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Biomedical subjects

M Tang

Publications and source records attributed to M Tang.

At least 127 records · Page 7Linked to original sources
PubMed1994

Fibroblast growth factor receptor gene expression and immunoreactivity are elevated in human glioblastoma multiforme.

Glioblastomas were examined for abnormalities in fibroblast growth factor receptor (FGFR) expression by polymerase chain reaction and immunocytochemical analysis. Polymerase chain reaction analysis demonstrated that FGFR1 mRNA levels were significantly higher in glioblastomas than in normal brain adjacent to the tumor or in untransformed human brain. These results were consistent with immunocytochemical localization of FGFR1 protein in glioblastomas: glioblastoma cells exhibited intense FGFR1 immunoreactivity in frozen sections of tumor and low to undetectable FGFR1 immunoreactivity in adjacent normal brain or in normal white matter obtained from patients without neoplastic disease. Endothelial cells of capillaries and larger vessels within the tumor were devoid of FGFR1 immunoreactivity. All glioblastomas evaluated in the present study expressed FGFR1 mRNA and FGFR1 immunoreactivity. Examination of the FGFR1 gene by Southern blot analysis indicated that overexpression of FGFR1 mRNA in glioblastomas did not result from gene amplification. These results indicate that glioblastoma cells, in contrast to endothelial cells within the tumor, display increased levels of FGFR1. Therefore, FGFR1 signal transduction may be associated with increased autocrine growth activity of tumor cells and is probably not related to the increased endothelial cell proliferation associated with these tumors.

Base Sequence↗
PubMed1994

Cardiac blood flow studies in fetuses with haemoglobin Bart's disease.

Blood flow across the atrioventricular valves and outflow tracts was measured in 55 normal fetuses and 32 fetuses with haemoglobin (Hb) Bart's disease between 18 and 26 weeks of gestation. The mean velocities remained unchanged in both normal and affected fetuses over the gestations studied. The volume flow across both atrioventricular valves and outflow tracts increased as the gestation advanced in both normal and affected fetuses, but was significantly higher in affected than in normal fetuses. The same magnitude of increased flow was found in both hydropic and non-hydropic fetuses with Hb Bart's disease. These findings suggest that fetuses with severe and long-standing anaemia have a remarkable cardiac compensatory mechanism for the maintenance of tissue oxygenation. In response to anaemia and circulatory loading, the cardiac chambers and outflow tracts enlarge proportionately up to twice the normal values. Because of this response and the operation of the Frank-Starling mechanism, the heart is able to maintain a normal mean velocity of propulsion and the net output is increased to two to three times that in normal fetuses. Hydropic changes in these anaemic fetuses appear unrelated to cardiac failure as cardiac failure is not observed at the time that hydropic changes develop.

Blood Flow Velocity↗
PubMed1994

UBP5 encodes a putative yeast ubiquitin-specific protease that is related to the human Tre-2 oncogene product.

A gene from chromosome V of the yeast Saccharomyces cerevisiae has been cloned and sequenced. The deduced amino acid sequence encoded by this gene is similar to several ubiquitin-specific proteases from yeast, especially at the highly conserved domain. It is thus named UBP5. UBP5 is also closely related to the human Tre-2 and the mouse Unp oncogene products. This study adds a new member to the ubiquitin protease family and suggests that alteration of ubiquitin protease activity may result in cancer in mammals. However, disruption of the UBP5 gene in a haploid strain did not result in a noticeable phenotypic alteration.

Amino Acid Sequence↗
PubMed1994

Production and secretion of interferon-gamma (IFN-gamma) in children with atopic dermatitis.

IFN-gamma is known to be a major inhibitor of IgE synthesis in vitro. Recent studies demonstrating reduced production of IFN-gamma in children and adults with atopic dermatitis and elevated serum IgE suggest a similar role for this cytokine in vivo. The reasons for this reduced IFN-gamma production are not known. One possibility is that atopic individuals have a reduced population of cells producing IFN-gamma in vivo. Using a fluorescence-labelled antibody to detect intracellular IFN-gamma, the percentage of IFN-gamma-producing cells was determined in children with atopic dermatitis and in non-atopic controls. Children with atopic dermatitis had a greater percentage of IFN-gamma-producing cells in unstimulated cultures compared with controls, indicating in vivo activation of lymphocytes in the atopic group. This could reflect the significant degree of inflammation present in these children, or the presence of bacterial infection or colonization. Although secretion of IFN-gamma after stimulation with phorbol myristate acetate (PMA)/Ca was significantly lower in children with atopic dermatitis compared with controls, the percentage of IFN-gamma-producing cells in the stimulated cultures from this group was equivalent to controls. This demonstrates that the reduced ability of atopic children to secrete IFN-gamma in vitro does not relate to a lack of IFN-gamma-producing cells, but to a difference in the regulation of IFN-gamma production beyond the stage of signal transduction.

