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Biomedical subjects

J C Chang

Publications and source records attributed to J C Chang.

At least 73 records · Page 4Linked to original sources
PubMed1997

Mesenteric and portal venous obstruction associated with primary antiphospholipid antibody syndrome.

A 58-year-old Korean man who had a past history of appendicitis, superior mesenteric vein thrombosis and intestinal obstruction presented 7 years later suffering from colicky right upper quadrant pain, epigastric discomfort after fatty meals, nausea and vomiting. He was found to have thrombosis of the superior mesenteric and portal veins, portal hypertension with oesophageal varices, cholangitis, and a biliary stone. The serum anti-cardiolipin antibody (aCL) titres were 103 immunoglobulin (Ig)G antiphospholipid units (GPL) and 50 IgM antiphospholipid units (MPL) and the aCL-IgG titre was still high at 106 2 years after the initial diagnosis. No evidence of disease states known to be associated with antiphospholipid antibodies was found. We report a patient with mesenteric and portal venous obstruction associated with the primary antiphospholipid syndrome (APS).

Antiphospholipid Syndrome↗
PubMed1997

Antimicrobial susceptibility of flavobacteria as determined by agar dilution and disk diffusion methods.

A total of 106 clinical isolates of flavobacteria, including 41 isolates of Flavobacterium meningosepticum, 59 of Flavobacterium indologenes, and 6 of Flavobacterium odoratum were collected from January 1992 to December 1995 from patients in Taiwan. The in vitro activities of antimicrobial agents were determined concomitantly by the standard agar dilution and disk diffusion methods. More than 90% of the flavobacterial isolates were resistant to cephalothin, cefotaxime, ceftriaxone, moxalactam, aztreonam, imipenem, aminoglycosides, erythromycin, and glycopeptides. The majority of F. meningosepticum isolates were susceptible to piperacillin and to minocycline but resistant to ceftazidime, with MICs at which 90% of the isolates are inhibited being 8, 4, and > 128 microg/ml, respectively. Approximately half of the F. indologenes isolates were susceptible to piperacillin, cefoperazone, ceftazidime, and minocycline, with MICs at which 50% of the isolates are inhibited being 4, 16, 8, and 4 microg/ml, respectively. The majority of F. odoratum isolates were resistant to all the antimicrobial agents tested except minocycline, to which five of six isolates were susceptible. With least-squares regression analysis and error rate-bounded analysis methods, the following resistant and susceptible zone diameter breakpoints were established: < or = 12 and > or = 17 mm, respectively, for piperacillin against F. meningosepticum and F. indologenes; < or = 13 and > or = 18 mm, respectively, for ceftazidime against F. meningosepticum and F. indologenes, < or = 17 and > or = 21 mm, respectively, for ofloxacin against F. indologenes; < or = 16 and > or = 20 mm, respectively, for ciprofloxacin against F. meningosepticum. Valid breakpoints for the disk diffusion method could not be established for cefoperazone and ofloxacin against F. meningosepticum and for minocycline against F. meningosepticum and F. indologenes due to a poor correlation coefficient for the regression line or for cefoperazone and ciprofloxacin against F. indologenes due to the presence of remarkable error rates.

Anti-Bacterial Agents↗
PubMed1997

Comparison of Etest and agar dilution method for antimicrobial susceptibility testing of Flavobacterium isolates.

The Etest was evaluated as a possible alternative to the standard agar dilution method for susceptibility testing of nine antimicrobial agents against Flavobacterium species. In studies of 100 clinical isolates, the agreement between the MICs (+/-1 log2 dilution) obtained by the two methods was acceptable for cefotaxime, ceftazidime, amikacin, minocycline, ofloxacin, and ciprofloxacin (> 90%). Conversely, the agreement between the results obtained for piperacillin was limited (84%). The overall agreement was 92.5%.

Anti-Bacterial Agents↗
PubMed1997

Persistence of T-cell clones in psoriatic lesions.

