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Biomedical subjects

S Cheng

Publications and source records attributed to S Cheng.

At least 145 records · Page 8Linked to original sources
PubMed1998

New procedures to estimate water temperatures and water depths for application in climate-dengue modeling.

Two new approaches have been developed to estimate water temperatures and water depths in containers that commonly are used as breeding sites for mosquitoes, the primary vectors of dengue viruses. These estimates are incorporated in recently developed stochastic simulation models used to describe the daily dynamics of dengue virus transmission in the urban environment. Water temperature estimates are provided through a regression model that includes meteorological variables not previously used; results show that they are significantly better than those used in previous dengue transmission models. Water depth models use a climatic water budget approach which estimates moisture storage within containers. The water depth models are less precise than those developed for water temperature; however, results are superior to those used in previous models. These new approaches should improve estimates of the impact of water conditions on dengue vectors.

Aedes↗
PubMed1998

Clinical and economic outcomes of individuals with severe peptic ulcer hemorrhage and nonbleeding visible vessel: an analysis of two prospective clinical trials.

OBJECTIVE: We report the clinical outcomes and direct medical costs of 155 patients with severe peptic ulcer hemorrhage and a nonbleeding visible vessel at emergency endoscopy treated with endoscopic hemostasis or medical-surgical therapy. METHODS: In two consecutive, prospective, randomized, controlled trials, patients were randomly assigned to endoscopic hemostasis (heater probe, bipolar electrocoagulation, or injection sclerosis) or medical-surgical treatment. Study endpoints included the incidence of severe ulcer rebleeding and emergency surgery, length of hospital stay, blood transfusion requirements, mortality rate, and direct costs of utilized health care. Direct medical costs were estimated using combined fixed and variable institutional costs for consumed resources and Medicare reimbursement rates. RESULTS: Compared with medical-surgical treatment, endoscopically treated patients had significantly lower rates of severe ulcer rebleeding (p = 0.004), emergency surgery (p = 0.002 and p = 0.019, 0.024), and blood transfusions (p = 0.025). Observed inter-trial differences in ulcer rebleeding rates may be partially explained in a multivariate model by covariates of comorbid disease and inpatient ulcer bleeding. In both trials, length of hospital stay, mortality rates, and treatment-related complications were similar. Estimated median direct costs per patient differed: The first trial had lower costs with endoscopic hemostasis ($4254, vs $4620 for electrocoagulation and $5909 for medical-surgical treatment), yet the second trial yielded lower costs with medical-surgical treatment ($3169, vs $3477 for injection sclerosis and $4098 for heater probe). CONCLUSIONS: Compared with medical-surgical therapy, endoscopic hemostasis for severe ulcer hemorrhage and a nonbleeding visible vessel yielded significantly better patient outcomes and was safe. This procedure may or may not yield lower direct medical costs and cost savings.

Blood Transfusion↗
PubMed1998

Effect of nimodipine on memory after cerebral infarction.

OBJECTIVES: Epidemiological studies indicate widespread memory impairment in patients with stroke in the early post-ictal stage. Nimodipine may have psychopharmacological properties and may improve memory. We conducted a single-blind randomized controlled trial to determine whether nimodipine given 7-14 days after cerebral infarction improved memory. MATERIAL AND METHODS: One hundred patients with acute cerebral infarction were consecutively enrolled between D7 to D14. After stratification, patients were randomized to receive oral nimodipine 90 mg daily for 12 weeks, or no drug. Independent assessors administered Mini-Mental State Examination (MMSE) and Fuld Object-Memory Evaluation (FOME) at baseline, 6 weeks, and 12 weeks. RESULTS: Patients receiving nimodipine showed greater improvement in FOME mean scores at 12 weeks (P=0.0334), and also in FOME score change across time (P=0.0283). Patients with severe disability who received nimodipine also showed greater MMSE score change across time (P=0.0495). CONCLUSION: Nimodipine given 7-14 days after cerebral infarction for 3 months results in memory improvement.

Aged↗
PubMed1998

An integrated medical and psychosocial treatment program for psychotic disorders: patient characteristics and outcome.

