in half, pitted, sliced

Find ripe but firm avocados. ©Joyce Hays, Target Health Inc.

 

These are all the ingredients you need for the original California avocado toast. ©Joyce Hays, Target Health Inc.

  

The following ingredients are what I have been adding to the avocado toast idea:

Tomato slices

Orange and yellow pepper slices, cooked in oil a few minutes until soft

Red onion slices

Hearts of romaine

Turkey bacon, cooked first

Ahi salmon, chopped well

Nova salmon under avocado slices

 

In the future, I’ll be trying avocado slices or mashed avocado sprinkled with chopped rosemary pistachios. ©Joyce Hays, Target Health Inc.

 

Clockwise: Avocado slices, tomato slices, red onion slices, orange & yellow cooked peppers, turkey bacon (cooked), romaine hearts.  ©Joyce Hays, Target Health Inc.

 

Avocado mash: A variation on avocado toast is mash one or two avocados, add some cut up ripe tomatoes, squeeze as much fresh garlic as you like, add fresh lemon or lime juice, flax seeds, mix well and spread on your whole grain toast. Or, use this avocado mash, as topping to other toast ideas. This mash turned out very well. ©Joyce Hays, Target Health Inc.

 

Fry as many eggs as you want. ©Joyce Hays, Target Health Inc.

 

Go by your own palate and create as many different combinations, with toast and avocados. ©Joyce Hays, Target Health Inc.

 

When I was a kid, my mother used to break a soft boiled egg over whatever hot cereal I was eating for breakfast. To this day, I love runny yolks on top of many dishes like veal chops, veggies, salmon tartare and much more, so this variation, above, was a no-brainer and my first variation for avocado toast. This turned out to be a delicious lunch. ©Joyce Hays, Target Health Inc.

 

Delicious down to the last bite. ©Joyce Hays, Target Health Inc.

 

Avocado toast with red onion. Extremely tasty. ©Joyce Hays, Target Health Inc.

 

Avocado toast with ripe tomato – with or without some mashed avocado on top. ©Joyce Hays, Target Health Inc.

 

Avocado toast with crispy hearts of romaine, topped with avocado mash. ©Joyce Hays, Target Health Inc.

 

Avocado toast with turkey bacon (cooked first), then topped with avocado slices  and avocado mash. ©Joyce Hays, Target Health Inc.

 

Avocado toast, using soft cooked orange pepper, avocado slice, topped with avocado mash. ©Joyce Hays, Target Health Inc.

 

Avocado toast, mashed on site, with your fork, then topped with red onion rings. ©Joyce Hays, Target Health Inc.

 

Whole grain toast, slices of avocado, mashed at table with fork, topped with chopped raw ahi salmon, topped with another slice of avocado. When I do this particular variation again, I will top this sandwich with sprouts, preferably broccoli sprouts. ©Joyce Hays, Target Health Inc.

 

Whole grain toast, mashed avocado, chopped nova, topped with red onion ring. ©Joyce Hays, Target Health Inc.

 

Whole grain toast, plain avocado slices, mashed with fork, covered with raw ahi chopped salmon, topped with runny yolk fried egg. ©Joyce Hays, Target Health Inc.

 

Goodness Comes in Many Forms. Here is my favorite combo of all: Whole grain toast, layer of avocado slices mashed with fork, next layer chopped raw ahi salmon, topped with runny yolk fried egg, red onion ring(s). and sipping chilled white wine. ©Joyce Hays, Target Health Inc.

 

The very next day, at one of our favorite restaurants, I asked the chef to make salmon tartare with two runny eggs on top. The green you see (above) is seaweed in the salmon tartare. I created this dish, at this restaurant. -to die for! ©Joyce Hays, Target Health Inc.

 

This chilled white, went well with all variations of the avocado toast. Here’s another toast: good health, to all our friends and colleagues! ©Joyce Hays, Target Health Inc.

 

On Saturday we saw a play at one of our theater clubs, where we are patrons, called: Fulfillment Center. I hear it got good reviews; however, sorry to say, neither Jules nor I liked it.

The Big Apple is beautiful these days. We live near Central Park (luckily) and it’s lush these days, with all the rain we’re getting. Everything is in bloom. The park near the Planetarium is gorgeous, as is (Public Library) Bryant Park, near our offices. The Westside Highway is like driving through a park, so many trees have been planted there, plus the wild rose bushes are in full flower now adding to the pleasure of driving down the WSHighway.

The world is in chaos, but this was a relaxing beautiful weekend for us!

Be well, everyone

 

From Our Table to Yours

Bon Appetit!

 

Filed Under News, Target Healthy Eating (recipes) | Leave a Comment 

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