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Biomedical subjects

C W Yang

Publications and source records attributed to C W Yang.

At least 55 records · Page 3Linked to original sources
PubMed1998

Cyclosporin inhibits nitric oxide production in medullary ascending limb cultured cells.

BACKGROUND: Nitric oxide (NO) has been shown to play a role in cyclosporin (CsA) nephrotoxicity, but its mechanism of action is still unclear. As inducible NO synthase (iNOS) mRNA has been found to be expressed in rat medullary thick ascending limb (mTAL) cells, we investigated the effects of CsA on NO production in a model of mouse cultured mTAL cells. MATERIALS AND METHODS: The experiments were carried out on sub-cultured cells derived from isolated mTAL microdissected from the kidney of C57BL/6 mice. The identification of the iNOS mRNA in mTAL microdissected segment and cultured cell was confirmed by RT PCR and RsaI digestion. Nitrite (NO2) released by mTAL cells was determined using the modified Griess reagent method and taken as an index of nitric oxide production. The cultured cells were treated with various concentrations of CsA and different signal transduction regulators to assess the effect and possible pathway(s) of action of CsA on NO production in mTAL cells. RESULTS: The basal production of NO by mTAL cells increased by 1.8-fold following incubation with bacterial lipopolysaccaride (LPS). Both aminoguanidine and L-NAME inhibited NO production. CsA (10-300 ng/ml) also inhibited NO production in a dose-dependent manner and prevented its increase induced by LPS. Phorbol 12-myristate 13-acetate (PMA), a PKC stimulator, enhanced slightly the production of NO under basal conditions and prevented the inhibitory action of CsA on NO production. These results suggest that the NO secreted by mouse cultured mTAL cells is dependent on the PKC pathway. CONCLUSION: These results show that CsA may down-regulate the production of NO by cultured mTAL cells expressing iNOS mRNA and that the PKC pathway is involved in this process.

Animals↗
PubMed1998

Clinical course of cytomegalovirus (CMV) viremia with and without ganciclovir treatment in CMV-seropositive kidney transplant recipients. Longitudinal follow-up of CMV pp65 antigenemia assay.

This study was designed to evaluate the longitudinal history of cytomegalovirus (CMV) infection and to test the capacity of ganciclovir as effective therapy in CMV-seropositive renal transplant recipients. The CMV viremia was detected with CMV pp65 antigenemia assay in 153 renal transplants. The recipients were classified as having low-grade and high-grade CMV infections according to the severity of CMV infection. The recipients with low-grade CMV infections were observed without ganciclovir treatment, and the recipients with high-grade CMV infection were randomly assigned to ganciclovir-treated and untreated groups. The clinical course between low-grade and high-grade CMV infections was evaluated. All recipients with low-grade CMV infection (n = 62) showed spontaneous remission regardless of immunosuppresants. In high-grade CMV infection (n = 31), the ciclosporin A treated group (n = 11) showed no evidence of CMV disease, and the methylprednisolone-treated group (n = 8) showed CMV disease in 1 (25%) of 4 ganciclovir-untreated recipients. In the OKT3 group (n = 12), symptomatic CMV infection was observed in 6 (100%) ganciclovir-untreated recipients contrary to no CMV disease in the ganciclovir-treated group (p < 0.05). In conclusion, the CMV antigenemia assay is effective in monitoring CMV viremia, and ganciclovir treatment should be done during early CMV viremia in OKT3-treated recipients.

Adult↗
PubMed1998

Inhibition of calbindin D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria.

A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting.

Animals↗
PubMed1997

An image capture and communication system for emergency computed tomography.

An image capture and communication system for emergency computed tomography (CT) is presented. The system, named ICCS, integrates CT scanners, personal computers (PC), network systems, an IBM API gateway and an IBM mainframe platform. The ICCS was implemented in the emergency unit in the Taichung Veterans General Hospital (TCVGH) and has received considerable support from the doctors, nurses and staff of the TCVGH emergency unit who have shown great interest in ICCS. This is because ICCS allows physicians in the emergency unit to examine patients' images on image viewing stations immediately after the patients are CT scanned. It also makes remote consultation possible for doctors who can stay where they are and consult with radiologists through the system and a hot line without leaving the emergency unit. This advantage greatly reduces the consultation time and saves many unnecessary trips between the emergency unit and the Department of Radiology.

