PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “GASTROINTESTINAL SYSTEM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources

Ogilvie's syndrome after cesarean delivery.

Ogilvie's syndrome is a rare postsurgical complication that can be associated with cesarean delivery. It is characterized by massive dilation of the colon, much like that which occurs with an obstruction but in the absence of a mechanical obstruction. Early detection and intervention are necessary to avoid serious morbidity and/or mortality. Conservative treatment is effective in many cases, but surgical intervention may be required. Nursing assessment of the gastrointestinal system in the postsurgical patient is reviewed using a case report of a patient who developed Ogilvie's syndrome after a cesarean delivery.

Adult↗

Local challenge on oral mucosa with an alpha-gliadin related synthetic peptide in patients with celiac disease.

OBJECTIVE: Gluten-derived peptides (e.g., amino-acids 31-49 of alpha-gliadin) have been shown to cause changes typical of celiac disease in the gut. Gluten-derived peptides have mostly been used in in vitro studies. The easiest access to the gastrointestinal system may be the mouth. In the present study we were interested to see whether a synthetic peptide corresponding to amino-acids 31-49 of alpha-gliadin could induce inflammatory changes in the oral mucosa after a local challenge in celiac disease patients. METHODS: The challenge was made by injecting the peptide solution at a concentration of 10 microg/ml submucosally into the oral mucosa of 10 celiac disease patients after a gluten-free diet (GFD) and 12 healthy control subjects. B and CD45RO+ T cells, mast cells, CD3+, CD4+, CD8+ lymphocytes, and alphabeta and gammadelta T-cell receptor-bearing (TcR alphabeta, TcR gammadelta) lymphocytes were counted and HLA DR expression was determined. The expression of CD25 and Ki-67 antigen was also examined. RESULTS: The peptide significantly increased the total number of T cells in the lamina propria of the celiac disease patients. The expression of T-cell activation marker CD25 (IL-2 receptor), but not that of cell proliferation marker Ki-67, was also significantly increased in the lamina propria after peptide challenge. Such a reaction was not observed in the controls. The numbers of CD3+ and CD4+ T cells in the lamina propria were also increased in celiac disease patients after the challenge. The count of TcR gammadelta+ cells was very small in the oral mucosa in celiac disease and showed no increase when the oral mucosa was challenged with the peptide. The expression of HLA DR staining was enhanced after the submucosal peptide challenge in celiac disease; however, the difference was not statistically significant. CONCLUSIONS: The results show that in the celiac disease patients after the peptide challenge the oral mucosal lamina propria responds with a nonproliferative increase of lymphocytes. Thus, submucosal challenge with the peptide 31-49 can be used as an aid in the diagnosis of celiac disease. However, further studies with optimized methodology, including various concentrations of the peptide, adjuvants, other peptides, etc., are warranted, especially because the oral mucosa provides the easiest access to an in vivo peptide challenge in celiac disease.

Adult↗

In vitro characterization of novel peptide inhibitors of endomorphin-degrading enzymes in the rat brain.

Endomorphins, endogenous mu-opioid receptor ligands, have been shown to exert antinociceptive, antidepressant, anxiolytic, and neuromodulatory effects, as well as to influence cardiovascular, respiratory, and gastrointestinal systems. In the present study, we designed and synthesized a series of tetrapeptides and tripeptides (amides and peptide acids) of similar to endomorphins structure, but with low mu-opioid receptor affinity, and tested them as possible inhibitors of endomorphin-degrading enzymes. The obtained results indicate that the tripeptides Tyr-Pro-Ala-NH2 and Tyr-Pro-Ala-OH, which do not bind to the mu-opioid receptors, are potent inhibitors of endomorphin-degrading enzymes in the rat brain. We suggest that the in vivo administration of these novel analogs may enhance physiological effects of endogenous endomorphins by decreasing the rate of their enzymatic cleavage.

Amino Acid Sequence↗

SR 48968 selectively prevents faecal excretion following activation of tachykinin NK2 receptors in rats.

