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C W Yang

Publications and source records attributed to C W Yang.

At least 37 records · Page 2Linked to original sources
PubMed2001

Clinical significance of anti-endothelial cell antibody in renal transplant recipients.

In order to evaluate the role of anti-endothelial cell antibody (AECA) in acute rejection in renal transplantation, serum AECA IgG titers were measured in 68 healthy controls, 111 chronic hemodialysis (HD) patients and 58 first renal transplant recipients. The AECA titer in hemodialysis patients was higher than in healthy controls (13.9 +/- 5.0 vs. 4.8 +/- 2.3 U/mL, p < 0.01). In transplant recipients, AECA titers were not affected by dialysis mode (HD vs. CAPD vs. non-dialysis; 9.6 +/- 7.6 vs. 7.9 +/- 3.9 vs. 11.9 +/- 3.1 U/mL, p > 0.05). After renal transplantation, AECA titer was decreased significantly (vs. 4.7 +/- 3.6 U/mL. p < 0.01). The serum AECA IgG titers increased significantly in recipients with acute rejection (6.9 +/- 3.1 vs. 13.5 +/- 9.9 U/mL, p < 0.01), but decreased to 5.6 +/- 3.0 U/mL (p < 0.01) after formal rejection therapy. In the recipients with acute rejection (n = 27), the pre-renal transplant AECA titer was higher than in that without acute rejection (14.0 +/- 8.6 vs. 7.7 +/- 3.8 U/mL, p < 0.01). The results of this study lead us to conclude that pre- and post-renal transplant AECA titer might be a useful predictor for acute rejection and useful for monitoring acute rejection in renal transplant recipients.

Adult↗
PubMed2000

Cyclosporine stimulates Na+-K+-Cl- cotransport activity in cultured mouse medullary thick ascending limb cells.

BACKGROUND: Cyclosporine (CsA) has been shown to alter the activity of plasma membrane transporters in kidney epithelial cells. In this study, we have investigated the effects of CsA on Na+,K+-ATPase and Na+-K+-Cl- cotransport activities in cultured cells derived from microdissected mouse medullary thick ascending limb (mTAL) cells. METHODS: Experiments were carried out on subcultured confluent mouse TAL cells. Reverse transcription-polymerase chain reaction experiments showed that they expressed the mNKCC2 electroneutral Na+-K+-Cl- cotransporter and ROM-K1 and ROMK2 potassium channel mRNA. Western blotting also revealed the presence of the 40 kD ROMK protein using an anti-ROMK antibody. The effect of CsA (100 ng/mL) on ion transport was assessed by measuring the influx and efflux of rubidium (86Rb+) and 36Cl-, used as tracers of K+ and Cl- movements, on cells grown on Petri dishes or permeable filters. RESULTS: CsA inhibited by 38% the ouabain-sensitive component of 86Rb+ influx mediated by the Na+,K+-ATPase pumps. CsA also increased by 38% the ouabain-resistant furosemide-sensitive component (Or-Fs) of 86Rb+ influx, reflecting the Na+-K+-Cl- cotransport activity and stimulated the basolateral efflux of 36Cl- from mTAL cells grown on filters. The CsA-stimulated basal efflux of Cl- was prevented by the basal addition of the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino) benzoate (NPPB, 10-4 mol/L). Apical addition of the K+ channel blocking agent Ba2+ (10-4 mol/L) partially prevented the CsA-stimulated basal efflux of Cl-. Adding Ba2+ to the luminal side of cells grown on Petri dishes also prevented the rise in apical 86Rb+ efflux and the increased Or-Fs component of 86Rb+ influx caused by CsA. CONCLUSION: These results indicated that CsA may stimulate the Na+-K+-Cl- cotransport activity and also suggested that this immunosuppressive agent may interfere in the recycling of apical K+ in this model of cultured mouse TAL cells.

Animals↗
PubMed2000

Intestinal protein loss in patients with haemorrhagic fever with renal syndrome.

