Isoproterenol-induced gastric mucosal protection from bile acid. Role of endogenous prostaglandins.

Topical isoproterenol is a potent protective agent against bile acid-induced gastric mucosal injury in hypotensive and normotensive rats. This study was undertaken to ascertain what role endogenous prostaglandins and gastric mucosal blood flow play in isoproterenol-induced protection. Accordingly, anesthetized, fasted rats were given the cyclooxygenase inhibitor, indomethacin (5 mg/kg subcutaneously), 30 min prior to topical pretreatment with 3 ml of intragastric saline, isoproterenol (3 microM), or 16,16-dimethyl prostaglandin E2 (3 microM) for 15 min.

Transcription of the TCR-beta locus initiates in adult murine bone marrow.

Successful expression of the TCR beta-chain gene is a multistep process that involves: 1) initial transcription of multiple, unrearranged gene segments, 2) rearrangement of V, D, and J gene segments to form a complete beta-chain gene, and 3) transcription of the fully rearranged beta gene. All of these events have been shown to occur in the thymus, where the majority of T cell development takes place; however, the extent to which any of these events may occur prethymically has not been established. To examine prethymic TCR-beta gene expression, RNA was isolated from a precursor T cell-enriched population (Thy 1low CD3-) of C58/J mouse bone marrow, and analyzed by reverse transcriptase-PCR.

Quantitation of CD62, soluble CD62, and lysosome-associated membrane proteins 1 and 2 for evaluation of the quality of stored platelet concentrates.

Background: Platelets become activated during storage, which results in secretion of granules, vesiculation of microparticles, secretion of protein, and a number of other biochemical and morphologic processes that decrease the utility of platelet concentrates stored for transfusion.

Study Design And Methods: To evaluate the quality of stored platelet concentrates, the cell surface expression of specific activation-dependent antigens (CD62 and lysosome-associated membrane proteins 1 and 2 [LAMP-1, LAMP-2]) on platelets stored in a hospital blood bank over a 7-day period was examined. Relative microparticle counts and the expression of CD62 by microparticles, as well as platelet concentrate supernatant levels of soluble CD62, were determined.

The role of calcitonin gene-related peptide and nitric oxide in gastric mucosal hyperemia and protection.

It has been suggested that capsaicin-induced hyperemia and mucosal protection occurs via calcitonin-gene-related peptide (CGRP) release from gastric afferent sensory neurons and nitric oxide (NO)-mediated vasodilation. The purpose of this study was to determine whether capsaicin and/or bile acid induced hyperemia is mediated by CGRP and/or NO. Male Sprague-Dawley rats (280-350 g) were anesthetized, and the glandular stomach (blood supply intact) was chambered between two plastic rings.

Foregut revascularization via retrograde splenic artery perfusion after resection of a juxtaceliac mycotic aneurysm: complicated by pancreatic infarction because of cholesterol emboli.

A 66-year-old woman had development of a rapidly enlarging juxtaceliac mycotic aneurysm after therapy for lumbar osteomyelitis and a psoas abscess. The aneurysm was repaired through a thoracoabdominal approach with a Dacron aortic graft sewn end to end to the thoracic aorta and end to side to the infrarenal aorta. Perfusion was restored after oversewing the abdominal aorta above the superior mesenteric artery and oversewing the celiac trunk.

Capsaicin-induced gastric hyperemia and protection are NO- dependent.

Topical treatment of gastric mucosa with capsaicin (cap) increases gastric mucosal blood flow (GMBF) and protects the mucosa from injury by acidified bile salts. The purpose of this study was to test the hypothesis that this hyperemia related "cytoprotection" is mediated by nitric oxide. Male Sprague-Dawley rats were anesthetized and the glandular stomach (blood supply intact) was chambered between two plastic rings.

Salicylic acid, active oxygen species and systemic acquired resistance in plants.

