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Biomedical subjects

H Rich

Publications and source records attributed to H Rich.

13 recordsLinked to original sources
PubMed1999

The prevalence of sexually transmitted pathogens in patients presenting to a Casablanca STD clinic.

The objective of this study conducted at the sexually transmitted diseases (STD) clinic of the Pasteur Institute of Morocco (SCPIM) is to describe clinical complaints and biological findings in patients attending this facility. Two thousand two hundred sixty-four patients had visited the STD clinic from 1992 to 1996. The main reported symptom was genital discharge for men (44.5%) and women (68.6%). Genital eruption and ulcer were more frequent in men. The principal biological result shows a seroprevalence of 0.62% for human immunodeficiency virus (HIV), 3.05% for hepatitis B virus (HBV), 51.5% for chlamydiae and 13.2% for syphilis. Factors associated with clinical findings were age and Gonococcus for men (odds ratio (OR): 1.94 and 5.96, respectively) and Trichomonas and positive TPHA for women (OR: 9.49 and 0.25, respectively). This work describes for the first time the distribution of various germs involved in sexually transmitted diseases in Moroccan population and underlines the importance of studying its sexual behavior as well as determinants of STD incidence.

Adult↗
PubMed1998

"The slow code".

Explore the source record for details and available documents.

Attitude to Death↗
PubMed1997

Leukotrienes in acetylcholine-induced contraction of esophageal circular smooth muscle in experimental esophagitis.

BACKGROUND & AIMS: Phospholipase A2 (PLA2) participates in acetylcholine (ACh)-induced contraction of esophageal circular smooth muscle. Because PLA2, arachidonic acid, and its metabolites are involved in inflammatory responses, their role after induction of experimental esophagitis was examined. METHODS: Experiments were performed in esophageal smooth muscle cells (ESO) isolated by enzymatic digestion from the circular layer of normal and esophagitis animals. Content of peptidoleukotrienes (leukotriene [LT] C4, LTD4, and LTE4) was measured in esophageal circular muscle tissue. RESULTS: The cytosolic PLA2 antagonist trifluoromethyl ketone analogue of arachidonic acid inhibited ACh-induced contraction of normal and esophagitis ESO. Inhibition by secreted PLA2 antagonists AM5 and MJ33 was significantly greater in esophagitis ESO. The lipoxygenase inhibitor nordihydro-guaiaretic acid and the LTD4 antagonist ICI 198,615 inhibited ACh-induced contraction of esophagitis but not of normal ESO. Secreted PLA2 and LTD4 contracted normal ESO more than esophagitis ESO. However, in esophagitis, ESO contraction was increased by threshold diacylglycerol concentration. Resting levels of LTs were greater in esophagitis than in normal circular esophageal muscle and increased in response to ACh in esophagitis but not in normal esophageal muscle. CONCLUSIONS: Esophagitis shifts the signal transduction pathway activated by ACh. Esophagitis increased the contribution of secreted PLA2 and of LTs to ACh-induced contraction.

Acetylcholine↗
PubMed1997

Experimental esophagitis affects intracellular calcium stores in the cat lower esophageal sphincter.

We previously showed that lower esophageal spincter (LES) tone depends on spontaneous production of inositol 1,4,5-trisphosphate (IP3) and release of intracellular Ca2+ and that acute experimental esophagitis reduces LES tone and IP3 production, suggesting damage to mechanisms responsible for release of Ca2+ from intracellular stores. In the present investigation, we examined the possibility that mechanisms responsible for Ca2+ storage or uptake may also be damaged. LES circular muscle cells were isolated by enzymatic digestion. Contraction was measured in response to IP3 and thapsigargin, which enhances release of Ca2+ from intracellular stores, and in response to calmodulin and to diacylglycerol. In addition, normal cells were incubated in thapsigargin to assess the effect of depletion of intracellular Ca2+ stores on contractile response. Contraction in response to IP3 and thapsigargin was reduced in experimental esophagitis, but contraction in response to calmodulin or diacylglycerol was not. Acetylcholine (ACh)-induced contraction of normal cells was inhibited by the calmodulin antagonist CGS-9343B but not by 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine dihydrochloride (H-7). In contrast, in cells from animals with esophagitis or in thapsigargin-treated cells from normal animals, ACh-induced contraction was inhibited by H-7 and not by CGS-9343B. We conclude that experimental esophagitis may damage intracellular Ca2+ stores in the LES and change the intracellular contractile pathways activated by ACh from calmodulin dependent in normal cells to protein kinase C dependent in esophagitis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Acute experimental esophagitis activates a second signal transduction pathway in cat smooth muscle from the lower esophageal sphincter.

In single cells, isolated by enzymatic digestion from the circular muscle layer of the lower esophageal sphincter (LES), acute experimental esophagitis (AE) alters signal transduction in response to a maximally effective dose of acetylcholine. In normal LES contraction was inhibited by M3 >> M1 or M2 antagonists. In AE inhibition by M2 antagonists increased significantly so that contraction was inhibited by M3 > M2 > M1 antagonists. In normal cells permeabilized by saponin, contraction was antagonized by antibodies against Gq/11, by the phosphatidylinositol-specific phospholipase C (PI-PLC) antagonist U 73122, but not by the phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor D609, or by the phospholipase D pathway inhibitor propranolol. In AE contraction was reduced by Gq/11 and Gi3 antibodies and by U73122, propranolol and D609. After thapsigargin treatment of normal cells to reduce intracellular Ca++ stores, contraction was inhibited by M2 and M3 antagonists, by antibodies against Gq/11 and Gi3, by U73122, D609 and propranolol, suggesting that depletion of Ca++ stores reproduces the changes induced by AE. We conclude that in normal LES smooth muscle cells acetylcholine-induced contraction is mediated by M3 receptors linked to Gq/11 and PI-PLC, whereas in AE, contraction through this pathway is reduced, perhaps because of reduction in Ca++ stores, and a second pathway is activated by M2 receptors linked to Gi3, PC-PLC and phospholipase D.