Emergency Service, Hospital↗
PubMed1997

Leptospirosis: an ignored cause of acute renal failure in Taiwan.

Leptospirosis, caused by a spirochete, is the most common zoonosis in domestic or wild animals. Animals excrete infected urine in soil or water and may cause human infections through abrased wound, mucosa, conjunctiva, or by swallowing contaminated water. Clinical presentations of leptospirosis are mostly subclinical. Five to ten percent of leptospirosis are fatal, causing fever, hemorrhage, jaundice, and acute renal failure (Weil's syndrome). Leptospirosis has been ignored as a cause of acute renal failure in Taiwan. We report two patients with leptospirosis who presented with high fever, abdominal pain, jaundice, and acute renal failure. Patient 1 died on day 12 of admission of multiple organ failure associated with pancytopenia, hypogammaglobulinemia, and reactive hemophagocytosis. Leptospirosis was recognized after death. Patient 2 was admitted with similar presentations 2 weeks later. Penicillin and doxycycline were given early in the course, and azotemia, jaundice, respiratory failure, and aseptic meningitis gradually improved. Renal biopsy showed interstitial nephritis. Several tubular clearance tests showed proximal tubular defect with severe bicarbonate wasting (FeHCO3- 20.9%) and incomplete type II renal tubular acidosis without affecting the distal nephron. After 80 days of treatment, this patient was discharged with recovery of conscious level and renal function. This is the first leptospirosis patient with detailed tubular functional and morphological studies of the kidney. Diagnosis of leptospirosis was made by microscopic agglutination test (MAT) for antibody to leptospira and by polymerase chain reaction (PCR) for leptospira DNA in blood and urine (interrogans serogroup australis in case 1 and Leptospira borgpetersenii serogroup ballum in case 2). Because active surveillance has resulted in 13 cases diagnosed as leptospirosis islandwide thereafter, underestimation and ignorance of leptospirosis as a cause of acute renal failure may occur in Taiwan. Therefore, an area with a low leptospirosis incidence may actually have a very high incidence. Leptospirosis should be suspected in febrile patients with jaundice and renal failure when pathogens cannot be identified by traditional culture for microorganisms.

Abdominal Pain↗
PubMed1997

Poor pre-dialysis glycaemic control is a predictor of mortality in type II diabetic patients on maintenance haemodialysis.

BACKGROUND: In type II diabetic patients, a better glycaemic control has been reported to slow down the progression of nephropathy. The effect of pre-dialysis glycaemic control on the long term prognosis in type II diabetics on haemodialysis is still uncertain. The purpose of this study is to evaluate the effect of glycaemic control before starting maintenance haemodialysis on the clinical outcome in type II diabetic haemodialysis patients. METHODS: One hundred and thirty-seven type II diabetics receiving regular haemodialysis in a single university hospital were enrolled. The patients were classified as either good or poor glycaemic control group according to their glycaemic control within 6 months before starting haemodialysis. Serum albumin, haematocrit, cholesterol, triglyceride, residual renal function, diabetic complications, and patient survival were analysed in both groups. RESULTS: There was no significant difference in age, gender, predialysis albumin level, cholesterol level, triglyceride level, and residual renal function between the two groups. The 1-year (94.5% vs 80.0%), 3-year (82.9% vs 58.1%), and 5-year (75.8% vs 21.8%) cumulative survival rates were lower in the poor glycaemic control group than in the good glycaemic control group (P < 0.001). The poor glycaemic control group also had more cardiovascular morbidity during the period of dialysis (P < 0.001). The increase in cardiovascular complications also accounted for the increased mortality during the course of haemodialysis. CONCLUSIONS: We conclude that poor glycaemic control before starting dialysis is a strong predictor of cardiovascular morbidity and survival for type II diabetics on haemodialysis. These results imply that better glycaemic control before dialysis might be important in improving the long-term prognosis in type II diabetics on haemodialysis.

Aged↗
PubMed1997

Evaluation of acute renal failure in bacterial allograft pyelonephritis using abdominal CT and graft biopsy.

