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Biomedical subjects

A De

Publications and source records attributed to A De.

At least 37 records · Page 2Linked to original sources
PubMed2001

Prevalence of gram negative anaerobic bacilli in routine clinical specimens.

A total of 206 gram negative anaerobic bacilli were isolated from 2591 routine clinical specimens. Majority of them (78.2%) were part of a mixed flora. A high incidence of gram negative anaerobic bacilli was found in post-operative wound infections and diabetic foot infections (30.1%), followed by necrotizing fasciitis and crush injuries (18%), pus of empyema and lung abscesses (14.5%) and aspirates from other deep abscesses (10.7%). Bacteroides fragilis was the most frequently recognized species (42.2%), followed by Fusobacterium sp. (17.4%), Prevotella sp. (15.1%) and Porphyromonas sp. (11.2%). Neomycin blood agar plate yielded the maximum number (72.8%) of strains in pure culture. Gram negative anaerobic bacilli in infective processes are significantly on the rise and so suspected cultures should be processed for both aerobic and anaerobic organisms.

Bacteriological Techniques↗
PubMed2000

Intradialytic subjective sleepiness and oral body temperature.

STUDY OBJECTIVES: Hemodialysis (HD) patients are often observed to sleep during treatment. Because of the well-described, inverse association between body temperature and sleep propensity, the purpose of this study was to describe the course of intradialytic (during HD) subjective sleepiness and examine its relationship to oral body temperature. In addition, we sought to determine if that relationship varied with dialysis treatment time of day. DESIGN: Subjective sleepiness and oral body temperature were recorded every 15 minutes through the entire course of HD. SETTING: The study was conducted at two large, inner-city dialysis units. PATIENTS OR PARTICIPANTS: The sample included 60 chronic HD patients, 20 on each of three shifts based on treatment time of day (shift 1-6:00A.M. to 10:00A.M.; shift 2-10:00A.M. to 2:00P.M.; and shift 3-2:00P.M. to 6:00P.M.. MEASUREMENTS AND RESULTS: Subjects on shift 1 were found to have a mean intradialytic sleepiness level greater than those on shift 2 (p<.04) and shift 3 (p<.003). Irrespective of shift, sleepiness increased during the first half of dialysis and decreased slightly as treatment progressed, a significant quadratic trend (p<.001). During the same period, temperature initially increased, subsequently dropped in temporal proximity to maximal sleepiness and increased again, a significant quadratic trend (p<.02). The relationship between sleepiness and temperature revealed a significant negative correlation (r=-.59, p<.03) and did not vary with treatment time of day. CONCLUSIONS: The results argue that sleep propensity increases during HD, an effect that may be related to treatment induced alterations in arousal and/or thermoregulatory processes. The effect is unrelated to treatment time of day.

Body Temperature↗
PubMed2000

Hypo-osmolar oral rehydration salts solution in dehydrating persistent diarrhoea in children: double-blind, randomized, controlled clinical trial.

UNLABELLED: A double-blind, randomized, controlled trial was conducted to compare the clinical efficacy of hypo-osmolar oral rehydration salts (ORS) solution (224 mmol/L) and standard ORS solution (311 mmol/L) in children with persistent diarrhoea who were prone to develop dehydration. Initially, 95 children aged between 3 and 24 mo were included in the study for overnight observation. Of these, 70 children who passed stool more than 2 g/kg/h were finally enrolled in the study and were randomly assigned either standard ORS or hypo-osmolar ORS. After decoding the identity of ORS, it was observed that 37 children were in the standard ORS group and 33 in the hypo-osmolar ORS group. Clinical parameters and microbiological findings of stool samples were comparable in the two groups at the time of enrolment. Total stool output (2.5+/-1.1 vs 3.2+/-1.6 kg; p = 0.04), duration of diarrhoea (114.8+/-38.3 vs 145.4+/-40.0 h; p = 0.002), total intake of ORS (5.4+/-1.6 vs 7.8+/-1.8 l; p = 0.002) and total fluid intake (7.9+/-2.6 vs 10.0+/-4.1 l, p = 0.01) were significantly less in the hypo-osmolar ORS group compared to the standard ORS group. However, the percentage of weight gain on recovery in the hypo-osmolar group was less compared to that of the standard ORS group, though the difference was statistically insignificant. Thirty-five (95%) children in the standard ORS and 33 (100%) children in the hypo-osmolar group recovered within 10 d of initiation of therapy and modified dietary management. CONCLUSION: Our findings suggest that hypo-osmolar ORS has beneficial effects on the clinical course of dehydrating persistent diarrhoea.

