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Biomedical subjects

J Chang

Publications and source records attributed to J Chang.

At least 289 records · Page 16Linked to original sources
PubMed1997

[Primary structure and variability of partial sequences in nonstructural gene 5 region of hepatitis G virus].

OBJECTIVE: To sequence partial genome of hepatitis G virus (HGV) in the sera of patients with different chronic liver disease and paid donors. METHODS: Total nucleic acids were extracted from the sera of 3 paid donors, 2 patients with liver cirrhosis, and 1 patient with non-A-E chronic hepatitis, then subjected to reverse transcriptase-nested-polymerase chain reaction (PCR) with primers derived from the putative nonstructural gene 5 (NS5). PCR products were directly sequenced after purification. RESULTS: Partial HGV NS5 gene of 6 isolates exhibited 87.2% to 93.9% nucleotide sequence identities with 3 reported HGV isolates (GBV-C, PNF2161, R10291) while the nucleotide homologies among the 6 isolates were 90.1% to 93.8%. And 93.6% to 98.7 homolies were found at the deduced amino acid level when comparing the 6 isolates with 3 reported ones, while 93.61% to 98.40% amino acid identities were found among 6 isolates. In the region sequenced, there were 16 conserved proline residues and 8 conserved cysteine residues. CONCLUSIONS: Six isolates of HGV were obtained from different cases and donors. The partial nucleotide sequences, as well as amino acid sequences, of the putative NS5 region of HGV were relatively conserved. This region of the genome may be suitable for the development of diagnosis reagents.

Adult↗
PubMed1997

Primary structure and variability of partial nonstructural gene 5 region of hepatitis G virus.

OBJECTIVE: To sequence partial nonstructural 5 (NS5) gene of hepatitis G virus (HGV) in the sera of Chinese patients with chronic non-A-E hepatitis or hepatitis B virus (HBV) infection. METHODS: Total nucleic acid was extracted from the sera of 35 patients with chronic non-A-E hepatitis and 20 patients with HBV infection, then it was subjected to reverse transcriptase-nested-polymerase chain reaction (RT-nested-PCR) with primers derived from the putative nonstructural gene 5 (NS5) region of HGV. The positive PCR products (994 bp in length) were directly sequenced using the Sang's method after purification. RESULTS: HGV RNA was detected in 1 of the 35 patients (2.9%) with chronic non-A-E hepatitis and 5 of the 20 patients (25%) with HBV infection. All the 6 positive samples were sequenced. These 6 Chinese isolates exhibited 87.21% to 93.92% nucleotide sequence identities with 3 reported isolates (GBV-C, PNF2161, R10292) over the 994 nucleotides examined, while the nucleotide homologies among the 6 isolates were 90.09% to 93.82%. And 93.61% to 98.72% homologies were found at the deduced amino acid level in comparing the 6 isolates with 3 reported ones, while 93.61% to 98.40% amino acid identities were found among the 6 isolates. In the region sequenced, there existed 16 conserved proline residues and 8 conserved cysteine residues. CONCLUSIONS: Six isolates of HGV were obtained from different Chinese patients in this study. The partial nucleotide sequences, as well as amino acid sequences, of the putative NS5 region of HGV in Chinese patients are relatively conserved. The overall degree of nucleotide conservation (90.09% to 93.82%) among Chinese isolates may make this region of the genome suitable for the development of diagnosis reagents.

Amino Acid Sequence↗
PubMed1997

Studies on the transmission potential of filariasis in controlled areas of Henan Province.

OBJECTIVE: To study the regular pattern of growth and declination or the transmission potential of filariasis after the disease was basically (the microfilarial rate was lower than 1%) in Henan Province in 1987. METHODS: According to the distribution of filaria species and original microfilarial rate, in 7 surveillance sites in 7 counties (cities) the etiology and mosquito vector surveys were carried out continuously during 1988-1995 and no control measurement for pathogen was taken. RESULTS: Ten residual microfilaremias became negative gradually in the first 6 years and no new microfilaremias occurred during 1988-1995. During 1993 to 1995, the microfilaremias rate of population in the sites was 0. The natural infection rates of filarial larvae in vector mosquito were 0.1%-0. During the 8 years, 15 vector mosquitos were positive with a total of 18 filarial larvae which were all of first or second-stage larvae. The C. pipiens pallens was the main vector, the second was A. sinensis, with a small number of C. fatigans and A. anthropophagus. The man-biting rates of mosquitoes for outdoor sleepers fluctuated greatly, the highest one was 360.6 mosquitoes/person per night and the lowest, 7.2. The man-biting rates of mosquitoes for sleepers inside mosquito-net was about 1 mosquito/person per night. The proportion of multiparous mosquitoes also fluctuated more greatly, the highest one was 88.1% and the lowest 27. 2% According to the data described above, the man-biting rate of vector mosquito which contained filarial L3 was 0. CONCLUSIONS: The results suggested that after the microfilarial rate was lower than 1%, the residual microfilaremias became negative gradually in 3-6 years, and the transmission of the disease was blocked. Therefore, in the areas where filariasis was basically controlled, elimination of the disease was attainable within sight.

