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At least 73 records · Page 4Linked to original sources
PubMed1993

Heterogeneous isoactin gene expression in the adult rat gastrointestinal tract.

BACKGROUND: Normal gastrointestinal development is a complex process involving the precise integration of multiple cell types. To gain a better understanding of these processes, the present study examined isoactin gene expression in the adult rat gastrointestinal tract. METHODS: Northern blot analysis was performed on specified segments of the adult rat esophagus, stomach, small intestine, cecum, colon, rectum, and anus using actin isoform-specific complementary DNAs for all six vertebrate isoactins. RESULTS: Smooth muscle and cytoplasmic isoactins were heterogeneously coexpressed in a segment-specific manner throughout the gastrointestinal tract. In addition, striated muscle isoactin expression was also detected in segments of the adult rat esophagus, stomach, colon, cecum, rectum, and anus. Histological analysis indicated that the adult rat esophagus, stomach, and anus contained significant quantities of skeletal muscle, providing a source for the striated muscle isoactins detected in these gut segments. A similar source of striated muscle isoactin expression in the cecum, colon, and rectum was not identified. Both coordinate and independent regulation of isoactin gene expression was observed in the gastrointestinal tract, although distinct patterns of autoregulation were absent. CONCLUSIONS: This study represents the first complete analysis of isoactin gene expression in the adult rat gastrointestinal tract and provides the basis for future studies designed to investigate the factors responsible for these processes.

Actins↗
PubMed2003

Localization of protein kinase C theta immunoreactivity to interstitial cells of Cajal in guinea-pig gastrointestinal tract.

In the gastrointestinal tract, interstitial cells of Cajal (ICC) are located between nerve fibres and muscle cells and have a role in neuromuscular transmission and muscle contractility. Protein kinase C (PKC) is involved in modulation of muscle contractility by neurotransmitters, but it is not known if PKC has a role in ICC. There are 11 different PKC isoforms. The presence of PKC isoforms in ICC in guinea-pig gastrointestinal tract was examined using fluorescence immunohistochemistry and confocal microscopy. Segments of guinea-pig stomach, duodenum, ileum, proximal and distal colon were fixed in zambonis fixative. Frozen sections and wholemounts were incubated with anti-PKC antibodies (alpha, beta, delta, epsilon, gamma, iota, lambda, mu, theta) followed by fluorescent secondary antibody. Only PKC theta (theta) immunoreactivity was found in ICC. None of the other PKC isoforms (alpha, beta, delta, epsilon, gamma, iota, lambda, mu) localized to the ICC. PKC theta immunoreactivity was prominent in ICC located between the circular and longitudinal muscle layers (ICC-MY) in all regions except stomach and within the circular muscle (ICC-IM) in the large intestine. PKC theta was not present in ICC in the deep muscular plexus in either duodenum or ileum. PKC theta immunoreactivity was present in the cell body and proximal processes of the ICC. The cells containing PKC theta also contained cKit confirming the cells were ICC. ICC-MY in the ileum also contained the neurokinin (NK) 1 receptor. In conclusion, PKC theta is present in pacemaker ICC, but its function is not yet known. Functional studies will be needed to determine the role of this kinase in ICC. Knowing the second messenger cascades and being able to manipulate subpopulations of ICC will add to our understanding of the molecular and cell biology of ICC networks within the gastrointestinal tract and may ultimately help in understanding the aetiology of some gastrointestinal motor pathologies.

Animals↗
PubMed2004

Gastrointestinal tract.

The developing gastrointestinal tract from conception to adolescence is in constant direct interaction with an increasingly complex environment. This sets up the potential for unrecognized acute as well as chronic disorders, some of which may be difficult to pinpoint in a developing infant and child, given the wide variations that exist. It is startling to note how early some environmental toxins can come into contact with the developing human, where vulnerability may be heightened and maturation of detoxifying pathways may be incomplete. Although the complex process of recognizing, detoxifying, and avoiding the toxic substance by the body has presumably evolved over a substantial period of time, in this rapidly changing world, the array of novel toxins that make their way into the gastrointestinal tract is increasing. There remain many gaps in understanding the effects of environmental toxins on all of the developmental stages from conception to adolescence. Although threshold levels have typically been derived from adult or animal data, factors such as size, relative differences in consumption in proportion to size especially in infancy, and variable physiologic maturation of metabolic pathways are not well understood. The vulnerability may be further accentuated by physical factors that alter with maturity, such as permeability and critical times during organogenesis or organ maturation. Also of concern is how little is known about low-dose, long-term exposure, as well as any interplay with common illnesses. This article focuses on environmental toxins that have been shown to have toxic effects on the gastrointestinal tract.

Child↗
PubMed2006

Prion diseases and the gastrointestinal tract.

