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Archive for the ‘Metabolomics’ Category


Live 11:00 AM- 12:00 Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health : Opening Remarks October 19, 2018

Reporter: Stephen J. Williams, Ph.D.

11:00 Welcome

 

 

Prof. Antonio Giordano, MD, PhD.

Director and President of the Sbarro Health Research Organization, College of Science and Technology, Temple University

Welcome to this symposium on Italian lifestyle and health.  This is similar to a symposium we had organized in New York.  A year ago Bloomberg came out with a study on higher longevity of the italian population and this study was concluded that this increased longevity was due to the italian lifestyle and diet especially in the southern part of Italy, a region which is older than Rome (actually founded by Greeks and Estonians).  However this symposium will delve into the components of this healthy Italian lifestyle which contributes to this longevity effect.  Some of this work was done in collaboration with Temple University and sponsored by the Italian Consulate General in Philadelphia ( which sponsors programs in this area called Ciao Philadelphia).

Greetings: Fucsia Nissoli Fitzgerald, Deputy elected in the Foreign Circumscription – North and Central America Division

Speaking for the Consulate General is Francesca  Cardurani-Meloni.   I would like to talk briefly about the Italian cuisine and its evolution, from the influence of the North and South Italy, economic factors, and influence by other cultures.  Italian cooking is about simplicity, cooking with what is in season and freshest.  The meal is not about the food but about comfort around the table, and comparible to a cullinary heaven, about sharing with family and friends, and bringing the freshest ingredients to the table.

Consul General, Honorable Pier Attinio Forlano, General Consul of Italy in Philadelphia

 

11:30 The Impact of Environment and Life Style in Human Disease

Prof. Antonio Giordano MD, PhD.

 

 

 

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

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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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  1. Lungs can supply blood stem cells and also produce platelets: Lungs, known primarily for breathing, play a previously unrecognized role in blood production, with more than half of the platelets in a mouse’s circulation produced there. Furthermore, a previously unknown pool of blood stem cells has been identified that is capable of restoring blood production when bone marrow stem cells are depleted.

 

  1. A new drug for multiple sclerosis: A new multiple sclerosis (MS) drug, which grew out of the work of UCSF (University of California, San Francisco) neurologist was approved by the FDA. Ocrelizumab, the first drug to reflect current scientific understanding of MS, was approved to treat both relapsing-remitting MS and primary progressive MS.

 

  1. Marijuana legalized – research needed on therapeutic possibilities and negative effects: Recreational marijuana will be legal in California starting in January, and that has brought a renewed urgency to seek out more information on the drug’s health effects, both positive and negative. UCSF scientists recognize marijuana’s contradictory status: the drug has proven therapeutic uses, but it can also lead to tremendous public health problems.

 

  1. Source of autism discovered: In a finding that could help unlock the fundamental mysteries about how events early in brain development lead to autism, researchers traced how distinct sets of genetic defects in a single neuronal protein can lead to either epilepsy in infancy or to autism spectrum disorders in predictable ways.

 

  1. Protein found in diet responsible for inflammation in brain: Ketogenic diets, characterized by extreme low-carbohydrate, high-fat regimens are known to benefit people with epilepsy and other neurological illnesses by lowering inflammation in the brain. UCSF researchers discovered the previously undiscovered mechanism by which a low-carbohydrate diet reduces inflammation in the brain. Importantly, the team identified a pivotal protein that links the diet to inflammatory genes, which, if blocked, could mirror the anti-inflammatory effects of ketogenic diets.

 

  1. Learning and memory failure due to brain injury is now restorable by drug: In a finding that holds promise for treating people with traumatic brain injury, an experimental drug, ISRIB (integrated stress response inhibitor), completely reversed severe learning and memory impairments caused by traumatic brain injury in mice. The groundbreaking finding revealed that the drug fully restored the ability to learn and remember in the brain-injured mice even when the animals were initially treated as long as a month after injury.

