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Biomedical subjects

S C Wang

Publications and source records attributed to S C Wang.

At least 127 records · Page 7Linked to original sources
PubMed1994

Intravesical instillation of gentamicin sulfate: in vitro, rat, canine, and human studies.

OBJECTIVE: Intravesical instillation of gentamicin sulfate has been used empirically as prophylaxis and to treat bacilluria in spinal-cord-injured patients undergoing clean intermittent catheterization. To assess the risks of absorption and the effects of storage conditions on antimicrobial potency, a series of studies were conducted. METHODS: Four studies were carried out: (1) An infected fulgurated rat bladder model was created to determine the effects of inflammation and infection on absorption. (2) A canine model with bilateral vesicoureteral reflux and elevated bladder pressures (> 40 cmH2O) assessed the effects of reflux and storage pressure. (3) The effects in patients with associated conditions including renal transplantation, myelomeningocele, vesicoureteral reflux, and bladder augmentation, were analyzed. (4) To determine the effects of storage conditions, solutions of gentamicin sulfate (480 mg gentamicin sulfate in 1 L 0.9% NaCl) were made that controlled for pH, storage temperature, and duration. RESULTS: (1) Increased absorption was found in 43 percent of rat serum samples. (2) None of the dogs demonstrated measurable absorption. (3) None of the patients likewise had measurable absorption. (4) All solutions were equally potent when tested against a panel of common urinary pathogens. Storage up to two months at room temperature without alkalinization had no effect on potency. CONCLUSIONS: Instilled intravesical gentamicin sulfate has a low risk of absorption and is highly effective. Severe bladder inflammation can increase transvesical absorption. It has prolonged stability without special storage conditions and should be considered as a route of prophylaxis in patients who perform intermittent catheterization.

Absorption↗
PubMed1994

Suppression of lipopolysaccharide-induced macrophage nitric oxide and cytokine production in vitro by a novel lipopolysaccharide antagonist.

BACKGROUND: Many of the physiologic derangements resulting in septic shock are caused by inflammatory mediators such as nitric oxide (NO) and cytokines produced in response to bacterial endotoxin or, more specifically, lipopolysaccharide. The recent development of a novel class of lipopolysaccharide antagonists offers the opportunity to block this response selectively. In this article we investigated the ability of one of these antagonists, B464 (Eisai), to block lipopolysaccharide-induced release of macrophage NO and cytokines. METHODS: The mouse macrophage cell line RAW264.7 was grown in vitro and exposed to (1) media control, (2) B464 alone, (3) lipopolysaccharide alone, or (4) lipopolysaccharide plus graded concentrations of B464. Supernatants were assayed for nitrite plus nitrate, the stable end products of NO, as well as tumor necrosis factor-alpha and interleukin-6. Total cellular RNA was examined for inducible NO synthase and interleukin-6 mRNA. RESULTS: Lipopolysaccharide-stimulated increases in NO, tumor necrosis factor, and interleukin-6 production were blocked by B464. Reduction of NO was also seen at the level of inducible NO synthase mRNA. Induction of interleukin-6 mRNA was also suppressed. CONCLUSION: B464 is a novel potent specific antagonist of lipopolysaccharide-induced macrophage NO and cytokine production.

Amino Acid Oxidoreductases↗
PubMed1994

Use of esmolol to prevent hemodynamic changes during intubation in general anesthesia.

To assess the minimal effective dosage of esmolol to prevent hypertension and tachycardia during laryngoscopy and endotracheal intubation in fentanyl-pretreated anesthesia, a double-blinded, randomized study was conducted. Two hundred patients undergoing elective, noncardiac surgeries were randomly allocated into four groups: group A received saline, group B esmolol 20 mg, group C esmolol 40 mg and group D esmolol 60 mg intravenously. General anesthesia was induced with 0.1 mg/kg vecuronium, 5 micrograms/kg fentanyl and 0.3 mg/kg etomidate. Heart rates (HR), systolic blood pressures (SBP), mean arterial pressures (MAP) and diastolic blood pressures (DBP) were recorded before induction, after induction, before intubation, 30 seconds, 1 minute, 2 minutes, 4 minutes, 6 minutes, and 10 minutes after intubation. After intubation HR and SBP increased significantly in group A (86.7 beats/min, 166.6 mmHg) in comparison with groups C (77.6 beats/min, 153.9 mmHg) and D (73.4 beats/min, 153.4 mmHg) (p < 0.05). Tachycardia (HR > 100) was found in 13 of 50(26%) patients in group A, 10 of 50(20%) patients in group B, 7 of 50(14%) patients in group C and 2 of 50(4%) patients in group D. Hypertension (SBP > 180) was found in 18(36%) patients in group A, 19(38%) patients in group B, 9(18%) patients in group C, and 6(12%) patients in group D. When compared with group A, only group D had significantly lower incidence of these adverse events (p < 0.05). In conclusion, fentanyl 5 micrograms/kg could not completely prevent the hemodynamic changes associated with endotracheal intubation, and 60 mg esmolol was observed to have positive effect in helping to control these changes.

