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Archive for the ‘Micronutrients’ Category


Live 12:00 – 1:00 P.M  Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health : October 19, 2018

Reporter: Stephen J. Williams, Ph.D.

12.00 The Italian Mediterranean Diet as a Model of Identity of a People with a Universal Good to Safeguard Health?

Prof. Antonino De Lorenzo, MD, PhD.

Director of the School of Specialization in Clinical Nutrition, University of Rome “Tor Vergata”

It is important to determine how our bodies interacts with the environment, such as absorption of nutrients.

Studies shown here show decrease in life expectancy of a high sugar diet, but the quality of the diet, not just the type of diet is important, especially the role of natural probiotics and phenolic compounds found in the Mediterranean diet.

The WHO report in 2005 discusses the unsustainability of nutrition deficiencies and suggest a proactive personalized and preventative/predictive approach of diet and health.

Most of the noncommunicable diseases like CV (46%) cancer 21% and 11% respiratory and 4% diabetes could be prevented and or cured with proper dietary approaches

Italy vs. the US diseases: in Italy most disease due to environmental contamination while US diet plays a major role

The issue we are facing in less than 10% of the Italian population (fruit, fibers, oils) are not getting the proper foods, diet and contributing to as we suggest 46% of the disease

The Food Paradox: 1.5 billion are obese; we notice we are eating less products of quality and most quality produce is going to waste;

  •  growing BMI and junk food: our studies are correlating the junk food (pre-prepared) and global BMI
  • modern diet and impact of human health (junk food high in additives, salt) has impact on microflora
  • Western Diet and Addiction: We show a link (using brain scans) showing correlation of junk food, sugar cravings, and other addictive behaviors by affecting the dopamine signaling in the substantia nigra
  • developed a junk food calculator and a Mediterranean diet calculator
  • the intersection of culture, food is embedded in the Mediterranean diet; this is supported by dietary studies of two distinct rural Italian populations (one of these in the US) show decrease in diet
  • Impact of diet: have model in Germany how this diet can increase health and life expectancy
  • from 1950 to present day 2.7 unit increase in the diet index can increase life expectancy by 26%
  • so there is an inverse relationship with our index and breast cancer

Environment and metal contamination and glyphosate: contribution to disease and impact of maintaining the healthy diet

  • huge problem with use of pesticides and increase in celiac disease

12:30 Environment and Health

Dr. Iris Maria Forte, PhD.

National Cancer Institute “Pascale” Foundation | IRCCS · Department of Research, Naples, Italy

Cancer as a disease of the environment.  Weinberg’s hallmarks of Cancer reveal how environment and epigenetics can impact any of these hallmarks.

Epigenetic effects

  • gene gatekeepers (Rb and P53)
  • DNA repair and damage stabilization

Heavy Metals and Dioxins:( alterations of the immune system as well as epigenetic regulations)

Asbestos and Mesothelioma:  they have demonstrated that p53 can be involved in development of mesothelioma as reactivating p53 may be a suitable strategy for therapy

Diet, Tomato and Cancer

  • looked at tomato extract on p53 function in gastric cancer: tomato extract had a growth reduction effect and altered cell cycle regulation and results in apoptosis
  • RBL2 levels are increased in extract amount dependent manner so data shows effect of certain tomato extracts of the southern italian tomato (     )

Antonio Giordano: we tested whole extracts of almost 30 different varieties of tomato.  The tomato variety  with highest activity was near Ravela however black tomatoes have shown high antitumor activity.  We have done a followup studies showing that these varieties, if grow elsewhere lose their antitumor activity after two or three generations of breeding, even though there genetics are similar.  We are also studying the effects of different styles of cooking of these tomatoes and if it reduces antitumor effect

please see post https://news.temple.edu/news/2017-08-28/muse-cancer-fighting-tomatoes-study-italian-food

 

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Please see related articles on Live Coverage of Previous Meetings on this Open Access Journal

Real Time Conference Coverage for Scientific and Business Media: Unique Twitter Hashtags and Handles per Conference Presentation/Session

LIVE – Real Time – 16th Annual Cancer Research Symposium, Koch Institute, Friday, June 16, 9AM – 5PM, Kresge Auditorium, MIT

Real Time Coverage and eProceedings of Presentations on 11/16 – 11/17, 2016, The 12th Annual Personalized Medicine Conference, HARVARD MEDICAL SCHOOL, Joseph B. Martin Conference Center, 77 Avenue Louis Pasteur, Boston

Tweets Impression Analytics, Re-Tweets, Tweets and Likes by @AVIVA1950 and @pharma_BI for 2018 BioIT, Boston, 5/15 – 5/17, 2018

BIO 2018! June 4-7, 2018 at Boston Convention & Exhibition Center

LIVE 2018 The 21st Gabay Award to LORENZ STUDER, Memorial Sloan Kettering Cancer Center, contributions in stem cell biology and patient-specific, cell-based therapy

