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Biomedical subjects

S Liao

Publications and source records attributed to S Liao.

At least 109 records · Page 6Linked to original sources
PubMed1996

Absence of an effect of levofloxacin on warfarin pharmacokinetics and anticoagulation in male volunteers.

Some fluoroquinolone drug-drug interactions involving inhibition of the hepatic metabolism of agents such as theophylline and caffeine have been identified. This study was designed to investigate the potential interaction of the fluoroquinolone levofloxacin in a standard multiple-dose regimen with the oral anticoagulant warfarin. Sixteen healthy male volunteers were given a single oral dose of 30 mg warfarin sodium during a multiple-dose regimen of placebo or levofloxacin 500 mg twice daily, in a placebo-controlled, randomized, double-blind, two-way crossover design. Plasma R(+) and S(-) warfarin concentrations and prothrombin times were measured for 6 days after administration of each warfarin dose. The pharmacokinetic parameters of both enantiomers of warfarin were comparable in the absence and presence of levofloxacin, with no significant differences noted in warfarin peak plasma concentration, time to peak plasma concentration, apparent total body clearance, and terminal disposition half-life. Levofloxacin also had no significant effect on warfarin pharmacodynamics, as assessed by baseline-corrected maximum prothrombin time, time to maximum prothrombin time, and area under the prothrombin time-versus-time curve. The lack of pharmacokinetic or pharmacodynamic interaction observed in this study suggests that a clinically important effect of levofloxacin on warfarin is unlikely to occur during concurrent therapy.

Administration, Oral↗
PubMed1996

Protective effect of interleukin-1 receptor antagonist on oleic acid-induced lung injury.

OBJECTIVE: To observe the changes of interleukin-1 (IL-1), nitric oxide (NO) and nitric oxide synthase (NOS) in mice with oleic acid-induced acute lung injury (ALI) and the protective effects of interleukin-1 receptor antagonist (IL-1ra). MATERIAL AND METHODS: Male Kunming mice were divided into control, oleic acid and IL-1ra groups. The control group mice were injected saline; the oleic acid group mice were injected oleic acid (0.2 ml/kg): and the IL-1ra group mice were injected the IL-1ra (20 mg/kg). Lung index, lung wet-to-dry weight ratio, and total protein, cell analysis, nitric oxide measurement, NOS activity in BALF, lung pathology examination were made after an hour of administration of drug. RESULTS: Preadministration of IL-1ra to the mouse with ALI decreased the lung index, lung wet-to-dry weight ratio and leakage of protein from pulmonary capillary, elevated PaO2, and attenuated lung histologic injury. It was found that in bronchoalveolar lavage fluid (BALF), NO amount and lung NOS activity increased in oleic acid group, BALF NO amount and lung NOS activity decreased obviously after given IL-1ra. CONCLUSIONS: This study demonstrated the protective effect of IL-1ra on oleic acid-induced lung injury, NO may participate in the pathological process of lung injury.

Animals↗
PubMed1995

Selective inhibition of steroid 5 alpha-reductase isozymes by tea epicatechin-3-gallate and epigallocatechin-3-gallate.

Inhibitors of 5 alpha-reductase may be effective in the treatment of 5 alpha-dihydrotestosterone-dependent abnormalities, such as benign prostate hyperplasia, prostate cancer and certain skin diseases. The green tea catechins, (-)epigallocatechin-3-gallate and (-)epicatechin-3-gallate, but not (-)epicatechin and (-)epigallocatechin, are potent inhibitors of type 1 but not type 2 5 alpha-reductase. (-)Epigallocatechin-3-gallate also inhibits accessory sex gland growth in the rat. These results suggest that certain tea gallates can regulate androgen action in target organs.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1995

Growth inhibition and regression of human prostate and breast tumors in athymic mice by tea epigallocatechin gallate.

The human prostate cancer cell lines, PC-3 (androgen-insensitive) and LNCaP 104-R (androgen-repressed) were inoculated subcutaneously into nude mice to produce prostate tumors. Intraperitoneal injection of green tea (-)epigallocatechin-3-gallate but not structurally related catechins, such as (-)epicatechin-3-gallate, inhibited the growth and rapidly reduced the size of human prostate tumors in nude mice. (-)Epigallocatechin-3-gallate also rapidly inhibited the growth of tumor growth formed by the human mammary cancer cell line MCF-7 in nude mice. It is possible that there is a relationship between the high consumption of green tea and the low incidence of prostate and breast cancers in some Asian countries.

Animals↗
PubMed1995

Leu-676-Pro mutation of the androgen receptor causes complete androgen insensitivity syndrome in a large Hutterite kindred.

