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B Leslie

Publications and source records attributed to B Leslie.

14 recordsLinked to original sources
PubMed1992

Nosocomial urinary tract infections at a pediatric hospital.

Although the epidemiology of nosocomial urinary tract infections (NUTIs) is well-described in the adult population, there is little information on children. We therefore reviewed all our patients with NUTIs, to determine their age, underlying diagnoses, microorganisms involved, use of catheters and secondary bacteremias. During a 2-year period at our institution, NUTIs accounted for 10% of all nosocomial infections (0.8 infections/100 admissions). Of 44,948 patients admitted during this period 0.7% (n = 318) acquired 351 episodes of NUTI. The patient ages ranged from 5 days to 21 years. The highest rates of NUTIs per ward (NUTI/100 admissions or transfers to the ward) were seen in the neonatal surgery (4.8), hematology/oncology (2.7), infant neurosurgery (2.1) and neonatal intensive care units (1.9). The most common organisms isolated were Escherichia coli (26%), Enterococcus sp. (15%), Pseudomonas sp. (13%), Klebsiella sp. (10%) and coagulase-negative Staphylococcus (9%). Catheterrelated infections accounted for 48% of all the NUTIs. Secondary bacteremia occurred rarely, with an incidence of 2.9% (n = 7). We conclude that NUTIs represent an important proportion (10%) of nosocomial infections in our population of hospitalized children, but secondary bacteremia is uncommon.

Adolescent↗
PubMed1991

Standard and low molecular weight heparin have no effect on tissue plasminogen activator induced plasma clot lysis or fibrinogenolysis.

Although heparin is often given as an adjunct to tissue plasminogen activator (t-PA), the effect of heparin on t-PA induced fibrin(ogen)olysis is controversial. To address this controversy, we examined the effects of standard and low molecular weight heparin (enoxaparine) on both t-PA induced clot lysis and t-PA mediated fibrinogenolysis in a human plasma system. Accordingly, 125I-labeled fibrin clots were incubated in t-PA containing citrated plasma in the presence or absence of these glycosaminoglycans, and the extent of thrombolysis was determined by measuring residual radioactivity of the clots, while B beta 1-42 levels were used as a specific index of fibrinogenolysis. Over a wide range of t-PA concentrations (0.1 to 1.6 micrograms/ml), neither heparin nor enoxaparine influences either t-PA induced clot lysis or t-PA mediated B beta 1-42 generation. These findings suggest that either agent could be used as an adjunct to t-PA without compromising either the thrombolytic potential of t-PA or its clot-selectivity.

Drug Interactions↗
PubMed1991

Soluble fibrin degradation products potentiate tissue plasminogen activator-induced fibrinogen proteolysis.

Despite its affinity for fibrin, tissue plasminogen activator (t-PA) administration causes systemic fibrinogenolysis. To investigate the mechanism, t-PA was incubated with plasma in the presence or absence of a fibrin clot, and the extent of fibrinogenolysis was determined by measuring B beta 1-42. In the presence of fibrin, there is a 21-fold increase in B beta 1-42 levels. The potentiation of fibrinogenolysis in the presence of fibrin is mediated by soluble fibrin degradation products because (a) the extent of t-PA induced fibrinogenolysis and clot lysis are directly related, (b) once clot lysis has been initiated, fibrinogenolysis continues even after the clot is removed, and (c) lysates of cross-linked fibrin clots potentiate t-PA-mediated fibrinogenolysis. Fibrin degradation products stimulate fibrinogenolysis by binding t-PA and plasminogen because approximately 70% of the labeled material in the clot lysates binds to both t-PA- and plasminogen-Sepharose, and only the bound fractions have potentiating activity. The binding site for t-PA and plasminogen is on the E domain because characterization of the potentiating fragments using gel filtration followed by PAGE and immunoblotting indicates that the major species is (DD)E complex, whereas minor components include high-molecular weight derivatives containing the (DD)E complex and fragment E. In contrast, D-dimer is the predominant species found in the fractions that do not bind to the adsorbants, and it has no potentiating activity. Thus, soluble products of t-PA-induced lysis of cross-linked fibrin potentiate t-PA-mediated fibrinogenolysis by providing a surface for t-PA and plasminogen binding thereby promoting plasmin generation. The occurrence of this phenomenon after therapeutic thrombolysis may explain the limited clot selectivity of t-PA.

