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Nathan Goodyear

Effects of Polyunsaturated Fatty Acids in Growth Medium on Lipid Composition and on Phy... - 0 views

www.ncbi.nlm.nih.gov/...PMC321255

PUFA poly unsaturated fatty acids GI dysbiosis bacteria microbiota

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Nathan Goodyear on 01 May 12
     
    PUFA shown to effect GI bacterial balance.  Altering adhesion of lactobacillus to intestinal surface.  Also, lactobacilli species shown to alter PUFA metabolism in GI.  This article reveals the effect that diet can have on GI bacterial balance.
Nathan Goodyear

Gastrointestinal Symptoms in a sample of children with Pervasive Developmental Disorders - 0 views

mercola.fileburst.com/...symptoms%20in%20PDD%20Yale.pdf

ASD autism PDD GI gastrointestinal symptoms inflammation anxiety children

shared by Nathan Goodyear on 30 Jan 12 - No Cached
  • Nathan Goodyear on 30 Jan 12
     
    This study didn't find major differences between children with/without GI symptoms in those with PDD. But some differences were identified: more anxiety, more listlessness, and more refractory to medical therapy in children with PDD and GI symptoms.
Nathan Goodyear

Frontiers | Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of... - 0 views

journal.frontiersin.org/...full

LPS lipopolysaccharides Alzheimer's disease brain inflammation

shared by Nathan Goodyear on 23 Sep 17 - No Cached
  • lipopolysaccharides (LPS), either alone or in combination, have indicated that when compared, bacterial LPSs exhibit the strongest induction of pro-inflammatory signaling in human neuronal–glial cells in primary coculture of any single inducer, and different LPS extracts from different gastrointestinal (GI)-tract resident Gram-negative bacteria appeared to have different pro-inflammatory potential
  • powerful inducer of the NF-κB
  • In both neocortex and hippocampus, LPS has been detected to range from a ~7- to ~21-fold increase abundance in AD brain
  • ...15 more annotations...
  • Major Gram-negative bacilli of the human GI-tract, such as the abundant B. fragilis and Escherichia coli (E. coli), are capable of discharging a remarkably complex assortment of pro-inflammatory neurotoxins
  • (i) bacterial amyloids (10, 21); (ii) endotoxins and exotoxins (5, 12); (iii) LPS (12, 18); and (iv) small non-coding RNAs (sncRNAs)
  • integral components of the outer leaflet of the outer membrane of Gram-negative bacteria, LPS
  • LPS, the major molecular component of the outer membrane of Gram-negative bacteria normally serves as a physical barrier providing the bacteria protection from its surroundings
  • LPS is also recognized by the immune system as a marker for the detection of bacterial pathogen invasion and responsible for the development of inflammatory response is perhaps the most potent stimulator and trigger of inflammation known
  • AD-affected brains have remarkably large loads of bacterial-derived toxins compared to controls. The transfer of noxious, pro-inflammatory molecules from the GI-tract microbiome to the CNS may be increasingly important during the course of aging when both the GI-tract and blood–brain barriers become significantly more permeable
  • first evidence of a perinuclear association of LPS with AD brain cell nuclei
  • LPS-mediated stimulation of chronic inflammation, beta-amyloid accumulation, and episodic memory decline in murine models of AD (39, 40) and a biophysical association of LPS with amyloid deposits and blood vessels in human AD patients
  • Strong adherence of LPS to the nuclear periphery has recently been shown to inhibit nuclear maturation and function that may impair or block export of mRNA signals from brain cell nuclei, a highly active organelle with extremely high rates of transcription, mRNA processing, and export into the cytoplasm
  • LPS may be further injurious to the nuclear membrane just as LPS contributes to cerebrovascular endothelial cell membrane injury
  • high intake of dietary fiber is a strong inhibitor of B. fragilis abundance and proliferation in the intact human GI-tract and as such is a potent inhibitor of the neurotoxic B. fragilis-derived amyloids, LPS, enterotoxins, and sncRNAs.
  • GI-tract microbiome-derived LPS may be an important initiator and/or significant contributor to inflammatory degeneration in the AD CNS
  • LPS has been recently localized to the same anatomical regions involved in AD-type neuropathology
  • a known pro-inflammatory transcription factor complex that triggers the expression of pathogenic pathways involved in neurodegenerative inflammation
  • pro-inflammatory amyloids, endo- and exotoxins, LPSs, and sncRNAs but also serve as potent sources of membrane-disrupting agents
  • Nathan Goodyear on 23 Sep 17
     