HUBweek 2018, October 8-14, 2018, Greater Boston – “We The Future” – coming together, of breaking down barriers, of convening across disciplinary lines to shape our future

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Benefits of Fiber in Diet

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

UPDATED on 1/15/2019

This is How Much Daily Fiber to Eat for Better Health – More appears better in meta-analysis — as in more than 30 g/day

by Ashley Lyles, Staff Writer, MedPage Today

In the systematic review, observational data showed a 15% to 30% decline in cardiovascular-related death, all-cause mortality, and incidence of stroke, coronary heart disease, type 2 diabetes, and colorectal cancer among people who consumed the most dietary fiber compared to those consuming the lowest amounts.

Whole grain intake yielded similar findings.

Risk reduction associated with a range of critical outcomes was greatest when daily intake of dietary fibre was between 25 g and 29 g. Dose-response curves suggested that higher intakes of dietary fibre could confer even greater benefit to protect against cardiovascular diseases, type 2 diabetes, and colorectal and breast cancer.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(18)31809-9.pdf

Eating more dietary fiber was linked with lower risk of disease and death, a meta-analysis showed.

According to observational studies, risk was reduced most for a range of critical outcomes from all-cause mortality to stroke when daily fiber consumption was between 25 grams and 29 grams, reported Jim Mann, PhD, of University of Otago in Dunedin, New Zealand, and colleagues in The Lancet.

By upping daily intake to 30 grams or more, people had even greater prevention of certain conditions: colorectal and breast cancer, type 2 diabetes, and cardiovascular diseases, according to dose-response curves the authors created.

Quantitative guidelines relating to dietary fiber have not been available, the researchers said. With the GRADE method, they determined that there was moderate and low-to-moderate certainty of evidence for the benefits of dietary fiber consumption and whole grain consumption, respectively.

Included in the systematic review were 58 clinical trials and 185 prospective studies for a total of 4,635 adult participants with 135 million person-years of information (one trial in children was included, but analyzed separately from adults). Trials and prospective studies assessing weight loss, supplement use, and participants with a chronic disease were excluded.

 

Food is digested by bathing in enzymes that break down its molecules. Those molecular fragments then pass through the gut wall and are absorbed in our intestines. But our bodies make a limited range of enzymes, so that we cannot break down many of the tough compounds in plants. The term “dietary fiber” refers to those indigestible molecules. These dietary fibers are indigestible only to us. The gut is coated with a layer of mucus, on which sits a carpet of hundreds of species of bacteria, part of the human microbiome. Some of these microbes carry the enzymes needed to break down various kinds of dietary fibers.

 

Scientists at the University of Gothenburg in Sweden are running experiments that are yielding some important new clues about fiber’s role in human health. Their research indicates that fiber doesn’t deliver many of its benefits directly to our bodies. Instead, the fiber we eat feeds billions of bacteria in our guts. Keeping them happy means our intestines and immune systems remain in good working order. The scientists have recently reported that the microbes are involved in the benefits obtained from the fruits-and-vegetables diet. Research proved that low fiber diet decreases the gut bacteria population by tenfold.

 

Along with changes to the microbiome there were also rapid changes observed in the experimental mice. Their intestines got smaller, and its mucus layer thinner. As a result, bacteria wound up much closer to the intestinal wall, and that encroachment triggered an immune reaction. After a few days on the low-fiber diet, mouse intestines developed chronic inflammation. After a few weeks, they started putting on fat and developing higher blood sugar levels. Inflammation can help fight infections, but if it becomes chronic, it can harm our bodies. Among other things, chronic inflammation may interfere with how the body uses the calories in food, storing more of it as fat rather than burning it for energy.

 

In a way fiber benefits human health is by giving, indirectly, another source of food. When bacteria finished harvesting the energy in the dietary fiber, they cast off the fragments as waste. That waste — in the form of short-chain fatty acids — is absorbed by intestinal cells, which use it as fuel. But the gut’s microbes do more than just make energy. They also send messages. Intestinal cells rely on chemical signals from the bacteria to work properly. The cells respond to the signals by multiplying and making a healthy supply of mucus. They also release bacteria-killing molecules. By generating these responses, gut bacteria help to maintain a peaceful coexistence with the immune system. They rest on the gut’s mucus layer at a safe distance from the intestinal wall. Any bacteria that wind up too close get wiped out by antimicrobial poisons.

 

A diet of fiber-rich foods, such as fruits and vegetables, reduces the risk of developing diabetes, heart disease and arthritis. Eating more fiber seems to lower people’s mortality rate, whatever be the cause. Researchers hope that they will learn more about how fiber influences the microbiome to use it as a way to treat disorders. Lowering inflammation with fiber may also help in the treatment of immune disorders such as inflammatory bowel disease. Fiber may also help reverse obesity. They found that fiber supplements helped obese people to lose weight. It’s possible that each type of fiber feeds a particular set of bacteria, which send their own important signals to our bodies.