Adrenergic beta-Antagonists↗
PubMed1994

Innervation of the ligament of the femoral head in the formosan rock monkey: a retrograde HRP tracing and ultrastructural study.

The innervation of the ligament attached to the femoral head of the Formosan rock monkey (Macaca cyclopis, Swinhoe) was investigated by means of the retrograde HRP tracing method and by electron microscopy. WGA/HRP was injected into the ligament of the left femoral head. Numerous neurons labelled with HRP were found in the ipsilateral lumbar sympathetic ganglia, from L1 to L7, with a peak in the L3 to L5 region. Labelled neurons were also found in the ipsilateral spinal dorsal root ganglia, from L1 to L7 and concentrated at L4. Ultrastructurally, the nerve fascicles to the ligament had an average diameter at 32.8 microns. They contained both myelinated and unmyelinated axons and accompanied the blood vessels. Sensory receptors were not found in the ligamentum proprium but free nerve endings were observed in the walls of the blood vessels. The present results indicate that the nerve fibres to the ligament of the femoral head may be involved in regulating blood vessel calibre in addition to having a sensory function.

Animals↗
PubMed1993

Molecular cloning and expression of inducible nitric oxide synthase from human hepatocytes.

Nitric oxide is a short-lived biologic mediator for diverse cell types. Synthesis of an inducible nitric oxide synthase (NOS) in murine macrophages is stimulated by lipopolysaccharide (LPS) and interferon gamma. In human hepatocytes, NOS activity is induced by treatment with a combination of tumor necrosis factor, interleukin 1, interferon gamma, and LPS. We now report the molecular cloning and expression of an inducible human hepatocyte NOS (hep-NOS) cDNA. hep-NOS has 80% amino acid sequence homology to macrophage NOS (mac-NOS). Like other NOS isoforms, recognition sites for FMN, FAD, and NADPH are present, as well as a consensus calmodulin binding site. NOS activity in human 293 kidney cells transfected with hep-NOS cDNA is diminished by Ca2+ chelation and a calmodulin antagonist, reflecting a Ca2+ dependence not evident for mac-NOS. Northern blot analysis with hep-NOS cDNA reveals a 4.5-kb mRNA in both human hepatocytes and aortic smooth muscle cells following stimulation with LPS and cytokines. Human genomic Southern blots probed with human hep-NOS and human endothelial NOS cDNA clones display different genomic restriction enzyme fragments, suggesting distinct gene products for these NOS isoforms. hep-NOS appears to be an inducible form of NOS that is distinct from mac-NOS as well as brain and endothelial NOS isozymes.

Amino Acid Oxidoreductases↗
PubMed1993

Cytokines, endotoxin, and glucocorticoids regulate the expression of inducible nitric oxide synthase in hepatocytes.