Enzyme Activation↗
PubMed1990

Urokinase has direct catalytic activity against fibrinogen and renders it less clottable by thrombin.

Recently, we demonstrated that tissue plasminogen activator directly releases fibrinopeptides A and B (FPA and FPB) from fibrinogen. The purpose of this study was to determine whether urokinase has similar activity. Incubation of urokinase with fibrinogen or heparinized plasma results in concentration-dependent FPB release unaccompanied by FPA cleavage. For equivalent amidolytic activity, high molecular weight urokinase releases twofold more FPB than the low molecular weight species. In contrast, prourokinase does not release FPB until activated to urokinase. Contaminating thrombin or plasma is not responsible for urokinase-mediated FPB release because this activity is unaccompanied by FPA or B beta 1-42 cleavage, and is unaffected by heparin, hirudin, a monospecific antibody against thrombin, aprotinin, or alpha 2-antiplasmin. FPB release reflects a direct action of urokinase on fibrinogen because release is completely inhibited by a monospecific antibody against the enzyme. Further, urokinase releases FPB from the FPB-containing substrate B beta 1-42, thus confirming its specificity for the B beta 14 (Arg)-B beta 15 (Gly) bond. In addition to FPB release, SDS-PAGE analysis of the time course of urokinase-mediated fibrinogenolysis indicates progressive proteolysis of both the A alpha- and B beta-chains of fibrinogen that occurs after FPB release is completed. As a consequence of urokinase-mediated fibrinogenolysis, there is progressive prolongation of the thrombin clotting time. These studies indicate that urokinase has direct catalytic activity against fibrinogen. By releasing FPB, a potent chemoattractant, and by rendering fibrinogen less clottable by thrombin, urokinase may participate in processes extending beyond fibrinolysis.

Blood Coagulation↗
PubMed1988

Flexor tendon ruptures in patients with rheumatoid arthritis.

One hundred fifteen flexor tendon ruptures were reviewed in 43 hands with rheumatoid arthritis, one hand with psoriatic arthritis, and one hand with lupus erythematosis. Ninety-one tendons were ruptured at the wrist, four ruptures occurred at the palm, and 20 ruptures occurred within the digits. At the wrist level, 61 ruptures were caused by attrition on a bone spur and 30 were caused by direct invasion of the tendon by tenosynovium. All ruptures distal to the wrist were caused by invasion of the tendon by tenosynovium. Patients whose ruptures were caused by attrition regained better motion than those whose ruptures were caused by invasion by tenosynovitis; however, motion overall was poor. Patients with isolated ruptures in the palm or at the wrist had the best functional results. Those patients with multiple ruptures within the carpal canal had a worse prognosis. Ruptures of both tendons within the fibro-osseous canal had the worst prognosis. The severity of the patient's disease and the degree of articular involvement had a great effect on the outcome of surgery. Prevention of tendon ruptures by early tenosynovectomy and removal of bone spurs should be the cornerstone of treatment.

Adult↗
PubMed1988

Human tissue-type plasminogen activator releases fibrinopeptides A and B from fibrinogen.

In five patients with venous thromboembolic disease treated with recombinant tissue-type plasminogen activator (rt-PA), there was a marked increase in the mean concentrations of fibrinopeptide A (from 0.6 to 5.9 nM; P less than 0.0001) and desarginine fibrinopeptide B (from 5.6 nM to 24.1 nM; P less than 0.01) 30 min after a bolus of rt-PA (0.6 mg/kg). Thrombin was unlikely to be responsible because the levels of desarginine fibrinopeptide B exceeded those of fibrinopeptide A and the changes occurred despite concomitant heparin therapy. The purpose of this study therefore, was to determine whether rt-PA directly releases the fibrinopeptides from fibrinogen. Incubation of rt-PA with heparinized plasma or purified fibrinogen resulted in time and dose-dependent release of both fibrinopeptide A and B. Contaminating thrombin was not responsible for this activity by the following criteria: the rate of rt-PA mediated fibrinopeptide B release was considerably faster than that of fibrinopeptide A, and fibrinopeptide release was unaffected by heparin, hirudin, or a monospecific antithrombin IgG. Aprotinin also had no effect on fibrinopeptide release, indicating that this activity was not plasmin mediated. Fibrinopeptide release was shown to be due to rt-PA because this activity was completely blocked by a monoclonal antibody against the enzyme. Further, the specificity of rt-PA for the thrombin cleavage sites on fibrinogen was confirmed by the demonstration that rt-PA released fibrinopeptide A or fibrinopeptide B from fibrinopeptide A or B-containing substrates, respectively. These studies thus demonstrate that (a) rt-PA releases fibrinopeptides A and B from fibrinogen thereby indicating that this enzyme is not specific for plasminogen, and (b) plasma fibrinopeptide A and desarginine fibrinopeptide B levels are not specific markers of thrombin action on fibrinogen in patients receiving rt-PA.

