Gastritis Stress-Induced Publications (48)

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Gastritis Stress-Induced Publications

2016Dec
Clin Transl Med
Clin Transl Med 2016 Dec 23;5(1):35. Epub 2016 Aug 23.
National Cancer Institute (NCI), the National Institutes of Health (NIH), Bethesda, MD, USA.

Longevity and accumulation of multiple context-dependent signaling pathways of long-standing inflammation (antigen-load or oxidative stress) are the results of decreased/altered regulation of immunity and loss of control switch mechanisms that we defined as Yin and Yang of acute inflammation or immune surveillance. Chronic inflammation is initiated by immune disruptors-induced progressive changes in physiology and function of susceptible host tissues that lead to increased immune suppression and multistep disease processes including carcinogenesis. The interrelated multiple hypotheses that are presented for the first time in this article are extension of author's earlier series of 'accidental' discoveries on the role of inflammation in developmental stages of immune dysfunction toward tumorigenesis and angiogenesis. Read More

Detailed analyses of data on chronic diseases suggest that nearly all age-associated illnesses, generally categorized as 'mild' (e.g., increased allergies), 'moderate' (e.g., hypertension, colitis, gastritis, pancreatitis, emphysema) or 'severe' (e.g., accelerated neurodegenerative and autoimmune diseases or site-specific cancers and metastasis) are variations of hypersensitivity responses of tissues that are manifested as different diseases in immune-responsive or immune-privileged tissues. Continuous release/presence of low level histamine (subclinical) in circulation could contribute to sustained oxidative stress and induction of 'mild' or 'moderate' or 'severe' (immune tsunami) immune disorders in susceptible tissues. Site-specific cancers are proposed to be 'severe' (irreversible) forms of cumulative delayed hypersensitivity responses that would induce immunological chaos in favor of tissue growth in target tissues. Shared or special features of growth from fetus development into adulthood and aging processes and carcinogenesis are briefly compared with regard to energy requirements of highly complex function of Yin and Yang. Features of Yang (growth-promoting) arm of acute inflammation during fetus and cancer growth will be compared for consuming low energy from glycolysis (Warburg effect). Growth of fetus and cancer cells under hypoxic conditions and impaired mitochondrial energy requirements of tissues including metabolism of essential branched amino acids (e.g., val, leu, isoleu) will be compared for proposing a working model for future systematic research on cancer biology, prevention and therapy. Presentation of a working model provides insightful clues into bioenergetics that are required for fetus growth (absence of external threat and lack of high energy-demands of Yin events and parasite-like survival in host), normal growth in adulthood (balance in Yin and Yang processes) or disease processes and carcinogenesis (loss of balance in Yin-Yang). Future studies require focusing on dynamics and promotion of natural/inherent balance between Yin (tumoricidal) and Yang (tumorigenic) of effective immunity that develop after birth. Lawless growth of cancerous cells and loss of cell contact inhibition could partially be due to impaired mitochondria (mitophagy) that influence metabolism of branched chain amino acids for biosynthesis of structural proteins. The author invites interested scientists with diverse expertise to provide comments, confirm, dispute and question and/or expand and collaborate on many components of the proposed working model with the goal to better understand cancer biology for future designs of cost-effective research and clinical trials and prevention of cancer. Initial events during oxidative stress-induced damages to DNA/RNA repair mechanisms and inappropriate expression of inflammatory mediators are potentially correctable, preventable or druggable, if future studies were to focus on systematic understanding of early altered immune response dynamics toward multistep chronic diseases and carcinogenesis.

2016May
Cochrane Database Syst Rev
Cochrane Database Syst Rev 2016 May 19(5):CD010714. Epub 2016 May 19.
Department of Pediatrics, West China Second University Hospital, West China Women's and Children's Hospital, No. 17 Section Three, Ren Min Nan Lu Avenue, Chengdu, Sichuan, China, 610041.