BACKGROUND: In haemorrhagic fever with renal syndrome (HFRS) vascular dysfunction has been observed in various organs, but the involvement of the intestine has not yet been reported. This study was performed to evaluate the association of intestinal protein loss in this disease with other clinical parameters reflecting vascular permeability or disease severity. METHODS: Twenty patients with HFRS were included in this study. Intestinal protein loss was measured by (99m)Tc-human serum albumin ((99m)Tc-HSA) scintigraphy in the acute stage, and quantitative analysis of protein loss was measured by the faecal clearance of alpha 1-antitrypsin (C(AT)) in the acute and the recovery stages. C(AT) was then compared with clinical parameters reflecting disease activity and vascular permeability. RESULTS: (99m)Tc-HSA scintigraphy was positive in 13 (65%) patients, and C(AT) in the acute stage was significantly increased as compared with C(AT) in the recovery stage (40.5+/-24.1 vs 9.2+/-4.2 ml/day, P<0.001). C(AT) was associated with serum albumin levels, frequency of hypotensive episodes, severity of acute renal failure, and degree of thrombocytopenia. CONCLUSIONS: Our data suggest that the increased vascular permeability of HFRS is associated with the increased intestinal loss of plasma proteins, which might represent one of the parameters of disease severity in HFRS.

Adult↗
PubMed2000

A case of Goodpasture's syndrome with massive pulmonary hemorrhage.

We present a typical case of Goodpasture's syndrome with massive pulmonary hemorrhage and acute deterioration of renal function. A 20-year-old male was admitted due to severe azotemia (blood urea nitrogen 214.7 mg/dL, serum creatinine 30.2 mg/dL) and was treated with emergency hemodialysis. On the 4th hospital day, a sudden onset of pulmonary hemorrhage developed. The circulating level of anti-glomerular basement membrane antibody was then elevated highly, and the kidney biopsy showed crescentic glomerulonephritis and linear deposition of IgG along the glomerular capillary. The patient was treated with intravenous high dose-steroid, oral cyclophosphamide and plasma exchanges. The pulmonary hemorrhage improved with the therapy, however, his renal function did not improve. He is currently on a regular schedule of hemodialysis.

Adult↗
PubMed2000

Comparison of acquired cystic kidney disease between hemodialysis and continuous ambulatory peritoneal dialysis.

OBJECTIVES: ACKD has been described mainly in patients treated with hemodialysis(HD), and there are only a few reports about the prevalence of ACKD in continuous ambulatory peritoneal dialysis (CAPD) patients. Therefore, we compared the prevalence of ACKD in patients receiving HD and CAPD, and evaluated the possible factors which may affect the development of ACKD. METHODS: Forty nine HD and 49 CAPD patients who had received dialysis therapy for at least 12 months were enrolled in this cross-sectional study. Patients who had a past history of polycystic kidney disease and had acquired cystic kidney disease on predialysis sonographic exam were excluded. Detection of ACKD was made by ultrasonography and ACKD was defined as 3 or more cysts in each kidney. RESULTS: The prevalence of ACKD was about 31% (30/98) and there was no significant difference between HD and CAPD patients(27% vs. 34%, p > 0.05). The prevalence of ACKD was not associated with age, sex, primary renal disease, the levels of hemoglobin, BUN, and serum creatinine. However, the duration of dialysis was significantly related to the development of ACKD (presence of ACKD, 74.4 +/- 42.4 months vs. absence of ACKD, 37.8 +/- 24.1 months, p < 0.05). CONCLUSION: The prevalence of ACKD is not different according to the mode of dialysis, and the major determinant of acquired cyst formation is duration of dialysis.

Adolescent↗
PubMed2000

Total creatinine appearance as indicator of risk of infectious complication in peritoneal dialysis.