Infection of plants, particularly by a necrotizing pathogen, usually induces a long-lasting, broad-based, systemic resistance to secondary pathogen attack. Many studies implicate salicylic acid as an essential signal in the development of such systemic acquired resistance in several plant species. Salicylic acid appears to mediate plant defence by binding to and inhibiting catalase, thus increasing the concentration of H(2)O(2) and other active oxygen species.

Capsaicin-induced gastric mucosal hyperemia and protection: the role of calcitonin gene-related peptide.

Background: Topical capsaicin augments gastric mucosal blood flow and is cytoprotective. This phenomenon is blocked by nitric oxide (NO) synthase and cyclooxygenase inhibition. Capsaicin-sensitive neurons store and release calcitonin gene-related peptide (CGRP).

Cocaine metabolites in the neonate: potential for toxicity.

Recent reports indicate that cocaine metabolites have biologic activity and could be toxic. To explore this possibility, two studies were initiated. The first study aimed to define the distribution of cocaine species by quantifying levels of cocaine and its metabolites norcocaine, benzoylecgonine, and benzoylnorecgonine in newborn cord blood and meconium.

Sensory neuron-mediated gastric mucosal protection is blocked by cyclooxygenase inhibition.

Background: Sensory neurons have been proposed to play a critical role in the protection of the gastric mucosa from a variety of necrotizing agents. The purposes of this study were (1) to investigate the effect of topical capsaicin, a sensory neuron stimulant, on the gastric mucosal injury caused by the topical application of low concentrations of bile acid and (2) to determine whether local neuronal blockade with topical lidocaine or cyclooxygenase blockade with systemic indomethacin has any effect during pretreatment with capsaicin.

Methods: Before injury with topical 5 mmol/L acidified taurocholate (pH 1.

Topical prostaglandin E2 and isoproterenol reduce bile acid-induced gastric mucosal injury in shocked rats.

In shocked animals, topical application of bile acids at low pH to gastric mucosa results in gross mucosal injury. Both systemic prostaglandins and isoproterenol reduce this injury, but side effects may limit their clinical usefulness. The purpose of this study was to determine the effect of topical pretreatment with isoproterenol and prostaglandin E2 on gastric mucosal injury induced by low concentrations of bile acid in shocked and normotensive rats.

Effect of local acid-base status on gastric mucosal blood flow and surface cell injury by bile acid.

Topical application of 5 mM sodium taurocholate (5 TC, pH 1.2) to canine gastric mucosa results in luminal hydrogen ion (H+) loss and surface epithelial cell (SEC) injury. However, gross mucosal injury does not occur because of a protective increase in gastric mucosal blood flow (GMBF).

Sphincterlike thoracoabdominal high pressure zone after esophagogastrectomy.

Background: The contribution of the crural diaphragm to the gastroesophageal high pressure zone (HPZ) may be important in prevention of gastroesophageal reflux. The purpose of this study was to investigate the manometric characteristics of the thoracoabdominal junction in patients after surgical removal of the lower esophageal sphincter.

Methods: Ten patients with prior esophagogastrectomy were studied manometrically.

The expression of CD4 by T cell precursors resident in both the thymus and the bone marrow.

A very small fraction of thymocytes has recently been identified that expresses low levels of CD4 in the absence of CD8, CD3, or a TCR. These CD4lo thymocytes appear to be the precursors of the early CD4-CD8-CD3- thymic subset and contain most of the T cell progenitor activity found within the thymus. Here, we examined adult bone marrow for the presence of a similar population of cells and found that 0.

Effects of topical isoproterenol on bile acid-induced gastric mucosal injury.

Topical isoproterenol protects the gastric mucosa from the severe necrosis induced by 100 per cent ethanol. Its effect on gastric mucosal blood flow is unknown. The purpose of this study was to determine the effect of topical isoproterenol on gastric mucosal blood flow and on the less severe gastric mucosal injury caused by dilute bile acid.

Selective lipoxygenase inhibitor reduces bile acid-induced gastric mucosal injury.