The causes of acute renal failure in bacterial allograft pyelonephritis were evaluated using abdominal CT and graft biopsy. Twenty-one recipients, who showed a poor response to antibiotic therapy, comprised this study group. The diagnostic approach taken with this poor responder group was first to perform abdominal CT. If a focal lesion was identified on abdominal CT, a diagnosis of acute focal bacterial nephritis or renal abscess was made. If no focal lesion was found, a graft biopsy was performed for diagnosis. Abdominal CT revealed focal lesions in 9 of the 21 recipients, and renal biopsy showed superimposed acute rejection in 8 of the 12 recipients biopsied. In conclusion, acute renal failure in allograft pyelonephritis is associated with not only severe infection but also a superimposed acute rejection process. Therefore, imaging study and graft biopsy are recommended in the poor responder group.

Acute Kidney Injury↗
PubMed1997

Inhibition of cellular proliferation by cyclosporin A during compensatory renal growth: flow cytometric analysis.

Cell cycle analysis using flow cytometer (FCMX) was performed to evaluate the influence of cyclosporin A (CsA) on cellular proliferation during compensatory renal growth (CRG) in uninephrectomized (Ux) rats. CsA (50 mg/kg/day) was administered subcutaneously for 7 days and animals were scarificed 0, 12, 24, 48, 72, 120 and 168 h after Ux. The percent changes in the S (DNA synthesis) and G2M (DNA replication) phases in the contralateral kidney were analyzed. The cortical cells entering the S and G2M phases showed significant differences between CsA and vehicle groups (p = 0.0001, p = 0.001, respectively), but the medullary cells entering the S and G2M phases showed no significant differences between the 2 groups (p = 1.000, respectively). In the cortex, the CsA group showed a significant decrease in the S (at 12, 72 and 120 h) and G2M phases (at 24, 72 and 120 h) compared to the vehicle group (p < 0.05, respectively), but there was no significant difference in the medulla. In conclusion, cellular proliferation is suppressed in cortical cells by CsA.

Animals↗
PubMed1997

Glomerular transforming growth factor-beta1 mRNA as a marker of glomerulosclerosis-application in renal biopsies.

As transforming growth factor-beta1 (TGF-beta1) is implicated in the pathogenesis of glomerulosclerosis, the aim of the study was to demonstrate if levels of glomerular TGF-beta1 mRNA in renal biopsies correlated with glomerulosclerosis. Glomeruli were collected by microdissection from renal biopsies in patients with membranous nephropathy, lupus nephritis, diabetic nephropathy, minimal change disease and IgA nephropathy presented by proteinuria when serum creatinine was <3 mg%. Glomerular mRNAs were reverse transcribed and TGF-beta1, alpha2(IV) collagen, beta-actin cDNA quantitated by competitive polymerase chain reaction (PCR). By semiquantitative electron microscopy, a 3.5-fold increase of glomerular TGF-beta1/beta-actin mRNA ratio in the moderate sclerotic group (n = 23, p < 0.01) and a 1.5-fold increase in the mild sclerotic group (n = 22, p < 0.05) were observed when compared to the minimal sclerotic group (n = 12). A concordant increase of glomerular alpha2(IV) collagen mRNA was found with 2.2- and 1.3-fold in moderate and mild sclerotic groups, respectively. The TGF-beta1/beta-actin mRNA ratios were highest in membranous nephropathy (466.4 +/- 133.4, n = 11), followed by lupus nephritis (394.9 +/- 94.8, n = 12) and diabetic nephropathy (333.2 +/- 97.6, n = 10). Patients with minimal change disease(233.1 +/- 54.1, n = 15)and IgA nephropathy(185.3 +/- 39.6, n = 9) had low levels. The degree of glomerulosclerosis in each group followed the TGF-beta1/beta-actin mRNA ratios indicating that the level is the major determinant ofglomerulosclerosis but not the disease entities. Glomerular TGF-beta1/beta-actin mRNA ratio did not correlate with clinical parameters such as the urinary protein excretion and creatinine clearance. These results suggest that glomerular TGF-beta1/beta-actin mRNA ratio may be used as a marker of glomerulosclerosis in renal biopsy to reflect the local sclerotic process.

Actins↗
PubMed1997

Acute myopathy induced by colchicine in a cyclosporine-treated renal transplant recipient--a case report and review of the literature.