Body Weight↗
PubMed2000

Opposing actions of two transforming growth factor-beta isoforms on pituitary lactotropic cell proliferation.

Three transforming growth factor-beta protein isoforms (TGFbeta1, TGFbeta2, and TGFbeta3) have been identified in mammals. These isoforms appear to have similar actions on cell growth in various tissues. In rat pituitary tissue, TGFbeta1 is localized in PRL-secreting lactotropes and has been shown to act on lactotropes to inhibit estradiol-induced cell proliferation. The steroid inhibits the production and secretion of TGFbeta1. It is not known whether the other two isoforms are produced in and/or act on lactotropes. Using immunocytochemical detection techniques, we determined that, like TGFbeta1, TGFbeta3 is colocalized with PRL in the anterior pituitary of Fischer-344 female rats. Administration of estradiol increased TGFbeta3-immunoreactive cell numbers, TGFbeta3 protein, and TGFbeta3 messenger RNA levels in the pituitary. Determinations of TGFbeta3 actions in vitro in primary cultures of pituitary cells indicated that TGFbeta3 concentration dependently increases lactotropic cell proliferation. The growth-promoting action of TGFbeta3 was potentiated by estradiol. Immunoneutralization studies indicated that although TGFbeta1 antibody failed to prevent estradiol's mitogenic action, it potentiated the mitogenic action of TGFbeta3. In contrast, TGFbeta3-neutralizing antibody inhibited lactotropic cell proliferation by estradiol. These data indicate that unlike many other tissues, TGFbeta1 and TGFbeta3 have opposite actions on lactotropic proliferation in the pituitary. Furthermore, TGFbeta1 and TGFbeta3 may be involved in estradiol's mitogenic action on lactotropes.

Animals↗
PubMed1999

Effect of ethanol on calcium regulation in rat fetal hypothalamic cells in culture.

The effects of acute exposure to ethanol on calcium regulation in primary cultures of rat fetal hypothalamic cells was studied with the use of the calcium indicator fura-2 and digital imaging techniques. We found that ethanol caused cytoplasmic calcium to increase in a dose-dependent and reversible manner, and these increases could be observed at pharmacologically relevant doses (34 mM). At 170 mM ethanol 65% of 1059 cells examined responded to ethanol with an increase in cytoplasmic calcium. Removing bath calcium eliminated the ethanol-induced calcium response in most cells (76% of 427 cells). In most cells exposure to thapsigargin (20 nM) had no significant effect on the ethanol-induced calcium increase (87% of 67 cells examined). The ethanol-induced calcium increase was reduced by 79+/-5% (n=110 cells) by the P/Q-type calcium channel blocker omega-agatoxin-TK (20 nM), by 51+/-10% (n=115 cells) by the N-type calcium channel blocker omega-conotoxin-GVIA (100 nM), and by 26+/-3% (n=90 cells) by the T-type calcium channel blocker flunarizine (1 microM). The L-type calcium channel blocker nifedipine (1 microM) had complex actions, sometimes inhibiting and sometimes increasing the calcium response. These results demonstrate that ethanol can directly modulate cytoplasmic calcium levels in hypothalamic cells mostly by a pathway that involves extracellular calcium and voltage-dependent calcium channels, and that this response may participate in the biological effects of acute ethanol exposure.

Animals↗
PubMed1999

Use of delayed pushing with epidural anesthesia: findings from a randomized, controlled trial.