BACKGROUND: We previously demonstrated a clonal dominance in the V beta 13.1 messages isolated from the lesional CD8+ T cells of psoriasis vulgaris, which suggested an interaction of V beta 13.1+ CD8+ T cells with skin antigens. OBJECTIVES: To determine whether the clonality observed accurately reflected a clonal population of infiltrating T cells or was skewed by an overabundance of messages from a small number of cells, and to extend our study of V beta gene usage by lesional CD8+ T cells to 9 new patients. DESIGN: Case study. SETTING: Patients were enrolled at the Psoriasis Research Institute in Palo Alto, Calif, and samples were analyzed at The Immune Response Corporation in Carlsbad, Calif. MAIN OUTCOME MEASURES: For the 2 previous patients, skin samples were sorted directly for V beta 13.1+ T cells, for which the T-cell receptors were sequenced. For the 9 new patients, CD8+ T cells were sorted and their T-cell receptor V beta gene usage measured using semiquantitative polymerase chain reaction with V beta-specific primers. RESULTS: The directly sorted V beta 13.1+ T cells exhibited clonal dominance in both patients. The dominant V beta 13.1 clone in each patient was the same as that found in the previous 2 biopsy specimens for which CD8+ T cells were sorted. Additionally, in 8 of the 9 new patients examined, we again found a preferential usage of V beta 3 and/or V beta 13.1 genes by the lesional CD8+ T cells. CONCLUSIONS: The clonality, which was found in the V beta messages of the sorted CD8+ T cells, accurately reflects the dominance of these clones in the infiltrating T cells. Moreover, the persistence in the same patient of the same clone for as long as 15 months and the overrepresentation of V beta 3 and/or V beta 13.1 in lesional CD8+ T cells in the new patients examined support the pathogenic role of T cells bearing these V betas.

Adult↗
PubMed1997

Genetic localization of the type I trimethoprim resistance gene and its dissemination in urinary tract isolates in Taiwan.

In a total of 425 urinary isolates of E. coli, Enterobacter spp., and Klebsiella spp. selected, there were 169 (45.4%) isolates harbouring type I dihydrofolate reductase (DHFR) gene among 374 trimethoprim-resistant isolates. In these 169 isolates, only 17.2% hybridized with the Tn7 probe. According to another probe specific for the integrase gene of integron, 87.6% showed a positive reaction. Further analysis by restriction mapping proved that the type I DHFR gene was inserted into a integron-like structure. These results indicate that the type I DHFR gene that was initially observed in association with transposable element Tn7 is becoming associated with an integrase function similar to integrons in most instances. Further analysis of the distribution of Tn21-like integrase gene in clinical isolates indicated that the prevalence rates were 86.4%, 84.8%, and 76.7% respectively in E. coli, Enterobacter spp., and Klebsiella spp.. Furthermore, the integrase gene found in our clinical isolates proved to be mediated by a plasmid, demonstrated by Southern hybridization. Thus, the trimethoprim-resistant gene that developed under selective pressure from the double drug trimethoprim and sulphonamide was transmitted by insertion into integron-like structure and then mediated by plasmid transfer for dissemination.

Animals↗
PubMed1997

Bilateral multicystic kidney dysplasia in a fetus with neonatal pulmonary hyaline membrane disease: a case report.

Multicystic kidney disease is the most common cause of neonatal renal mass and either the most or second most common neonatal abdominal mass. This disease is a congenital dysplasia of the kidney characterized by large nonhomogeneous dilations of the collecting tubules. It may occur unilaterally or bilaterally, and the incidence is about 1 out of 5,000 to 10,000 births. Severe bilateral defects are lethal. Partial dysplastic involvement of both kidneys eventually leads to renal function impairment. This is a case of bilateral multicystic kidney dysplasia diagnosed prenatally at 34 weeks of gestation. Hyaline membrane disease was found in both lungs after delivery. The antenatal diagnostic criteria for multicystic kidney disease and treatment after diagnosis are also discussed.

Adult↗
PubMed1996

NRF2, a member of the NFE2 family of transcription factors, is not essential for murine erythropoiesis, growth, and development.

The locus control region of the beta-globin gene is composed of four erythroid-specific hypersensitive sites. Hypersensitive site 2 has been shown to be a powerful enhancer and contains a tandem repeat sequence for the transcription factors AP1 and NFE2 (activating protein 1 and nuclear factor erythroid 2, respectively). The human NRF2 (NFE2 related factor 2) has been isolated by bacterial expression screening using this core sequence as a probe. p45-NFE2, NRF1, and NRF2 belong to the CNC ("cap 'n' collar") subfamily of the basic region-leucine zipper transcription factors, which exhibits strong homology at specific regions such as the "CNC" and the DNA binding and leucine zipper domains. Although the erythroid-specific p45-NFE2 has been implicated in globin gene regulation, p45-NFE2 null mice succumb to bleedings due to lack of platelets and those that survive exhibit only a mild anemia. To determine the function of NRF2, which we found to be widely expressed in vivo, we have characterized the genomic structure of the mouse NRF2 gene, disrupted the Nrf2 gene by homologous recombination in mouse embryonic stem cells (ES cells), and generated NRF2-/- mice. Homozygous mutant mice developed normally, were not anemic, reached adulthood, and reproduced. Our studies indicate that NRF2 is dispensable for mouse development.