 

  1. Regulatory T cells induce stem cells for promoting hair growth: In a finding that could impact baldness, researchers found that regulatory T cells, a type of immune cell generally associated with controlling inflammation, directly trigger stem cells in the skin to promote healthy hair growth. An experiment with mice revealed that without these immune cells as partners, stem cells cannot regenerate hair follicles, leading to baldness.

 

  1. More intake of good fat is also bad: Liberal consumption of good fat (monounsaturated fat) – found in olive oil and avocados – may lead to fatty liver disease, a risk factor for metabolic disorders like type 2 diabetes and hypertension. Eating the fat in combination with high starch content was found to cause the most severe fatty liver disease in mice.

 

  1. Chemical toxicity in almost every daily use products: Unregulated chemicals are increasingly prevalent in products people use every day, and that rise matches a concurrent rise in health conditions like cancers and childhood diseases, Thus, researcher in UCSF is working to understand the environment’s role – including exposure to chemicals – in health conditions.

 

  1. Cytomegalovirus found as common factor for diabetes and heart disease in young women: Cytomegalovirus is associated with risk factors for type 2 diabetes and heart disease in women younger than 50. Women of normal weight who were infected with the typically asymptomatic cytomegalovirus, or CMV, were more likely to have metabolic syndrome. Surprisingly, the reverse was found in those with extreme obesity.

 

References:

 

https://www.ucsf.edu/news/2017/12/409241/most-popular-science-stories-2017

 

https://www.ucsf.edu/news/2017/03/406111/surprising-new-role-lungs-making-blood

 

https://www.ucsf.edu/news/2017/03/406296/new-multiple-sclerosis-drug-ocrelizumab-could-halt-disease

 

https://www.ucsf.edu/news/2017/06/407351/dazed-and-confused-marijuana-legalization-raises-need-more-research

 

https://www.ucsf.edu/news/2017/01/405631/autism-researchers-discover-genetic-rosetta-stone

 

https://www.ucsf.edu/news/2017/09/408366/how-ketogenic-diets-curb-inflammation-brain

 

https://www.ucsf.edu/news/2017/07/407656/drug-reverses-memory-failure-caused-traumatic-brain-injury

 

https://www.ucsf.edu/news/2017/05/407121/new-hair-growth-mechanism-discovered

 

https://www.ucsf.edu/news/2017/06/407536/go-easy-avocado-toast-good-fat-can-still-be-bad-you-research-shows

 

https://www.ucsf.edu/news/2017/06/407416/toxic-exposure-chemicals-are-our-water-food-air-and-furniture

 

https://www.ucsf.edu/news/2017/02/405871/common-virus-tied-diabetes-heart-disease-women-under-50

 

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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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The Biologic Roles of Leptin in Metabolism, Leptin Physiology and Obesity: On the Mechanism of Action of the Hormone in Energy Balance

Reporter: Aviva Lev-Ari, PhD, RN

 

More than $140 billion is spent each year in the United States to treat obesity-related diseases, according to the CDC.

Worldwide obesity rates have doubled since 1980, and most people now live in countries where more deaths are caused by overweight and obesity than by malnourishment, according to the World Health Organization.

Treatment with leptin was approved in the United States in 2014 for use in congenital leptin deficiency as well as in an unusual syndrome of lipodystrophy, but the protein has not been readily available for clinical experiments.

These are the conclusions in a commentary published June 22 in Cell Metabolism by Harvard Medical School metabolism experts Jeffrey Flier and Eleftheria Maratos-Flier.

Flier, the HMS George Higginson Professor of Physiology and Medicine, and Maratos-Flier, HMS professor of medicine at Beth Israel Deaconess Medical Center, have made significant contributions to the understanding of the metabolism of obesity and starvation in general, and of leptin in particular.

The role for leptin as a starvation signal is now well established. [T]he physiologic role of leptin in most individuals may be limited to signaling the response to hunger or starvation, and then reversing that signal as energy stores are restored

Conclusion

“We continue to believe that healthy and lean individuals exist who resist obesity at least in part through their leptin levels, and that some individuals develop obesity because they have insufficiently elevated leptin levels or cellular resistance to leptin,” Flier said.