The gastrointestinal (GI) tract plays a central role in the pathogenesis of transmissible spongiform encephalopathies. These are human and animal diseases that include bovine spongiform encephalopathy, scrapie and Creutzfeldt-Jakob disease. They are uniformly fatal neurological diseases, which are characterized by ataxia and vacuolation in the central nervous system. Although they are known to be caused by the conversion of normal cellular prion protein to its infectious conformational isoform (PrPsc) the process by which this isoform is propagated and transported to the brain remains poorly understood. M cells, dendritic cells and possibly enteroendocrine cells are important in the movement of infectious prions across the GI epithelium. From there, PrPsc propagation requires B lymphocytes, dendritic cells and follicular dendritic cells of Peyer's patches. The early accumulation of the disease-causing agent in the plexuses of the enteric nervous system supports the contention that the autonomic nervous system is important in disease transmission. This is further supported by the presence of PrPsc in the ganglia of the parasympathetic and sympathetic nerves that innervate the GI tract. Additionally, the lymphoreticular system has been implicated as the route of transmission from the gut to the brain. Although normal cellular prion protein is found in the enteric nervous system, its role has not been characterized. Further research is required to understand how the cellular components of the gut wall interact to propagate and transmit infectious prions to develop potential therapies that may prevent the progression of transmissible spongiform encephalopathies.

Autonomic Nervous System↗
PubMed2003

The gastrointestinal tract as target of steroid hormone action: quantification of steroid receptor mRNA expression (AR, ERalpha, ERbeta and PR) in 10 bovine gastrointestinal tract compartments by kinetic RT-PCR.

We have examined the tissue-specific mRNA expression pattern of androgen receptor (AR), both estrogen receptor (ER) subtypes ERalpha and ERbeta and progestin receptor (PR) in 10 bovine gastrointestinal compartments. Goal of this study was to evaluate the deviating tissue sensitivities and the influence of the estrogenic active preparation Ralgro on the compartment-specific expression regulation. Ralgro contains Zeranol which shows strong estrogenic and anabolic effects. Eight heifers were treated for 8 weeks with Ralgro at different dosages (0, 1, 3, and 10 times). To quantify the very low abundant steroid receptor mRNA transcripts sensitive and reliable real-time (kinetic) reverse transcription (RT)-PCR quantification methods were validated on the LightCycler. Expression results indicate the existence of AR and both ER subtypes in all 10 gastrointestinal compartments. PR receptor was expressed at very low abundancy. Gastrointestinal tissues exhibit a specific ERalpha and ERbeta expression pattern with high expression levels for both subtypes in rectum, colon and ileum. With increasing Zeranol concentrations a significant down-regulation for ERalpha and ERbeta was observed in jejunum (P<0.001 and <0.05, respectively). Significant up-regulations under estrogen treatment could be shown in abomasum for ERalpha (P<0.05) and in rectum for ERbeta (P<0.001). The authors conclude, that especially estrogens and the expression of their corresponding receptor subtypes may play an important role in the modulation and regulation in gastric as well as gut functions, cell proliferation and possibly in the pathophysiology of cell cancer. The different expression patterns of ERalpha and ERbeta can be regarded as support of the hypothesis that the subtype proteins may have different biological functions in the gastrointestinal tract. AR and PR seem to be not estrogen dependent.

Animals↗
PubMed1978

Cyclic changes in the osmolality and electrolyte composition in the gastrointestinal tract of the rock hyrax.

The rock hyrax has been shown to have a very unusual and complex digestive tract. The gastrointestinal tract is comparable to that of the simple and complex stomach of mammals as well as to that of birds. Determinations of osmolality and electrolytes have been made in different sections of the gut of the hyrax. However, with the exception of the elevated potassium levels observed in the cranial stomach, the hyrax poses no unusual osmotic or electrolyte concentrations when compared to man or other mammals. The greater cation concentration and hypertonicity of the cranial stomach was largely accounted for by the elevated potassium load in this gut segment. Sodium and potassium comprised the major cations present throughout the gastrointestinal tract. Chloride was the major anion observed in the foregut; however, the electroneutrality of the mid and hindgut of the hyrax was primarily maintained by the presence of large concentrations of volatile fatty acids produced in these portions of the gut. Volatile fatty acid also accounted for the high anion concentration and hypertonicity of the cranial stomach.

Animals↗
PubMed2006

Taste receptors in the gastrointestinal tract. IV. Functional implications of bitter taste receptors in gastrointestinal chemosensing.