We tested the ability of SR 48968, (S)-N-methyl-N(4-(4-acetylamino-4-phenylpiperidino)-2-(3,4-dichloropheny l)butyl ) benzamide, a non-peptide antagonist highly selective for tachykinin NK2 receptors, to prevent defecation induced in rats by several agents. The tachykinin agonists substance P, [MePhe7]neurokinin B and [beta-Ala8]neurokinin A (4-10) all promoted defecation and increased faecal water content, the last compound being over ten times more potent than the other two (intraperitoneal dose inducing the excretion of 1 g faeces dry weight = 6.7 micrograms kg-1). SR 48968 given either orally (p.o.) or subcutaneously (s.c.) was similarly potent in dose-dependently inhibiting faecal output stimulated by the selective NK2-agonist [beta-Ala8]neurokinin A (4-10) (doses causing 50% inhibition 0.4 microgram kg-1, p.o. and 0.3 microgram kg-1, s.c.). This inhibition was long-lasting (more than 18 h after 1 microgram kg-1 SR 48968 either s.c. or p.o.). At the higher doses tested, SR 48968 also significantly prevented the increase in faecal water content produced by [beta-Ala8]neurokinin A (4-10). In rats treated with SR 48968, stimulation of faecal output by the alpha 2-adrenergic antagonist idazoxan and by salmonella endotoxin (LPS), but not by the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin, 5-HT, carbachol or platelet-activating factor, was partially prevented. The present results suggest that activation of intestinal NK2 receptors, either directly by the selective agonist [beta-Ala8]neurokinin A (4-10) or indirectly through the release of endogenous neurokinin A (by idazoxan or LPS), promotes defecation, presumably as a consequence of increased gut motility or secretion, or both. SR 48968 should therefore be useful for studying the role of neurokinin A-dependent mechanisms in health and disease, including those of the gastrointestinal system, and possibly for developing new therapeutic agents.

Animals↗

Evaluation of antibiotic therapies for eradication of Helicobacter hepaticus.

The newly recognized murine pathogen Helicobacter hepaticus is known to colonize the ceca and colons of several strains of mice from a variety of commercial suppliers. Additionally, the organism persistently infects mice, causes a chronic hepatitis, and is linked to hepatic tumors in the A/JCr inbred mouse strain. For this reason, eradication of the organism from infected mouse colonies is desirable. Treatment modalities for eradication of H. hepaticus from the gastrointestinal system consisted of oral administration of various antibiotic combinations previously evaluated for eradication of experimental H. felis gastric infection in mice. A/JCr mice (8 to 10 weeks old) naturally infected with H. hepaticus were divided into six treatment groups of 10 animals each. Animals received monotherapy of amoxicillin, metronidazole, or tetracycline or triple therapy of amoxicillin-metronidazole-bismuth (AMB) or tetracycline-metronidazole-bismuth (TMB). All medications were administered by oral gavage three times daily for 2 weeks. One month after the final treatment, mice were euthanatized and livers, ceca, and colons were cultured for H. hepaticus. All untreated control animals had H. hepaticus isolated from the cecum and/or colon. H. hepaticus was not recovered from the livers, ceca, or colons of the AMB or TMB treatment groups. All animals receiving the various antibiotic monotherapies had H. hepaticus isolated from the cecum and colon. We conclude that at the doses and the route evaluated, AMB and TMB triple therapies are effective for eradication of H. hepaticus in 8- to 10-week old A/JCr mice.

Amoxicillin↗

Induction of resistance to azole drugs in Trypanosoma cruzi.