A large Manitoba Hutterite kindred with X-linked receptor negative complete androgen insensitivity syndrome (CAIS) was studied. In attempts to identify all carriers of the syndrome in this kindred, using the androgen receptor (AR) cDNA, we have found a novel diagnostic MspI polymorphic pattern, which cosegregates with the disease. This polymorphism was not detected in 79 unrelated X-chromosomes of which 22 were from Hutterite controls. We were able to localize the polymorphism to exon 4, which is known to encode part of the androgen receptor hormone binding domain. A single base substitution (T-->C) was detected, which creates a new MspI site. This novel transition mutation replaces Leu-676 with Pro at a site which is conserved in numerous members of the steroid receptor gene family. Sequencing all 8 exons of the AR revealed the Leu-676-->Pro mutation as the only change in the primary structure of the receptor. Transfection of COS-1 cells with an expression vector of the mutant AR demonstrates that this point mutation of nucleotide 2558 abolishes receptor binding activity. The mutation can easily be detected by MspI digestion of the polymerase chain reaction (PCR) amplified exon 4 product.

Amino Acid Sequence↗
PubMed1995

Recovery trends over three years following pediatric traumatic brain injury.

This cohort study investigated the magnitude of neurobehavioral, academic, and "real world" deficits over the course of 3 years in children with mild, moderate, and severe traumatic brain injury (TBI), and their individually matched controls. This series of analyses addresses the history of recovery, tracing changes in performance over time. Data on 72 case-control pairs (mild, n = 40; moderate, n = 17; severe, n = 15) were available for three testing times: 3 weeks, 1 year, and 3 years after the resolution of post-traumatic amnesia. The same standardized battery of tests was used at all testing times. The dependent variables in these analyses included individual test results, a variable summarizing results within each of 10 neurobehavioral domains, and an overall score across all domains. Three statistics were calculated for each variable: (1) the "grand" mean across the three testing times; (2) the slope (expressing the linear trend in performance); and (3) the change in slope over time (expressing the change in the rate of recovery). Use of the differences between case and control scores controlled for premorbid factors, maturation, and test-retest effects. Results indicate the chronicity of neurobehavioral deficits across all 3 years for moderately and severely injured children. They show a strong improvement rate during the first year, but a negligible rate of change during the following 2 years postinjury in most domains. All three of the time components--grand mean, slope, and change in slope--have significant Spearman correlations with severity ranging up to rho = -.5. Over time, the recovery rate slows down more for those with greater brain injury severity. The greatest slowing of recovery occurs in Performance IQ, adaptive problem solving, memory, and motor skills, as well as on a summary score of overall performance. Given this "plateauing" of recovery, achievement of parity with peers by the moderately and severely injured seems unlikely. Mildly injured children, however, exhibit negligible deficits or change in performance over time.

Activities of Daily Living↗
PubMed1995

Medial neovascularization in abdominal aortic aneurysms: a histopathologic marker of aneurysmal degeneration with pathophysiologic implications.

PURPOSE: The purpose of this study was to characterize the distribution of aortic wall microvessels in normal aorta, atheroocclusive disease (AOD), and abdominal aortic aneurysms (AAA) and to evaluate whether medial neovascularization (MNV) is a reliable histopathologic marker of aneurysmal degeneration. METHODS: Aortic tissue specimens (9 normal, 10 AOD, and 10 AAA) were examined for elastin with Verhoeff-van Gieson stain and for Ulex europaeus type I lectin, an endothelial-specific antigen, and laminin, a marker of basement membranes, by immunohistochemistry. The density of MNV was determined by morphometry of aortic sections stained for endothelium. The spatial distribution of aortic microvessels was compared with that of elastin destruction and chronic inflammation. RESULTS: Evidence of medial neovascularization was generally not observed in normal aorta or AOD, whereas AAAs showed strong spatial correlations between MNV, disruption and degradation of elastin, and chronic inflammation in the outer aortic wall. Several specimens of AOD had focal areas of MNV associated with localized elastin fragmentation and monocytic infiltration located at the interface between the atherosclerotic plaque and the inner media. The density of MNV was about fifteenfold higher in AAA compared with normal aorta and about threefold higher compared with AOD (microvessels per high-power field): normal aorta, 0.77 +/- 0.28; AOD, 3.40 +/- 0.51; AAA, 11.32 +/- 1.58 (ANOVA, p < 0.001). CONCLUSIONS: The presence and density of MNV in the abdominal aorta is a consistent histopathologic marker of aneurysmal degeneration that is spatially correlated with the destruction of elastin and chronic inflammation. The observation of focal MNV in some specimens of AOD, associated with partial elastin disruption, raises the possibility that early changes of aneurysm disease might develop by an extension of angiogenic/inflammatory processes from the atherosclerotic plaque into the aortic media.