OBJECTIVE: To compare outcomes between women receiving epidural anesthesia assigned to a group following either a 1-hour "delayed" pushing protocol or directed to initiate pushing at full cervical dilation. STUDY DESIGN: Using a randomized, controlled design, multivariate analyses were used to evaluate second stage labor duration and Apgar scores. An estimated odds ratio equation evaluated fetal descent progress. RESULTS: A 13.68-minute difference occurred in second stage labor length (p = 0.225). No differences were found in Apgar scores (p > 0.09). An estimated odds ratio, that progress in terms of one fetal station unit would occur for control group subjects as compared with subjects with similar progress in the experimental group, was 1.51 (95% confidence interval: 1.16, 1.95). CONCLUSION: Second stage labor was not significantly lengthened, and a similar rate of fetal descent occurred in the absence of directed pushing. Findings support further research on the potential advantages of minimizing the duration of pushing in labor.

Anesthesia, Epidural↗
PubMed1999

Effects of ethanol on alpha-adrenergic and beta-adrenergic agonist-stimulated beta-endorphin release and cAMP production in hypothalamic cells in primary cultures.

We have previously shown that low concentrations of ethanol rapidly stimulate beta-endorphin (beta-EP) release from hypothalamic neurons in primary cultures and that chronic exposures to these concentrations of ethanol desensitize beta-EP neurons to ethanol challenges. We have also shown that chronic ethanol desensitizes dibutyryl cAMP-, adenosine-, and prostaglandin E1-stimulated beta-EP release and the cAMP content in hypothalamic neurons. In this study, we determined the effects of ethanol (50 mM) on beta-adrenergic agonist (isoproterenol) or alpha-adrenergic agonist (l-phenylephrine)-induced beta-EP release and cellular contents of cAMP to identify whether ethanol causes heterologous desensitization of the adenylate cyclase system in this neuronal cell population. Both isoproterenol and l-phenylephrine increased beta-EP levels in culture media and elevated the cAMP content in cell extracts in a concentration (0.1 and 10 microM)-dependent fashion between 3 to 6 hr. A 50 mM dose of ethanol increased beta-EP and cAMP levels at 3 hr, but it did not elevate beta-EP and cAMP levels after 48 hr of exposure. Acute exposure (3 hr) of these cells to ethanol moderately enhanced the isoproterenol-stimulated and l-phenylephrine-stimulated levels of media beta-EP and intracellular levels of cAMP. However, chronic exposure (48 hr) to ethanol reduced the magnitude of both alpha- and beta-adrenergic receptor agonist-stimulated beta-EP release and cAMP production. These results confirm our previous findings that the ethanol action on beta-EP secretion is mediated by the cAMP system and further suggest that chronic ethanol causes heterologous desensitization of the adenylate cyclase system in the beta-EP neuronal cell population.

Adrenergic alpha-Agonists↗
PubMed1999

Effect of voltage-dependent calcium channel blockers on ethanol-induced beta-endorphin release from hypothalamic neurons in primary cultures.

The voltage-dependent calcium channel (VDCC) has been shown to mediate calcium entry into neurons that regulates neurotransmission in many neuronal cells. Four major types of VDCCs (three high-voltage-activated L-, N-, and P-types and one low-voltage-activated T-type) have been identified in neurons. Involvement of the VDCC in ethanol-stimulated beta-endorphin (beta-EP) release from hypothalamic neurons has not been studied. In the present study, the role of VDCC on basal and ethanol-induced beta-EP release was determined by using rat fetal hypothalamic cells in primary cultures. Treatments with a 50 mM dose of ethanol for 3 hr increased immunoreactive beta-EP (IR-beta-EP) release from hypothalamic cells maintained in cultures for 9 days. Ethanol-induced IR-beta-EP release was inhibited by a P/Q-type channel blocker omega-agatoxin TK (0.1-1 microM), an N-type channel blocker omega-conotoxin (0.1-1 microM), an L-type blocker nifedipine (1-10 microM), and a T-type blocker flunarizine (1-10 microM). The minimal effective doses of these blockers that blocked the ethanol response produced no significant effects on basal release of IR-beta-EP; neither did these doses of the blockers produce any significant effects on cell viability. These results suggest that ethanol-stimulated IR-beta-EP release is regulated by extracellular calcium involving P-, N-, L- and T-type channels.

Animals↗
PubMed1998

Hormonal control of pituitary prolactin-secreting tumors.