Aging↗
PubMed1996

Chemokine expression by intraepithelial gamma delta T cells. Implications for the recruitment of inflammatory cells to damaged epithelia.

T cells expressing gamma delta TCR may have evolved to recognize Ag in a different manner as well as perform a broader set of functions than T cells with alpha beta TCR. In this study, we tested the hypothesis that dendritic epidermal T cells (DETC) bearing the invariant V gamma 3V delta 1 TCR may be able to signal the migration of peripheral alpha beta T cells to the epidermis by secreting specific chemokines. Expression of macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, RANTES, and lymphotactin was inducible in DETC 7-17 cells, whereas mRNA for monocyte chemoattractant protein (MCP)-1 could not be detected. Strikingly, lymphotactin was the most abundant chemokine produced by activated DETC 7-17 cells. Activated primary DETC cultures also produced copious amounts of lymphotactin mRNA. Similarly, freshly isolated and activated intestinal intraepithelial T cells (i-IEL) with gamma delta TCR expressed high levels of lymphotactin mRNA. In contrast, lymphotactin mRNA was present in activated spleen gamma delta T cells at low basal levels. Migration of CD8+ T cells induced by culture supernatants from stimulated DETC 7-17 cells was strongly reduced in the presence of a neutralizing anti-lymphotactin antiserum and to a lesser extent by neutralizing anti-MIP-1 alpha, anti-MIP-1 beta, or anti-RANTES antiserum. The presence of lymphotactin in supernatants from activated DETC 7-17 cultures was directly demonstrated by Western blot analysis. These observations are consistent with a model in which gamma delta IEL play an active multi-faceted role in the maintenance of epithelia homeostasis.

Animals↗
PubMed1996

Selective killing of AFP-positive hepatocellular carcinoma cells by adeno-associated virus transfer of the herpes simplex virus thymidine kinase gene.

The use of viral thymidine kinase (TK) gene coupled with the administration of ganciclovir to render cancer cell death has been studied extensively. Many of these experiments utilized retrovirus to transfer the TK gene under the control of a nonspecific promoter. Because nonspecific expression of the viral TK gene may cause death of proliferating cells, other than cancer cells, we explored the use of a liver-specific promoter and a tumor-specific AFP enhancer to achieve regulated viral TK gene expression for treatment of hepatocellular carcinoma. We also used the adeno-associated virus (AAV) as vector for the delivery of the TK gene because this virus is not associated with any pathological consequences in humans. Because it can infect nondividing S-phase cells, AAV can transfer genes into noncycling tumor cells. A recombinant AAV virus was constructed to include the selectable marker neoR gene and the herpes simplex virus (HSV)-TK gene driven by the human AFP enhancer and the albumin promoter. The liver-predominant expression pattern of the TK gene was observed when this construct was tested in transgenic mice. When human hepatocellular carcinoma cell lines displaying different levels of AFP and albumin and nonhepatocyte tumor cell lines were infected with the recombinant AAV virus, ganciclovir treatment caused only AFP and albumin-positive hepatocellular carcinoma cells death, but not nonhepatocyte tumor cells or AFP and albumin-negative hepatic tumor cells. Moreover, the dose required to kill the cancer cells was inversely proportional to the level of AFP expression in the cells.

Albumins↗
PubMed1996

Postoperative thrombotic thrombocytopenic purpura following cardiovascular surgeries.

Among 47 patients with thrombotic thrombocytopenic purpura (TTP), 8 patients were diagnosed to have postoperative-TTP. Two patients underwent vascular surgery, 5 patients coronary artery bypass grafts, and 1 patient resection of myocardial sarcoma. Prior to surgery, all patients except one had normal hemograms and platelet counts, and blood smears showed no schistocytes. Five to 19 days after surgery, all 8 patients developed postoperative TTP, which clinical feature was characterized by unexplained progressive encephalopathy, thrombocytopenia, and microangiopathic hemolytic anemia. In addition, in 3 patients, progressive gangrene of the toes also developed. Four patients achieved complete remission following exchange plasmapheresis and 1 patient spontaneous remission. Due to complicated surgical settings after surgery, recognition of TTP was often delayed and it contributed to death in 3 patients despite treatment with exchange plasmapheresis. In view of occurrence of postoperative TTP following cardiac and vascular surgeries, pathogenic mechanism for postoperative TTP may be explained on the basis of injury of diseased endothelial surface and release of a humoral factor(s) that results in platelet aggregation in the capillaries and arterioles. Our experience with these cases indicates that TTP may occur as a serious complication of cardiac and vascular surgeries, and early recognition of the diagnosis and institution of exchange plasmapheresis are of paramount importance for favorable outcome.

