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Biomedical subjects

W L Tang

Publications and source records attributed to W L Tang.

7 recordsLinked to original sources

[Clinical trial of indapamide in the management of central diabetes insipidus].

To investigate antidiuretic effect of indapamide, ten patients with central diabetes insipidus (CDI) were observed with the treatment of 2.5-7.5 mg of indapamide per day. After the third day of therapy, their mean daily urine output reduced by about 50%, and urine osmolality increased 1.36 times. No further change was seen in urine volume and urine osmolality on the sixth day of treatment. This antidiuretic effect was similar to that of 50-75 mg dihydrochlorothiazide per day. No adverse reaction was observed in blood pressure and serum potassium concentration during indapamide therapy. These data suggest that indapamide may be a new drug in the management of CDI.

Adolescent

The murine lymphotoxin gene promoter. Characterization and negative regulation.

Murine lymphotoxin (LT; TNF-beta) gene upstream regulatory elements were identified by linking fragments of 5' DNA to the chloramphenicol acetyl transferase gene. Fragment LT1 (-293 to +77 in relation to the proximal cap site) exhibited promoter activity which drove CAT expression in transfected murine fibroblasts and T lymphomas. Primer extension analysis of endogenous LT message confirmed that LT1 contained the necessary elements required for promoter function. Promoter activity was not observed when LT2 (-662 to +77), LT3 (-1186 to +77), or LT3 delta AX (-1186 to +77 (delta-662/-269)) were ligated to the chloramphenicol acetyl transferase gene and transfected into fibroblasts or T lymphomas. At least one upstream repressor element is postulated to account for this promoter inhibition. In contrast to the results obtained with fibroblast and T cell transfectants, LT1 was inactive in the B cell transfectants A20 and P3X63. This suggests that some B cells express a repressor factor that inhibits the LT promoter and/or they lack the necessary positive regulatory factors.

Animals

Lymphotoxin activation by human T-cell leukemia virus type I-infected cell lines: role for NF-kappa B.

Human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of biologically active lymphotoxin (LT; tumor necrosis factor-beta) protein and LT mRNA. To understand the regulation of LT transcription by HTLV-I, we analyzed the ability of a series of deletions of the LT promoter to drive the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells. The smallest LT promoter fragment (-140 to +77) that was able to drive CAT activity contained a site that was similar to the immunoglobulin kappa-chain NF-kappa B-binding site. Since the HTLV-I tax gene activates the nuclear form of NF-kappa B, this finding suggested a possible means of HTLV-I activation of LT production. We found that the LT kappa B-like site specifically formed a complex with NF-kappa B-containing nuclear extract from MT-2, C81-66-45, and other activated T cells. Mutation of the LT kappa B site in the context of the LT promoter (-293 to +77) (mutant M1) reduced the ability of the promoter to drive the CAT gene in HTLV-I-infected and noninfected human T-cell lines. These data suggest a general role for NF-kappa B activation in the induction of LT gene transcription. Activation of LT in HTLV-I-infected cells may explain the pathology associated with HTLV-I infection, including the hypercalcemia that is prevalent in adult T-cell leukemia.

Base Sequence

Amniotic fluid lecithin/sphingomyelin ratio in high risk pregnancy.

The amniotic fluid lecithin/sphingomyelin (L/S) ratio from 128 cases of high risk pregnancies were measured by using high performance liquid chromatography (HPLC). The L/S ratio was found to be increased in patients with pre-eclampsia, hypertension, intrauterine growth retardation (IUGR), prolonged rupture of membranes (PROM), and twin gestation, but decreased in patients with diabetes from gestational diabetes to class C. In patients with placenta previa, the L/S ratio was not affected.

Amniotic Fluid

Lymphotoxin: cloning, regulation and mechanism of killing.

The gene for murine lymphotoxin (MuLT) has been cloned from a cDNA library prepared using poly(A)+ RNA from an activated murine IL-2-maintained cloned T cell line (21C11). This was accomplished with a MuLT BamHI fragment isolated from a murine genomic library by hybridization to a human LT cDNA probe. Northern blot analysis with RNA from 21C11, an L3T4+ (CD4+-equivalent) ovalbumin-specific class II-restricted T cell line, revealed a 15S band that hybridized to this MuLT fragment. A cDNA library prepared with poly(A)+ RNA from 21C11 cells contained 36 colonies that hybridized with the MuLT BamHI fragment. A full-length cDNA has been isolated, sequenced, expressed in COS-1 cells and used to map MuLT to mouse chromosome 17. The sequence and structure of the MuLT gene has been determined. MuLT cDNA has been used to analyse mRNA expression in several L3T4+ and Lyt-2+ (CD8+-equivalent) T cell clones activated with antigen, mitogen, or antibody to the T cell receptor. LT is expressed by both class I- and class II-restricted T cells. The mechanism of killing by both LT and the functionally related molecule TNF-alpha includes the induction of DNA fragmentation in the target cell.

Animals

Validity of lung correction algorithms.

Our studies have compared the "effective tissue-air ratio (TAR) method" (ICRU Report No. 24), "equivalent TAR method," and the "generalized Batho method" (currently used by the TP-11 computer treatment planning system) with measured results for different energy photon beams using two lung inhomogeneities to simulate a lateral chest field. Significant differences on the order of 3%-15% were found when comparing these various methods with measured values.

Algorithms