OBJECTIVES: To provide an overview of a comprehensive and integrated case-management program that incorporates principles of assertive community treatment and combines effective medical and psychosocial interventions and to present the results of a process and outcome evaluation of the program, with particular emphasis on its impact on service utilization and consumer satisfaction. METHOD: Data on demographic, clinical, and several outcome measures were collected on all patients who received care in the program for a minimum of 6 months. For process evaluation we assessed the extent to which the program adhered to its goals and satisfied the patients, their families, and community-service agencies. Outcome-evaluation data on the number and length of hospital admissions were compared for each subject with individual historical data for a period equal to the time spent in the program. In addition, relapses of psychotic symptoms that did not result in hospital admissions were calculated for each patient while in the program. RESULTS: Demographic, clinical, and treatment characteristics of clients show that the program has succeeded in maintaining its focus on providing services to relatively chronically ill patients with psychotic disorders over a mean period of 3 years. The process-evaluation data indicated a high level of satisfaction by patients, families, and other service agencies with the services received. Information on outcome variable showed that the program achieved significantly lower rates of hospital admissions and relapse of psychosis than expected. There was a highly significant reduction achieved in the utilization of inpatient hospital resources for patients receiving care in the program. Most of the inpatient service utilization was attributed to patients either who were resistant to treatment with antipsychotic agents or who refused to accept or comply with medication. CONCLUSIONS: It is possible to provide effective continuity of care from inpatient treatment to community adjustment for most individuals with psychotic disorders across the spectrum by blending hospital and community resources within an integrated case-management model of care.

Adult↗
PubMed1998

A multilocus genotyping assay for cardiovascular disease.

In our efforts to develop diagnostic tests for complex multifactorial disorders, and to assist the research community in evaluating genetic markers for predisposition to cardiovascular disease, we have developed a prototype assay to genotype up to 35 variable sites among 15 genes. The candidate markers in this panel were selected from biological pathways likely to contribute to the development and progression of cardiovascular disease. Each sample is amplified in two multiplex polymerase chain reactions that are then hybridized to an array of immobilized oligonucleotide probes. The assay has been applied to a population-based cohort representing 238 families; allele frequencies observed among 455 unrelated parents from this cohort agree with available literature values. Data from a cohort of 142 lipid-clinic patients were used to explore locus associations with arterial occlusion, as measured by quantitative angiography. This prototype assay provides a research tool for studies to assess the association of multiple markers with disease, and for clinical studies to evaluate marker association with patient responsiveness to experimental therapies.

Adult↗
PubMed1998

[Influence of ischemic preconditioning of heart on ischemia/reperfusion injury of rabbit lung].

The influence of ischemic preconditioning of heart on ischemia-reperfusion injury of 16 Japanese big-ear-rabbit lungs were studied. The results showed: 1. Experimental group had a significant reduction in wet/dry weight ratio; 2. It had a significant increase in PaO2. 3. It had a minimal intraalveolar neutrophil infiltration in comparison with the control group. These data suggestes that the ischemic preconditioning of heart can lighten the ischemia-reperfusion injury of rabbit lungs.

Animals↗
PubMed1998

[The studies on MTS1/p16 gene deletion during transformation of human bronchial epithelial cells].

OBJECTIVE: To detect the deletion of MTS1/p16 and the expression of P16 protein during the transformation of human bronchial epithelial cell line M. METHODS: Dual-color fluo-rescence in situ hybridization (FISH), immunohistochemical staining and western blot analysis were carried out. RESULTS: No deletion of MTS1/p16 gene was found in MP18 cells of the cell line M. But partial deletions occurred in the MP36 and MP120 cells of the cell line M. Immunohistochemical analysis and western blot test showed lower expression of P16 protein in the MP120 cells than in MP20 cells. CONCLUSIONS: MTS1/p16 gene deletion contributes to the malignant transformation of the human bronchial epithelial cell line M. Also FISH is a useful technique in detecting gene deletion.

Bronchi↗
PubMed1998

[Cloning and mapping of the rpoB gene in M. tuberculosis].

