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Biomedical subjects

D Tran

Publications and source records attributed to D Tran.

At least 55 records · Page 3Linked to original sources
PubMed2000

Eosinophilic gastroenteritis mimicking acute appendicitis.

Eosinophilic gastroenteritis is a rare entity that can be treated successfully with glucocorticoid therapy if the appropriate diagnosis is made. However, it may present with symptomatology mimicking acute surgical conditions. We present the case of a 26-year-old man who presented with diffuse epigastric pain, nausea, vomiting, and diarrhea. Extensive workup including upper endoscopy and imaging study revealed gastritis with ulcer and ascites. The patient developed right lower quadrant pain with localized peritonitis and leukocytosis. He underwent appendectomy and small bowel biopsy. Pathology revealed eosinophilic cellular infiltrate of both the appendiceal and small intestinal wall. The unique features of this condition are reviewed and surgical approaches are discussed.

Abdomen, Acute↗
PubMed1999

A cyclic antimicrobial peptide produced in primate leukocytes by the ligation of two truncated alpha-defensins.

Analysis of rhesus macaque leukocytes disclosed the presence of an 18-residue macrocyclic, tridisulfide antibiotic peptide in granules of neutrophils and monocytes. The peptide, termed rhesus theta defensin-1 (RTD-1), is microbicidal for bacteria and fungi at low micromolar concentrations. Antibacterial activity of the cyclic peptide was threefold greater than that of an open-chain analog, and the cyclic conformation was required for antimicrobial activity in the presence of 150 millimolar sodium chloride. Biosynthesis of RTD-1 involves the head-to-tail ligation of two alpha-defensin-related nonapeptides, requiring the formation of two new peptide bonds. Thus, host defense cells possess mechanisms for synthesis and granular packaging of macrocyclic antibiotic peptides that are components of the phagocyte antimicrobial armamentarium.

Amino Acid Sequence↗
PubMed1999

Different mutator phenotypes in Mlh1- versus Pms2-deficient mice.

Deficiencies in DNA mismatch repair (MMR) result in increased mutation rates and cancer risk in both humans and mice. Mouse strains homozygous for knockouts of either the Pms2 or Mlh1 MMR gene develop cancer but exhibit very different tumor spectra; only Mlh1(-/-) animals develop intestinal tumors. We carried out a detailed study of the microsatellite mutation spectra in each knockout strain. Five mononucleotide repeat tracts at four different chromosomal locations were studied by using single-molecule PCR or an in vivo forward mutation assay. Three dinucleotide repeat loci also were examined. Surprisingly, the mononucleotide repeat mutation frequency in Mlh1(-/-) mice was 2- to 3-fold higher than in Pms2(-/-) animals. The higher mutation frequency in Mlh1(-/-) mice may be a consequence of some residual DNA repair capacity in the Pms2(-/-) animals. Relevant to this idea, we observed that Pms2(-/-) mice exhibit almost normal levels of Mlh1p, whereas Mlh1(-/-) animals lack both Mlh1p and Pms2p. Comparison between Mlh1(-/-) animals and Mlh1(-/-) and Pms2(-/-) double knockout mice revealed little difference in mutator phenotype, suggesting that Mlh1 nullizygosity is sufficient to inactivate MMR completely. The findings may provide a basis for understanding the greater predisposition to intestinal cancer of Mlh1(-/-) mice. Small differences (2- to 3-fold) in mononucleotide repeat mutation rates may have dramatic effects on tumor development, requiring multiple genetic alterations in coding regions. Alternatively, this strain difference in tumor spectra also may be related to the consequences of the absence of Pms2p compared with the absence of both Pms2p and Mlh1p on as yet little understood cellular processes.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Smoking and lipid cardiovascular risk factors in Vietnamese refugees in Australia.

BACKGROUND: The effects of smoking and sex on lipid risk factors for cardiovascular disease were examined among Vietnamese people newly arrived in Australia. METHODS: Immigrants recruited through Refugee Screening had anthropometric data recorded and blood collected to measure total cholesterol (TC), high-density lipoprotein cholesterol (HDL), and triglyceride (TG) by Reflotron; apolipoprotein A-1 (apo A-1) and apolipoprotein B-100 (apo B) by immunoturbidimetric analyses (Turbitimer); and lipoprotein (a) (LP (a)) by ELISA. A questionnaire determined behavioral variables known to influence cardiovascular risk and Statview, Minitab, and SPSS were employed for data analysis. RESULTS: Lipoprotein profiles of men (n = 242) and women (n = 159) were compared. Crude TC and apo B were similar; HDL, apo A-1, and LP (a) were higher in women, TG was higher in men. After adjustment (age, BMI, WHR, years of smoking, and drinks per week), only apo A-1 and LP (a), were higher in women. "At risk" levels of TC or apo B did not differ by gender; risk of low apo A-1 was higher among men. Smokers had a significant risk (crude and adjusted) of low HDL, low apo A-1, and high LP (a). The sex difference in HDL was removed by a single adjustment for smoking; male smokers had higher LP (a) than male nonsmokers. CONCLUSION: Male and female Vietnamese immigrants had similar adjusted lipid profiles. Smoking had a marked detrimental effect on lipids.