Peritonitis and exit-site infections are the main causes of complications in peritoneal dialysis. Death due to infectious complication is also one of the major causes of drop-out. The underlying cause of infection may include malnutrition. Total creatinine appearance (TCA) may reflect overall nutritional status. We determined TCA from the daily dialysate, urine, and estimated gut creatinine of patients and normalized it to actual body weight (nTCA). We examined the relationship between nTCA and the incidence of infection, and between nTCA and infection-related survival. The study included 323 adult patients in a single dialysis center. The mean nTCA of all patients was 19.73 +/- 4.75 mg/kg/day. The patients with an nTCA below 1 standard deviation from the mean (nTCA < 14.98 mg/kg/day) had a significantly higher peritonitis and exit-site infection rate (p < 0.01) and a higher chance of drop-out owing to infection-related complications (p < 0.0001). Our study concluded that the adult patient with malnutrition (nTCA < 14.98 mg/kg/day) has higher risk of infection.

Bacterial Infections↗
PubMed1999

The possible role of c-fos protein in hypothalamus in sleep disturbance in chronic uremic rats.

Sleep disturbance is very common in patients with chronic renal failure, but its mechanism is not clear. The activity of c-fos protein (FOS) in ventrolateral preoptic neurons (VLPO) is associated with the sleep pattern. The purpose of this study was to evaluate the relationship between sleep disturbance and the expression of FOS in VLPO of chronic uremic rats. Chronic uremia was induced by the 5/6 nephrectomized model. The movements of the rats were measured with infrared monitoring during the daytime (8.00-20.00) and nighttime (20.00-8.00). Rats were killed at 10.00 or 16.00 h for the daytime (uremic rats 7, control 8) and at 22.00 h for the nighttime (uremic rats 7, control 9). The expression of FOS in VLPO was examined with the immunohistochemical method. The number of recorded daytime movements in uremic rats was significantly higher than in control rats (458 +/- 185 vs. 222 +/- 41, p < 0.001), but the number of recorded nighttime movements in uremic rats was lower than in control rats (949 +/- 430 vs. 1,618 +/- 261, p < 0.001). In the daytime, the number of FOS immunoreactive cells in uremic rats was lower than in control rats (18.4 +/- 5.3 vs. 42.8 +/- 6.3, p < 0. 001), but there was no difference between two groups in the nighttime (10.8 +/- 8.4 vs. 12.5 +/- 5.1, p = 0.62). There was a strong negative correlation between the number of recorded movements and the number of FOS immunoreactive cells in VLPO (r = -0.700, p < 0.001). This finding suggests that sleep disturbances in chronic uremic rats might be related to the decreased expression of FOS in VLPO.

Animals↗
PubMed1998

Local vaginal anesthesia during high-dose-rate intracavitary brachytherapy for cervical cancer.

PURPOSE: To evaluate the clinical efficacy of local vaginal lidocaine application for pain relief during high-dose-rate (HDR) intracavitary brachytherapy for patients with cervical cancer, and to investigate sequential changes in serum levels of lidocaine during the procedures. METHODS AND MATERIALS: This prospective study was designed to examine the analgesic effect, physical response, and side effects of local anesthesia during HDR intracavitary brachytherapy. Forty patients were enrolled. All patients received 10-15 MV X-rays to the pelvis with a total dose of 45-59.4 Gy 5-6 weeks before undergoing HDR intracavitary brachytherapy. All patients underwent first intracavitary brachytherapy under general anesthesia. These patients were randomly allocated to receive one of two different treatment protocols as follows: (1) treatment session - control session - treatment session - control session; or (2) control session - treatment session- control session - treatment session. In the treatment sessions, topical anesthesia was administered using 4 ml of 10% lidocaine solution sprayed liberally on the cervix and vagina during intracavitary brachytherapy. In the control sessions, a placebo was administered in the same manner during brachytherapy. The Hensche's applicators for brachytherapy were inserted into the cervix and vagina 5 min after lidocaine application. The visual analogue scale (VAS) was used to assess pain and discomfort during brachytherapy. Blood pressure and heart rates were measured to evaluate the physiological response. Another prospective study was then performed to investigate the sequential changes of serum lidocaine levels during the anesthetic procedure. Eleven additional patients with similar disease state and demographic characteristics were enrolled and blood samples were obtained before, and 5, 15, 30, and 45 min after the initiation of lidocaine application. RESULTS: The mean VAS values recorded during the treatment sessions and control sessions were 49.9 +/- 24.1 versus 60.1 +/- 24.8, respectively. The value of VAS in the treatment session was significantly lower than that of the control session (p < 0.001). No statistically significant differences were found in the changes of blood pressure and heart rate and in the incidence of side effects during these two types of sessions (p > 0.05). In the drug-level study, serum levels of lidocaine reached a peak 5 min after the initiation of local anesthesia. The mean peak concentrations (Cmax) of lidocaine were 0.50 +/- 0.45 microg/ml. CONCLUSION: Local vaginal anesthesia with 10% lidocaine solution can significantly decrease the degree of painful sensation during HDR intracavitary brachytherapy, and is safe to administer for the procedure for cervical cancer.