Changes in the luminal contents of the gastrointestinal tract modulate gastrointestinal functions, including absorption of nutrients, food intake, and protection against harmful substances. The current notion is that mucosal enteroendocrine cells act as primary chemoreceptors by releasing signaling molecules in response to changes in the luminal environment, which in turn activate nerve terminals. The recent discovery that taste receptors and G protein subunits alpha-gustducin and alpha-transducin, involved in gustatory signal transduction, are expressed in the gastrointestinal mucosa supports the concept of a chemosensory machinery in the gastrointestinal tract. An understanding of luminal sensing processes responsible for the generation of the appropriate functional response to specific nutrients and nonnutrients is of clinical importance since aberrant or unsteady responses to changes in luminal contents might result in disease states ranging from intoxication to feeding disorders and inflammation. The purpose of this theme article is to discuss the functional implications of bitter taste signaling molecules in the gastrointestinal tract deduced by their localization in selected populations of epithelial cells and their relationship with neural pathways responsible for the generation of specific responses to luminal contents.

Animals↗
PubMed1993

HTLV-I associated and non-associated primary T-cell lymphoma of gastrointestinal tract.

The gastrointestinal (GI) tract is the common extranodal site for non-Hodgkin's lymphoma (NHL), and primary lymphoma of GI tract are mostly of B-cell origin. We have treated 16 patients with primary lymphoma of GI tract between 1981 and 1991, of whom 10 (62%) were of B-cell origin, while 6 (38%) were of T-cell origin. The incidence of T-cell phenotype in our hospital was considered to be much higher than that of previous reports and these 6 patients with primary T-cell lymphoma of GI tract were carefully studied. The primary sites were stomach in 4, ileocecum in 1, and duodenum in 1 case. Their T-cell nature was confirmed by immunohistochemical methods. All were peripheral T-cell lymphomas; one was CD 3+ 4- 8- and the other 5 were CD 3+ 4+ 8-. The antibody against human T-cell leukemia virus type I (HTLV-I) was positive in 3 cases (HTLV-I associated), but negative in 3 (HTLV-I non-associated). The integration of HTLV-I proviral DNA in HTLV-I associated patients was demonstrated by Southern blot analysis after DNA amplification by means of polymerase chain reaction (PCR). The clinical features of the HTLV-I associated and HTLV-I non-associated primary T-cell lymphoma of the GI tract were quite different. HTLV-I associated patients showed leukemic manifestations and tumor involvement of the skin at a later stage of the disease. These observations indicated that HTLV-I can play an important role in the occurrence of primary T-cell lymphoma of GI tract.

Adult↗
PubMed1998

Enteric reovirus infection as a probe to study immunotoxicity of the gastrointestinal tract.

The gastrointestinal (GI) tract contains a complex immune system that defends the host against a wide range of pathogens and toxins. The GI tract is also exposed to many environmental toxins that could adversely affect intestinal immunity, and few systems to study immunotoxicity of the GI tract have been described. We demonstrate that intestinal reovirus infection can be used as a system to assess the effects of toxins on intestinal and systemic immunity. Mice were given various doses of cyclophosphamide (CY) for 5 days at doses ranging from 100 to 500 mg/kg by the oral route or 200 mg/kg by the intraperitoneal route. On day 3 of dosing, mice were orally infected with reovirus serotype 1, strain Lang. The effects of CY on viral clearance, intestinal and systemic immune responses, and distribution of intestinal lymphocytes were assessed. Mice treated with CY failed to clear the virus in a dose-dependent manner, and serum anti-reovirus antibody titers were suppressed. Virus-specific IgA in cultures of intestinal tissue from CY-treated mice was significantly reduced compared to controls, although total IgA production was not affected. The virus-specific cytotoxic T-cell response in spleen was also suppressed in CY-treated animals. Cyclophosphamide treatment reduced the number and percentage of B-cells in Peyer's patches. Reovirus infection did not increase cellularity of Peyer's patches in CY-treated mice. Cyclophosphamide treatment also had little effect on the phenotype of intestinal intraepithelial lymphocytes. These data demonstrate that intestinal reovirus infection is useful in studying exposure of the GI tract to immunotoxic agents.

Animals↗
PubMed1995

The gastrointestinal tract after anaesthesia.

Gastrointestinal tract motility may be reduced markedly after surgery with delay in gastric emptying. these alterations are induced partly by surgery, partly by the residual effects of anaesthetic agents, and particularly by opioids administered for post-operative pain relief. These changes may be antagonized to a certain extent by administration of prokinetic agents such as cisapride. Post-operative ileus reduces the rate of mobilization and may also reduce or delay absorption of drugs administered by the gastrointestinal tract. Furthermore, post-operative nausea and vomiting, multi-factorial in aetiology, may ensue and also be responsible for delayed mobilization, subjective discomfort and delay in administration of oral agents post-operatively. A serious problem may be leakage from bowel anastomoses. Although the causes are primarily surgical, an increase in bowel contractility may be deleterious and it has been suggested that neostigmine and morphine may be implicated in anastomotic dehiscence.

Anesthesia↗