Adult↗
PubMed1999

Involvement of dendritic cells in long-term aortocoronary saphenous vein bypass graft failure.

Antigen-presenting dendritic cells are present in atherosclerotic lesions in human arterial intima, but have not been investigated in atherosclerotic and hyperplastic stenotic lesions that affect vein grafts used as arterial conduits. This study was undertaken to examine whether dendritic cells are present in aortocoronary artery saphenous vein bypass grafts affected by high-grade atheromatous stenosis. Stenotic saphenous vein coronary artery bypass grafts (angiographic luminal stenosis > 75%) were harvested from 10 patients (nine male, one female), aged 4271 years (mean 56.5) at re-do operation. The mean time interval from bypass surgery to the excision of stenotic grafts was 11.5 years (range 2-21). The specimens were fixed in 10% buffered formalin, embedded in paraffin blocks and the sections stained with antibodies to S-100 (to identify dendritic cells), CD3 (T cells), CD68 (macrophages), von Willebrand factor (endothelial cells) and alpha-smooth muscle actin (smooth muscle cells) using avidin-biotin complex immunoperoxidase technique. Normal veins were obtained during saphenous vein femoro-popliteal grafting. The stenotic venous grafts showed histological features typical of extensive arterialization, intimal hyperplasia, atherosclerotic plaque-like lesions, calcification and thrombosis. In areas of intimal hyperplasia, S-10O-positive cells were distributed irregularly among smooth muscle cells. S-100-positive dendritic cells were seen most frequently within atherosclerotic plaque-like lesions where they co-localized with CD3+ cells and CD68+ cells. S-100-positive dendritic cells were also seen accumulating within calcific foci. No S-100-positve cells were found in normal, ungrafted saphenous veins. We conclude that dendritic cells are present in aortocoronary saphenous vein bypass grafts affected by high grade stenosis. Dendritic cells are probably involved in immune mechanisms of atherogenesis through their interactions with T cells and macrophages. The accumulation of dendritic cells within calcific foci suggests their contribution to the calcification of stenotic venous grafts.

Adult↗
PubMed1999

Substance P antagonists: the next breakthrough in treating depression?

Several lines of evidence implicate the neuropeptide substance P in depression, either in the pathogenesis or as a novel target for amelioration of symptoms. NK1 (substance P) receptor antagonists have been reported to have antidepressant-like actions in animal models. The first clinical trial of an NK1 antagonist showed promising results. A second trial, using a more potent compound, is underway. If the clinical trials show that NK1 (substance P) antagonism represents a well-tolerated, distinct mechanism for antidepressant activity, novel antidepressant agents will emerge as mono- or adjunct-therapy.

Animals↗
PubMed1999

Peptide localization and gene structure of cryptdin 4, a differentially expressed mouse paneth cell alpha-defensin.

Paneth cells in crypts of the small intestine express antimicrobial peptides, including alpha-defensins, termed cryptdins in mice. Of the known Paneth cell alpha-defensins, the cryptdin 4 gene is unique, because it is inactive in the duodenum and expressed at maximal levels in the distal small bowel (D. Darmoul and A. J. Ouellette, Am. J. Physiol. 271:G68-G74, 1996). With a cryptdin 4-specific antibody, immunohistochemical staining of ileal Paneth cells was strong and specific for cytoplasmic granules, demonstrating that this microbicidal peptide is a secretory product of Paneth cells in the distal small intestine. Consistent with the pattern of cryptdin 4 mRNA distribution along the length of the gut, the cryptdin 4 peptide was not detected in duodenum. Structurally, the cryptdin 4 gene resembles other Paneth cell alpha-defensin genes. Its two exons, transcriptional start site, intron, splice sites, and 3' flanking sequences are characteristic of the highly conserved mouse alpha-defensin genes. However, in the region upstream of the transcriptional initiation site, the cryptdin 4 gene contains a repeated 130-bp element that is unique to this alpha-defensin gene. Every independent cryptdin 4 genomic clone examined carries the repeated element, which contains putative recognition sequences for TF-IID-EIIA, cMyc-RS-1, and IgHC.2/CuE1.1; the repeat proximal to the start of transcription replaces DNA at the corresponding position in other mouse alpha-defensin genes. We speculate that this unique duplicated element may have a cis-acting regulatory role in the positional specificity of cryptdin 4 gene expression.