Anesthesia, Local↗
PubMed1998

Aminoguanidine reduces glomerular inducible nitric oxide synthase (iNOS) and transforming growth factor-beta 1 (TGF-beta1) mRNA expression and diminishes glomerulosclerosis in NZB/W F1 mice.

Over-expression of iNOS is implicated in the pathogenesis of glomerulonephritis in animal models of systemic lupus erythematosus. The aim of this study was to evaluate the effect of aminoguanidine, a selective inhibitor of iNOS, for the protection from glomerulosclerosis in NZB/W F1 mice. Female NZB/W F1 mice (n = 8) were treated with aminoguanidine (1 g/l) in drinking water for 4 months starting at age 2 months before the onset of glomerulonephritis. Controls were age- and sex-matched mice (n = 10) without aminoguanidine treatment. By glomerular microdissection and reverse-transcription competitive polymerase chain reaction, we found that glomerular iNOS/beta-actin and TGF-beta1/beta-actin mRNA ratios were reduced 15.1% (P<0.05) and 61.3% (P<0.01), respectively, in aminoguanidine-treated mice. Aminoguanidine significantly reduced the glomerular iNOS staining, urinary nitrite production and degree of glomerulosclerosis. In addition, the glomerular volume and mean glomerular cell number were reduced 33.2% (P<0.01) and 32.8% (P<0.01), respectively. Likewise, the urinary proteinuria was also significantly reduced by aminoguanidine. These results indicate that administration of aminoguanidine may reduce the progression of glomerulosclerosis in NZB/W F1 mice, possibly through inhibition of glomerular nitric oxide production.

Animals↗
PubMed1998

Trimethyltin stimulates protein kinase C translocation through receptor-mediated phospholipase C activation in PC12 cells.

Trimethyltin (TMT) is a potent neurotoxic compound that initiates a delayed neuronal cell death. Previously we have shown that TMT-induced cytotoxicity is associated with protein kinase C (PKC) translocation and activation. The present study investigates the mechanism underlying TMT-stimulated PKC translocation in PC12 cells. TMT exposure led to a rapid increase in intracellular levels of inositol 1,4,5-trisphosphate (IP3), a product of phospholipase C (PLC). This was significantly decreased by pretreating cells with antagonists to either the cholinergic muscarinic receptor (atropine) or the glutamatergic metabotropic receptor [(+)-alpha-methyl-4-carboxyphenylglycine; (+)-MCPG]. Furthermore, the rise in IP3 level was blocked by pretreating cells with a PLC inhibitor (U-73122) or by a combination of atropine and (+)-MCPG. This pretreatment also significantly decreased TMT-stimulated PKC translocation, indicating that TMT-mediated PKC translocation was related to PLC activation, presumably through formation of diacylglycerol, an endogenous activator of PKC and product of PLC. It is interesting that atropine and (+)-MCPG did not provide protection against TMT-induced cytotoxicity in these cells. However, these data suggest that TMT causes the release of cellular constituents that activate G protein-coupled receptors, ultimately leading to PKC translocation.

Animals↗