 

References:

 

https://www.nytimes.com/2018/01/01/science/food-fiber-microbiome-inflammation.html

 

 

https://www.ncbi.nlm.nih.gov/pubmed/29276171

 

https://www.ncbi.nlm.nih.gov/pubmed/29276170

 

https://www.ncbi.nlm.nih.gov/pubmed/29486139

 

https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fiber/art-20043983

 

https://nutritiouslife.com/eat-empowered/high-fiber-diet/

 

http://www.eatingwell.com/article/287742/10-amazing-health-benefits-of-eating-more-fiber/

 

http://www.cookinglight.com/eating-smart/nutrition-101/what-is-a-high-fiber-diet

 

https://www.helpguide.org/articles/healthy-eating/high-fiber-foods.htm

 

https://www.gicare.com/diets/high-fiber-diet/

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

The trillions of microbes in the human gut are known to aid the body in synthesizing key vitamins and other nutrients. But this new study suggests that things can sometimes be more adversarial.

 

Choline is a key nutrient in a range of metabolic processes, as well as the production of cell membranes. Researchers identified a strain of choline-metabolizing E. coli that, when transplanted into the guts of germ-free mice, consumed enough of the nutrient to create a choline deficiency in them, even when the animals consumed a choline-rich diet.

 

This new study indicate that choline-utilizing bacteria compete with the host for this nutrient, significantly impacting plasma and hepatic levels of methyl-donor metabolites and recapitulating biochemical signatures of choline deficiency. Mice harboring high levels of choline-consuming bacteria showed increased susceptibility to metabolic disease in the context of a high-fat diet.

 

DNA methylation is essential for normal development and has been linked to everything from aging to carcinogenesis. This study showed changes in DNA methylation across multiple tissues, not just in adult mice with a choline-consuming gut microbiota, but also in the pups of those animals while they developed in utero.

 

Bacterially induced reduction of methyl-donor availability influenced global DNA methylation patterns in both adult mice and their offspring and engendered behavioral alterations. This study reveal an underappreciated effect of bacterial choline metabolism on host metabolism, epigenetics, and behavior.

 

The choline-deficient mice with choline-consuming gut microbes also showed much higher rates of infanticide, and exhibited signs of anxiety, with some mice over-grooming themselves and their cage-mates, sometimes to the point of baldness.

 

Tests have also shown as many as 65 percent of healthy individuals carry genes that encode for the enzyme that metabolizes choline in their gut microbiomes. This work suggests that interpersonal differences in microbial metabolism should be considered when determining optimal nutrient intake requirements.

 

References:

 

https://news.harvard.edu/gazette/story/2017/11/harvard-research-suggests-microbial-menace/

 

http://www.cell.com/cell-host-microbe/fulltext/S1931-3128(17)30304-9

 

https://www.ncbi.nlm.nih.gov/pubmed/23151509

 

https://www.ncbi.nlm.nih.gov/pubmed/25677519

 

http://mbio.asm.org/content/6/2/e02481-14

 

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Using “Cerebral Organoids” to Trace the Elemental Composition of a Developing Brain

Curator: Marzan Khan, B.Sc

A research focused on the detection of micronutrient accumulation in the developing brain has been conducted recently by a team of scientific researchers in Brazil(1). Their study was comprised of a cutting-edge technology human cerebral organoids, which are a close equivalent of the embryonic brain, in in-vitro models to identify some of the minerals essential during brain development using synchroton radiation(1). Since the majority of studies done on this matter have relied on samples from animal models, the adult brain or post-mortem tissue, this technique has been dubbed the “closest and most complete study system to date for understanding human neural development and its pathological manifestations”(2).

Cerebral organoids are three-dimensional miniature structures derived from human pluripotent stem cells that further differentiate into structures closely resembling the developing brain(2). Concentrating on two different time points during the developmental progression, the researchers illustrated the micronutrient content during an interval of high cell division marked on day 30 as well as day 40 when the organoids were starting to become mature neurons that secrete neurotransmitters, arranging into layers and forming synapses(2).

Synchrotron radiation X-ray fluorescence (SR-XRF) spectroscopy was used to discern each type of element present(2). After an incident beam of X-ray was directed at the sample, each atom emitted a distinct photon signature(2). Phosphorus (P), Potassium (P), Sulphur (S), Calcium (Ca), Iron (Fe), and Zinc (Zn) were found to be present in the samples in significant concentrations(2). Manganese (Mn), Nickel (Ni) and Copper (Cu) were also detected, but in negligible amounts, and therefore tagged as “ultratrace” elements(2). The distribution of these minerals, their concentration as well as their occurrence in pairs were examined at each interval(2).