Amino Acid Sequence↗
PubMed1999

Visualization of cell surface vasopressin V1a receptors in rat hepatocytes with a fluorescent linear antagonist.

To visualize cell surface V1a vasopressin receptors in rat hepatocytes in the absence of receptor-mediated endocytosis, we used a high-affinity fluorescent linear antagonist, Rhm8-PVA. Epifluorescence microscopy (3CCD camera) and fluorescence spectroscopy were used. Rhm8-PVA alone did not stimulate Ca2+ signals and competitively blocked Ca2+ signals (Kinact of 3.0 nM) evoked by arginine vasopressin (vasopressin). When rat hepatocytes were incubated with 10 nM of Rhm8-PVA for 30 min at 4C, the fluorescent antagonist bound to the surface of cells, presumably the plasma membrane. The V1a receptor specificity of Rhm8-PVA binding was confirmed by its displacement by the nonfluorescent antagonist V4253 and by the natural hormone vasopressin at 4C. Prior vasopressin-mediated endocytosis of V1a receptors at 37C abolished binding of the labeled antagonist, whereas in non-preincubated cells, Rhm8-PVA labeled the cell surface of rat hepatocytes. When cells labeled with Rhm8-PVA at 4C were warmed to 37C to initiate receptor-mediated internalization of the fluorescent complex, Rhm8-PVA remained at the cell surface. Incubation temperature at 4C or 37C had little effect on binding of Rhm8-PVA. We conclude that Rhm8-PVA is unable to evoke receptor-mediated endocytosis and can readily be used to visualize cell surface receptors in living cells.

Animals↗
PubMed1999

Distribution of signaling molecules involved in vasopressin-induced Ca2+ mobilization in rat hepatocyte multiplets.

In freshly isolated rat hepatocyte multiplets, Ca2+ signals in response to vasopressin are highly organized. In this study we used specific probes to visualize, by fluorescence and confocal microscopy, the main signaling molecules involved in vasopressin-mediated Ca2+ responses. V1a receptors were detected with a novel fluorescent antagonist, Rhm8-PVA. The Galphaq/Galpha11, PLCbeta3, PIP2, and InsP3 receptors were detected with specific antibodies. V1a vasopressin receptors and PIP2 were associated with the basolateral membrane and were not detected in the bile canalicular domain. Galphaq/Galpha11, PLCbeta3, and InsP3 receptors were associated with the basolateral membrane and also with other intracellular structures. We used double labeling, Western blotting, and drugs (cytochalasin D, colchicine) known to disorganize the cytoskeleton to demonstrate the partial co-localization of Galphaq/Galpha11 with F-actin.

Actins↗
PubMed1999

Understanding and managing common baldness.

BACKGROUND: Society places importance on physical attributes especially the appearance of our hair. Common baldness or androgenetic alopecia is a normal physiological process of hair loss in genetically predisposed individuals. Premature or accelerated hair loss can engender considerable negative thoughts and anxiety associated with feelings of diminished attractiveness. OBJECTIVE: To enable general practitioners to recognise the various treatment options available, therefore offering patients reasonable hope and informed choices. DISCUSSION: Common baldness can be prevented by currently available mediums and regrowth may be achieved in a significant percentage of cases. Correct use of these agents requires an understanding of the pathogenesis of androgenetic alopecia, its natural history and the time course of response to treatment.

Alopecia↗
PubMed1999

[Paul-Louis Simond and the Marchoux mission in Brazil].