Trypanosoma cruzi is the protozoan parasite that causes Chagas' disease, a frequently fatal illness affecting the heart and gastrointestinal systems. An estimated 16 million to 18 million people in Latin America and 50,000 to 100,000 people in the United States are infected with this pathogen. Treatment options for T. cruzi infections are suboptimal due to the toxicities and limited effectiveness of the available drugs. Azole antimicrobial agents have been discovered to have antitrypanosomal activity by inhibition of ergosterol synthesis. The triazole itraconazole was recently shown to produce a parasitologic cure rate of 53% in chronically infected patients (W. Apt et al., Am. J. Trop. Med. Hyg. 59:133-138, 1998), a result which may lead to more use of this family of drugs for the treatment of T. cruzi infections. In the experiments reported on here, resistance to azoles was induced in vitro by serial passage of mammalian-stage parasites in the presence of fluconazole for 4 months. These parasites were cross resistant to the other azoles, ketoconazole, miconazole, and itraconazole. They remained susceptible to benznidazole and amphotericin B. The azole-resistant phenotype was stable for more than 2 months of in vitro serial passage without fluconazole. In addition, the parasites resisted treatment in mice receiving ketoconazole. The rapid development of azole resistance in T. cruzi in vitro suggests that resistance to azole drugs has the potential to occur in patients and may pose an impediment to the progress being made in the treatment of T. cruzi infection.

Animals↗

Effects of common forage phenolic acids on Escherichia coli O157:H7 viability in bovine feces.

Ruminant animals are carriers of Escherichia coli O157:H7, and the transmission of E. coli O157:H7 from cattle to the environment and to humans is a concern. It is unclear if diet can influence the survivability of E. coli O157:H7 in the gastrointestinal system or in feces in the environment. Feces from cattle fed bromegrass hay or corn silage diets were inoculated with E. coli O157:H7, and the survival of this pathogen was analyzed. When animals consumed bromegrass hay for <1 month, viable E. coli O157:H7 was not recovered after 28 days postinoculation, but when animals consumed the diet for >1 month, E. coli O157:H7 cells were recovered for >120 days. Viable E. coli O157:H7 cells in feces from animals fed corn silage were detected until day 45 and differed little with the time on the diet. To determine if forage phenolic acids affected the viability of E. coli O157:H7, feces from animals fed corn silage or cracked corn were amended with common forage phenolic acids. When 0.5% trans-cinnamic acid or 0.5% para-coumaric acid was added to feces from silage-fed animals, the E. coli O157:H7 death rate was increased significantly (17-fold and 23-fold, respectively) compared to that with no addition. In feces from animals fed cracked corn, E. coli O157:H7 death rates were increased significantly with the addition of 0.1% and 0.5% trans-cinnamic acid (7- and 13-fold), 0.1% and 0.5% p-coumaric acid (3- and 8-fold), and 0.5% ferulic acid (3-fold). These data suggest that phenolic acids common to forage plants can decrease viable counts of E. coli O157:H7 shed in feces.

Animal Feed↗

Clinical and immunological features of 65 Iranian patients with common variable immunodeficiency.

Common variable immunodeficiency (CVID) is a primary immunodeficiency disease characterized by hypogammaglobulinemia and recurrent bacterial infections. The records of 65 patients with CVID (37 males and 28 females) in the age range of 24 to 537 months were reviewed. By the year 2003, 11 patients had died and seven patients could not be located. The total follow-up period was 221 patient-years. The median diagnostic delay (time between onset and diagnosis) in our patient group was 60 months. At the time of diagnosis, the baseline serum immunoglobulin G (IgG), IgM, and IgA levels were below the level normal for the patients' age; the medians for this group were 120, 10, and 0 mg/dl, respectively. All of the patients presented with infectious diseases at the time of onset, the most common of which were otitis media, diarrhea, pneumonia, and sinusitis. Acute and recurrent infections were also found in almost all of the patients, particularly involving respiratory and gastrointestinal systems. The most common infections, before diagnosis and during follow-up, were pneumonia, acute diarrhea, acute sinusitis, and otitis media. CVID should be considered in any patient with a history of recurrent infections and decreased levels of all serum immunoglobulin isotypes.

Adolescent↗

Pure botulinum neurotoxin is absorbed from the stomach and small intestine and produces peripheral neuromuscular blockade.