“But in science, belief and knowledge are two different things, and as much as we may lean toward this belief, we ought to develop evidence for this hypothesis or abandon it in favor of new potential mechanisms for the regulation of body weight,” he said.

SOURCES

Leptin’s Physiologic Role: Does the Emperor of Energy Balance Have No Clothes?

Jeffrey S. Flier'Correspondence information about the author Jeffrey S. Flier

,

Eleftheria Maratos-Flier
Publication stage: In Press Corrected Proof

Seeking evidence for anti-obesity claim – Does the Emperor Have Clothes?

Importance of leptin signaling and signal transducer and activator of transcription-3 activation in mediating the cardiac hypertrophy associated with obesity

Maren Leifheit-Nestler12, Nana-Maria Wagner13, Rajinikanth Gogiraju1,Michael Didié14, Stavros Konstantinides15, Gerd Hasenfuss1and Katrin Schäfer1*

J Translational Medicine: Cardiovascular, Metabolic and Lipoprotein Translation. 2013; 11:170.  http://www.translational-medicine.com/content/11/1/170

http://dx.doi.org/10.1186/1479-5876-11-170

 

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

 

Leptin signaling in mediating the cardiac hypertrophy associated with obesity

Larry H Bernstein, MD, FCAP, Reviewer, and Aviva Lev-Ari, PhD, RN

 

Leptin and Puberty

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

 

Pregnancy with a Leptin-Receptor Mutation

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

 

New Insights into mtDNA, mitochondrial proteins, aging, and metabolic control

Curator: Larry H. Bernstein, MD, FCAP

Adipocyte Derived Stroma Cells: Their Usage in Regenerative Medicine and Reprogramming into Pancreatic Beta-Like Cells

Curator: Evelina Cohn, PhD

Fat Cells Reprogrammed to Make Insulin

Curator: Larry H. Bernstein, MD, FCAP

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Functional Analysis of the Microbiome for Development of Potential Therapeutic Approaches to Weight Regain

Reporter: Aviva Lev-Ari, PhD, RN

 

Transplanting fecal microbes to prevent recurring obesity

Finally, the researchers used these insights to develop new treatments for recurrent obesity. They implanted formerly obese mice with gut microbes from mice that had never been obese. This fecal microbiome transplantation erased the “memory” of obesity in these mice when they were re-exposed to a high-calorie diet, preventing excessive recurrent obesity.

Gut Microbes Contribute to Recurrent ‘Yo-Yo’ Obesity, Study Shows

By Einat Paz-Frankel, NoCamels December 18, 2016

Researchers at Israel’s Weizmann Institute of Science have shown in mice that intestinal microbes – collectively termed the gut microbiome – play an unexpectedly important role in exacerbated post-dieting weight gain, and that this common phenomenon may in the future be prevented or treated by altering the composition or function of the microbiome.

“We’ve shown in obese mice that following successful dieting and weight loss, the microbiome retains a ‘memory’ of previous obesity,” Elinav said in a statement. “This persistent microbiome accelerated the regaining of weight when the mice were put back on a high-calorie diet or ate regular food in excessive amounts.”

http://nocamels.com/2016/12/gut-microbes-recurrent-obesity-diet/

 

Original Research

Persistent microbiome alterations modulate the rate of post-dieting weight regain

Nature (2016) doi:10.1038/nature20796

Corrected online

28 November 2016

Article tools

Abstract

In tackling the obesity pandemic, significant efforts are devoted to the development of effective weight reduction strategies, yet many dieting individuals fail to maintain a long-term weight reduction, and instead undergo excessive weight regain cycles. The mechanisms driving recurrent post-dieting obesity remain largely elusive. Here, we identify an intestinal microbiome signature that persists after successful dieting of obese mice, which contributes to faster weight regain and metabolic aberrations upon re-exposure to obesity-promoting conditions and transmits the accelerated weight regain phenotype upon inter-animal transfer. We develop a machine-learning algorithm that enables personalized microbiome-based prediction of the extent of post-dieting weight regain. Additionally, we find that the microbiome contributes to diminished post-dieting flavonoid levels and reduced energy expenditure, and demonstrate that flavonoid-based ‘post-biotic’ intervention ameliorates excessive secondary weight gain. Together, our data highlight a possible microbiome contribution to accelerated post-dieting weight regain, and suggest that microbiome-targeting approaches may help to diagnose and treat this common disorder.