Nitric oxide (NO.) is a short-lived mediator which can be induced in a variety of cell types and produces many physiologic and metabolic changes in target cells. The inducible or high-output NO. synthase (NOS) pathway was first characterized in macrophages activated by lipopolysaccharide (LPS) and interferon gamma (IFN-gamma). Hepatocytes also express an inducible NOS following exposure to the combination of endotoxin (LPS) and tumor necrosis factor (TNF), interleukin 1 (IL-1), and IFN-gamma. In this study, to identify which of these cytokines, if any, was acting to induce the gene expression for hepatocyte NOS, we measured the levels of rat hepatocyte NOS mRNA by Northern blot analysis after stimulation by various combinations of endotoxin and cytokines in vitro. We found the mRNA for hepatocyte NOS to be a single band at approximately 4.5 kilobases which was maximally up-regulated (approximately 70-fold) by the combination of TNF, IL-1, IFN-gamma, and LPS. Abundance of NOS mRNA peaked 6-8 hr after stimulation and then declined by 25% at 24 hr. Unstimulated hepatocytes in vitro showed only a trace mRNA band after prolonged autoradiographic exposure. As single agents, TNF and IL-1 were the most effective inducers of hepatocyte NOS mRNA. Combinations of two or three stimuli revealed strong synergy between TNF, IL-1, and IFN-gamma. The increased mRNA levels correlated with elevated nitrogen oxide release and cGMP levels in the culture supernatants. Dexamethasone and cycloheximide inhibited induction of mRNA for hepatocyte NOS in a dose-dependent fashion. The addition of NG-monomethyl-L-arginine had no effect on mRNA levels but effectively blocked NO. formation. The inducible hepatocyte NOS mRNA was also detected in rat hepatocytes following chronic hepatic inflammation triggered by Corynebacterium parvum injection in vivo. These data demonstrate that the inducible NOS is functional in rat hepatocytes both in vitro and in vivo and that this pathway is under complex control. Endotoxin and inflammatory cytokines act synergistically to up-regulate gene expression for hepatocyte NOS, whereas glucocorticoids down-regulate the mRNA.

Amino Acid Oxidoreductases↗
PubMed1993

Induction of hepatocyte lipopolysaccharide binding protein in models of sepsis and the acute-phase response.

Lipopolysaccharide binding protein (LBP) is a serum glycoprotein that complexes with lipopolysaccharide (LPS) to facilitate macrophage response to endotoxin. To determine the conditions that stimulate LBP production in vivo, we measured the induction of LBP in models of inflammation produced by LPS, Corynebacterium parvum, and turpentine injection. Plasma aspartate aminotransferase and alanine aminotransferase concentrations and hepatocyte fibrinogen synthesis were elevated in all models. Northern blot analysis revealed 17-, 14-, and 20-fold upregulation of hepatocyte LBP mRNA following treatment with LPS, C parvum, and turpentine, respectively. Peritoneal macrophage interleukin 6 and tumor necrosis factor production following endotoxin stimulation was augmented by cultured hepatocyte supernatants, suggesting increased LBP synthesis in these groups. The results show that LBP mRNA is induced during hepatic inflammation and suggest that LBP is an acute-phase protein important in regulating the in vivo response to endotoxin.

Acute-Phase Proteins↗
PubMed1993

Nitric oxide synthase expression is induced in hepatocytes in vivo during hepatic inflammation.

Nitric oxide (NO.) is a short-lived biologic mediator produced by the enzyme NO. synthase (NOS) which exists in constitutive and inducible isoforms. Previously, we have shown that hepatocytes express an inducible NOS in vitro following exposure to the combination of lipopolysaccharide and inflammatory cytokines. The purpose of the present study is to characterize the induction of NOS in vivo in rat hepatocytes during chronic hepatic inflammation triggered by Corynebacterium parvum injection and to correlate NO. synthesis with the timing of liver injury. Using Northern blot hybridization, hepatocyte-inducible NOS mRNA was detected 3 days after C. parvum administration and was not found in normal hepatocytes. Hepatocyte NOS activity was significantly increased 3 to 7 days after C. parvum. Plasma concentrations of nitrite and nitrate (NO2- + NO3-), the stable end products of NO. oxidation, increased from a basal concentration of 21.0 +/- 2.5 to 2439.6 +/- 364.2 microM 3 days after injection. Urinary excretion of NO2- + NO3- also increased in a parallel manner. Plasma liver injury enzymes were elevated three to sixfold in vivo at 3 to 5 days following C. parvum and coincided with the period of maximal NO production. The results show that NO. is produced directly by hepatocytes in vivo during hepatic inflammation and suggest a role for NO. in mediating the hepatic response to inflammatory stimuli.

Amino Acid Oxidoreductases↗
PubMed1993

Evidence for early Th 2 T cell predominance in xenoreactivity.