Leukotriene receptor blockade attenuates topical bile acid-induced gastric mucosal injury, suggesting that peptidyl-leukotrienes may be mediators of this injury. The purpose of this study was to test the hypothesis that a selective 5-lipoxygenase inhibitor protects against bile acid-induced gastric epithelial injury in the rat. Prior to injury with 10 and 20 mM acidified taurocholate (pH 1.

In vitro growth of bone marrow-resident T cell precursors supported by mast cell growth factor and IL-3.

The growth requirements of bone marrow-resident cells that are able to differentiate along the T cell lineage (pre-T cells) have not been well established. We recently have shown that the T cell-derived lymphokine IL-3 is able to maintain pre-T cells in vitro for at least 2 weeks. However, in our initial studies, we were not able to ascertain whether IL-3 induced pre-T cell growth during culture, or whether IL-3 simply maintained the viability of these progenitors.

High-yield recovery of recombinant DNA from poorly growing cosmid and lambda genomic clones.

Certain genomic sequences cannot be recovered efficiently in cosmid or lambda bacteriophage clones, presenting a barrier to efforts to construct a contiguous cloned library of a genome. We have encountered such sequences during our efforts to isolate cosmid and bacteriophage lambda clones carrying members of the human type 2 cystatin gene family. Several cosmid clones constructed in the pWE 15 vector did not survive purification, and using standard techniques, we were unable to obtain significant amounts of cosmid DNA from those clones we could purify.

Do leukotrienes mediate bile acid-induced gastric mucosal injury?

Leukotrienes C4 and D4 are potent vasoconstrictors and have been proposed as mediators of the severe gastric mucosal injury caused by a variety of necrotizing agents. The purpose of this study was to investigate the role of leukotrienes on the less severe gastric mucosal injury caused by low concentrations of bile acid. Prior to injury with 5 mM acidified taurocholate (pH 1.

Effect of capsaicin on gastric mucosal injury and blood flow following bile acid exposure.

Topical bile acid at low pH stimulates gastric mucosal blood flow (GMBF), thereby limiting injury to surface epithelial cells (SEC). Capsaicin-sensitive afferent neurons (ASN) are possible mediators of the GMBF response and, therefore, of mucosal protection. In order to investigate the effect of topical capsaicin (ASN stimulant) and topical lidocaine (ASN inhibitor) on SEC exfoliation and GMBF, vascularized wedges of canine gastric corpus were mounted in lucite chambers.

Characterization of the progeny of precursor-T (pre-T) cells maintained in vitro by interleukin-3 (IL-3). Development of T-cell function in vivo.

We have recently described a bone marrow culture system which is able to maintain a portion of the precursor-T (pre-T) cell compartment of adult murine marrow in vitro, in the presence of interleukin-3 (IL-3), for at least 2 weeks. However, because growth in IL-3 might also induce the differentiation of the pre-T cells, it is necessary to determine the extent to which the developmental potential of the pre-T cells is altered during their residency in vitro. Previously, we analysed the progeny of cultured pre-T cells and compared their intrathymic development, their appearance in the periphery, and their V beta gene utilization to that of the progeny of fresh pre-T cells.

Do sensory neurons mediate adaptive cytoprotection of gastric mucosa against bile acid injury?

Pretreatment with the mild irritant 1 mmol acidified taurocholate protects the gastric mucosa from the injury induced by the subsequent application of 5 mmol acidified taurocholate, a phenomenon referred to as "adaptive cytoprotection." How this occurs remains an enigma. The purpose of this study was to investigate the role of sensory neurons and mucus secretion in this phenomenon.

Leukotriene receptor blockade reduces bile acid-induced superficial gastric mucosal injury.

Leukotriene C4 and D4 are putative mediators of the severe gastric mucosal injury caused by a variety of topical irritants. The purpose of this present study was (1) to investigate the effect of pretreatment with topical leukotriene C4 and D4 on the more superficial injury caused by low concentrations of bile acid and (2) to determine the effect of leukotriene receptor blockade, alone and during leukotriene pretreatment, on this injury. Prior to injury with topical 5 mM acidified taurocholate (pH 1.