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Biomedical subjects

R M Huang

Publications and source records attributed to R M Huang.

6 recordsLinked to original sources
PubMed2005

Tuberculosis mortality trends in Taiwan: a resurgence of non-respiratory tuberculosis.

SETTING: Population-based study in Taiwan. OBJECTIVE: To determine the tuberculosis (TB) mortality trends in Taiwan by site and age. DESIGN: Mortality data for the years 1972 to 2001 were used to calculate the age/site-specific mortality rate (deaths per 100000 population). The year of change in the slope of mortality trends was estimated by iterative piecewise regression analysis. RESULTS: A levelling off in mortality trends was noted in the late 1980s for all age groups except those aged 75 and above. Except in the age group 25-44 years, the trends in respiratory TB mortality showed a smooth decline. However, for non-respiratory TB mortality, a reversal of the decline was noted for all age groups since 1994-1995. A twofold increase in the number of deaths from central nervous system (CNS) and 'other' TB was noted. A marked increase in the number of deaths from old TB was noted since 1992-1996. CONCLUSION: TB mortality trends in Taiwan have not declined as expected over the past decade. The slowing down of the decline in TB mortality was mainly attributable to a levelling off of respiratory TB mortality in the age group 25-44 and a reversal of non-respiratory TB mortality trends, especially in the 25-44 and > or =65 years age groups.

Adolescent↗
PubMed2005

Patient and health system delays in the diagnosis and treatment of tuberculosis in Southern Taiwan.

SETTING: Tainan city, Tainan county and 13 townships of Kaohsiung county, Southern Taiwan. OBJECTIVE: To measure delays in the diagnosis and treatment of sputum-positive tuberculosis (TB) and to determine factors associated with delays in seeking health care (patient delay) and in starting anti-tuberculosis treatment (health system delay). DESIGN: A population-based patient interview study. RESULTS: Median patient delay was 7 days (range 0-730). Median health system delay was 23 days (range 0-489), 13 for smear-positive patients and 37 for smear-negative patients (P < 0.005). Median total delay was 44 days (range 0-730). Age <65 years was associated with longer patient delay. Negative smear, absence of haemoptysis, not having a chest radiograph at the first medical consultation and visiting clinics for first consultation were associated with a longer health system delay. Age <65 years, negative smear and cough as the only presenting symptom were associated with longer total delay. CONCLUSION: Patient delay was substantially shorter than health system delay. To reduce health system delay, clinics need to be involved and the referral mechanism must be strengthened. Physicians should maintain high alert for TB and perform prompt sputum smear examinations.

Adolescent↗
PubMed1999

Identification of a new member of the tumor necrosis factor family and its receptor, a human ortholog of mouse GITR.

The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate diverse biological functions, including cell proliferation, differentiation, and survival [1] [2] [3]. We have identified a new TNF-related ligand, designated human GITR ligand (hGITRL), and its human receptor (hGITR), an ortholog of the recently discovered murine glucocorticoid-induced TNFR-related (mGITR) protein [4]. The hGITRL gene mapped to chromosome 1q23, near the gene for the TNF homolog Fas/CD95 ligand [5]. The hGITR gene mapped to chromosome 1p36, near a cluster of five genes encoding TNFR homologs [1] [6]. We found hGITRL mRNA in several peripheral tissues, and detected hGITRL protein on cultured vascular endothelial cells. The levels of hGITR mRNA in tissues were generally low; in peripheral blood T cells, however, antigen-receptor stimulation led to a substantial induction of hGITR transcripts. Cotransfection of hGITRL and hGITR in embryonic kidney 293 cells activated the anti-apoptotic transcription factor NF-kappaB, via a pathway that appeared to involve TNFR-associated factor 2 (TRAF2) [7] and NF-kappaB-inducing kinase (NIK) [8]. Cotransfection of hGITRL and hGITR in Jurkat T leukemia cells inhibited antigen-receptor-induced cell death. Thus, hGITRL and hGITR may modulate T lymphocyte survival in peripheral tissues.

Amino Acid Sequence↗
PubMed1992

[Hybridization experiments using Anopheles minimus from Guangxi and Yunnan].

Hybridization experiments were conducted by forced mating between Anopheles minimus from Guangxi (G) and Yunnan (Y). F1 hybrid females were all fertile with normally developed ovaries. (Y female x G male) F1 males were all sterile, with abnormally enlarged testes. (G female x Y male) F1 males, though fertile, showed somewhat atrophic testes, and when they were back crossed with parental females, the latter produced eggs with very low hatching rate. Ovarian nurse cell polytene chromosomes from F1 hybrid females showed partial asynapsis in X chromosome as well as in autosonles, asynapsis at 38 zone in 3L being the most constant. It was obvious that there was definite, though partial, reproductive isolation between An minimus from Guangxi and that from Yunnan. Whether they are sibling species remains to be further investigated (Figs. 1-8).

Animals↗
PubMed1989

Septic pulmonary emboli: CT-radiographic correlation.

Radiographic and CT findings in 15 patients with clinically documented septic pulmonary emboli were compared retrospectively. In most cases, radiographic changes were nonspecific. In comparison, on CT a combination of specific signs could be identified in all patients. These included peripheral nodules with clearly identifiable feeding vessels associated with metastatic lung abscesses (10 [67%] of 15 cases), and subpleural, wedge-shaped densities with and without necrosis caused by septic infarcts (11 [73%] of 15 cases). Ancillary pleural, mediastinal, axillary, and pericardial abnormalities also were more easily identified with CT. We conclude that CT is complementary to other imaging techniques in the recognition of septic pulmonary emboli.

Adult↗