Gastrointestinal bleeding refers to loss of blood from any site of the digestive tract. In paediatric clinical practice, it is usually a complaint of children attending the emergency department as a symptom of diseases such as ulcers, gastric or oesophageal varices, gastritis, Mallory-Weiss tears, anorectal fissures, allergic colitis, infectious colitis, intussusception, Henoch-Schonlein purpura, and Meckel's diverticulum; it also occurs with high incidence in critically ill children hospitalised in intensive care units and is caused by stress-induced gastropathy. No matter what the cause of gastrointestinal bleeding, fasting is believed to be necessary due to the fear that eating may affect haemostasis or aggravate bleeding. Read More


To assess the effects and safety of fasting for haemostasis in gastrointestinal bleeding in children.
We searched EBM Reviews - the Cochrane Central Register of Controlled Trials (CENTRAL) (May 2016), Ovid MEDLINE(R) (1946 to 3 May 2016), EMBASE (1980 to 2016 Week 18), Chinese Biomedical Database (CBM) (1978 to 3 May 2016), China National Knowledge Infrastructure (CNKI) (1979 to 3 May 2016), VIP Database (1989 to 4 May 2016) and Wanfang Data (1990 to 4 May 2016). We used no restrictions on language or study setting and limited searches in CNKI and Wanfang Data to the medical field.
Randomised controlled trials (RCTs) or quasi-RCTs in children with gastrointestinal bleeding that compared fasting with feeding.
Two review authors independently screened the literature search results, and there were no disagreements.
We identified no RCTs or quasi-RCTs that compared the effects and safety of fasting with feeding for haemostasis in children with gastrointestinal bleeding. No study fulfilled the criteria for considering studies for our review.
There is currently no information available from RCTs or quasi-RCTs to support or refute the use of fasting for haemostasis in children with gastrointestinal bleeding.

2014Sep
J Ethnopharmacol
J Ethnopharmacol 2014 Sep 30;155(2):1001-10. Epub 2014 Jun 30.
Department of Botany, Faculty of Science, University of Peradeniya, Peradeniya, Sri Lanka.

Biotite mica enriched with Fe(2+) ions are widely used as a major mineral ingredient in traditional pharmaceutical science of alchemy (Rasashastra). Abhrak bhasma (mica ash), a pharmaceutical product containing treated mica, is utilized, for example, in Ayurvedic treatments for ailments such as gastritis, renal disease, skin disease and mainly in rejuvenation formulations. However, the untreated mica minerals may be harmful when used directly, as they carry considerably high amounts of trace-elements that can cause undesirable effects in the human body. Read More

In order to remove toxic factors and produce readily absorbable materials having high nutrient capacity, specific thermal and chemical treatments (purification, detoxification, particle size reduction and incineration) are performed during the preparation of Rasashastra. This review evaluates the chemical and pharmacological aspects of mica ash as well as the technological aspects of mica ash production.
The detailed literature review on the chemistry and scientific basis of mica ash, its preparation techniques, mica alterations and pharmaceutical applications was carried out by using published Ayurvedic text books and research articles, available from Science Direct, on mica minerals, mica ash and their physico-chemical alteration processes and pharmacological applications.
During the purification and detoxification procedures, heating followed by quenching (in ionic medium) influences the structural distortion and the development of stress-induced cracks and spallations of the micaceous plates. Thus, the efficient diffusion of the external medium takes place at successive heating and quenching steps. Acidic organic liquids and animal byproducts can enhance the cation exchange capacity and solubility of mica. Further, these natural compounds facilitate the removal of toxic-elements in the structure. When treated-mica and paddy husks are tied up in a cloth and squeezed, particle size reduction and further detoxification takes place. Leaching out of oxidized iron coatings is accelerated when the mixtures are immersed in acidic media, by which the filtrate is enriched with oxidized iron-silicate particles. These nano-oxide particles are converted into a more favorable oxidation form for human consumption when the herbometallic mixture is incinerated in closed vessels. Recent analytical data reveals that major and minor elements in mica ash are within the limits of pharmacopoeial standards for Ayurvedic formulations. Further, recent studies show that mica ash has hypoglycemic, hepatoprotective, anthelminthic and antimicrobial properties.
Chemical and structural modifications in mica occur during mica-based drug preparation in traditional medicine. Purification steps particularly influence the structural distortion while heating and quenching can form nano-size particles. Carboxylic acids and other organic molecules present in quenching media serve as chemical modifiers of mica. At the same time the toxic elements are leached out from mica to the quenching media through an ion exchange process. Mica ash has been successfully used for treating liver, kidney and skin related ailments in traditional medicine, and mica ash alone or its herbo-metallic formulations have different applications. Further, the recent toxicological and analytical studies validate the traditional uses of mica ash and mica ash bearing products. Further scientific studies are needed to fully establish that mica-based pharmaceuticals are safe and devoid of toxic and long term side effects.