Adult↗
PubMed1995

Production and localization of 92-kilodalton gelatinase in abdominal aortic aneurysms. An elastolytic metalloproteinase expressed by aneurysm-infiltrating macrophages.

Abdominal aortic aneurysms (AAA) are characterized by disruption and degradation of the elastic media, yet the elastolytic proteinases involved and their cellular sources are undefined. We examined if 92-kD gelatinase, an elastolytic matrix metalloproteinase, participates in the pathobiology of AAA. Gelatin zymography of conditioned medium from normal, atheroocclusive disease (AOD), or AAA tissues in organ culture showed that all tissues produced 72-kD gelatinase. AOD and AAA cultures also secreted 92-kD gelatinase, but significantly more enzyme was released from AAA tissues. ELISA confirmed that AAA tissues released approximately 2-fold more 92-kD gelatinase than AOD tissue and approximately 10-fold more than normal aorta. Phorbol ester induced a 5.3-fold increase in 92-kD gelatinase secretion by normal aorta and AOD and an 11.5-fold increase by AAA. By immunohistochemistry, 92-kD gelatinase was not detected in normal aorta and was only occasionally seen within the neointimal lesions of AOD tissue. In all AAA specimens, however, 92-kD gelatinase was readily localized to numerous macrophages in the media and at the adventitial-medial junction. The expression of 92-kD gelatinase mRNA by aneurysm-infiltrating macrophages was confirmed by in situ hybridization. These results demonstrate that diseased aortic tissues secrete greater amounts of gelatinolytic activity than normal aorta primarily due to increased production of 92-kD gelatinase. In addition, the localization of 92-kD gelatinase to macrophages in the damaged wall of aneurysmal aortas suggests that chronic release of this elastolytic metalloproteinase contributes to extracellular matrix degradation in AAA.

Aorta↗
PubMed1995

Inhibition of growth of human ovarian cancer in nude mice by luteinizing hormone-releasing hormone antagonist Cetrorelix (SB-75).

OBJECTIVE: To report on the in vitro and in vivo inhibitory effects of LH-releasing hormone (LH-RH) antagonist Cetrorelix (SB-75; Asta Medica, Frankfurt-Main, Germany) against a panel of human ovarian carcinomas. INTERVENTIONS IN VITRO STUDIES: the effect of SB-75 was measured using a standardized chemosensitivity assay in the following ovarian cancer cell lines: UCI 101; UCI 107; PA-1; NIH: OVCAR 3; UCLA: 222; A2780, parental; A2780-CR, cisplatin resistant; A2780-DR, doxorubicin resistant; and the human breast cancer cell line, MCF-7. Results were expressed as percent growth inhibition determined by crystal violet photometric analysis. In vivo studies: the antiproliferative effect of this agent was examined using UCI-107, a primary epithelial ovarian carcinoma cell line, in a nude mouse model. On day 0, 10 x 10(6) UCI 107 cells were implanted subcutaneously into 20 intact female athymic nude mice (5 to 6 weeks old). On day 8, the mice were randomly divided into two groups of 10; control mice were implanted with miniosmotic pumps filled with a vehicle solution consisting of 5.2% mannitol in saline; and treated animals received pumps filled to deliver continuous administration of SB-75 at 60 micrograms per mouse per day. RESULTS IN VITRO STUDIES: direct inhibition of cell proliferation by SB-75 was not observed at concentrations ranging from 1 nM to 100 microM (exposure lasting three to four cell doublings) with the exception of MCF-7, which demonstrated a 33% inhibition at the latter concentration. In vivo studies: on day 16, caliper measurements were taken from subcutaneous tumor nodules in SB-75-treated and untreated mice and a significant difference of 270% in mean tumor volume was observed. End point was determined, on day 30, when control tumor volume approached 10,000 mm3. At that time the difference in mean tumor volumes increased to 600%, indicating a substantial antiproliferative effect had been achieved in the SB-75-treated group. CONCLUSION: Our in vitro findings show direct inhibition by SB-75 on proliferation of human breast cancer cells. This direct inhibition in vitro was not observed in our ovarian cancer cell lines. However, in vivo SB-75 caused a significant inhibition of growth of human epithelial ovarian cancer. This may be a result of inhibition of the pituitary gonadal axis and gonadotropin secretion. Our results warrant further investigation.

Animals↗
PubMed1995

Surgical management of breast masses in pregnant women.