Prolactin secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans. Prolactinomas have been linked to estrogen exposure in humans and animals. However, the mechanism by which estrogen increases mitogenesis in lactotropes, as well as other estrogen responsive cells, is not well understood. Given the complex nature of steroid hormones and their wide array of actions, it seems plausible that there are multiple ways in which estrogen can exert its cell-transforming actions. Estrogen has a wide range of actions on cells depending on the cell type, receptor levels, and other factors present in the cell. A defect at any point could play a potential role in cell transformation. The source of such defects could be the result of any of a wide range of possibilities, including genetic predisposition, prolonged exposure to sufficient levels of the steroid hormone, or other insults to the cell which lead to altered responsiveness to estrogen in some way. This review discusses the recent advances that have been made in the area of understanding estrogen action in transformation of pituitary lactotropes.

Animals↗
PubMed1998

Mg2+ mediated sequence-specific binding of transcriptional activator protein C of bacteriophage Mu to DNA.

The contributions from the secondary structure of the transcriptional activator protein C of bacteriophage Mu to its specific DNA binding and the influence of various factors, viz., electrolytes, and minor groove and major groove binders on this protein-DNA interaction have been addressed. Circular dichroism (CD) spectral results suggest that, in the absence of Mg2+, C protein exhibits a beta-pleated sheetlike structure and Mg2+ changes the conformation to a more alpha-helical structure which could provide specific geometrical constraints complementary to those of DNA-helix. Thus, Mg2+ acts as a cofactor for the binding of the C protein to its specific site in DNA by inducing conformational changes in the protein. Competitive binding studies with minor and major groove binding drugs, viz., distamycin A and methyl green, respectively, and the DMS footprinting data indicate that the C protein recognizes the major groove of DNA during complex formation. Further, upon major groove binding, C protein brings about changes in DNA conformation; such conformational changes could have implications in the transcription process.

Amino Acid Sequence↗
PubMed1998

Role of transforming growth factor (TGF)-beta Type I and TGF-beta type II receptors in the TGF-beta1-regulated gene expression in pituitary prolactin-secreting lactotropes.

Transforming growth factor beta1 (TGF-beta1) inhibits pituitary lactotrope proliferation and secretion of PRL in an autocrine/paracrine manner. In this study, the role of TGF-beta1 type I (TbetaR-I) and TGF-beta type II (TbetaR-II) receptors in TGF-beta1-regulated gene expression in lactotropes was determined using anterior pituitary cells known to be responsive to TGF-beta1 growth inhibition and using a transformed PR1 cell line known to be nonresponsive to TGF-beta1 growth inhibition. Treatment with TGF-beta1 inhibited cell proliferation and decreased PRL mRNA levels in anterior pituitary cells, but in PR-1 cells, the treatment caused only decreased PRL mRNA levels. Affinity labeling of TGF-beta binding proteins indicated that anterior pituitary cells contain several TGF-beta-binding protein complexes, including the 65 kDa size TbetaR-I and 95 kDa size TbetaR-II. In the PR1 cells, the major complex found was similar to the 65 kDa size of TbetaR-I. Immunocytochemistry identified TbetaR-I and TbetaR-II receptor proteins in lactotropes but detected primarily TbetaR-I receptor protein in PR1 cells. RT-PCR detection of TbetaR-I and TbetaR-II mRNA identified both receptor mRNA transcripts in anterior pituitary cells and in PR1 cells but the levels of TbetaR-II and TbetaR-I mRNA transcripts in PR1 cells was much lower than that in anterior pituitary cells. Determination of the TGF-beta1 gene responses in PR1 cells following TbetaR-I and TbetaR-II gene transfection indicated that PR1 cells transactivate transcription of the TGF-beta-responsive p3TP-Lux reporter in the absence of cotransfected TbetaR-II receptor. The introduction of the TbetaR-II receptor alone or in combination with TbetaR-I confer ligand-independent reporter transactivation in these cells. When only TbetaR-I was introduced along with reporter, a ligand-dependent transactivation was observed. These data suggest for the first time that the TGF-beta1-mediated transcriptional activation response can be distinguished from the growth response in lactotropes. Furthermore, the TGF-beta1 gene-transcription response is less dependent on TbetaR-II receptor expression than is the TGF-beta1 growth-inhibitory response.