Phosphorus was discovered to be the most abundant element in the cerebral organoid samples(3). Between the two time points at 30 days (cell proliferation) and 45 days (neuronal maturation) there was a marked decrease in P content(2). Since phosphorus is a major component of nucleotides and phospholipids, this reduction was clarified as a shift from a stage of cell division that requires the production of DNA and phospholipids, to a migratory and differentiation phase(2). Potassium levels were maintained during both phases, substantiating its role in mitotic cell division as well as cell migration over long distances(2). Sulfur levels were reportedly high at 30 days and 45 days(2). It was hypothesized that this element was responsible for the patterning of the organoids(2). Calcium, known to control transcription factors involved in neuronal differentiation and survival were detected in the micromolar range, along with zinc and iron(2). Zinc commits the differentiation of pluripotent stem cells into neuronal cells and iron is necessary for neuronal tissue expansion(2).

The cells in an embryo start to differentiate very early on- the neural plate is formed on the 16th day of contraception, which further folds and bulges out to become the nervous system (containing the brain and spinal cord regions)(3). Nutrients obtained from the mother are the primary sources of diet and energy for a developing embryo to fully differentiate and specialize into different organs(2). Lack of proper nutrition in pregnant mothers has been linked to many neurodegenerative diseases occurring in their progeny(2). Spina bifida which is characterized by the incomplete development of the brain and spinal cord, is a classic example of maternal malnutrition(2,4). Paucity of minerals in the diet of pregnant women are known to hamper learning and memory in children(2). Even Schizophrenia, Parkinson’s and Huntington’s disease have been associated to malnourishment(2). By showing the different types of elements present in statistically significant concentrations in cerebral organoids, the results of this study underscore the necessity of a healthy nourishment available to mothers during pregnancy for optimal development of the fetal brain(2).

References:

1.Kenny Walter. 02/10/2017. Study focuses on Microcutrients in Human Minibrains. RandDMagazine.http://www.rdmag.com/article/2017/02/study-focuses-micronutrients-human-minibrains?et_cid=5825577&et_rid=461755519&type=cta&et_cid=5825577&et_rid=461755519&linkid=conten

2.Sartore RC, Cardoso SC, Lages YVM, Paraguassu JM, Stelling MP, Madeiro da Costa RF, Guimaraes MZ, Pérez CA, Rehen SK.(2017)Trace elements during primordial plexiform network formation in human cerebral organoids. PeerJ 5:e2927https://doi.org/10.7717/peerj.292

3.Fetal Development: Baby’s Nervous System and Brain; What to expect; 20/07/201. http://www.whattoexpect.com/pregnancy/fetal-brain-nervous-system/

4. Spina Bifida Fact Sheet; National Institute of Neurological Disorders and Stroke National Institutes of Health, Bethesda, MD 20892

https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Spina-Bifida-Fact-Sheet

Other related articles published in this Open Access Online Scientific Journal include the following:

 

Zinc-Finger Nucleases (ZFNs) and Transcription Activator–Like Effector Nucleases (TALENs)

Reporter: Larry H Bernstein, MD, FCAP

https://pharmaceuticalintelligence.com/2013/03/04/talens-and-zfns/

 

Calcium Regulation Key Mechanism Discovered: New Potential for Neuro-degenerative Diseases Drug Development

Reporter: Aviva Lev-Ari, PhD., RN

https://pharmaceuticalintelligence.com/2013/01/17/calcium-regulation-key-mechanism-discovered-new-potential-for-neuro-degenerative-diseases-drug-development/

 

How Methionine Imbalance with Sulfur-Insufficiency Leads to Hyperhomocysteinemia

Curator: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2013/04/04/sulfur-deficiency-leads_to_hyperhomocysteinemia/

 

Erythropoietin (EPO) and Intravenous Iron (Fe) as Therapeutics for Anemia in Severe and Resistant CHF: The Elevated N-terminal proBNP Biomarker

Co-Author of the FIRST Article: Larry H. Bernstein, MD, FCAP

Reviewer and Curator of the SECOND and of the THIRD Articles: Larry H. Bernstein, MD, FCAP

Article Architecture Curator: Aviva Lev-Ari, PhD., RN

https://pharmaceuticalintelligence.com/2013/12/10/epo-as-therapeutics-for-anemia-in-chf/

 

The relationship of S amino acids to marasmic and kwashiorkor PEM

Larry H. Bernstein, MD, FCAP, Curator

https://pharmaceuticalintelligence.com/2015/10/24/the-relationship-of-s-amino-acids-to-marasmic-and-kwashiorkor-pem/

 

Mutations in a Sodium-gated Potassium Channel Subunit Gene related to a subset of severe Nocturnal Frontal Lobe Epilepsy