OBJECTIVE: To clone the rpoB gene of M. tuberculosis. METHODS: Screening the rpoB gene of M. tuberculosis from M. tuberculosis genomic DNA library by using the rpoB gene conservative region PCR product as a probe. RESULTS: 411 bp products were seen after amplification of H37Ra DNA. The cloning and sequencing results indicated that the 411 bp products were homogeneous to M. tuberculosis rpoB gene. 12,000 clones of M. tuberculosis genomic DNA library were screened by hybridization using the 411 bp product as a probe and 7 clones seemed positive, 3 clones were real positive after the second hybridization. 1 of them carried a 3.8 kb insert fragment. The preliminary restriction map of the 3.8 kb segment was made. The regions which were found homogeneous to the probe to the end of this cloned fragment were 1 and 2.8 kb. CONCLUSION: In comparison with the open reading frame of H37Rv rpoB gene, the 3.8 kb segment cloned here covers larger portion of entire rpoB gene of M. tuberculosis. This study will provide a useful tool to study the resistant mechanism of rifampin and other rifamycin compounds to M. tuberculosis.

Antibiotics, Antitubercular↗
PubMed1998

[Virilizing and feminizing adrenal syndrome].

OBJECTIVE: To inquire into diagnosis, differential diagnosis and treatment of virilizing and feminizing adrenal syndrome especially differential diagnosis between benign and malignant of sex hormone producing adrenal neoplasma and treatment principles of congenital adrenal hyperplasia (CAH). METHOD: Eight cases of CAH and five cases of sex hormone producing adrenal neoplasma were presented during 1986-1996. The former included 3 rare cases of 17 alpha hydroxylase deficiency and others. The latter included 3 cases of feminizing adrenal tumors and 2 cases of virilizing adrenal tumors. RESULT: Weight and diameter of tumor, DHEA, 17-ks and sex hormone levels, appearance of CT imaging, infiltration and metastasis, were closely related to differentiation of benign and malignant tumors. CONCLUSION: Some standards are not absolute because of limited practice, follow-up is very important. Adrenal virilizing and feminizing neoplasms were surgically resected by different incision. Modified subcostal incision is recommended as a best choice for huge adrenal mass. Corticoadrenal hormone treatment of CAH should select different kind of corticoadrenal medicine for different kind of CAH. Treatment of sex hormones is not suitable for children suffered from 17 hydroxylase deficiency until prepuberty.

Adrenal Gland Neoplasms↗
PubMed1997

Tumor suppressor p53 is a negative regulator in thyroid hormone receptor signaling pathways.

Thyroid hormone nuclear receptors (TRs) are ligand-dependent transcription factors which regulate growth, differentiation, and development. The molecular mechanisms by which TRs mediate these diverse effects are unclear. One emerging hypothesis suggests that TRs could mediate these diverse effects via cooperation with different transcription factors/receptors. Indeed, we have recently shown that the human TR subtype beta1 (h-TRbeta1) interacts with the tumor suppressor p53. p53 is a transcription factor that plays a critical role in cell cycle regulation and tumor development. To assess the physiological relevance of the interaction of h-TRbeta1 with p53, the present study addressed the question as to whether the functions of h-TRbeta1 could be modulated by p53. We first compared the h-TRbeta1-mediated transcriptional activity in two pairs of isogenic cell lines, RKO/RKO E6 and MCF-7/MCF-7 E6. RKO and MCF-7 cells are colon and breast carcinoma cell lines, respectively, that contain p53 but lack TRbeta1. The isogenic RKO E6 and MCF-7 E6 cells are stable clones expressing high levels of papillomavirus type 16 E6 protein. In these cells, the level of p53 protein was lower than the parental cells. The impairment of p53 functions in these E6-containing cells led to an activation of TRbeta1-mediated transcriptional activity. Furthermore, in a growth hormone-producing cell line in which the expression of the growth hormone gene is positively regulated by TRs, overexpression of the wild-type p53 led to repression in the expression of the growth hormone gene. Thus, TRs could cross-talk with p53 in its signaling pathways to regulate gene regulatory functions. The present findings further strengthen the hypothesis that mediation of the pleiotropic effects of T3 requires the cooperation of TRs with a large network of transcription factors.

Adenoviridae↗
PubMed1997

HLA-DQB1 polymorphism determines incidence, onset, and severity of collagen-induced arthritis in transgenic mice. Implications in human rheumatoid arthritis.