Activin Receptors, Type I↗
PubMed1998

C-reactive protein and buffy coat smear in early diagnosis of childhood septicemia.

Out of 200 cases of septicemia in children (age group 0-14 years), 111 had positive C-Reactive Protein (CRP > 12 mg/l) and 84 were buffy coat smear positive. Blood culture was positive in 98 cases, with predominant organism being Klebsiella pneumoniae, followed by Staphylococcus aureus. CRP test showed 100% sensitivity and 87.3% specificity, while buffy coat smear showed 76.5% sensitivity and 91.2% specificity. As blood culture reports are not available before 48-72 hours, combination of CRP test and buffy coat smear examination will be very helpful in early diagnosis of childhood septicemia.

Bacteremia↗
PubMed1997

Over expression of vascular endothelial growth factor and its receptor during the development of estrogen-induced rat pituitary tumors may mediate estrogen-initiated tumor angiogenesis.

Estrogens, which have been associated with several types of human and animal cancers, can induce tumor angiogenesis in the pituitary of Fischer 344 rats. The mechanistic details of tumor angiogenesis induction, during estrogen carcinogenesis, are still unknown. To elucidate the role of estrogen in the regulation of tumor angiogenesis in the pituitary of female rats, the density of blood vessels was analysed using factor VIII related antigen (FVIIIRAg) immunohistochemistry and the expression of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) was examined by Western blot and immunohistochemical analysis. The expression of VEGF receptor (VEGFR-2/Flk-1/KDR) was also examined by immunohistochemistry. The results demonstrated that 17beta-estradiol (E2) induces neovascularization, as well as the growth and enlargement of blood vessels after 7 days of exposure. The high tumor angiogenic potential was associated with an elevated VEGF/VPF protein expression in the E2 exposed pituitary of ovariectomized (OVEX) rats. VEGF/VPF and FVIIIRAg immunohistochemistry and endothelial specific lectin (UEA1) binding studies, indicate that the elevation of VEGF protein expression initially occurred in both blood vessels and non-endothelial cells. After 15 days of E2 exposure, VEGF/VPF protein expression, in the non-endothelial cell population, sharply declined and was restricted to the blood vessels. The function of non-endothelial-derived VEGF is not clear. Furthermore, immunohistochemical studies demonstrated that VEGFR-2 (flk-1/KDR), expression was elevated significantly in the endothelial cells of microblood vessels after 7 days of E2 exposure. These findings suggest that over expression of VEGF and its receptor (VEGFR-2) may play an important role in the initial step of the regulation of estrogen induced tumor angiogenesis in the rat pituitary.

Animals↗
PubMed1997

Use of protein A gene fusions for the analysis of structure-function relationship of the transactivator protein C of bacteriophage Mu.

A sensitive dimerization assay for DNA binding proteins has been developed using gene fusion technology. For this purpose, we have engineered a gene fusion using protein A gene of Staphylococcus aureus and C gene, the late gene transactivator of bacteriophage Mu. The C gene was fused to the 3' end of the gene for protein A to generate an A-C fusion. The overexpressed fusion protein was purified in a single step using immunoglobulin affinity chromatography. Purified fusion protein exhibits DNA binding activity as demonstrated by electrophoretic mobility shift assays. When the fusion protein A-C was mixed with C and analyzed for DNA binding, in addition to C and A-C specific complexes, a single intermediate complex comprising of a heterodimer of C and A-C fusion proteins was observed. Further, the protein A moiety in the fusion protein A-C does not contribute to DNA binding as demonstrated by proteolytic cleavage and circular dichroism (CD) analysis. The assay has also been applied to analyze the DNA binding domain of C protein by generating fusions between protein A and N- and C-terminal deletion mutants of C. The results indicate a role for the region towards the carboxy terminal of the protein in DNA binding. The general applicability of this method is discussed.

Amino Acid Sequence↗
PubMed1996

Pituitary lactotrope expresses transforming growth factor beta (TGF beta) type II receptor mRNA and protein and contains 125I-TGF beta 1 binding sites.