Animals↗
PubMed1996

The inhibition of HIV replication in monocytes by interleukin 10 is linked to inhibition of cell differentiation.

The effect of exogenous recombinant interleukin 10 on the replication of low-passage HIV-1 strains in blood-derived monocytes and monocyte-derived-macrophages (MDMs) was examined at various stages of cell maturation after adherence to the plastic substrate. Interleukin 10 inhibited extracellular production of HIV-1 to a greater degree in monocytes infected within 24 hr of adherence than those infected at 5-7 days. Inhibition of viral production as extracellular p24 antigen was most marked when interleukin 10 was preincubated with monocytes for 24-96 hr (optimum, 48 hr), and increased between 2 and 100 ng/ml. Neutralizing antibody to IL-10 reversed the inhibition. Inhibition of HIV production from monocytes and macrophages was maximal at 1 week after a single addition of cytokine, but then HIV production rose to control levels. Interleukin 10 was also found to inhibit reversibly the normal increase in size and maturation of both uninfected and HIV-infected monocytes during 10-15 days of adherence. In addition, cytoplasmic and membrane expression of CD26, a marker of macrophage maturation, was markedly inhibited but the proportion of detaching, apoptotic, or necrotic cells was also not increased. Hence, interleukin 10 reversibly inhibits both monocyte maturation and HIV production from infected monocytes with similar kinetics, suggesting that inhibition of monocyte maturation by IL-10 may have a marked effect of HIV production by these cells.

CD4 Antigens↗
PubMed1996

Inhibition of human immunodeficiency virus replication in differentiating monocytes by interleukin 10 occurs in parallel with inhibition of cellular RNA expression.

The mechanism of inhibition of HIVBa-L replication by interleukin 10 (IL-10) in primary monocytes and macrophages at various stages of maturation was investigated using semiquantitative PCR for reverse-transcribed HIV DNA, and Northern hybridization for HIV mRNA expression in comparison with extracellular p24 antigen. Pretreatment of monocytes with IL-10 markedly inhibited expression of both unspliced and spliced HIV RNA, reaching a nadir at 7 days and recovering to normal levels by 10 days after a single application. The optimum inhibitory concentration was 25 ng/ml. Less inhibition of HIV RNA expression was observed when IL-10 was added after HIV infection of monocytes and the inhibitory effect progressively declined to negligible levels as monocytes matured into macrophages over 10 days. IL-10 also downregulated the expression of cellular genes, including the transferrin receptor, 28S rRNA, and GAPDH. The kinetics of the inhibition of cellular mRNAs correlated with the inhibition of HIV RNA and also declined as monocytes matured into macrophages. In contrast, IL-10 did not inhibit cellular mRNA expression in the macrophage cell line THP-1. Neutralizing polyclonal antibody to IL-10 reversed all its inhibitory effects. Interaction of IL-10 and TNF-alpha in combination were generally antagonistic in their effects on HIV transcription. IL-10 prevented stimulation of HIV RNA expression by TNF-alpha after preincubation with monocytes for 48 hr. IL-10 had no effect on the levels of HIV cDNA or the process of initiation and completion of reverse transcription. The inhibitory effect of IL-10 on HIV replication in maturing monocytes was probably mediated mainly by inhibition of cellular gene expression and inhibition of maturation of monocytes into macrophages and their activation, with consequent downregulation of HIV mRNA.

Cell Differentiation↗
PubMed1996

Inactivation of mouse alpha-globin gene by homologous recombination: mouse model of hemoglobin H disease.

We have disrupted the 5' locus of the duplicated adult alpha-globin genes by gene targeting in the mouse embryonic stem cells and created mice with alpha-thalassemia syndromes. The heterozygous knockout mice (.alpha/alpha alpha) are asymptomatic like the silent carriers in humans whereas the homozygous knockout mice (.alpha/.alpha) show hemolytic anemia. Mice with three dysfunctional alpha-globin genes generated by breeding the 5' alpha-globin knockouts (.alpha/alpha alpha) and the deletion type alpha-thalassemia mice (../alpha alpha) produce severe hemoglobin H disease and they die in utero. These results indicate that the 5' alpha-globin gene is the predominant locus in mice, and suggest that it is even more dominant than its human homologue.