Reporter: Aviva Lev-Ari, PhD., RN

https://pharmaceuticalintelligence.com/2012/10/22/mutations-in-a-sodium-gated-potassium-channel-subunit-gene-to-a-subset-of-severe-nocturnal-frontal-lobe-epilepsy/

 

Copper and its role on “progressive neurodegeneration” and death

Reported by: Dr. Venkat S. Karra, Ph.D.

https://pharmaceuticalintelligence.com/2012/08/14/copper-and-its-role-on-progressive-neurodegeneration-and-death/

 

Metabolomics, Metabonomics and Functional Nutrition: the next step in nutritional metabolism and biotherapeutics

Reviewer and Curator: Larry H. Bernstein, MD, FCAP 

https://pharmaceuticalintelligence.com/2014/08/22/metabolomics-metabonomics-and-functional-nutrition-the-next-step-in-nutritional-metabolism-and-biotherapeutics/

 

Nutrition and Aging

Curator: Larry H Bernstein, MD, FCAP

https://pharmaceuticalintelligence.com/2015/10/25/nutrition-and-aging/

 

The Three Parent Technique to Avoid Mitochondrial Disease in Embryo

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

https://pharmaceuticalintelligence.com/2016/10/07/the-three-parent-technique-to-avoid-mitochondrial-disease-in-embryo/

 

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“Minerals in Medicine” –  40 Minerals that are crucial to Human Health and Biomedicine: Exhibit by NIH Clinical Center and The Smithsonian Institution National Museum of Natural History

Reporter: Aviva Lev-Ari, PhD, RN

 

Friday, September 9, 2016

NIH Clinical Center and The Smithsonian Institution partner to launch Minerals in Medicine Exhibition

What

The National Institutes of Health Clinical Center, in partnership with The Smithsonian Institution National Museum of Natural History, will open a special exhibition of more than 40 minerals that are crucial to human health and biomedicine. “Minerals in Medicine” is designed to enthrall and enlighten NIH Clinical Center’s patients, their loved ones, and the NIH community. Media are invited into America’s Research Hospital, the NIH Clinical Center, to experience this unique exhibition during a ribbon cutting ceremony on Monday September 12 at 4pm.

Beyond taking in the minerals’ arresting beauty, spectators can learn about their important role in keeping the human body healthy, and in enabling the creation of life-saving medicines and cutting edge medical equipment that is used in the NIH Clinical Center and healthcare facilities worldwide. The exhibition, which is on an eighteen-month loan from the National Museum of Natural History, includes specimens that were handpicked from the museum’s vast collection by NIH physicians in partnership with Smithsonian Institution geologists. Some of the minerals on display were obtained regionally as they are part of the Maryland and Virginia landscape.

Who

  • John I. Gallin, M.D., Director of the NIH Clinical Center
  • Jeffrey E. Post, Ph.D., Smithsonian Institution National Museum of Natural History, Chair of the Department of Mineral Sciences and Curator of the National Gem and Mineral Collection

When

Monday, September 12, 2016, 4:00 – 5:00 p.m.

Where

NIH Clinical Center (Building 10), 10 Center Drive, Bethesda, MD, 20892; 1st Floor near Admissions

How

RSVP encouraged, but not required, to attend in person. NIH Visitors Map: http://www.ors.od.nih.gov/maps/Pages/NIH-Visitor-Map.aspx

About the NIH Clinical Center: The NIH Clinical Center is the clinical research hospital for the National Institutes of Health. Through clinical research, clinician-investigators translate laboratory discoveries into better treatments, therapies and interventions to improve the nation’s health. More information: http://clinicalcenter.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

SOURCE

https://www.nih.gov/news-events/news-releases/nih-clinical-center-smithsonian-institution-partner-launch-minerals-medicine-exhibition

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Selye’s Riddle solved

Larry H. Bernstein, mD, FCAP, Curator

LPBI

 

Mathematicians Solve 78-year-old Mystery

Mathematicians developed a solution to Selye's riddle which has puzzled scientists for almost 80 years.
Mathematicians developed a solution to Selye’s riddle which has puzzled scientists for almost 80 years.

In previous research, it was suggested that adaptation of an animal to different factors looks like spending of one resource, and that the animal dies when this resource is exhausted. In 1938, Hans Selye introduced “adaptation energy” and found strong experimental arguments in favor of this hypothesis. However, this term has caused much debate because, as it cannot be measured as a physical quantity, adaptation energy is not strictly energy.