Transforming growth factor beta 1 (TGF beta 1) has recently been shown to be produced in the prolactin (PRL)-secreting lactotropes of the pituitary gland. TGF beta 1 inhibits lactotropic secretion and proliferation, and the production of TGF beta 1 in lactotropes is reduced during lactotropic growth following estrogen treatment in ovariectomized rats. In many estrogen-responsive tissues, TGF beta 1 has been shown to exert its effect by binding to TGF beta 1 type II receptors (T beta R II) at the cell surface. In this study, we sought to ascertain whether T beta R II is involved in TGF beta 1 action on lactotropes by determining the changes of T beta R II mRNA and protein levels and specific 125I-TGF beta 1 binding sites on the lactotropes during estrogen-induced proliferation of lactotropes in Fischer 344 rats. Double immunohistochemical procedures were employed to identify immunoreactive T beta R II in PRL-reactive cells. The majority of T beta R II-reactive cells in the anterior pituitary were observed to be lactotropes. Dual immunohistochemistry and in situ hybridization procedures also indicated that lactotropes were the major cell types containing T beta R II mRNA hybrids. Both the levels of immunoreactive T beta R II protein and in situ T beta R II mRNA hybrids in the pituitary were significantly decreased in ovariectomized rats after 15 days of estrogen treatment. Determination of 125I-TGF beta 1 binding sites in lactotropes by double immunohistochemistry and receptor autoradiography also revealed specific binding sites of 125I-TGF beta 1 in lactotropes in the anterior pituitary. 125I-TGF beta 1 binding in the anterior pituitary was also reduced following estrogen treatment in ovariectomized rats. These data suggest that down-regulation of T beta R II may be an important mechanism of estrogen action on lactotropic cell growth and PRL secretion, and further support the notion that TGF beta 1 controls lactotropic function by autocrine/paracrine mechanisms.

Animals↗
PubMed1995

Reduction in the expression and action of transforming growth factor beta 1 on lactotropes during estrogen-induced tumorigenesis in the anterior pituitary.

We have previously shown that transforming growth factor beta 1 (TGF-beta 1) receptor and TGF-beta type II receptor (T beta R-II) are produced in lactotropes, and that TGF-beta 1 inhibits the growth of these anterior pituitary cells by an autocrine mechanism. To study the changes of the expression and function of this growth factor during tumorigenesis, we have measured the levels of TGF-beta 1 and T beta R-II mRNAs and proteins in the normal and tumor anterior pituitary cells in vivo and in vitro and have compared the cell growth responses to TGF-beta 1 in normal and tumor pituitary cells in vitro. Treatment with estradiol-17 beta for 1, 2, 4, and 8 weeks caused a time-dependent increase in pituitary protein, prolactin, and prolactin mRNA levels and in plasma prolactin levels, suggesting that estrogen enhanced lactotropic proliferation in anterior pituitary glands. The levels of TGF-beta 1 protein and mRNA in anterior pituitary tissues were reduced over time after estrogen treatment during the development of pituitary tumors. The mRNA and protein levels of T beta R-II decreased markedly during the development of pituitary tumors. In addition, two transformed lactotropes, GH3 and PR1 cell lines, showed markedly reduced levels of TGF-beta 1 as well as T beta R-II mRNA. Comparison of the antiproliferative effects of TGF-beta in transformed and normal lactotropes in cultures revealed that the sensitivity of GH3 cells is reduced, and that PR1 cells are virtually resistant to TGF-beta 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Characterisation of the single copy trefoil peptides intestinal trefoil factor and pS2 and their ability to form covalent dimers.

A bacterial recombinant expression system was established to produce biologically active rat Intestinal Trefoil Factor (rITF). Characterisation of purified rITF shows that both monomers and dimers can be observed under reducing and non-reducing conditions, respectively. Site-directed mutagenesis studies show that Cys57 is necessary for rITF dimer formation. Samples of human gastrointestinal tissue following biopsy also demonstrated the presence of reducible human pS2 and ITF covalent dimers. Three-dimensional models for pS2 and ITF support the hypothesis that both pS2 and ITF can exist as disulphide-linked dimers in vivo and that any proposed function for these peptides must take dimer formation into account.

Amino Acid Sequence↗