We report a case of colchicine-induced myopathy related to short-term, customary administration of colchicine. A 49-year-old male was admitted because of muscle weakness and myalgia that had developed 10 days previously. He had received renal transplantation 5 years previously and took cyclosporine as an immunosuppressant. Two weeks before admission, gout was developed and he took colchicine (1.2 mg b.i.d) by himself for three days. Colchicine-induced myopathy was clinically suspected, and colchicine intake was stopped immediately. After that, clinical symptoms gradually improved and serum muscle enzyme returned to normal. In this case, mild renal dysfunction and drug interaction between cyclosporine and colchicine wee suggested to be the precipitating factors of colchicine-induced myopathy.

Colchicine↗
PubMed1997

Serum and urine soluble HLA class I antigen concentrations are increased in patients with hemorrhagic fever with renal syndrome.

OBJECTIVES: In order to evaluate the association between the Hantaan virus-induced cellular-immune response and clinical severity in patients with hemorrhagic fever with renal syndrome (HFRS). METHODS: We serially measured the serum (n = 16) and urine (n = 6) concentrations of soluble HLA class 1 antigen (sHLA-l) and clinical powameters in patients with HFRS. RESULTS: Serum sHLA-I concentrations in patients with HFRS were significantly higher than those in controls throughout all clinical phases (p < 0.01). The highly elevated Serum sHLA-I concentrations peaked in the oliguric phase and declined gradually through the phases of HFRS. Serum sHLA-l concentrations in patients with hypotensive episode were higher than in those without the episode (5,85 +/-2,184 vs. 2,389 +/- 860 ng/ml in oliguric phase, 4.11 +/- 1,952 vs. 1,502 +/- 592 ng/ml in diuretic phase, p < 0.05), and serum sHLA-l levels showed a significant correlation with blood WBC count (r = 0.75 in the febrile and hypotensive phase, p < 0.01) and serum creatinine concentrations (r = 0.64 in the oliguric phase, p < 0.01), respectively, Urine sHLA-I levels in the oliguric phase were significantly higher than those in the diuretic phase (390 +/- 155 vs. 214 +/- 45 ng/mg Cr, p < 0.05) and urine sHLA-I levels are associated with severe illness in patients with HFRS. The higher serum sHLA-I are associated with severe illness in patients with HFRS. The persistent elevation of serum sHLA-I during all phases of HFRS might be related to increased production due to prolonged cellular immunologic stimulation by the Hantaan virus rather than decreased excretion of sHLA-I through the kidney. CONCLUSION: We suggest that the serum and urine sHLA-I concentrations can be used as a stable and objective parameter for monitoring clinical severity and renal dysfunction in patients with HFRS.

Adult↗
PubMed1997

Differential expression of glomerular extracellular matrix and growth factor mRNA in rapid and slowly progressive glomerulosclerosis: studies in mice transgenic for native or mutated growth hormone.

We found that mice transgenic for native bovine growth hormone (bGH) gene had increased body size and rapidly progressive glomerulosclerosis, whereas mice transgenic for a mutated bGH gene (bGH-m11) had near normal body size and slowly progressive glomerulosclerosis. The aim of this study was to determine whether rapidly and slowly progressive glomerulosclerosis had distinct glomerular extracellular matrix (ECM) and growth factor mRNA levels. ECM and growth factors were quantitated by competitive reverse transcriptase-PCR in microdissected glomeruli from bGH, bGH-m11, and nontransgenic littermate control mice. In rapid progressors (bGH mice) at 2 to 3 months, the levels of mRNA-coding for some glomerular ECM and growth factors were increased (alpha 1(IV) collagen, 7.3-fold; laminin B1, 3.9-fold; tenascin, 8-fold; and tumor growth factor (TGF)-beta 1, 3.4-fold). These levels underwent a further 2.3-fold increase at 6 to 9 months. Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). PDGF-B levels were normal. At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. The labeling index and PDGF levels were not increased at any time. The levels of expression of several glomerular ECM mRNA and growth factors of rapid progressors at 2 to 3 months of age was nearly double that of slow progressors, nearly doubling again by 6 to 9 months. In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. Thus, the initial levels of these mRNA and their rate of change correlated with the severity of glomerulosclerosis.

Aging↗
PubMed1996

Thin foil preparation of metal particles in brittle ceramic matrices.