2014Apr
Chonnam Med J
Chonnam Med J 2014 Apr 22;50(1):6-14. Epub 2014 Apr 22.
Department of Biochemistry, Chonnam National University Medical School, Gwangju, Korea.

This study was designed to evaluate the efficacy of an orally administered aqueous extract of glutinous rice (GRE) to protect against acute gastric mucosal lesions induced by ethanol, indomethacin, and water immersion restraint stress in rats and to characterize the active substances responsible for the protection. GRE was shown to dose-dependently prevent the gastric lesions induced by the above ulcerogenic treatments at doses of 30 to 300 mg/kg. GRE treatment increased the gastric mucin content and partially blocked the ethanol-induced depletion of the gastric mucus layer. Read More

Also, it increased the nonprotein sulfhydryl concentration in the gastric mucosa. The gastroprotective action of GRE was markedly enhanced by co-treatment with 4-8 mg/kg tea extracts. The activity of GRE was completely lost by heat treatment at 80℃ for 3 min or treatment with 0.01% pepsin at 37℃ for 1 h. Protein extraction studies indicated that prolamins are involved in the gastroprotective activity of GRE. Our results suggest that glutinous rice proteins are useful for the prevention and treatment of gastritis and peptic ulcer.

The administration of exogenous β-hydroxybutyrate (β-HB), as well as fasting and caloric restriction, is a condition associated with β-HB abundance and decreased appetite in animals. Increased β-HB and decreased appetite exist simultaneously in some diseases, such as bovine left displaced abomasums (LDA) and human chronic gastritis. However, the effects of β-HB on stomach injuries have not been explored. Read More

To elucidate the possible effects of exogenous β-HB on the stomach, mice were injected intraperitoneally with β-HB, and bovine abomasum smooth muscle cells (BSMCs) were treated with different concentrations of β-HB. We found that β-HB induced BSMCs endoplasmic reticulum- and mitochondria-mediated apoptotic cell death. β-HB promoted Bax expression and caspase-12, -9, and -3 activation while blocking Bcl-2 expression. β-HB also promoted AIF, EndoG release and p53 expression. β-HB acted on key molecules in the apoptotic cell death pathway and increased p38 and c-June NH2-terminal kinase phosphorylation while inhibiting ERK phosphorylation and PCNA expression. β-HB upregulated P27 and P21 mRNA levels while downregulating cyclin and CDK mRNA levels, arresting the cell cycle. These results suggest that BSMCs treated with β-HB can induce oxidative stress, which can be prevented by intracellular calcium chelators BAPTA/AM but not antioxidant NAC. Additionally, these results suggest that β-HB causes ROS generation through a Ca2+-dependent mechanism and that intracellular Ca2+ levels play a critical role in β-HB -induced apoptotic cell death. The impact of β-HB on programmed cell death and oxidative stress in vivo was confirmed in murine experiments. For the first time, we show oxidative stress effects of β-HB on smooth muscle. We propose that β-HB is a possible cause of some stomach diseases, including bovine LDA.

2014Mar

Although Hans Selye is mostly known for his discovery & development of the stress concept, he also introduced the first physiologically sound, structure-activity classification of steroids that was also based on the chemical structure of steroids in 1943. He not only introduced the names of glucocorticoids & mineralocorticoids but discovered the anti- & pro-inflammatory properties, respectively, of these steroids in animal models. Furthermore, he not only described the first stress-induced gastric ulcers in rats (1936) & characterized the first human 'stress ulcers' during the air-raids in London during World War 11 (1943). Read More

Thus, Selye was a much more productive & creative scientist than it is generally considered.