Certain HLA-DR alleles have been associated with predisposition to human rheumatoid arthritis (RA). There is also evidence that certain HLA-DQ alleles may also be important in determining susceptibility to RA. We have previously demonstrated that mice transgenic for HLA-DQ8, a DQ allele associated with susceptibility to RA, develop severe arthritis after type II collagen immunization. To investigate the influence of polymorphic difference at the DQ loci on susceptibility to arthritis, we generated mice transgenic for HLA-DQ6, an allele associated with a nonsusceptible haplotype. The DQ6 mice were found to be resistant to collagen-induced arthritis. We also assessed the combined effect of an RA-susceptible and an RA nonassociated DQ allele by producing double-transgenic mice expressing DQ6 and DQ8 molecules, representing the more prevalent condition found in humans where heterozygosity at the DQ allele is common. The double-transgenic mice developed moderate CIA when immunized with CII when compared with the severe arthritis observed in DQ8 transgenic mice, much like RA patients bearing both susceptible and nonsusceptible HLA haplotypes. These studies support a role for HLA-DQ polymorphism in human RA.

Age Factors↗
PubMed1997

The tumor suppressor p53 is a negative regulator of estrogen receptor signaling pathways.

The estrogen receptor (ER) is a ligand-dependent transcription factor which regulates growth, development, differentiation and reproduction. To test the hypothesis that the diverse effects of the ER could be mediated by interacting with other transcription factors/oncogenes, the present study assessed its interaction with the tumor suppressor p53. p53 is a transcription factor which is involved in cell cycle regulation and apoptosis. We found that the wild-type p53 physically interacted with ER in vivo and repressed the estrogen-activated transcriptional activity. However, p53 mutants had no or reduced repression effect, depending on the sites of mutation. These findings suggest that p53 can cross talk with the ER in hormone-activated signaling pathways in cells.

Endometrial Neoplasms↗
PubMed1997

The gene regulating activity of thyroid hormone nuclear receptors is modulated by cell-type specific factors.

To understand whether the transcriptional activity of thyroid hormone nuclear receptors (TRs) is modulated by cell-type specific factors, full length TR subtype alpha1 (TRalpha1) and beta1 (TRbeta1) cDNAs were cloned from human hepatoma cell lines: HA22T, SK-Hep-1 and HepG2. The cloned receptor bound to the thyroid hormone 3,3',5-triiodo-L-thyronine (T3) and the thyroid hormone response elements (TREs) similarly to those cloned from other tissues. They exhibited T3- and TRE-dependent transactivation activities, indicating these TRs were transcriptionally active. The lipogenic malic enzyme (ME), a T3-target gene in liver, was stimulated approximately 3- and 1.5-fold by T3 in HA22T and SK-Hep-1, respectively. The T3-stimulated ME gene expression was inhibited in HA22T, but stimulated in SK-Hep-1 cells by insulin. These results suggest that the gene regulating activity of TRs was modulated by cell-type specific factors. Furthermore, these cell-type specific factors could modulate the cross talk between TR- and insulin receptor-mediated pathways.

Carcinoma, Hepatocellular↗
PubMed1997

Expression of mucin-associated tumor antigens is altered by cell density.

Mucin-associated sialylated Lewis antigens are implicated in tumor cell metastasis and are used in several tests for pancreatic cancer. Despite their clinical importance, little is known about the structures of the oligosaccharides of pancreatic cancer mucins or about the regulation of their synthesis or of the synthesis of their protein cores. In this study, we examined the effects of culture at high cell density on the expression of these antigens in the SW1990 human pancreatic cancer cell line. Mucins from cells that were 2.5 weeks post-confluent had increased expression of sialyl-Lewis(a) and Lewis(x) antigens but reduced expression of the DU-PAN-2 antigen (NeuAc alpha2,3Galbeta1,3GlcNAc-Gal-R) when compared to mucins from 1 day post-confluent cells. Sialyl-Lewis antigens differ from the DU-PAN-2 antigen by the presence of an additional fucose. Mucins from 2.5-week cells also had increased binding to lectins specific for fucose, such as AAL and UEAI, with no apparent change in the binding of lectins specific for sialic acids. Metabolically radiolabeled O-linked oligosaccharides with sialyl-Lewis(a) antigenic reactivity eluted from Bio-Gel P-10 in the region of sialylated and sulfated oligosaccharides. Oligosaccharides eluted from QAE-Sephadex (2 mM Tris base) in a pattern suggesting the presence of 1, 2 and 3 or more negative charges per oligosaccharide. Even after desialylation and desulfation, oligosaccharides eluted from Bio-Gel P-10 with apparent molecular sizes greater than glucose oligomers of 12 units. Culture of SW 1990 cells at high density also increased the steady-state levels of mRNA for mucins MUC1, 2, 4, 5 and 6. In summary, after prolonged culture at high cell density, SW1990 cells have qualitative changes in their oligosaccharides that may be due to up-regulation of fucosyltransferases.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1997

Modulation of hormone-dependent transcriptional activity of the glucocorticoid receptor by the tumor suppressor p53.