In 1900 the role of a particular mosquito called Stegomyia fasciata in the transmission of yellow fever was proved by a board of American medical officers. This discovery was the beginning of several scientific missions in South America, mostly in Brazil. As yellow fever was increasing in its West African colonies, the French government decided to send a scientific mission to Rio de Janeiro, to find new ways of prevention against the disease. Under the authority of the Institut Pasteur, Paul-Louis Simond, who had just discovered the role of the flea in the transmission of plague, was designated to carry through this mission together with Emile Marchoux and Alexandre Salimbeni, eminent Pasteurians like him. From November 1901 to May 1905, the three men studied the epidemiological and clinical aspects of the disease in Rio. They worked on the intermediate host's entomology, the Stegomyia female mosquito, improving the knowledge of yellow fever and its means of transmission. They also realized experiments on 25 healthy volunteers, submitting them to the bite of infected mosquitoes. They were among the first to proceed to yellow féver vaccinations by means of virulent serum heated to 55 degrees C or filtered. Their work led to the establishment of new sanitary rules to prevent the spread of the disease. This contributed to the success of the "yellow fever campaign" initiated by Oswaldo Cruz in the town of Rio. One of the most original contribution of their studies was to show that the yellow fever agent (which was still unknown) could be transmitted from an infected female Stegomyia to its eggs and larvaes. After this mission, the French authorities were able to fight yellow fever efficiently in their African colonies as well as in the West Indies and French Guyana.

Animals↗
PubMed1998

Anti-HIV-1 activity of indolicidin, an antimicrobial peptide from neutrophils.

Indolicidin is a tridecapeptide amide isolated from the cytoplasmic granules of bovine neutrophils. It has potent, broad spectrum microbicidal activities in vitro that are thought to be related to the membrane-disruptive properties of the peptide. Based on the putative membrane-targeted mode of action, we postulated that indolicidin would be active against HIV-1, an enveloped virus. Indolicidin was reproducibly virucidal against HIV-1 at a concentration of 333 microg/mL (174 microM) with a 50% inhibitory dose between 67 and 100 microg/mL. At 37 degrees C, killing was rapid with >50% killing of HIV occurring within 5 min, and nearly 100% viral inactivation achieved by 60 min. The anti-HIV activity of indolicidin was temperature-sensitive, a finding consistent with a membrane-mediated antiviral mechanism. Parallel experiments revealed that indolicidin lysed cultured lymphoblastoid cells at concentrations similar to those required for antiviral activity. However, a des-R13-amide indolicidin analog (R12-OH), previously shown to have less antibacterial activity than indolicidin, was significantly less active against HIV and was non-toxic to lymphoid target cells at concentrations up to 333 microg/mL, the highest level tested.

Animals↗
PubMed1998

Preliminary studies on the amoebicidal efficacy of contact lens disinfection systems.

PURPOSE: This preliminary study evaluated the efficacy of contact lens disinfection systems against Acanthamoeba castellanii, tested with and without co-incubation with Pseudomonas aeruginosa. METHODS: First, disinfection systems containing 3% hydrogen peroxide, 0.00005% polyaminopropyl biguanide or 0.001% polyquaternium were challenged with A. castellanii for 72 h. Surviving cells were enumerated. Second, A. castellanii were co-incubated with P. aeruginosa for 48 h, then exposed to the disinfectants for 6 h. RESULTS: There was zero survival of A. castellanii in hydrogen peroxide and variable survival in multipurpose systems. Following co-incubation, A. castellanii survival increased significantly (P = 0.015). CONCLUSIONS: Multipurpose systems have variable anti-amoeba activity and storage cases contaminated by bacteria may enhance amoeba survival.

Acanthamoeba↗
PubMed1998

[Intracellular calcium channels, hormone receptors and intercellular calcium waves].