Chromatography, High Pressure Liquid↗
PubMed1985

Social and anamnestic correlates of consensus in diagnosing schizophrenia.

One hundred and twenty patients with a clinical diagnosis of schizophrenia (mean age 38.2 years; 73 women, 47 men) were evaluated by means of 13 systems for diagnosing schizophrenia. The sample included only patients classified as schizophrenic by at least one system. Data analyses indicated that the number of systems that diagnosed patients as schizophrenic (i.e., a variable that ranged from one to 13 points) was larger for persons who suffered from their symptoms in a more chronic manner (r = .47), were more frequently diagnosed as schizophrenic in hospitals in the past (r = .44), were more frequently hospitalized before (r = .31), and whose last hospitalization was more recent (r = .24). They were also less likely to be presently employed in higher-ranking positions (r = .32) and to own a house (r = .32).

Adult↗
PubMed1984

Intraosseous blood supply of the capitate and its correlation with aseptic necrosis.

Isolated capitate fractures that result in the development of aseptic necrosis of the proximal pole are uncommon. Five patients were treated who developed aseptic necrosis of the proximal pole. Four had a history of trauma with radiographic evidence of nonunion. In vitro arterial injection studies were done to correlate clinical problem with intraosseous capitate vascularity. Palmar vessels were found to contribute the majority of the blood supply to the capitate. Three patterns of intraosseous blood supply were seen. In each pattern, the proximal pole received its blood supply exclusively in a retrograde fashion across the capitate waist analogous to the proximal scaphoid. Aseptic necrosis without collapse of the proximal pole was successfully managed with curettage and bone grafting in three patients. The remaining two patients, with collapse and pericapitate degenerative changes, were managed with intercarpal fusion.

Adult↗
PubMed1982

Monocyte function in cirrhosis.

Monocyte function has been studied in a total of 51 patients with biopsy-proven cirrhosis and 35 controls. There was significantly reduced monocyte spreading (p less than 0.05), chemotaxis (p less than 0.02), bacterial phagocytosis (p less than 0.05) and bacterial killing (p less than 0.02) in the cirrhotics compared to the controls. Monocytes from patients with cirrhosis produced significantly less of the lysosomal enzymes N-acetyl beta-glucosaminidase and beta-glucuronidase than those obtained from the controls (p less than 0.02). There was no significant difference in the number of monocytes obtained, the number of macrophage precursors, and the nitro-blue tetrazoline (NBT) reduction between the cirrhotic and the controls. The reduced function appeared to be mainly due to a circulating inhibitory factor and could be corrected by incubation of the cirrhotic cells in serum from control subjects. The response of monocytes from patients with cirrhosis did not differ from the controls in their response to added endotoxin or latex particles suggesting that they are capable of a normal response in the absence of the inhibitory factor. Paired specimens of portal and systemic serum were collected from patients with no evidence of liver disease undergoing vascular surgery. When added to normal human monocytes the portal serum caused a significant reduction in bacterial killing (p less than 0.02) and chemotaxis (p less than 0.05) compared to results obtained in the paired systemic serum. Mixing experiments suggests the presence of an active inhibitor in the portal serum. The results suggest that monocyte function is reduced in cirrhosis apparently due to a serum inhibitor which may have originated from the portal vein. The abnormalities may account in part for the increased susceptibility of these patients to infection.

Acetylglucosaminidase↗
PubMed1979

Shigellosis: analysis of 176 isolations.

Shigellosis, a worldwide epidemiological problem, is caused usually by six serotypes of Shigella. Man is the principal host, often infected by person-to-person contact. The number of reported cases of shigellosis has progressively increased during the past decade. Because of the observation, the authors reviewed all isolations of Shigella species in patients at Howard University Hospital. There were 176 isolations from 53 patients during the 4½ year period of the study. The study emphasizes the scope and distribution of the disease and the effectiveness of isolation and identification procedures.

Adolescent↗
PubMed1972

Care of the hair.

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Beauty Culture↗