 

Evolution of adaptation mechanisms: Adaptation energy, stress, and oscillating death

Alexander N. Gorbana, , Tatiana A. Tyukinaa, Elena V. Smirnovab, Lyudmila I. Pokidyshevab,

Highlights

•   We formalize Selye׳s ideas about adaptation energy and dynamics of adaptation.
•   A hierarchy of dynamic models of adaptation is developed.
•   Adaptation energy is considered as an internal coordinate on the ‘dominant path’ in the model of adaptation.
•   The optimal distribution of resources for neutralization of harmful factors is studied.
•   The phenomena of ‘oscillating death’ and ‘oscillating remission’ are predicted.       

In previous research, it was suggested that adaptation of an animal to different factors looks like spending of one resource, and that the animal dies when this resource is exhausted.

In 1938, Selye proposed the notion of adaptation energy and published ‘Experimental evidence supporting the conception of adaptation energy.’ Adaptation of an animal to different factors appears as the spending of one resource. Adaptation energy is a hypothetical extensive quantity spent for adaptation. This term causes much debate when one takes it literally, as a physical quantity, i.e. a sort of energy. The controversial points of view impede the systematic use of the notion of adaptation energy despite experimental evidence. Nevertheless, the response to many harmful factors often has general non-specific form and we suggest that the mechanisms of physiological adaptation admit a very general and nonspecific description.

We aim to demonstrate that Selye׳s adaptation energy is the cornerstone of the top-down approach to modelling of non-specific adaptation processes. We analyze Selye׳s axioms of adaptation energy together with Goldstone׳s modifications and propose a series of models for interpretation of these axioms. Adaptation energy is considered as an internal coordinate on the ‘dominant path’ in the model of adaptation. The phenomena of ‘oscillating death’ and ‘oscillating remission’ are predicted on the base of the dynamical models of adaptation. Natural selection plays a key role in the evolution of mechanisms of physiological adaptation. We use the fitness optimization approach to study of the distribution of resources for neutralization of harmful factors, during adaptation to a multifactor environment, and analyze the optimal strategies for different systems of factors.

In this work, an international team of researchers, led by Professor Alexander N. Gorban from the University of Leicester, have developed a solution to Selye’s riddle, which has puzzled scientists for almost 80 years.

Alexander N. Gorban, Professor of Applied Mathematics in the Department of Mathematics at the University of Leicester, said: “Nobody can measure adaptation energy directly, indeed, but it can be understood by its place already in simple models. In this work, we develop a hierarchy of top-down models following Selye’s findings and further developments. We trust Selye’s intuition and experiments and use the notion of adaptation energy as a cornerstone in a system of models. We provide a ‘thermodynamic-like’ theory of organism resilience that, just like classical thermodynamics, allows for economics metaphors, such as cost and bankruptcy and, more importantly, is largely independent of a detailed mechanistic explanation of what is ‘going on underneath’.”

Adaptation energy is considered as an internal coordinate on the “dominant path” in the model of adaptation. The phenomena of “oscillating death” and “oscillating remission,” which have been observed in clinic for a long time, are predicted on the basis of the dynamical models of adaptation. The models, based on Selye’s idea of adaptation energy, demonstrate that the oscillating remission and oscillating death do not need exogenous reasons. The developed theory of adaptation to various factors gives the instrument for the early anticipation of crises.

Professor Alessandro Giuliani from Istituto Superiore di Sanità in Rome commented on the work, saying: “Gorban and his colleagues dare to make science adopting the thermodynamics style: they look for powerful principles endowed with predictive ability in the real world before knowing the microscopic details. This is, in my opinion, the only possible way out from the actual repeatability crisis of mainstream biology, where a fantastic knowledge of the details totally fails to predict anything outside the test tube.1

Citation: Alexander N. Gorban, Tatiana A. Tyukina, Elena V. Smirnova, Lyudmila I. Pokidysheva. Evolution of adaptation mechanisms: Adaptation energy, stress, and oscillating death. Journal of Theoretical Biology, 2016; DOI:10.1016/j.jtbi.2015.12.017. Voosen P. (2015) Amid a Sea of False Findings NIH tries Reform, The Chronicle of Higher Education.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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Inflammatory Disorders: Articles published @ pharmaceuticalintelligence.com

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN

This is a compilation of articles on Inflammatory Disorders that were published 

@ pharmaceuticalintelligence.com, since 4/2012 to date

There are published works that have not been included.  However, there is a substantial amount of material in the following categories:

  1. The systemic inflammatory response
    https://pharmaceuticalintelligence.com/2014/11/08/introduction-to-impairments-in-pathological-states-endocrine-disorders-stress-hypermetabolism-cancer/
    https://pharmaceuticalintelligence.com/2014/11/09/summary-and-perspectives-impairments-in-pathological-states-endocrine-disorders-stress-hypermetabolism-cancer/
    https://pharmaceuticalintelligence.com/2015/12/19/neutrophil-serine-proteases-in-disease-and-therapeutic-considerations/
    https://pharmaceuticalintelligence.com/2014/03/21/what-is-the-key-method-to-harness-inflammation-to-close-the-doors-for-many-complex-diseases/
    https://pharmaceuticalintelligence.com/2012/08/20/therapeutic-targets-for-diabetes-and-related-metabolic-disorders/
    https://pharmaceuticalintelligence.com/2012/12/03/a-second-look-at-the-transthyretin-nutrition-inflammatory-conundrum/
    https://pharmaceuticalintelligence.com/2012/07/08/zebrafish-provide-insights-into-causes-and-treatment-of-human-diseases/
    https://pharmaceuticalintelligence.com/2016/01/25/ibd-immunomodulatory-effect-of-retinoic-acid-il-23il-17a-axis-correlates-with-the-nitric-oxide-pathway/
    https://pharmaceuticalintelligence.com/2015/11/29/role-of-inflammation-in-disease/
    https://pharmaceuticalintelligence.com/2013/03/06/can-resolvins-suppress-acute-lung-injury/
    https://pharmaceuticalintelligence.com/2015/02/26/acute-lung-injury/
  2. sepsis
    https://pharmaceuticalintelligence.com/2012/10/20/nitric-oxide-and-sepsis-hemodynamic-collapse-and-the-search-for-therapeutic-options/
  3. vasculitis
    https://pharmaceuticalintelligence.com/2015/02/26/acute-lung-injury/
    https://pharmaceuticalintelligence.com/2012/11/26/the-molecular-biology-of-renal-disorders/
    https://pharmaceuticalintelligence.com/2012/11/20/the-potential-for-nitric-oxide-donors-in-renal-function-disorders/
  4. neurodegenerative disease
    https://pharmaceuticalintelligence.com/2013/02/27/ustekinumab-new-drug-therapy-for-cognitive-decline-resulting-from-neuroinflammatory-cytokine-signaling-and-alzheimers-disease/
    https://pharmaceuticalintelligence.com/2016/01/26/amyloid-and-alzheimers-disease/
    https://pharmaceuticalintelligence.com/2016/02/15/alzheimers-disease-tau-art-thou-or-amyloid/
    https://pharmaceuticalintelligence.com/2016/01/26/beyond-tau-and-amyloid/
    https://pharmaceuticalintelligence.com/2015/12/10/remyelination-of-axon-requires-gli1-inhibition/
    https://pharmaceuticalintelligence.com/2015/11/28/neurovascular-pathways-to-neurodegeneration/
    https://pharmaceuticalintelligence.com/2015/11/13/new-alzheimers-protein-aicd-2/
    https://pharmaceuticalintelligence.com/2015/10/31/impairment-of-cognitive-function-and-neurogenesis/
    https://pharmaceuticalintelligence.com/2014/05/06/bwh-researchers-genetic-variations-can-influence-immune-cell-function-risk-factors-for-alzheimers-diseasedm-and-ms-later-in-life/
  5. cancer immunology
    https://pharmaceuticalintelligence.com/2013/04/12/innovations-in-tumor-immunology/
    https://pharmaceuticalintelligence.com/2016/01/09/signaling-of-immune-response-in-colon-cancer/
    https://pharmaceuticalintelligence.com/2015/05/12/vaccines-small-peptides-aptamers-and-immunotherapy-9/
    https://pharmaceuticalintelligence.com/2015/01/30/viruses-vaccines-and-immunotherapy/
    https://pharmaceuticalintelligence.com/2015/10/20/gene-expression-and-adaptive-immune-resistance-mechanisms-in-lymphoma/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
  6. autoimmune diseases: rheumatoid arthritis, colitis, ileitis, …
    https://pharmaceuticalintelligence.com/2016/02/11/intestinal-inflammatory-pharmaceutics/
    https://pharmaceuticalintelligence.com/2016/01/07/two-new-drugs-for-inflammatory-bowel-syndrome-are-giving-patients-hope/
    https://pharmaceuticalintelligence.com/2015/12/16/contribution-to-inflammatory-bowel-disease-ibd-of-bacterial-overgrowth-in-gut-on-a-chip/
    https://pharmaceuticalintelligence.com/2016/02/13/cytokines-in-ibd/
    https://pharmaceuticalintelligence.com/2016/01/23/autoimmune-inflammtory-bowl-diseases-crohns-disease-ulcerative-colitis-potential-roles-for-modulation-of-interleukins-17-and-23-signaling-for-therapeutics/
    https://pharmaceuticalintelligence.com/2014/10/14/autoimmune-disease-single-gene-eliminates-the-immune-protein-isg15-resulting-in-inability-to-resolve-inflammation-and-fight-infections-discovery-rockefeller-university/
    https://pharmaceuticalintelligence.com/2015/03/01/diarrheas-bacterial-and-nonbacterial/
    https://pharmaceuticalintelligence.com/2016/02/11/intestinal-inflammatory-pharmaceutics/
    https://pharmaceuticalintelligence.com/2014/01/28/biologics-for-autoimmune-diseases-cambridge-healthtech-institutes-inaugural-may-5-6-2014-seaport-world-trade-center-boston-ma/
    https://pharmaceuticalintelligence.com/2015/11/19/rheumatoid-arthritis-update/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
    https://pharmaceuticalintelligence.com/2013/07/31/confined-indolamine-2-3-dehydrogenase-controls-the-hemostasis-of-immune-responses-for-good-and-bad/
    https://pharmaceuticalintelligence.com/2012/09/13/tofacitinib-an-oral-janus-kinase-inhibitor-in-active-ulcerative-colitis/
    https://pharmaceuticalintelligence.com/2013/03/05/approach-to-controlling-pathogenic-inflammation-in-arthritis/
    https://pharmaceuticalintelligence.com/2013/03/05/rheumatoid-arthritis-risk/
    https://pharmaceuticalintelligence.com/2012/07/08/the-mechanism-of-action-of-the-drug-acthar-for-systemic-lupus-erythematosus-sle/
  7. T cells in immunity
    https://pharmaceuticalintelligence.com/2015/09/07/t-cell-mediated-immune-responses-signaling-pathways-activated-by-tlrs/
    https://pharmaceuticalintelligence.com/2015/05/14/allogeneic-stem-cell-transplantation-9-2/
    https://pharmaceuticalintelligence.com/2015/02/19/graft-versus-host-disease/
    https://pharmaceuticalintelligence.com/2014/10/14/autoimmune-disease-single-gene-eliminates-the-immune-protein-isg15-resulting-in-inability-to-resolve-inflammation-and-fight-infections-discovery-rockefeller-university/
    https://pharmaceuticalintelligence.com/2014/05/27/immunity-and-host-defense-a-bibliography-of-research-technion/
    https://pharmaceuticalintelligence.com/2013/08/04/the-delicate-connection-ido-indolamine-2-3-dehydrogenase-and-immunology/
    https://pharmaceuticalintelligence.com/2013/07/31/confined-indolamine-2-3-dehydrogenase-controls-the-hemostasis-of-immune-responses-for-good-and-bad/
    https://pharmaceuticalintelligence.com/2013/04/14/immune-regulation-news/