The hormone-mediated intercellular Ca2+ waves were analyzed in multiplets of rat hepatocytes by video imaging of fura2 fluorescence. These multicellular systems are composed of groups of several cells (doublets to quintuplets) issued from the liver cell plate, a one cell-thick cord of about 20 hepatocytes long between portal and centrolobular veins. When the multiplets were homogeneously bathed with the glycogenolytic agonists vasopressin, noradrenaline, angiotensin II and ATP, they showed highly organized Ca2+ signals. Surprisingly, for a given agonist, the primary rises in intracellular Ca2+ concentration ([Ca2+]i) originated invariably in the same hepatocyte, then was propagated in a sequential manner to the nearest connected cells (cell 2, then 3, cell 4 in a quadruplet, for example). The sequential activation of the cells appeared to be an intrinsic property of multiplets of rat hepatocytes. The same sequence was observed at each train of oscillations occurring between cells. The order of [Ca2+]i responses was modified neither by repeated additions of hormones nor by the hormonal dose. The mechanical disruption of an intermediate cell did not prevent the activation of the next cell. These results suggest that each hepatocyte in the multiplet displays its own sensitivity to the hormone and that a gradient of sensitivity between each cell could be responsible for directing the intercellular Ca2+ wave. To test this hypothesis, we selectively isolated rat hepatocytes from periportal (PP) and perivenous (PV) areas of the liver cell plate. Periportal (PP) and perivenous (PV) rat hepatocyte suspensions were loaded with quin2/AM and hormonal responses were studied in a spectrofluorimeter. Noradrenaline, angiotensin II, and vasopressin-induced [Ca2+]i rises were greater in PV than in PP hepatocytes. In contrast, PP cells were more responsive than PV cells to ATP. The function of the InsP3 receptor (InsP3R) was also studied by measuring the InsP3-mediated 45Ca2+ release from permeabilized PP and PV hepatocytes. In permeabilized PP and PV hepatocytes, internal Ca2+ stores displayed the same loading-kinetics, the responses to InsP3 were similar, and the sizes of InsP3-sensitive compartment were not different. In a further study, we investigated by video microscopy in fura2-loaded multicellular systems of rat hepatocytes, the mechanisms controlling intercellular propagation of the Ca2+ wave and coordination of Ca2+ signals induced by the different hormones. Using focal microperfusion which allows local perfusion of any cell of the multiplet, rapid agonist removal during the Ca2+ response and microinjection, we found that second messengers and [Ca2+]i rises in one hepatocyte cannot trigger Ca2+ responses in connected adjacent cells, suggesting that diffusion across gap junctions, while required for coordination, is not sufficient by itself for the propagation of the intercellular Ca2+ wave. In addition, focal microperfusion and intermediate cell disruption experiments revealed very fine functional differences (hormonal delay, frequency of [Ca2+]i oscillations) between hormone-induced Ca2+ signals, even between two adjacent connected hepatocytes. Recent unpublished results performed in suspensions of PP and PV rat hepatocytes supported the view of a major role played by vasopressin receptors (V1a) in genesis and orientation of the Ca2+ wave. Vasopressin binding sites, V1a mRNAs detected by RNAse Protection Assay, and vasopressin-induced InsP3 production, were more abundant in PV than in PP cells. A gradient of hormone receptors could orientate the propagation of the Ca2+ wave in multicellular systems and in liver cell plate. These results suggest that the intercellular Ca2+ wave in multicellular systems of rat hepatocytes is propagated through mechanisms involving at least three factors. (ABSTRACT TRUNCATED)

Animals↗
PubMed1997

Cyclin G2 is up-regulated during growth inhibition and B cell antigen receptor-mediated cell cycle arrest.

Human cyclin G2 together with its closest homolog cyclin G1 defines a novel family of cyclins (Horne, M. C., Goolsby, G. L., Donaldson, K. L., Tran, D., Neubauer, M., and Wahl, A. F. (1996) J. Biol. Chem. 271, 6050-6061). Cyclin G2 is highly expressed in the immune system where immunologic tolerance subjects self-reactive lymphocytes to negative selection and clonal deletion via apoptosis. Here we investigated the effect of growth inhibitory signals on cyclin G2 mRNA abundance in different maturation stage-specific murine B cell lines. Upon treatment of wild-type and p53 null B cell lines with the negative growth factor, transforming growth factor beta1, or the growth inhibitory corticosteroid dexamethasone, cyclin G2 mRNA levels were increased in a time-dependent manner 5-14-fold over control cell levels. Unstimulated immature B cell lines (WEHI-231 and CH31) and unstimulated or IgM B cell receptor (BCR) -stimulated mature B cell lines (BAL-17 and CH12) rapidly proliferate and express low levels of cyclin G2 mRNA. In contrast, BCR-stimulated immature B cell lines undergo growth arrest and coincidentally exhibit an approximately 10-fold increase in cyclin G2 transcripts and a decrease in cyclin D2 message. Costimulation of WEHI-231 and CH31 cells with calcium ionophores and protein kinase C agonists partially mimics anti-IgM stimulation and elicits a strong up-regulation of cyclin G2 mRNA and down-regulation of cyclin D2 mRNA. Signaling mutants of WEHI-231 that are deficient in the phosphoinositide signaling pathway and consequently resistant to the BCR stimulus-induced growth arrest did not display a significant increase in cyclin G2 or decrease in cyclin D2 mRNAs when challenged with anti-IgM antibodies. The two polyclonal activators lipopolysaccharide and soluble gp39, which inhibit the growth arrest response of immature B cells, suppressed cyclin G2 mRNA expression induced by BCR stimulation. These results suggest that in murine B cells responding to growth inhibitory stimuli cyclin G2 may be a key negative regulator of cell cycle progression.

Amino Acid Sequence↗