2014Jun
Gastroenterology
Gastroenterology 2014 Jun 13;146(7):1739-51.e14. Epub 2014 Feb 13.
Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address:

The gastric cancer-causing pathogen Helicobacter pylori up-regulates spermine oxidase (SMOX) in gastric epithelial cells, causing oxidative stress-induced apoptosis and DNA damage. A subpopulation of SMOX(high) cells are resistant to apoptosis, despite their high levels of DNA damage. Because epidermal growth factor receptor (EGFR) activation can regulate apoptosis, we determined its role in SMOX-mediated effects. Read More


SMOX, apoptosis, and DNA damage were measured in gastric epithelial cells from H. pylori-infected Egfr(wa5) mice (which have attenuated EGFR activity), Egfr wild-type mice, or in infected cells incubated with EGFR inhibitors or deficient in EGFR. A phosphoproteomic analysis was performed. Two independent tissue microarrays containing each stage of disease, from gastritis to carcinoma, and gastric biopsy specimens from Colombian and Honduran cohorts were analyzed by immunohistochemistry.
SMOX expression and DNA damage were decreased, and apoptosis increased in H. pylori-infected Egfr(wa5) mice. H. pylori-infected cells with deletion or inhibition of EGFR had reduced levels of SMOX, DNA damage, and DNA damage(high) apoptosis(low) cells. Phosphoproteomic analysis showed increased EGFR and erythroblastic leukemia-associated viral oncogene B (ERBB)2 signaling. Immunoblot analysis showed the presence of a phosphorylated (p)EGFR-ERBB2 heterodimer and pERBB2; knockdown of ErbB2 facilitated apoptosis of DNA damage(high) apoptosis(low) cells. SMOX was increased in all stages of gastric disease, peaking in tissues with intestinal metaplasia, whereas pEGFR, pEGFR-ERBB2, and pERBB2 were increased predominantly in tissues showing gastritis or atrophic gastritis. Principal component analysis separated gastritis tissues from patients with cancer vs those without cancer. pEGFR, pEGFR-ERBB2, pERBB2, and SMOX were increased in gastric samples from patients whose disease progressed to intestinal metaplasia or dysplasia, compared with patients whose disease did not progress.
In an analysis of gastric tissues from mice and patients, we identified a molecular signature (based on levels of pEGFR, pERBB2, and SMOX) for the initiation of gastric carcinogenesis.

2013May
Food Chem. Toxicol.
Food Chem Toxicol 2013 May 26;55:353-7. Epub 2013 Jan 26.
Bioevaluation Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongwon, Chungbuk 363-883, Republic of Korea.
2013Jan
PLoS ONE
PLoS One 2013 17;8(1):e54811. Epub 2013 Jan 17.
Research Unit of Translational Neurogastroenterology, Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.

Environmental enrichment (EE) has a beneficial effect on rodent behaviour, neuronal plasticity and brain function. Although it may also improve stress coping, it is not known whether EE influences the brain response to an external (psychological) stressor such as water avoidance stress (WAS) or an internal (systemic) stressor such as gastrointestinal inflammation. This study hence explored whether EE modifies WAS-induced activation of the mouse corticolimbic system and whether this stress response is altered by gastritis or colitis. Read More

Male C67BL/6N mice were housed under standard or enriched environment for 9 weeks, after which they were subjected to a 1-week treatment with oral iodoacetamide to induce gastritis or oral dextran sulfate sodium to induce colitis. Following exposure to WAS the expression of c-Fos, a marker of neuronal activation, was measured by immunocytochemistry. EE aggravated experimentally induced colitis, but not gastritis, as shown by an increase in the disease activity score and the colonic myeloperoxidase content. In the brain, EE enhanced the WAS-induced activation of the dentate gyrus and unmasked an inhibitory effect of gastritis and colitis on WAS-evoked c-Fos expression within this part of the hippocampus. Conversely, EE inhibited the WAS-evoked activation of the central amygdala and prevented the inhibitory effect of gastritis and colitis on WAS-evoked c-Fos expression in this region. EE, in addition, blunted the WAS-induced activation of the infralimbic cortex and attenuated the inhibitory effect of gastritis and colitis on WAS-evoked c-Fos expression in this area. These data reveal that EE has a region-specific effect on stress-induced c-Fos expression in the corticolimbic system, which is likely to improve stress resilience. The response of the prefrontal cortex - amygdala - hippocampus circuitry to psychological stress is also modified by the systemic stress of gut inflammation, and this interaction between external and internal stressors is modulated by the housing environment.