Clostridium botulinum serotype A produces a neurotoxin composed of a 100-kDa heavy chain and a 50-kDa light chain linked by a disulfide bond. This neurotoxin is part of a ca. 900-kDa complex, formed by noncovalent association with a single nontoxin, nonhemagglutinin subunit and a family of hemagglutinating proteins. Previous work has suggested, although never conclusively demonstrated, that neurotoxin alone cannot survive passage through the stomach and/or cannot be absorbed from the gut without the involvement of auxiliary proteins in the complex. Therefore, this study compared the relative absorption and toxicity of three preparations of neurotoxin in an in vivo mouse model. Equimolar amounts of serotype A complex with hemagglutinins, complex without hemagglutinins, and purified neurotoxin were surgically introduced into the stomach or into the small intestine. In some experiments, movement of neurotoxin from the site of administration was restricted by ligation of the pylorus. Comparison of relative toxicities demonstrated that at adequate doses, complex with hemagglutinins, complex without hemagglutinins, and pure neurotoxin can be absorbed from the stomach. The potency of neurotoxin in complex was greater than that of pure neurotoxin, but the magnitude of this difference diminished as the dosage of neurotoxin increased. Qualitatively similar results were obtained when complex with hemagglutinins, complex without hemagglutinins, and pure neurotoxin were placed directly into the intestine. This work establishes that pure botulinum neurotoxin serotype A is toxic when administered orally. This means that pure neurotoxin does not require hemagglutinins or other auxiliary proteins for absorption from the gastrointestinal system into the general circulation.

Absorption↗

Gene targeting reveals a crucial role for MTG8 in the gut.

The MTG8 (ETO) locus is involved in a reciprocal exchange with runx1 in the t(8;21) of acute myeloid leukemia. It is a member of a small gene family encoding transcriptional regulators that interact with corepressors and histone deacetylase. However, the physiologic cellular processes controlled by MTG8 are not known. In order to gain an insight into the latter, we have generated mutant mice with an insertional inactivation at the locus, which disrupts transcription of exon 2. The postnatal viability of homozygous mutants was greatly reduced. In approximately 25% the midgut was missing, whereas practically all pups surviving past the first 2 days showed severe growth impairment, which was likely due to a gross disruption of the gut architecture. The latter phenotype could be traced back to late embryonic development. No difference in gut cell differentiation or proliferation was found compared to wild-type littermates. Levels of factors known to be involved in gut morphogenesis were also unchanged. MTG8 is expressed in the outermost layers of the developing gut from at least E9.5. Thus, MTG8 plays a novel, essential role in the gastrointestinal system.

Animals↗

Secretory IgA: immune defence pattern in ankylosing spondylitis and klebsiella.

Saliva secretory IgA (sIgA), secretory component (SC); serum immunoglobulins (IgG, IgA, IgM), complement (C3, C4), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were performed in 32 patients with ankylosing spondylitis and 29 normal controls. They were investigated for carriage in the faeces of Klebsiella spp. on 3 occasions over the previous months. Throat swabs and urine were cultured at the same time as immunological estimations were done. 24-hour urine sIgA specimens were studied in 13 patients and 12 normal controls. Significantly raised mean values of saliva sIgA and serum IgG, IgA, C3, and C4 were found in patients with raised values of serum ESR and CRP levels when correlated with controls. Raised values of sIgA in saliva, which is an important factor of the local immune defence mechanism of mucosal surfaces, suggests the presence of an antigenic stimulus from the gastrointestinal system in ankylosing spondylitis during activity of disease.

Adult↗

A double blind multicentre study of OM-8980 and auranofin in rheumatoid arthritis.

The therapeutic efficacy of the immunomodulator OM-8980 in rheumatoid arthritis was compared with that of auranofin, an oral gold salt, in a double blind, randomised multicentre study lasting six months. Seventy patients were treated with auranofin and 75 with OM-8980. The patients of both groups improved significantly at three and six months for all the clinical parameters observed: Ritchie index, number of swollen joints, morning stiffness, pain, grip strength, intake of non-steroidal anti-inflammatory drugs, and erythrocyte sedimentation rate. No serious side effects were observed in either group. The patients receiving auranofin had more adverse reactions, mainly affecting the gastrointestinal system.

Adjuvants, Immunologic↗

Bladder smooth muscle dysfunction in patients with irritable bowel syndrome.