    LPS links gut to inflammation in Alzheimer's disease
Nathan Goodyear

Acute and "chronic" phase reaction-a mother of disease - 0 views

www.journals.elsevierhealth.com/...abstract

immune system GI gastrointestinal

shared by Nathan Goodyear on 28 Jun 11 - No Cached
  • Nathan Goodyear on 28 Jun 11
     
    This study describes how important the GI system is to overall health: estimated that 75% of the immune support of the body lines the GI system
Nathan Goodyear

The use of fecal calprotectin and la... [Acta Gastroenterol Belg. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24261027

calprotectin lactoferrin inflammation IBD IBS inflammatory bowel disease

shared by Nathan Goodyear on 06 Jan 14 - No Cached
  • Nathan Goodyear on 06 Jan 14
     
    Useful biomarkers: calprotectin and lactoferrin used to follow GI inflammation.  Calprotectin is useful to follow inactive/active IBD.  It also has been show to predict recurrence and can aid in differentiation between IBD and IBS.  Lactoferrin appears to be a biomarker more useful in GI inflammation.
Nathan Goodyear

Resolution of cryptosporidiosis with probiotic treatment - 0 views

pmj.bmj.com/...112.full.pdf

probiotic GI gastrointestinal probiotics

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Nathan Goodyear on 01 May 12
     
    probiotic treatment has efficacy against active GI infection with cryptosporidium.
Nathan Goodyear

Cell Host and Microbe - Microbiota Regulate Intestinal Absorption and Metabolism of Fat... - 0 views

www.cell.com/...S1931312812002740

gut GI microbiota dysbiosis metabolism energy balance

shared by Nathan Goodyear on 13 Sep 12 - No Cached
  • Nathan Goodyear on 13 Sep 12
     
    You are what you eat...you are what your gut eats.  Confirmation of the influence of the GI microbiota on calorie utilization.   We shouldn't be surprised by this: what do we do to cattle?  we give them antibiotics which increases their weight and time to market.  What are we doing to ourselves?
Nathan Goodyear

clinical presentation and Histologic Findings at Ileocolonoscopy in children with Autis... - 0 views

mercola.fileburst.com/...Krigsman%20proof.pdf

autism ASD inflammation GI

shared by Nathan Goodyear on 29 Jan 12 - No Cached
  • Nathan Goodyear on 29 Jan 12
     
    Ileal and colonic inflammation found in children with autism. Prominent GI symptoms were found in this chart review of 143 children with autism and developmental disorders.
Nathan Goodyear

The intestinal epithelial barrier: how to dist... [Semin Immunol. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17324587

TLR toll-like receptors NODs GI gut immunity inflammation microbiota bacteria dysbiosis

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    TLRs and NODs play important role in GI mucosal immunity.
Nathan Goodyear

ALCAT Test results in the treatment of respiratory... [Rocz Akad Med Bialymst. 1995] - ... - 0 views

www.ncbi.nlm.nih.gov/...8775317

ALCAT test treatment arthritis bronchitis GI hives urticaria

shared by Nathan Goodyear on 16 Jun 11 - No Cached
  • Nathan Goodyear on 16 Jun 11
     
    ALCAT Test shown to reduce arthritis, hives, bronchitis, and GI symptoms as well as other symptoms
Nathan Goodyear

Duration of Breastfeeding and Risk of Overweight: A Meta-Analysis - 0 views

aje.oxfordjournals.org/...397.abstract

breast feeding obesity overweight pediatrics children GI bifidobacteria

shared by Nathan Goodyear on 25 Aug 11 - No Cached
  • Nathan Goodyear on 25 Aug 11
     
    the longer breast feeding occurs, the lower the risk of obesity/overweight in the child.  One role is the resultant GI colonization with bifidobacteria.
Nathan Goodyear

Long-term impacts of antibiotic exposure on the human intestinal microbiota - 0 views

mic.sgmjournals.org/...3216

antibiotics microbiome GI system imbalance probiotic exposure

shared by Nathan Goodyear on 25 Aug 11 - No Cached
  • Nathan Goodyear on 25 Aug 11
     
    antibiotics reduce the bacterial population, microbiome, in the GI system. antibiotic induced imbalance remained for years.
Nathan Goodyear