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metabolomics-seriesdindividualred-page2

Metabolic Genomics & Pharmaceutics

2015

http://www.amazon.com/dp/B012BB0ZF0

 

Author, Curator and Editor

Larry H Bernstein, MD, FCAP

Chief Scientific Officer

Leaders in Pharmaceutical Business Intelligence

Larry.bernstein@gmail.com

Chapter 1: Metabolic Pathways

1.1            Carbohydrate Metabolism

1.2            Studies of Respiration Lead to Acetyl CoA

1.3            Pentose Shunt, Electron Transfer, Galactose, more Lipids in brief

1.4            The Multi-step Transfer of Phosphate Bond and Hydrogen Exchange Energy

1.5            Diabetes Mellitus

1.6            Glycosaminoglycans, Mucopolysaccharides, L-iduronidase, Enzyme Therapy

Chapter 2: Lipid Metabolism

2.1            Lipid Classification System

2.2            Essential Fatty Acids

2.3            Lipid Oxidation and Synthesis of Fatty Acids

2.4            Cholesterol and Regulation of Liver Synthetic Pathways

2.5            Sex hormones, Adrenal cortisol, Prostaglandins

2.6            Cytoskeleton and Cell Membrane Physiology

2.7            Pharmacological Action of Steroid hormone

Chapter 3: Cell Signaling

3.1            Signaling and Signaling Pathways

3.2            Signaling Transduction Tutorial

3.3            Selected References to Signaling and Metabolic Pathways in Leaders in Pharmaceutical Intelligence

3.4            Integrins, Cadherins, Signaling and the Cytoskeleton

3.5            Complex Models of Signaling: Therapeutic Implications

3.6            Functional Correlates of Signaling Pathways

Chapter 4: Protein Synthesis and Degradation

4.1            The Role and Importance of Transcription Factors

4.2            RNA and the Transcription of the Genetic Code

4.3            9:30 – 10:00, 6/13/2014, David Bartel “MicroRNAs, Poly(A) tails and Post-transcriptional Gene Regulation

4.4            Transcriptional Silencing and Longevity Protein Sir2

4.5            Ca2+ Signaling: Transcriptional Control

4.6            Long Noncoding RNA Network regulates PTEN Transcription

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

4.8            Cardiac Ca2+ Signaling: Transcriptional Control

4.9            Transcription Factor Lyl-1 Critical in Producing Early T-Cell Progenitors

4.10            Human Frontal Lobe Brain: Specific Transcriptional Networks

4.11            Somatic, Germ-cell, and Whole Sequence DNA in Cell Lineage and Disease

Chapter 5:  Sub-cellular Structure

5.1            Mitochondria: Origin from Oxygen free environment, Role in Aerobic Glycolysis and Metabolic Adaptation

5.2            Mitochondrial Metabolism and Cardiac Function

5.3            Mitochondria: More than just the “Powerhouse of the Cell”

5.4            Mitochondrial Fission and Fusion: Potential Therapeutic Targets?

5.5            Mitochondrial Mutation Analysis might be “1-step” Away

5.6            Autophagy-Modulating Proteins and Small Molecules Candidate Targets for Cancer Therapy: Commentary of Bioinformatics Approaches

5.7            Chromatophagy, A New Cancer Therapy: Starve The Diseased Cell Until It Eats Its Own DNA

5.8           A Curated Census of Autophagy-Modulating Proteins and Small Molecules Candidate Targets for Cancer Therapy

5.9           Role of Calcium, the Actin Skeleton, and Lipid Structures in Signaling and Cell Motility

Chapter 6: Proteomics

6.1            Proteomics, Metabolomics, Signaling Pathways, and Cell Regulation: a Compilation of Articles in the Journal http://pharmaceuticalintelligence.com