Adolescent↗
PubMed1994

Herpes simplex virus glycoproteins E and I facilitate cell-to-cell spread in vivo and across junctions of cultured cells.

Herpes simplex virus (HSV) glycoproteins E and I (gE and gI) can act as a receptor for the Fc domain of immunoglobulin G (IgG). To examine the role of HSV IgG Fc receptor in viral pathogenesis, rabbits and mice were infected by the corneal route with HSV gE- or gI- mutants. Wild-type HSV-1 produced large dendritic lesions in the corneal epithelium and subsequent stromal disease leading to viral encephalitis, whereas gE- and gI- mutant viruses produced microscopic punctate or small dendritic lesions in the epithelium and no corneal disease or encephalitis. These differences were not related to the ability of the gE-gI oligomer to bind IgG because the differences were observed before the appearance of anti-HSV IgG and in mice, in which IgG binds to the Fc receptor poorly or not at all. Mutant viruses produced small plaques on monolayers of normal human fibroblasts and epithelial cells. Replication of gE- and gI- mutant viruses in human fibroblasts were normal, and the rates of entry of mutant and wild-type viruses into fibroblasts were similar; however, spread of gE- and gI- mutant viruses from cell to cell was significantly slower than that of wild-type HSV-1. In experiments in which fibroblast monolayers were infected with low multiplicities of virus and multiple rounds of infection occurred, the presence of neutralizing antibodies in the culture medium caused the yields of mutant viruses to drop dramatically, whereas there was a lesser effect on the production of wild-type HSV. It appears that cell-to-cell transmission of wild-type HSV-1 occurs by at least two mechanisms: (i) release of virus from cells and entry of extracellular virus into a neighboring cell and (ii) transfer of virus across cell junctions in a manner resistant to neutralizing antibodies. Our results suggest that gE- and gI- mutants are defective in the latter mechanism of spread, suggesting the possibility that the gE-gI complex facilitates virus transfer across cell junctions, a mode of spread which may predominate in some tissues. It is ironic that the gE-gI complex, usually considered an IgG Fc receptor, may, through its ability to mediate cell-to-cell spread, actually protect HSV from IgG in a manner different than previously thought.

Animals↗
PubMed1994

Effects of pentoxifylline on choroidal blood flow in nonproliferative diabetic retinopathy.

OBJECTIVE: Diminished blood flow plays an important role in the progression of diabetic retinopathy. Since increased blood viscosity is a contributing factor to hypoperfusion, it was of interest to determine whether therapy intended to decrease blood viscosity and induce vasodilation could increase blood flow in patients with diabetic retinopathy. METHODOLOGY: Ten patients, 4 with nonproliferative diabetic retinopathy and 6 age-matched, nondiabetic controls, were studied by a noninvasive system to index choroidal blood flow. Pentoxifylline was administered daily at an oral dose of 400 mg tid in the diabetic patients for nine months. RESULTS: The control group had pulse amplitude = 2.87 +/- 0.67 mm Hg with pulsatile choroidal blood flow = 714 +/- 196 microL/minute. Reproducibility studies in the control group (6 patients measured on three separate occasions) demonstrated an intraclass correlation coefficient of reliability, r = 0.83. In the diabetic patients, pulsatile flow = 276 +/- 68 microL/minute, 61% lower than the age-matched nondiabetic subjects (P = 0.003). After nine months of pentoxifylline therapy the diabetic patients had an increase in pulsatile choroidal blood flow to 469 +/- 152 microL/minute (P < 0.002). CONCLUSIONS: Pentoxifylline therapy brought blood flow levels in the diabetic patients closer to those of the nondiabetic age-matched control population so that following therapy there was no statistically significant difference between the two groups although the former were still lower. The potential efficacy of pentoxifylline in improving ocular blood flow in patients with diabetic retinopathy should be tested in a large controlled clinical trial.

Adult↗
PubMed1994

Estrogen differentially affects c-jun expression in uterine tissue compartments.