Selenium in Human Health and Disease | Abstract - 0 views

online.liebertpub.com/...ars.2010.3275

selenium Se disease health prostate cancer GI cancer cancer diabetes CVD cardiovascular disease

shared by Nathan Goodyear on 10 Nov 14 - No Cached
  • Nathan Goodyear on 10 Nov 14
     
    Selenium deficiency has important implications in disease: including CVD, GI cancer, prostate cancer, and diabetes.
Nathan Goodyear

Bariatric Surgery Results in Cortical Bone Loss - 0 views

jcem.endojournals.org/...541.abstract

bariatric surgery bariatric surgery weight loss surgery overweight obesity

shared by Nathan Goodyear on 18 Feb 13 - No Cached
  • Nathan Goodyear on 18 Feb 13
     
    no surprise here.  Bariatric surgery was found to result in bone loss.  Disruption of the GI tract and absorption is going to result in malnutrition states and bone loss will be one of the side effects.
Nathan Goodyear

Zonulin Upregulation Is Associated With Increased Gut Permeability in Subjects With Typ... - 0 views

diabetes.diabetesjournals.org/...1443

zonulin diabetes

shared by Nathan Goodyear on 25 Jan 17 - No Cached
  • Nathan Goodyear on 25 Jan 17
     
    Increased Zonulin as a result of GI inflammation increases gut permeability and is associated with increased disease potential
Nathan Goodyear

Foods fail to suppress Ghrelin levels in obese humans - 0 views

jcem.endojournals.org/...2984.full.pdf+html

gherlin obesity overweight weight-loss hormone

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    Ghrelin is a hormone that is release to induce hunger and eating. Post meals, gherlin should decrease; but in obese individuals, a dysregulation between the GI system and the hypothalamus results in elevated gherlin resulting in overeating.
Nathan Goodyear

Blastocystis hominis and Endolimax nana Co-Infection Resulting in Chronic Diarrhea in a... - 0 views

www.ncbi.nlm.nih.gov/...PMC3383306

B hominis E nana diarrhea blastocystis hominis Endolimax nana

shared by Nathan Goodyear on 14 Oct 13 - No Cached
  • Nathan Goodyear on 14 Oct 13
     
    B hominis and E nana co-infection cause of GI disturbance in immunocompetent male
Nathan Goodyear

Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3448089

dysbiosis diet nutrition metabolic endotoxemia disease inflammation gut

shared by Nathan Goodyear on 27 Jul 14 - No Cached
  • The gut microbiota participates in the body’s metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders
  • Firmicutes and Bacteroidetes represent the two largest phyla in the human and mouse microbiota and a shift in the ratio of these phyla has been associated with many disease conditions, including obesity
  • In obese humans, there is decreased abundance of Bacteroidetes compared to lean individuals
  • ...21 more annotations...
  • weight loss in obese individuals results in an increase in the abundance of Bacteroidetes
  • there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios
  • Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects
  • While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.
  • targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet
  • The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp
  • It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity
  • In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis
  • LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism
  • early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences
  • increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp
  • mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio
  • microbial antigens through the innate immune system are involved in T1D progression
  • The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota
  • There is evidence that dietary and microbial antigens independently influence T1D
  • Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice
  • breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp
  • the composition of the gut microbiota strongly correlates with diet
  • In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp
  • diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity
  • “Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis
  • Nathan Goodyear on 27 Jul 14
     
    Nice discussion of how diet, induces gut bacterial change, that leads to metabolic endotoxemia and disease.
Nathan Goodyear

Chemotherapy-driven dysbiosis in the intestinal microbiome. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...26147207

gut gut flora gut microbiome gut microbiota chemotherapy cancer prostate men hormone hormones Testosterone

shared by Nathan Goodyear on 07 Jul 15 - No Cached
  • Nathan Goodyear on 07 Jul 15
     
    Gut microbiome effected by chemotherapy and the result is GI mucositis.  A decrease in Firmicutes and Actinobacteria was found.
Nathan Goodyear

Obestatin partially affects ghrelin stimulatio... [Endocrinology. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17204551

obestatin overweight obesity weight loss

shared by Nathan Goodyear on 02 Nov 11 - No Cached
  • Nathan Goodyear on 02 Nov 11
     
    obestatin inhibits food intake and slow GI motility.  THis is the opposite of ghrelin, which increases appetite
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