OBJECTIVE: The goal of this study was to review the outcomes of breast biopsies in pregnant women in order to plan optimum management strategies for pregnant women with breast masses. STUDY DESIGN: From January 1990 to October 1992, 17 pregnant women underwent breast biopsy at a university hospital. Parameters evaluated were (1) trimester at presentation, (2) timing of biopsy, (3) mode of anesthesia, (4) requirements for tocolytics, and (5) histology of the lesion. RESULTS: Antepartum biopsy was performed on all 11 patients who presented in the first or second trimester. Biopsy was accomplished postpartum in four of five patients presenting in the third trimester. Only one patient required tocolysis (associated with biopsy followed by immediate mastectomy). Histologic diagnosis was predominantly lactating adenoma (13 of 17 patients). CONCLUSION: These results demonstrate that breast biopsy can be safely performed on pregnant women. We recommend that women presenting with breast masses in the first or second trimester undergo antepartum biopsy. We recommend postpartum excision for masses presenting in the latter half of the third trimester. For those presenting in the first half of the third trimester, fine needle aspiration biopsy may be a suitable alternative, particularly for the mass suspicious for cancer.

Adenoma↗
PubMed1994

Ubiquitous receptor: a receptor that modulates gene activation by retinoic acid and thyroid hormone receptors.

The cDNA for a member of the nuclear receptor family was cloned and named ubiquitous receptor (UR), since UR protein and mRNA are detected in many cell types. Rat UR/human retinoid X receptor alpha (hRXR alpha) heterodimers bound preferentially to double-stranded oligonucleotide direct repeats having the consensus half-site sequence AGGTCA and 4-nt spacing (DR-4). Coexpression of UR in COS-1 cells inhibited the stimulation of chloramphenicol acetyltransferase (CAT) reporter gene expression by hRXR alpha and human retinoic acid receptor alpha in the presence of all-trans-retinoic acid when DR-4 (but not DR-5) was present upstream of the promoter of a CAT reporter gene (DR-4-CAT). UR expression also inhibited the activation of a DR-4-CAT reporter gene by hRXR alpha and 9-cis-retinoic acid or by thyroid hormone receptor beta in the presence of thyroid hormone. However, in the absence of 9-cis-retinoic acid, UR in combination with hRXR alpha stimulation DR-4-CAT expression. Coexpression of thyroid hormone receptor markedly reduced this stimulation in the absence of thyroid hormone. UR may play an important role in normal growth and differentiation by modulating gene activation in retinoic acid and thyroid hormone signaling pathways.

Amino Acid Sequence↗
PubMed1994

Secretory proteins move through the endoplasmic reticulum membrane via an aqueous, gated pore.

The environment of secretory proteins undergoing translocation across the ER membrane was determined by incorporating fluorescent probes into nascent chains during translation. Dyes were positioned at various locations across the entire bilayer and inside the ribosome, and in each case the probes were in an aqueous milieu, as shown both by their fluorescence lifetimes and by collisional quenching of their fluorescence by iodide ions introduced into the ER lumen. The nascent chain therefore occupies an aqueous pore that spans the entire membrane. Since the pore is sealed off from the cytoplasm, cotranslational translocation is effected topographically. This pore is not open to the lumen after targeting is completed; it opens only after the nascent chain length reaches about 70 residues.

Animals↗
PubMed1994

Loss of heterozygosity in cervical carcinoma: subchromosomal localization of a putative tumor-suppressor gene to chromosome 11q22-q24.

Infection of cervical epithelial cells with so-called "aggressive" subtypes of human papilloma virus (HPV) appears to be an important factor in the etiology of cervical carcinoma. However, mounting evidence suggests that additional genetic changes are required for progression to an invasive carcinoma. Functional studies have shown that human chromosome 11 contains a gene or genes capable of suppressing tumorigenicity in cell lines derived from different histopathological types of cervical carcinoma, suggesting that aberration of this gene(s) may represent at least one of the additional changes required for tumorigenic progression. To identify the likely chromosomal position of this gene(s), we have carried out a systematic genetic analysis of chromosome 11 in the primary tumors of 32 patients with cervical carcinoma. Sixteen highly polymorphic markers, 10 of which were based on simple sequence repeats typed by PCR, were used to compare matched DNA samples from noninvolved tissue and portions of tumor tissue highly enriched for neoplastic cells by the cryostat-sectioning technique. Of the 32 patients examined, 14 (44%) demonstrated clonal genetic alterations resulting in loss of heterozygosity for one or more markers. Seven of the clonal genetic alterations on chromosome 11 were specific to the long arm, and the overlap between these and other allelic deletions suggests that a suppressor gene(s) relevant to cervical carcinoma maps to chromosome 11q22-q24.

Alleles↗