Animals↗
PubMed1996

Selection of axial growth sites in yeast requires Axl2p, a novel plasma membrane glycoprotein.

Spa2p and Cdc10p both participate in bud site selection and cell morphogenesis in yeast, and spa2delta cdc10-10 cells are inviable. To identify additional components important for these processes in yeast, a colony-sectoring assay was used to isolate high-copy suppressors of the spa2delda cdc10-10 lethality. One such gene, AXL2, has been characterized in detail. axl2 cells are defective in bud site selection in haploid cells and bud in a bipolar fashion. Genetic analysis indicates that AXL2 falls into the same epistasis group as BUD3. Axl2p is predicted to be a type I transmembrane protein. Tunicamycin treatment experiments, biochemical fractionation and extraction experiments, and proteinase K protection experiments collectively indicate that Axl2p is an integral membrane glycoprotein at the plasma membrane. Indirect immunofluorescence experiments using either Axl2p tagged with three copies of a hemagglutinin epitope or high-copy AXL2 and anti-Axl2p antibodies reveal a unique localization pattern for Axl2p. The protein is present as a patch at the incipient bud site and in emerging buds, and at the bud periphery in small-budded cells. In cells containing medium-sized or large buds, Axl2p is located as a ring at the neck. Thus, Axl2p is a novel membrane protein critical for selecting proper growth sites in yeast. We suggest that Axl2p acts as an anchor in the plasma membrane that helps direct new growth components and/or polarity establishment components to the cortical axial budding site.

Amino Acid Sequence↗
PubMed1996

Potentiation of bradykinin-induced inositol phosphates production by cyclic AMP elevating agents and endothelin-1 in cultured astrocytes.

Cultured astrocytes express bradykinin (BK) receptors, which are coupled to phospholipase C (PLC) through G-protein to mediate phosphoinositide (PI) hydrolysis. The regulation of this BK receptor-G protein-PLC pathway by cAMP and endothelin-1 (ET-1) was explored by short-term (20 min) and long-term (24 h) treatment with 100 mu M dibutyryl cyclic AMP (dBcAMP) or 10 nM ET-1. Short-term treatment of cells with dBcAMP had no effect on BK-induced PI hydrolysis; however, long-term treatment resulted in potentiation of the BK response. Similar effects were seen after 10 mu M forskolin pretreatment of the cells. We further explored the site of action of 24 h dBcAMP pretreatment and found that AlF(4)-, ionomycin- or A3187-induced PI hydrolysis was not affected but (3H)BK binding was increased. These results indicate that the site of action of dBcAMP is the BK receptor and Scatchard plot analysis showed that the Bmax was increased but the Kd decreased. Cycloheximide (0.5 mu M) blocked the increase in (3H)BK binding, indicating that new synthesis of receptor protein might occur during 24 h pretreatment with dBcAMP. Twenty minutes pretreatment of cells with ET-1 resulted in desensitization of the ET-1 induced P1 response, while the BK response was unaffected. After 24 h pretreatment with ET-1, desensitization to ET-1 still occurred, while BK-induced PI hydrolysis was markedly potentiated. (3H)BK binding and AlF(4)--induced but not A23187- or ionomycin-induced PI hydrolysis were increased, indicating that the site of action of long-term ET-1 treatment was the BK receptor and G protein; Scatchard analysis showed an increase in Bmax but no effect on Kd. These effects were blocked by cycloheximide, indicating that new synthesis of both receptor protein and G protein might occur during 24 h pretreatment with ET-1. (3H)Thymidine uptake was inhibited or potentiated by dBcAMP and ET-1, respectively. Possible dBcAMP-induced differentiation and ET-1-induced proliferation may contribute to the increased expression of receptor proteins.

Aluminum Compounds↗
PubMed1996

Haloperidol prevents ketamine- and phencyclidine-induced HSP70 protein expression but not microglial activation.

Noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, inclu ding ketamine and phencyclidine (PCP), produce abnormal intracellular vacuoles in posterior cingulate and retrosplenial cortical neurons in the rat. Ketamine also induces 70-kDa heat shock protein (HSP70) expression in pyramidal neurons in the posterior cingulate and retrosplenial cortex and, as shown by this study, activates microglia in the retrosplenial cortex of the rat. Whereas HSP70 protein expression was induced with ketamine doses of 40 mg/kg (ip) and higher, doses of 80 mg/kg and higher were required to activate microglia. HSP70-positive neurons were observed in 30- to 90-day-old rats but not in younger, 10- to 20- day old animals following ketamine (80 mg/kg, ip). Pretreatment with the antipsychotic drug haloperidol at doses of 1.0 mg/kg and above abolished all HSP70 immunostaining produced by ketamine (80 mg/kg). However, a single dose of haloperidol (5 mg/kg, im) did not decrease the number of microglia activated in retrosplenial cortex by ketamine (80-140 mg/kg). Similarly, PCP (10 and 50 mg/kg, ip)-induced microglial activation in the posterior cingulate and retrosplenial cortex of adult rats was not blocked by haloperidol (10 mg/kg, im, 1 h prior to PCP). These results suggest that ketamine and PCP injure neurons in the posterior cingulate and retrosplenial cortex of adults rats. Though haloperidol may afford some protection against this injury since it inhibits induction of HSP70 expression, the failure to prevent microglial activation suggests that single doses of haloperidol do not completely protect neurons from NMDA antagonist toxicity.

Animals↗
PubMed1996

Epidemiology of herpes simplex virus type 2 infections in a high-risk adolescent population.

The seroprevalence of infection with type 2 herpes simplex virus (HSV-2) was determined in 135 adolescents detained in a juvenile detention facility. A total of 16% of enrollees were seropositive for HSV-2. Age of onset of sexual intercourse, number of lifetime partners, frequency of condom use, and history of sexually transmitted diseases did not predict HSV-2 seropositivity.

Adolescent↗
PubMed1996

Sequestration of type VI collagen in the pericellular microenvironment of adult chrondrocytes cultured in agarose.

The chondron represents the chondrocyte and its pericellular microenvironment and plays an important role in the progression of osteoarthritis. Type VI collagen is preferentially localized in the pericellular microenvironment of adult articular cartilage and increases during osteoarthritis. In this study, we characterized the pericellular sequestration of type VI collagen in long-term chondrocyte-agarose cultures, and assessed the action of interleukin-1 on type VI collagen deposition and assembly. Immunohistochemical and biochemical analysis showed that cultured chondrocytes initiate type VI collagen sequestration immediately upon plating and continue pericellular matrix sequestration in a time dependent manner. Confocal microscopy confirmed the cell surface localization and pericellular accumulation of type VI collagen, while image analysis identified a 'cargo-net like' organization of type VI collagen around each chondrocyte. Quantitative analysis revealed a primary phase of rapid cell division and low levels of type VI collagen sequestration, followed by a secondary phase of relative growth stability and high levels of type VI collagen deposition. Interleukin-1 treated cultures showed increased sequestration and retention of type VI collagen in an expanded microenvironment surrounding the chondrocytes. The data suggests a role for type VI collagen in the differentiation of the pericellular microenvironment in vitro. The increased type VI collagen sequestration promoted by interleukin-1 was consistent with previous studies on osteoarthritic cartilage, and implies a functional role for type VI collagen in the chondron remodeling associated with cartilage degradation.

Animals↗
PubMed1996

A study of ovarian cancer patients treated with dose-intensive chemotherapy supported with peripheral blood progenitor cells mobilised by filgrastim and cyclophosphamide.

We have shown that large numbers of haemopoietic progenitor cells are mobilised into the blood after filgrastim [granulocyte colony-stimulating factor (G-CSF)] alone and filgrastim following cyclophosphamide chemotherapy in previously untreated patients with ovarian cancer. These cells may be used to provide safe and effective haemopoietic rescue following dose-intensive chemotherapy. Using filgrastim alone (10 micrograms kg-1), the apheresis harvest contained a median CFU-GM count of 45 x 10(4) kg-1 and 2 x 10(6) kg-1 CD34+ cells. Treatment with filgrastim (5 micrograms kg-1) following cyclophosphamide (3 g m-2) resulted in a harvest containing 66 x 10(4) kg-1 CFU-GM and 2.4 x 10(6) kg-1 CD34+ cells. There was no statistically significant difference between these two mobilising regimens. We have also demonstrated that dose-intensive carboplatin and cyclophosphamide chemotherapy can be delivered safely to patients with ovarian cancer when supported by peripheral blood progenitor cells and filgrastim. Carboplatin (AUC 7.5) and cyclophosphamide (900 mg m-2) given at 3 weekly intervals with progenitor cell and growth factor support was well tolerated in terms of haematological and systemic side-effects. Double the dose intensity of chemotherapy was delivered compared with our standard dose regimen when the treatment was given at 3 weekly intervals. Median dose intensity could be further escalated to 2.33 compared with our standard regimen by decreasing the interval between treatment cycles to 2 weeks. However, at this dose intensity less than a third of patients received their planned treatment on time. All the delays were due to thrombocytopenia.