Acetylcholine↗
PubMed1996

The effects of a health newsletter for foster parents on their perceptions of the behavior and development of foster children.

Foster children have a high prevalence of medical, emotional, development, and behavioral problems originating both with events leading up to placement and as a consequence of the placement itself. Foster parents are often inadequately trained to understand and help with these difficulties. This may result in the persistence or aggravation of problems, and thereby increase the risk of placement failure. Because of the high demands on foster parents, any such training that is offered may be poorly attended. Methods to better inform these parents delivered in their own home may be more practical and better accepted. Parents at Heart is a quarterly health newsletter mailed to foster parents that deals with topics relevant to foster children. A questionnaire administered before the first issue determined some characteristics of these parents and ascertained their attitudes about a series of child development situations and behavior problems. A questionnaire after the fourth issue of Parents at Hear showed that many of these attitudes were influenced by the material in the newsletter.

Adult↗
PubMed1979

A collaborative study of infective endocarditis in the 1970s. Emphasis on infections in patients who have undergone cardiovascular surgery.

Twenty-six major cardiovascular centers participated in a cooperative study of all cases of infective endocarditis occurring during a single calendar year to obtain an overview of infective endocarditis. The study was designed to learn which patients appear to be at highest risk to develop this infection after palliative or reparative cardiovascular surgery. Of 278 patients developing infective endocarditis during the year at these medical centers, 63 (23%) had had previous cardiovascular surgery and 215 had not. Seventy percent of the 278 patients had recognized congenital or acquired heart disease before developing the infection. Rheumatic heart disease accounted for over half of the patients with underlying structural heart disease. A majority (55%) of the 63 patients who had been operated on before developing endocarditis had prosthetic valves inserted. Of those who did not require prosthetic valves, the majority had congenital heart disease with systemic artery-to-pulmonary artery shunts. Although these data were obtained from a selected group of patients, they confirm a significant risk of endocarditis in patients with prosthetic valves and suggest that in postoperative patients with non-valvular congenital heart disease, the highest risk appears to be in cyanotic patients with palliative pulmonary artery-to-systemic artery shunts.

Adolescent↗
PubMedDate not supplied

Signal transduction in esophageal and LES circular muscle contraction.

Contraction of normal esophageal circular muscle (ESO) in response to acetylcholine (ACh) is linked to M2 muscarinic receptors activating at least three intracellular phospholipases, i.e., phosphatidylcholine-specific phospholipase C (PC-PLC), phospholipase D (PLD), and the high molecular weight (85 kDa) cytosolic phospholipase A2 (cPLA2) to induce phosphatidylcholine (PC) metabolism, production of diacylglycerol (DAG) and arachidonic acid (AA), resulting in activation of a protein kinase C (PKC)-dependent pathway. In contrast, lower esophageal sphincter (LES) contraction induced by maximally effective doses of ACh is mediated by muscarinic M3 receptors, linked to pertussis toxin-insensitive GTP-binding proteins of the G(q/11) type. They activate phospholipase C, which hydrolyzes phosphatidylinositol bisphosphate (PIP2), producing inositol 1,4,5-trisphosphate (IP3) and DAG. IP3 causes release of intracellular Ca++ and formation of a Ca++-calmodulin complex, resulting in activation of myosin light chain kinase and contraction through a calmodulin-dependent pathway. Signal transduction pathways responsible for maintenance of LES tone are quite distinct from those activated during contraction in response to maximally effective doses of agonists (e.g., ACh). Resting LES tone is associated with activity of a low molecular weight (approximately 14 kDa) pancreatic-like (group 1) secreted phospholipase A2 (sPLA2) and production of arachidonic acid (AA), which is metabolized to prostaglandins and thromboxanes. These AA metabolites act on receptors linked to G-proteins to induce activation of PI- and PC-specific phospholipases, and production of second messengers. Resting LES tone is associated with submaximal PI hydrolysis resulting in submaximal levels of inositol trisphosphate (IP3-induced Ca++ release, and interaction with DAG to activate PKC. In an animal model of acute esophagitis, acid-induced inflammation alters the contractile pathway of ESO and LES. In LES circular muscle, after induction of experimental esophagitis, basal levels of PI hydrolysis are substantially reduced and intracellular Ca++ stores are functionally damaged, resulting in a reduction of resting tone. The reduction in intracellular Ca++ release causes a switch in the signal transduction pathway mediating contraction in response to ACh. In the normal LES, ACh causes release of Ca++ from intracellular stores and activation of a calmodulin-dependent pathway. After esophagitis, ACh-induced contraction depends on influx of extracellular Ca++, which is insufficient to activate calmodulin, and contraction is mediated by a PKC-dependent pathway. These changes are reproduced in normal LES cells by thapsigargin-induced depletion of Ca++ stores, suggesting that the amount of Ca++ available for release from intracellular stores defines the signal transduction pathway activated by a maximally effective dose of ACh.

Acetylcholine↗