6.2            A Brief Curation of Proteomics, Metabolomics, and Metabolism

6.3            Using RNA-seq and Targeted Nucleases to Identify Mechanisms of Drug Resistance in Acute Myeloid Leukemia, SK Rathe in Nature, 2014

6.4            Proteomics – The Pathway to Understanding and Decision-making in Medicine

6.5            Advances in Separations Technology for the “OMICs” and Clarification of Therapeutic Targets

6.6           Expanding the Genetic Alphabet and Linking the Genome to the Metabolome

6.7            Genomics, Proteomics and Standards

6.8            Proteins and Cellular Adaptation to Stress

6.9            Genes, Proteomes, and their Interaction

6.10           Regulation of Somatic Stem Cell Function

6.11           Scientists discover that Pluripotency factor NANOG is also active in Adult Organism

Chapter 7: Metabolomics

7.1            Extracellular Evaluation of Intracellular Flux in Yeast Cells

7.2            Metabolomic Analysis of Two Leukemia Cell Lines Part I

7.3            Metabolomic Analysis of Two Leukemia Cell Lines Part II

7.4            Buffering of Genetic Modules involved in Tricarboxylic Acid Cycle Metabolism provides Homeomeostatic Regulation

7.5            Metabolomics, Metabonomics and Functional Nutrition: The Next Step in Nutritional Metabolism and Biotherapeutics

7.6            Isoenzymes in Cell Metabolic Pathways

7.7            A Brief Curation of Proteomics, Metabolomics, and Metabolism

7.8            Metabolomics is about Metabolic Systems Integration

7.9             Mechanisms of Drug Resistance

7.10           Development Of Super-Resolved Fluorescence Microscopy

7.11            Metabolic Reactions Need Just Enough

Chapter 8.  Impairments in Pathological States: Endocrine Disorders; Stress Hypermetabolism and CAncer

8.1           Omega3 Fatty Acids, Depleting the Source, and Protein Insufficiency in Renal Disease

8.2             Liver Endoplasmic Reticulum Stress and Hepatosteatosis

8.3            How Methionine Imbalance with Sulfur Insufficiency Leads to Hyperhomocysteinemia

8.4            AMPK Is a Negative Regulator of the Warburg Effect and Suppresses Tumor Growth InVivo

8.5           A Second Look at the Transthyretin Nutrition Inflammatory Conundrum

8.6            Mitochondrial Damage and Repair under Oxidative Stress

8.7            Metformin, Thyroid Pituitary Axis, Diabetes Mellitus, and Metabolism

8.8            Is the Warburg Effect the Cause or the Effect of Cancer: A 21st Century View?

8.9            Social Behavior Traits Embedded in Gene Expression

8.10          A Future for Plasma Metabolomics in Cardiovascular Disease Assessment

Chapter 9: Genomic Expression in Health and Disease 

9.1            Genetics of Conduction Disease: Atrioventricular (AV) Conduction Disease (block): Gene Mutations – Transcription, Excitability, and Energy Homeostasis

9.2            BRCA1 a Tumour Suppressor in Breast and Ovarian Cancer – Functions in Transcription, Ubiquitination and DNA Repair

9.3            Metabolic Drivers in Aggressive Brain Tumors

9.4            Modified Yeast Produces a Range of Opiates for the First time

9.5            Parasitic Plant Strangleweed Injects Host With Over 9,000 RNA Transcripts

9.6            Plant-based Nutrition, Neutraceuticals and Alternative Medicine: Article Compilation the Journal

9.7            Reference Genes in the Human Gut Microbiome: The BGI Catalogue

9.8            Two Mutations, in the PCSK9 Gene: Eliminates a Protein involved in Controlling LDL Cholesterol

9.9            HDL-C: Target of Therapy – Steven E. Nissen, MD, MACC, Cleveland Clinic vs Peter Libby, MD, BWH

Summary 

Epilogue


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