Estrogen rapidly induces expression of the jun immediate early gene family in mature and immature rodent uteri, suggesting that these protooncogenes are directly involved in the proliferative response of the uterus to estrogen. The jun family mRNAs, however, have not been localized to specific uterine cell types. Furthermore, it is necessary to differentiate between the response of the immature vs. the mature rat uterus to 17 beta-estradiol (E2-17 beta), because in the former, all uterine cell types respond to estrogen with increased DNA synthesis, but in the latter, the proliferative response is restricted to the uterine epithelial cells. In the present study, in situ hybridization was used to determine the cell type-specific location of mRNA encoding the immediate early genes c-jun, jun-B, and jun-D after the administration of E2-17 beta to mature and immature rats. Estradiol stimulated jun-B and jun-D expression primarily in the uterine luminal and glandular epithelium. The pattern of c-jun expression, however, was strikingly different; E2-17 beta repressed c-jun mRNA levels in the uterine luminal epithelium and simultaneously increased c-jun expression in the uterine myometrium. In mature vs. immature uteri, the general cell type-specific patterns of jun-B and jun-D expression were similar after estrogen administration. The expression of c-jun was increased by estrogen in the uterine glands as well the uterine myometrium of immature rats; however, in mature rats, uterine glandular epithelial cells did not respond to E2-17 beta administration with increased c-jun expression. These experiments demonstrate for the first time positive and negative regulatory actions of estrogen on c-jun expression and suggest a role for tissue-specific factors in the control of c-jun expression. The lack of maturational effects on jun gene expression implies that the differential response of the immature vs. the mature uterus to estrogen, in terms of cell proliferation, involves a point of control other than that at the level of the jun protooncogene family.

Aging↗
PubMed1994

The apolipoprotein epsilon 4 allele in Parkinson's disease with and without dementia.

The epsilon 4 isoform of apolipoprotein E (Apo-E) may confer genetic susceptibility for familial and sporadic Alzheimer's disease (AD). Because dementia in AD and Parkinson's disease (PD) share many biologic and clinical features, we determined the Apo-E genotypes for 79 patients with PD, 22 of whom were demented, and for 44 age-matched healthy elderly controls from the same community. We hypothesized that if the dementia was similar to AD, there would be a higher allele frequency of apolipoprotein epsilon 4 (Apo epsilon 4) in demented PD patients compared with nondemented PD patients and controls. The epsilon 4 allele frequency for PD without dementia was 0.132, for PD with dementia, 0.068, and for controls, 0.102. There was no association between Apo epsilon 4 and dementia in the PD patients. We conclude that the biologic basis for dementia in PD may differ from that of AD.

Aged↗
PubMed1994

Changes in biliary (high-molecular-mass) and liver isoforms of alkaline phosphatase after baboon-to-human liver transplantation.

We report a case of hyperphosphatasemia in a 35-year-old patient with hepatitis B who underwent an orthotopic xenogeneic liver transplant. Marked increases in total alkaline phosphatase (ALP; EC 3.1.3.1) activity began 5 days posttransplantation (six times human normal) and increased to approximately 17 times normal at day 11. Increased ALP persisted for > 40 days and steadily increased to 75 times normal in the patient's last 30 days. Gel electrophoresis detected both liver (LALP) and biliary (high-molecular-mass, BALP) isoforms. LALP measured with ion-exchange columns revealed an activity time course pattern similar to that of total ALP. Results for BALP activity also obtained with ion-exchange columns exhibited broad variability, ranging from 2 to 428 times normal.

Adult↗
PubMed1993

Identification and deletion mutagenesis of the bovine herpesvirus 1 dUTPase gene and a gene homologous to herpes simplex virus UL49.5.

The gene encoding bovine herpesvirus 1 (BHV 1) deoxyuridine triphosphatase (dUTPase) was isolated by a PCR procedure using degenerate oligonucleotide primers whose sequences were based upon conserved motifs commonly present in dUTPase genes. This gene was found to reside between 0.059 and 0.066 map units in the BHV 1 Cooper strain. DNA sequence analysis of this region revealed an open reading frame of 975 base pairs capable of encoding 325 amino acids. The deduced amino acid sequence of the open reading frame exhibits significant homology with dUTPases of other herpesviruses (including human herpes simplex virus, varicella-zoster virus, and Epstein-Barr virus), and it contains five conserved amino acid motifs characteristics of all dUTPases identified to date. A mutant virus carrying a partial deletion of the putative dUTPase gene was made and was found to lack virus-encoded dUTPase activity. This further confirmed that we have identified the BHV 1 dUTPase gene. In addition, a further analysis of the genomic fragment which contains the dUTPase coding sequence revealed an additional 288-base-pair open reading frame which appears to be colinear with the HSV 1 UL49.5 gene. The deduced amino acid sequence of this open reading frame is significantly homologous to the HSV 1 UL49.5 gene product, and as with UL49.5, it contains a potential signal sequence and transmembrane domain characteristic of membrane-associated proteins. These results suggest that this open reading frame represents the BHV 1 homolog of the HSV 1 UL49.5 gene. Since our dUTPase negative mutant was fully viable and since the mutant was constructed such that the UL49.5 gene was also deleted, both the dUTPase and the UL49.5 gene homolog are not required for virus growth in cell culture.

Amino Acid Sequence↗
PubMed1993

Pneumatic retinopexy using only air.