Adult↗
PubMed1996

Evaluation of cytogenetic conversion to Ph- haemopoiesis in long-term bone marrow culture for patients with chronic myeloid leukaemia on conventional hydroxyurea therapy, on pulse high-dose hydroxyurea and on interferon-alpha.

Long-term bone marrow culture (LTBMC) has been used successfully in autologous transplantation in chronic myeloid leukaemia (CML). However, variation between patients in the recovery of Ph- cells in culture limits the application of this procedure to a minority. Treatment that effectively reduces in vivo tumour burden prior to initiation of LTBMC may improve the selection of Ph- cells in culture. To test this hypothesis we evaluated the frequency and degree of cytogenetic conversion to Ph- haemopoiesis in LTBMC from four independent groups of CML patients: Untreated (n = 19); conventional dosage of hydroxyurea (HU) (n = 10); pulse high-dose HU (P-HU) (n = 22) and interferon (IFN)-alpha (n = 12). In this study IFN-alpha therapy resulted in a significantly higher incidence of patients with detectable Ph- clonogenic cells in the marrow (P = 0.01) and with > or = 50% Ph- haemopoiesis in LTBMC as compared to newly diagnosed patients (P = 0.05). Also, sequential culture studies undertaken in 14 CML patients at diagnosis and following the start of pulse highdose HU therapy showed that in eight patients the average proportion of Ph- metaphases detected in LTBMC substantially increased from 1.7% (range 0-7) at diagnosis to levels of 71% (range 14-100) after treatment. Therefore we conclude that the use of IFN or pulse high-dose HU in early stage disease appears to create an opportunity to harvest the marrow for long-term culture (LTC) purging with reduced leukaaemic burden.

Adult↗
PubMed1996

Reasons for changing caffeinated coffee consumption: the Rancho Bernardo Study.

OBJECTIVE: To determine patterns of lifetime caffeinated and decaffeinated coffee use, focusing on frequency and determinants for curtailing caffeinated coffee. METHODS: Residents of Rancho Bernardo, a white, upper-middle class Southern California community, were surveyed about their lifetime coffee-drinking behavior; completed questionnaires were received from 69% (n = 2955; mean age was 64 years, age range: 30-105 years). Chi-square tests of differences between proportions in categorical data and t-tests for continuous data were used. Due to the large number of comparisons, statistical significance was defined as p or=5 cups/day only in those who curtailed caffeinated coffee on advice of a physician or for heart/circulatory problems. CONCLUSIONS: Curtailing of caffeinated coffee in this adult cohort was primarily due to health concerns, but few of those who curtailed caffeinated coffee attribute the change to the advice of a physician.

Adult↗
PubMed1996

The effect of tamoxifen and hormone replacement therapy on serum cholesterol, bone mineral density and coagulation factors in healthy postmenopausal women participating in a randomised, controlled tamoxifen prevention study.

BACKGROUND: The role of hormone replacement therapy (HRT) in women who have been treated for breast cancer remains controversial. The addition of tamoxifen may protect these women from any proliferative effect of exogenous oestrogen on the breast. The aim of this analysis was to determine if tamoxifen and HRT may be safely administered together. METHODS: We studied the interaction between HRT and tamoxifen on serum cholesterol, fibrinogen, antithrombin III (AT III) and bone mineral density (BMD) in postmenopausal healthy women enrolled in a randomised tamoxifen chemoprevention trial. RESULTS: Tamoxifen decreased serum cholesterol by a mean of 13% from pretreatment values (n = 153). The addition of HRT to tamoxifen did not result in further reduction in serum cholesterol (n = 20). HRT alone led to a reduction of serum cholesterol by a mean of 5% in 14 women on placebo. The addition of tamoxifen to HRT resulted in further reduction in serum cholesterol by a mean of 7% (n = 44). Significant reductions of plasma fibrinogen by 14% and AT III by 8% were seen in women who received tamoxifen. There were no further significant changes in these coagulation factors in women on tamoxifen/HRT combinations. Tamoxifen resulted in an annual increase in BMD of the femur and spine by 2% and 1.5%, respectively, when compared to placebo (n = 38). The addition of HRT to tamoxifen resulted in further 2% annual increase in BMD of the femur. CONCLUSIONS: We conclude that there were no significant adverse intereactions with tamoxifen and HRT in this small series of patients. The combination results in a reduction of serum cholesterol, increase in BMD especially in the femur and appears not to have any adverse effect on coagulation factors. Multicentre studies should be conducted to evaluate the effect of this combination on relieving menopausal symptoms, disease relapse and overall survival in women who have received treatment for breast cancer.

Aged↗