Proteomics, metabolomics and diabetes

https://pharmaceuticalintelligence.com/2015/11/16/reducing-obesity-related-inflammation/

https://pharmaceuticalintelligence.com/2015/10/25/the-relationship-of-stress-hypermetabolism-to-essential-protein-needs/

https://pharmaceuticalintelligence.com/2015/10/24/the-relationship-of-s-amino-acids-to-marasmic-and-kwashiorkor-pem/

https://pharmaceuticalintelligence.com/2015/10/24/the-significant-burden-of-childhood-malnutrition-and-stunting/

https://pharmaceuticalintelligence.com/2015/04/14/protein-binding-protein-protein-interactions-therapeutic-implications-7-3/

https://pharmaceuticalintelligence.com/2015/03/07/transthyretin-and-the-stressful-condition/

https://pharmaceuticalintelligence.com/2015/02/13/neural-activity-regulating-endocrine-response/

https://pharmaceuticalintelligence.com/2015/01/31/proteomics/

https://pharmaceuticalintelligence.com/2015/01/17/proteins-an-evolutionary-record-of-diversity-and-adaptation/

https://pharmaceuticalintelligence.com/2014/11/01/summary-of-signaling-and-signaling-pathways/

https://pharmaceuticalintelligence.com/2014/10/31/complex-models-of-signaling-therapeutic-implications/

https://pharmaceuticalintelligence.com/2014/10/24/diabetes-mellitus/

https://pharmaceuticalintelligence.com/2014/10/16/metabolomics-summary-and-perspective/

https://pharmaceuticalintelligence.com/2014/10/14/metabolic-reactions-need-just-enough/

https://pharmaceuticalintelligence.com/2014/11/03/introduction-to-protein-synthesis-and-degradation/

https://pharmaceuticalintelligence.com/2015/09/25/proceedings-of-the-nyas/

https://pharmaceuticalintelligence.com/2014/10/31/complex-models-of-signaling-therapeutic-implications/

https://pharmaceuticalintelligence.com/2014/03/21/what-is-the-key-method-to-harness-inflammation-to-close-the-doors-for-many-complex-diseases/

https://pharmaceuticalintelligence.com/2013/03/05/irf-1-deficiency-skews-the-differentiation-of-dendritic-cells/

https://pharmaceuticalintelligence.com/2012/11/26/new-insights-on-no-donors/

https://pharmaceuticalintelligence.com/2012/11/20/the-potential-for-nitric-oxide-donors-in-renal-function-disorders/

 

 

 

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