Urodynamic studies were carried out on 30 patients with irritable bowel syndrome and 30 matched controls. Fifty per cent of the irritable bowel patients compared with only 13% of the control group had evidence of bladder dysfunction (p = 0.006). In the irritable bowel group detrusor instability was observed in 10 patients compared with only one control subject (p = 0.008). A steep cystometrogram occurred in five irritable bowel patients and three controls (NS). Detrusor instability was most common in patients with a bowel habit characterised by alternating constipation and diarrhoea. This is the first study to provide objective evidence that patients with irritable bowel syndrome may have a disorder of smooth muscle or its innervation that is not confined to the gastrointestinal system.

Adult↗

Hyperemesis gravidarum: current concepts and management.

Hyperemesis gravidarum is a common problem for an obstetrician. Though nausea and vomiting are quite common in pregnancy, hyperemesis is found in only 1-20 patients per 1000. In this practical review, a general outline of the syndrome, its relation to the gastrointestinal system and thyroid, mild and rare severe complications, and conventional treatment versus newer options are discussed.

Antiemetics↗

Peptide signals regulating food intake and energy homeostasis.

The adiposity hormone leptin has been shown to decrease food intake and body weight by acting on neuropeptide circuits in the hypothalamus. However, it is not clear how this primary hypothalamic action of leptin is translated into a change in food intake. We hypothesize that the behavioral effect of leptin ultimately involves the integration of neuronal responses in the forebrain with those in the nucleus tractus solitarius in the caudal brainstem, where ingestive behavior signals are received from the gastrointestinal system and the blood. One example is the peptide cholecystokinin, which is released from the gut following ingestion of a meal and acts via vagal afferent nerve fibers to activate medial nucleus tractus solitarius neurons and thereby decrease meal size. While it is established that leptin acts in the arcuate nucleus in the hypothalamus to stimulate anorexigenic neurons that inhibit food intake while simulataneously inhibiting orexigenic neurons that increase food intake, the mechanisms linking these effects with regions of the caudal brainstem that integrate cues related to meal termination are unclear. Based on an increasing body of supportive data, we hypothesize that this integration involves a pathway comprising descending projections from neurons from the paraventricular nucleus to neurons within the nucleus tractus solitarius that are activated by meal-related satiety factors. Leptin's anorexic effect comprises primarily decreased meal size, and at subthreshold doses for eliciting an effect on food intake, leptin intensifies the satiety response to circulating cholecystokinin. The location of neurons subserving the effects of intracerebroventricular administration of leptin and intraperitoneal injection of cholecystokinin on food intake has been identified by analysis of Fos expression. These studies reveal a distribution that includes the paraventricular nucleus and regions within the caudal brainstem, with the medial nucleus tractus solitarius having the most pronounced Fos expression in response to leptin and cholecystokinin, and support the hypothesis that the long-term adiposity signal leptin and the short-term satiety signal cholecystokinin act in concert to maintain body weight homeostasis.

Animals↗

MR imaging of common and uncommon large pelvic masses.

Magnetic resonance (MR) imaging is often used in the detection and staging of large pelvic masses. Many large masses in the female pelvis arise from the reproductive organs (eg, uterus, cervix, ovaries, fallopian tubes). In addition, these masses may arise from the gastrointestinal system, urinary system, adjacent soft tissues, peritoneum, or retroperitoneum or from metastases. The majority of large masses in the female pelvis represent such commonly encountered entities as uterine fibroid tumor, dermoid tumor, ovarian cyst, and ovarian cancer. However, uncommon pelvic masses such as mesothelioma, adenocarcinoma, carcinosarcoma, leiomyosarcoma, and desmoid tumor may also be seen. Thus, the differential diagnosis for female pelvic masses is extensive. However, the site of origin, MR imaging characteristics, and clinical history may all help narrow the differential diagnosis. Although with large tumors it may not always be possible to determine the site of origin or distinguish between various tumors at radiology, familiarity with the clinicopathologic and MR imaging features of common and uncommon pelvic masses is important for diagnosis and treatment.

Female↗