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Biomedical subjects

M J Wu

Publications and source records attributed to M J Wu.

At least 73 records · Page 4Linked to original sources

Using red blood cell creatine concentration to evaluate the equine erythropoietic response.

Red blood cell creatine concentration was examined to determine its association with the equine erythropoietic response. Studies were conducted on 9 healthy horses, 4 healthy ponies, 24 anemia horses, and 2 horses in which anemia was experimentally induced. A modified Jaffe reaction was used to measure RBC creatine concentration. The mean RBC creatine concentration of the 9 healthy horses was 5.72 +/- 0.42 mg/dl, and that of the 4 healthy ponies was 2.59 +/- 0.31 mg/dl. Density-separation of erythrocytes from the healthy horses revealed significantly higher (P less than 0.001) creatine content (7.72 +/- 0.57 mg/dl) in the young RBC populations than in the old RBC populations (4.03 +/- 0.27 mg/dl). The RBC creatine content was assayed in 19 hot-blooded horses which were anemic due to a variety of causes. Of these anemic horses, 12 with PCV between 25% and 30% had a mean RBC creatine concentration of 6.12 +/- 0.46 mg/dl. The 7 other anemic horses with PCV less than 25% had a mean RBC creatine value of 6.07 +/- 0.12 mg/dl. Bone marrow films were examined from 5 anemic horses and in the 2 horses in which anemia was experimentally induced. The RBC creatine concentration correlated positively (P less than 0.001) with the reticulocyte count in the bone marrow and negatively with the myeloid-erythroid ratio (P less than 0.001).

Anemia↗

Amantadine hydrochloride pharmacokinetics in patients with impaired renal function.

To study the disposition of amantadine hydrochloride in patients with impaired renal function, 100 mg was administered orally to 13 patients with creatinine clearances ranging from 48 to 10 ml/min/1.73 m2 body surface area. Six adults with normal renal function served as controls. Plasma half-life averaged 68.5 +/- 9.5 SEM hours in the renal patients (range: 27 to 144), versus 12.6 +/- 1.7 hours in controls. Plasma half-life correlated significantly with serum creatinine (r = 0.8476, P less than 0.001) and serum urea nitrogen levels (r = 0.8791, P less than o.001). Similarly, plasma elimination constant correlated with creatinine clearance/1.73 m2 body surface area (r = 09201, P less than 0.001). Renal amantadine clearance also correlated with creatinine clearance/1.73 m2 body surface area (r = 0.8217, P less than 0.001). However, renal amantadine clearance regularly exceeded creatinine clearance, suggesting that tubular secretion plays a role in the elimination of this drug. Amantadine excretion is decreased in patients with impaired renal function. The amount by which dosage must be reduced can be estimated based on creatinine clearance.

Adult↗

Renal infarction with Gianturco wool coils. Use in the management of massive proteinuria.

A mechanical device was successfully used in therapeutic renal artery occlusion in a patient with renal amyloidosis and massive proteinuria (25 g/day). The serum albumin level increased from 1.8 to 3.4 g/dL after cessation of proteinuria. There has been no evidence of peripheral embolization, hypertension, or infection of the infarcted kidney for the past 20 months following the procedure.

Aged↗

Amantadine hydrochloride pharmacokinetics in hemodialysis patients.

To study the fate of amantadine hydrochloride in patients with renal failure, we gave 100 mg orally to 12 such patients immediately after hemodialysis. Plasma levels did not decrease between 24 and 44 hours after drug ingestion, suggesting an extremely poor total body clearance. Apparent volume of distribution was 5.1 +/- 0.2 (SEM) L/kg of body weight. Between 44 and 48 hours, as a result of 4 hours of hemodialysis, the mean plasma drug level decreased from 268 to 225 ng/mL (P less than 0.001). Dialyzer clearance was 67.0 +/- 3.9 mL of plasma per minute. The total quantity of drug removed by the dialysis treatment, however, was only 3.9 +/- 0.25 mg. The average half-life of amantadine in eight patients studied while receiving maintenance hemodialysis was 24.3 +/- 2.4 h of dialysis administered over approximately 13 days. Plasma half-life in six nonuremic control subjects was 12.2 +/- 1.6 h. Amantadine is poorly excreted in dialysis patients and has a large volume of distribution. The amount removed by a single dialysis is only a small fraction of the total body store.

Amantadine↗

Vasculitis in Goodpasture's syndrome.

Because of differing diagnostic criteria, a controversy exists as to whether vasculitis may occur in patients with Goodpasture's syndrome. Using strict criteria (pulmonary hemorrhage, glomerulonephritis, and antiglomerular basement membrane antibody), we found histological evidence of vasculitis in two of 18 patients with Goodpasture's syndrome. The vasculitis was found in kidney biopsy specimens. Clinically, these two patients did not differ from other patients who have Goodpasture's syndrome without vasculitis. The presence of vasculitis should not exclude the diagnosis of Goodpasture's syndrome.

Adolescent↗

Relapse in anti glomerular basement membrane antibody mediated crescentic glomerulonephritis.

Patients with crescentic glomerulonephritis and anti glomerular basement membrane antibody typically experience a rapidly progressive course. Remission and relapse in renal disease are unusual. We report two patients with this syndrome who remitted following immunosuppressive therapy and relapsed 20 and 48 months later, respectively. The pathogenesis of relapse is discussed. It is different from the initial insult in that antiglomerular antibody may not be important.

Antibodies↗

Use of pulsed-field gel electrophoresis in the analysis of recurrent Staphylococcus aureus infections in patients on continuous ambulatory peritoneal dialysis.

BACKGROUND/AIM: The purpose of this study was to evaluate pulsed-field gel electrophoresis (PFGE) for distinguishing between relapse and reinfection of Staphylococcus aureus infections in patients on continuous ambulatory peritoneal dialysis (CAPD). METHODS: Between July 1993 and May 1997, 4 patients with recurrent CAPD-associated infections caused by S. aureus we enrolled in this study. There were nine episodes of peritonitis, one episode of temporary double lumen catheter infection, and one episode of Hickman catheter infection. A total of eleven S. aureus isolates were collected from peritoneal fluid (n = 9) and blood (n = 2). PFGE typing was applied. RESULTS: In our study, from PFGE typing, the 11 S. aureus isolates were classified into seven patterns. Antibiogram profiling classified only four patterns. Patient A had a reinfection by another strain of S. aureus, and patient B had three episodes of peritonitis caused by the same strain of S. aureus due to exit site infections. Patient C had two episodes of CAPD peritonitis caused by two different strains, respectively. Patient D had four episodes of S. aureus infection (three CAPD peritonitis and one bacteremia); the first two episodes of peritonitis were caused by an identical strain of S. aureus, whereas the subsequent two infections were caused by other organisms. CONCLUSION: PFGE has a high discriminatory power and can be an assistant method to antibiogram profiling for distinguishing relapse from reinfection in CAPD-associated peritonitis.

Anti-Bacterial Agents↗