Adult↗
PubMed1996

Microleakage of a 4-methacryloxyethyl trimellitate anhydride bonding agent with amalgams.

Microleakage contributes to deterioration of materials, recurrent decay, growth of microorganisms at the interface, and postoperative tooth sensitivity. This study examined the microleakage between amalgams and tooth surfaces with a cavity liner, a 4-methacryloxyethyl trimellitate anhydride bonding agent (Amalgambond) and six different types of amalgams. Class 1 cavity preparations in extracted human molars were filled with different combinations of liners and amalgams and were stored at 37 degrees C in physiologic saline solution. After 1 week half of each amalgam restoration was removed. Within the same group the same cavity treatment was performed and the same type of amalgam was packed as before. Microleakage was determined after 2000 thermal cycles. Statistical analysis indicated that Amalgambond significantly reduced microleakage of different amalgams compared with the Copalite-lined and unlined controls. No microleakage was detected at the interface between the existing and replacement amalgams.

Dental Amalgam↗
PubMed1996

Review of quantitative standards and guidelines for fungi in indoor air.

Existing quantitative standards/guidelines for fungi in indoor air issued by governmental agencies are based primarily on baseline data (rather than health effects data), and are either absolute (numerical) or relative (indoor/outdoor comparisons) or a combination of the two. The Russian Federation is the only governmental agency that has binding quantitative regulations for bioaerosols. Recommended guidelines have been proposed or sponsored by North American and European governmental agencies and private professional organizations. A considerable number of frequently cited guidelines have been proposed by individuals based either on baseline data or on personal experience. Quantitative standards/guidelines range from less than 100 CFU/m3 to greater than 1000 CFU/m3 (total fungi) as the upper limit for non-contaminated indoor environments. Major issues with existing quantitative standards and guidelines are the lack of connection to human dose/response data, reliance on short term grab samples analyzed only by culture, and the absence of standardized protocols for data collection, analysis, and interpretation. Urgent research needs include the study of human responses to specific fungal agents, development and widespread use of standard protocols using currently available sampling methodologies, and the development of long term, time-discriminating personal samplers that are inexpensive, easy to use, and amenable to straightforward, relevant analysis.

Air Microbiology↗
PubMed1996

Effect of Mycobacterium tuberculosis and its components on macrophages and the release of matrix metalloproteinases.

BACKGROUND: Pulmonary tuberculosis is associated with caseating necrosis, parenchymal lung destruction, and cavity formation. It was hypothesised that tuberculous lung destruction is mediated, at least in part, by the participation of matrix metalloproteinases released by mononuclear phagocytes. METHODS: Cells of the myelomonocytic leukaemia cell line THP-1 were incubated with lipoarabinomannan (LAM), the major antigenic cell wall component, and with Mycobacterium tuberculosis and analysed by Northern blot analysis. Two patients with active cavitary tuberculosis also underwent bronchoalveolar lavage and the cells were analysed by Northern blotting. RESULTS: Incubation of THP-1 cells with LAM resulted in the stimulated release of matrix metalloproteinase-9 (MMP-9), a 92 kDa gelatinase, by 24 hours in a dose-dependent fashion. In addition, Northern analysis revealed that LAM upregulated the gene for MMP-9 by 24 hours, but not the gene for the 72 kDa gelatinase MMP-2. Heat killed M tuberculosis H37Ra also upregulated the MMP-9 gene. Bronchoalveolar lavage of the two patients with active cavitary tuberculosis showed striking upregulation of the MMP-9 gene compared with a normal control using Northern analysis. LAM also upregulated the type I interstitial collagenase (MMP-1) gene by 24 hours in both THP-1 cells and peripheral blood monocytes. CONCLUSIONS: These data suggest that M tuberculosis and its major cell antigenic component, LAM, stimulate the release of MMP-9 and upregulate the expression of genes for MMP-1 and MMP-9. It is possible that M tuberculosis and its components contribute directly to cavity formation by their ability to stimulate macrophages to release matrix metallo-proteinases that digest collagens I-IV, and indirectly by stimulating the release of the cytokines interleukin 1 beta and tumour necrosis factor alpha that induce fibroblasts to amplify the release of matrix metalloproteinases.

Antigens, Bacterial↗