Thin foil preparation for metal particles in brittle ceramic matrices is particularly difficult, due to differential thinning of the component materials. This paper considers the preparation of thin foils of stony meteorites. Stony meteorites have a composite nature consisting of small metal particles (< 200 microns) embedded in an inherently brittle silicate matrix. Specimens of this type are difficult to prepare as thin foils because the area of interest is limited to specific regions within the metal particles. The problems of thin foil preparation of metal particles in the stony meteorites were overcome by developing a technique involving electrochemical polishing prior to ion beam thinning. The metal particles were first separated from the silicate matrix and then embedded in Epo-Tek H20E silver epoxy. This specific epoxy was selected for its good electron conductivity which allowed the specimen to be thinned by the electrochemical polishing technique. Specimens prepared by this technique have permitted the direct observation and characterization of the metallic phases in stony meteorites.

Ceramics↗
PubMed1996

Cyanide-stimulated inositol 1,4,5-trisphosphate formation: an intracellular neurotoxic signaling cascade.

Cyanide-induced neurotoxicity is associated with altered cellular Ca2+ homeostasis resulting in sustained elevation of cytosolic Ca2+. In order to characterize the effect of cyanide on intracellular signaling mechanisms, the interaction of KCN with the inositol 1,4,5-trisphosphate Ca2+ signaling system was determined in the PC12 cell line. KCN in the concentration range of 1.0-100 microM produced a rapid rise in intracellular IP3 levels (peak level occurred within 60 sec); 10 microM KCN elevated intracellular levels of IP3 to 148% of control levels. This response was mediated by phospholipase C (PLC) since U73122, a specific PLC inhibitor, blocked the response. Removal of Ca2+ from the incubation medium and chelation of intracellular Ca2+ with BAPTA partially attenuate the cyanide-stimulated IP3 generation, showing that the response is partially Ca2+ dependent. Also, treatment of cells with nifedipine or LaCl3, Ca2+ channel blockers, partially blocked the generation of IP3. This study shows that cyanide in concentrations as low as 1 microM stimulates IP3 generation that may be mediated by receptor and nonreceptor IP3 production since they have differential dependence on Ca2+. It is proposed that this response is an early intracellular signaling action that can contribute to altered Ca2+ homeostasis characteristic of cyanide neurotoxicity.

Animals↗
PubMed1996

Peritoneal nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis.

Nitric oxide plays an important role in mediating the inflammatory process. The aim of this study was to evaluate if nitric oxide production was increased during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and the association with the prognosis. The study population comprised 21 patients with 22 episodes of peritonitis. Fifteen patients without peritonitis were controls. Nitrate was measured by HPLC and nitrite by the Griess method, to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from six patients during peritonitis and 1 week after treatment to study changes in dialysate:plasma ratio. In 15 patients, nitrite was measured during peritonitis and every 3 days for 2 weeks or until normalized for evolutional changes. The dialysate:plasma ratios of nitrate and nitrite during peritonitis were reduced 26% and 41.5%, respectively, after 1 week of treatment, indicating the peritoneal production of nitric oxide during peritonitis. In the evolutional study, a 5.1-fold increase of peak nitrite levels in bacterial peritonitis (n = 13) and a 2.5-fold increase in fungal peritonitis (n = 3) were observed compared to controls. Nitrite gradually declined to control levels (9.3 +/- 7.2 days) after effective antibiotic treatment, but took longer than to normalize leukocyte count in the peritoneal dialysate effluent (3.9 +/- 1.9 days). In four patients with refractory peritonitis (Candida infection in three, Acinetobacter infection in one), the nitrite levels remained elevated 2-fold despite treatment, and the catheters were removed. It is concluded that nitrite levels in peritoneal dialysate effluent may serve as a marker to assess treatment efficacy in CAPD patients with peritonitis.

Acinetobacter Infections↗
PubMed1996

Chronic granulomatous interstitial nephritis: unusual complication of acute pyelonephritis.

We describe an unusual complication of acute pyelonephritis in a 45-year-old diabetic female. She was admitted to our hospital due to fever and flank pain which had developed 10 days earlier. Urinalysis showed many WBC and urine culture revealed Escherichia coli. After adequate antibiotic treatment, clinical symptoms abated but renal failure and leukocyturia persisted. Abdominal CT showed bilateral focal bacterial nephritis and renal biopsy disclosed chronic granulomatous interstitial nephritis. On the 80th hospital day she was discharged with a serum creatinine of 299 mumol/l. In the outpatient clinic, renal dysfunction and leukocyturia persisted up to 1 year. In conclusion, this case raises the possibility of a chronic interstitial process of acute pyelonephritis.

Acute Disease↗