Two distinct subsets of CD4+ Th lymphocytes have been characterized by their cytokine profiles: Th 1 (TH1) and Th 2 (TH2). While TH1 cells predominate in cell-mediated responses, TH2 cells support the humoral response. We have examined the mRNA cytokine profile of normal mouse lymphocytes in response to alloantigen versus xenoantigen (rat) in MLC, and present evidence to suggest that early in proliferative responses, alloreactivity is dominated primarily by TH1-type lymphocytes, while xenoreactivity is predominantly TH2. Normal mouse lymphocyte-responding cells were cultured in a one-way MLR with either allo or xeno antigen and examined for production of mRNA for cytokines characteristically produced by TH1 (IL-2, IFN-gamma) or TH2 (IL-4, IL-10) cells. Semiquantitative reverse transcription-polymerase chain reaction analysis was performed for mouse IL-2, IL-4, IL-10, and IFN-gamma mRNA. In the mouse anti-rat xeno response, mRNA for TH2 gene products were upregulated, with greater levels of IL-4 and IL-10 at 24 and 48 hr when compared with controls. In contrast, upregulation of mRNA for TH1 gene products occurred in the mouse anti-mouse allo response, with higher levels of IL-2 and IFN-gamma at 24 and 48 hr. In the anti-xeno response, upregulation of all 4 cytokines occurred by day 4 and peak levels of mRNA for all cytokines examined were 2-3 times that seen for the peak anti-allogeneic response. These data suggest that early xenorecognition may differ from allorecognition by differential activation of the TH2 subset. A better understanding of the balance between Th subset function and cytokine profile in allo and xeno reactivity may allow a more targeted and specific approach to control the early events in xenograft rejection.

Animals↗
PubMed1993

A dual mechanism of immunosuppression by FK-506. Differential suppression of IL-4 and IL-10 levels in T helper 2 cells.

FK-506 is known to suppress the transcription of several genes encoding cytokines (e.g., IL-2, IFN-gamma) thought to play an important role in the allograft response. This general inhibition of cytokine gene transcription and protein production was previously thought to be the main mechanism by which FK-506 suppressed the immune response. We have studied the pattern of cytokine suppression caused by FK-506 in differentiated murine Th 2 cell lines. Supernatants from Th2 cells treated with FK-506 showed marked suppression of IL-4 but only moderate suppression of IL-10 levels. To determine whether this differential effect on IL-4 and IL-10 could also be seen at the mRNA level, total cellular RNA was isolated from cells treated with (1) media, (2) Con A (2 micrograms/ml), (3) FK-506 (50 ng/ml), or (4) Con A + FK-506. Reverse transcription-polymerase chain reaction and northern blot analysis were used to measure IL-4 and IL-10 mRNA. Similar to results at the protein level, FK-506 suppressed steady state levels of IL-4 mRNA markedly but had a lesser effect on steady state levels of IL-10 mRNA. Furthermore, FK-506 completely abrogated Con A-induced upregulation of IL-4 mRNA, but only slightly suppressed Con A-induced upregulation of IL-10 mRNA. IL-10 (cytokine synthesis inhibitory factor) is a cytokine with immunosuppressive properties that itself inhibits the production of IL-2 and IFN-gamma murine helper cells. IL-10 also downregulates MHC II expression and antigen presentation by monocytes. Therefore, the ability of FK-506 to differentially suppress the mRNA levels of immunostimulatory cytokines such as IL-2, IL-4, and IFN-gamma more than the mRNA levels of the immunosuppressive cytokine IL-10 suggests that the effective immunosuppression seen in vivo with FK-506 may be a combination of these 2 effects.

Animals↗
PubMed1993

Cytokine induction of interferon regulatory factor-1 in hepatocytes.

BACKGROUND: Interferon regulatory factor-1 (IRF-1) is a transcriptional factor originally cloned from fibroblasts that activates interferons and certain interferon-responsive genes. Because IRF-1 is an "early-immediate" nuclear protein, it can function acutely after trauma or septic stimuli. We have identified IRF-1 expression in hepatocytes in vivo in sepsis. The purpose of this study was to characterize the cytokine signals that up-regulate IRF-1 messenger RNA (mRNA) in cultured hepatocytes. METHODS: Rat hepatocytes were isolated by in situ collagenase perfusion and stimulated in vitro with cytokines. IRF-1 mRNA levels were determined by Northern blot hybridization with a DNA probe for hepatocyte IRF-1 generated with reverse transcription polymerase chain reaction with custom-designed oligonucleotide primers based on the known sequence for T-cell IRF-1. RESULTS: Northern blot of hepatocyte RNA showed a single IRF-1 mRNA band at approximately 2.4 Kb. The mRNA levels were markedly up-regulated (vs control hepatocytes) 2 hours after in vitro stimulation with the cytokines interferon-gamma (17-fold), tumor necrosis factor-alpha (3-fold), and interleukin-1 beta (2-fold). Lipopolysaccharide had no direct effect. CONCLUSIONS: The results showed that IRF-1 is up-regulated in hepatocytes primarily in response to interferon-gamma and to a lesser extent after tumor necrosis factor-alpha or interleukin-1 beta stimulation. This suggests that IRF-1 plays a role in regulating liver gene expression in sepsis; however, the specific genes controlled by IRF-1 remain to be determined.