The glucocorticoid receptor (GR) is a ligand-dependent transcription factor which regulates growth, development and metabolic functions. To test the hypothesis that the pleiotropic effect of the GR could be mediated by other transcription factors/oncogenes, the present study assessed its interaction with the tumor suppressor p53. p53 is a transcription factor which is involved in cell cycle regulation and apoptosis. We found that the wild-type p53 physically interacted with the GR and repressed the glucocorticoid-dependent transcriptional activity. In contrast, mutant p53 had no or a lesser effect depending on the type of p53 mutant. These findings raised the possibility that p53 may play an important role in modulating the activities of glucocorticoids in cells.

Cell Cycle↗
PubMed1997

Critical role of glutamine 252 in the hormone-dependent transcriptional activity of the thyroid hormone beta1 nuclear receptor.

To understand the molecular basis of the ligand-dependent transcriptional activity of thyroid hormone nuclear receptors (TRs), we investigated the effect of mutation of glutamine 252 (Q252) on the function of human TR subtype beta1 (wTRbeta1). Q252 is conserved in TRs in all species and is located in a region of the hormone binding domain that has been shown to undergo 3,3',5-triiodo-L-thyronine (T3) induced conformational changes. Q252 was mutated to Gly (Q252G) or Asn (Q252N) and their immunoreactivity, hormone, and DNA binding activities were characterized. Mutants Q252G and Q252N bound to T3 with similar affinity as the wTRbeta1. However, they failed to interact with a monoclonal anti-wTRbeta1 antibody whose epitope is located in the region of amino acids 248-256, suggesting that mutation of Q252 to Gly or Asn resulted in local structural alteration in TRbeta1. In addition, mutation of Glu to Gly or Asn led to increases in their binding to the thyroid hormone response elements (TREs) as homodimers and as heterodimers with the retinoid X receptor. Mutants Q252G and Q252N were more effective as repressors in the absence of T3, while both had a 1.5-2-fold higher T3-dependent transcriptional activity mediated by three TREs than the wTRbeta1. The increases in the transcriptional activity were not due to an increase in the expression of the mutant receptor proteins because the in vivo expression level of the mutant receptor proteins was identical to that of the wTRbeta1. Our data indicate that the T3-dependent transcriptional activity is not entirely dependent on the T3 binding activity of the receptor. The interplay of ligand and DNA binding domains plays a pivotal role in the transcriptional activity of the TRs.

Antibodies, Monoclonal↗
PubMed1997

Skeletal casein kinase activity defect in the HYP mouse.

The Hyp mouse, a model for human X-linked hypophosphatemia (XLH), is characterized by phosphate wasting and defective mineralization. Since osteopontin (OPN) is considered pivotal for biological mineralization, we examined the biosynthesis of OPN in osteoblasts of +/Y and Hyp/Y mice. Immunoprecipitation analyses using a specific antibody to OPN revealed that Hyp/Y and +/Y osteoblasts secrete similar levels of OPN as determined by [35S]-methionine biosynthetic labeling, but a reduced phosphorylation was noted after 32P-PO4 biosynthetic labeling. Northern blot hybridization analysis of +/Y and Hyp/Y mice osteoblast mRNAs, using a cDNA probe for mouse OPN, revealed no difference in the steady state levels of osteopontin mRNA. Analysis of casein kinase II activity in +/Y and Hyp/Y mice osteoblast, kidney, heart and liver membrane fractions revealed that casein kinase II activity in the Hyp/Y mice osteoblasts and kidney is only 35%-50%, respectively, of that of the +/Y mice tissues. The accumulated data are consistent with a post-translation defect in the Hyp/Y mouse osteoblast which results in the under-phosphorylation of osteopontin and subsequent under-mineralization of bone matrix.

Animals↗