Pneumatic retinopexy was performed using only air in an attempt to minimize vitreous disturbance and lower the incidence of postoperative proliferative vitreoretinopathy (PVR) and premacular membranes (PMM). Retinal cryopexy or laser treatment (in 2 cases) and intravitreal injection of 0.8 cc filtered air were performed on 45 rhegmatogenous retinal detachments with superior breaks and no preoperative vitreous hemorrhage or PVR. Reattachment was achieved in 39 (86.7%) eyes. The remaining 6 eyes were secondarily treated with scleral buckle surgery, which was successful in all cases. The average length of follow-up was 17.1 +/- 8.6 months, at which time visual acuity was the same or better in 44 (97.8%) eyes. In 1 case (2.2%) PVR developed, a PMM formed in 1 case (2.2%), and new or missed retinal breaks were found in 4 cases (8.8%). This technique achieves a high rate of reattachment, good visual outcome, and low incidence of PVR, PMM, and new or missed breaks, perhaps due to the short-acting, nonexpansile nature of air.

Adult↗
PubMed1993

IL-4 and interferon-gamma production in children with atopic disease.

In vitro studies have implicated reciprocal roles for IL-4 and interferon-gamma (IFN-gamma) in the regulation of IgE production. As elevated IgE is a major feature of atopic disease, an important question is whether an imbalance of IL-4 and IFN-gamma is present in vivo. The production of IL-4 and IFN-gamma in phytohaemagglutinin (PHA)-stimulated peripheral blood mononuclear cell cultures from atopic children was examined to determine if there is an increased production of IL-4 and/or a reduced production of IFN-gamma. Highly atopic children with IgE > 600 U/ml produced significantly more IL-4 and less IFN-gamma in vitro than age-matched non-atopic controls. Production of IL-4 and IFN-gamma in mildly atopic children was equivalent to controls. These findings indicate that highly atopic children have an imbalance of IL-4 and IFN-gamma production and that the degree of imbalance relates to severity of the atopic state. The ratio of in vitro IL-4: IFN-gamma production correlated positively with serum IgE, which suggests that the balance of these two cytokines is a factor in the regulation of IgE, in vivo. It remains to be determined whether this imbalance of IL-4 and IFN-gamma in the highly atopic children is the cause or result of the disease process.

Asthma↗
PubMed1993

Expression of glycoprotein gIII-human decay-accelerating factor chimera on the bovine herpesvirus 1 virion via a glycosyl phosphatidylinositol-based membrane anchor.

Mutants of bovine herpesvirus 1 that express a truncated envelope glycoprotein gIII or a gIII-human decay-accelerating factor (hDAF) chimeric protein (gIII.hDAF) were employed to evaluate the function of the transmembrane and cytoplasmic domains of the gIII molecule. Truncated gIII (i.e., lacking the transmembrane and cytoplasmic region) was readily released from infected cells and was not detected on mature virus particles. In contrast, replacement of the transmembrane and cytoplasmic domains with the carboxyl-terminal portion of hDAF restored the expression of gIII on the membranes of infected cells as well as on virion surfaces. The presence of the gIII.hDAF chimera on virus particles was also associated with normal gIII function, i.e., the mediation of virus attachment and penetration. The gIII-hDAF chimera, which is present on both infected cell surfaces and virions, could be cleaved by a phosphatidylinositol-specific phospholipase C, indicating that it was anchored in the membrane via glycosyl phosphatidylinositol. Our results from this study suggest that the transmembrane and cytoplasmic regions of the gIII molecule serve as a general membrane anchor, but they do not contain structural signals required for the specific assembly of envelope proteins into mature virions.

Animals↗
PubMed1992

Expression of the receptor-linked protein tyrosine phosphatase LAR: proteolytic cleavage and shedding of the CAM-like extracellular region.

The human transmembrane molecule LAR is a protein tyrosine phosphatase (PTPase) with a cell adhesion molecule-like extracellular receptor region. The structure of LAR hinted at its involvement in the regulation of tyrosine phosphorylation through cell-cell or cell-matrix interactions. We show here that LAR is expressed on the cell surface as a complex of two non-covalently associated subunits derived from a proprotein. The LAR E-subunit contains the cell adhesion molecule-like receptor region, while the LAR P-subunit contains a short segment of the extracellular region, the transmembrane peptide and the cytoplasmic PTPase domains. Proprotein processing occurs intracellularly. Analysis of LAR mutants suggested that cleavage occurs in the LAR extracellular region at a paired basic amino acid site by a subtilisin-like endoprotease. A single amino acid substitution at this site blocked LAR proprotein cleavage. The LAR E-subunit is shed during cell growth, suggesting that LAR receptor shedding may be a mechanism for regulating PTPase function. The use of immunohistochemistry techniques on human tissues demonstrated the expression of LAR by various cell lineages, including epithelial cells, smooth muscle cells and cardiac myocytes. The LAR gene is mapped to chromosome 1, region p32-33, which contains candidate tumor suppressor genes.

Amino Acid Sequence↗