Animals↗
PubMed1993

[The effect of streptomycin on energy metabolism in inner ear tissues in guinea pigs].

Fifty-four guinea pigs were divided into three groups. Group I was injected with streptomycin sulfate 200 mg/kg body wt.ip. for 8 days; group II was injected with streptomycin sulfate 200 mg/kg body wt. and Chinese angelica 2 ml/kg body wt. ip. for 8 days; group III, serving as control, was injected with corresponding volume of water for injection. Glucose and pyruvate levels were determined chemically, ATP, ADP and AMP were determined by HPLC. The hearing reflex thresholds were measured before injection of drug and sacrifice. The glucose content in inner ear tissues of group I and II was found to be lower than that of the control. The pyruvate content in group I and II was higher than that of the control. The ratio of pyruvate to glucose in the group I and II was significantly higher than that of the control, P < 0.05. ATP level in inner ear tissues in group I (50.3 +/- 39.0 micrograms/mg protein) decreased significantly as compared with the control (167.7 +/- 115.4 micrograms/mg protein), P < 0.05, but not in group II (151.6 +/- 124.3 micrograms/mg protein). The energy change in each group was in the range of 0.80-0.84. The hearing reflex threshold attenuation in group I 8 days after injection of drug was slightly lower than that prior to the injection of the drug. The results suggest that streptomycin might inhibit the uptake and metabolism of glucose and decrease the ATP level in the inner ear tissues, and that the inner ear tissues accelerate the metabolism of amino-acids for compensation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

Plasma endothelin levels in cirrhotic patients and their correlation with atrial natriuretic peptide.

Plasma levels of endothelin (ET) were determined by radioimmunoassay in 11 healthy volunteers and 34 patients with liver cirrhosis. The results revealed that mean ET plasma level was significantly lower in 34 cirrhotic patients than in normal subjects (40.21 +/- 4.38 ng/L vs 84.55 +/- 7.88 ng/L, P < 0.01). Plasma ET was 32.17 +/- 3.98 ng/L in 23 cirrhosis patients with ascites compared with 57.0 +/- 9.0 ng/L in patients without ascites (P < 0.01). Moreover, it is apparent that plasma levels of ET decreased with the increase of ascites volume, and increased after the disappearance of ascites. But plasma levels of atrial natriuretic peptide (ANP) in cirrhotic patients were markedly higher than those in the controls (830.12 +/- 72.18 ng/L vs 439.45 +/- 50.18 ng/L, P < 0.01). In patients with ascites, ET plasma levels were inversely correlated to ANP. The results suggest that deficiency of circulating ET might be one of the important factors involved in sodium and water retention in cirrhosis.

Adult↗
PubMed1993

[Strategics of medical centers and regional hospitals in response to new labour insurance fee schedule].

The purpose of this paper is to evaluate the medical centers and regional hospitals, strategic response to the implementation of new labour insurance fee schedule. This survey selects fifty-one medical centers and regional hospitals, with the response rate of 92.73%. This questionnaire was developed and evaluated by the authors and mailed to the questionnaire response by hospital's director or relative department director. We have selected Shortell et al. (1985) theory as the framework for evaluating and explaining hospital response to regulation environment (ex: change in the reimbursement system) at institutional-level response (ex: hospital association activity aimed at influencing regulation), managerial-level response (ex: increased physician participation in hospital-wide decision making; starting or expanding a planning department) and technical-level response (ex: shared clinical services such as lab., X-ray, pharmacy). The result found that hospitals with the characteristics as non-public ownership, medical centers, bigger size, and more administrative staff are more inclined to adopt institutional-level response. And a technical-level response occurs to hospital when market competibility becomes more intense which leads to higher reimbursement resource dependency.

Fee Schedules↗