Interstitial and vascular pancreas rejection in relation to graft survival

To examine the incidence of interstitial and vascular rejection in pancreas allografts and its impact on graft survival, we studied 36 percutaneous pancreas biopsies and 10 pancreas transplantectomy specimens from 32 patients who had undergone simultaneous pancreas-kidney transplantation. Interstitial rejection (IR) was predominantly found in the biopsies, while vascular rejection (VR) was most prominent in the transplantectomies. Pancreas graft survival was significantly decreased for pancreas grafts that had suffered from vascular rejection when compared to those with only interstitial rejection. Potential rejection markers, i. e., serum amylase, glucose, creatinine, and urinary amylase, did not correlate with histological signs of rejection, although increased levels of serum amylase were, in all but one case, associated with rejection.We conclude that a percutaneous pancreas biopsy remains the most reliable method to determine pancreas rejection, and that by distinguishing between IR andVR, a pancreas biopsy may provide important diagnostic as well as prognostic information. Received: 6 March 1997 Received after revision: 5 June 1997 Accepted: 30 June 1997     

Traumatic rupture of the corpus cavernosum: evaluation and management

Rupture of the corpus cavernosum is a rare but probably under-reported entity. It truly represents a urological emergency and current recommendations are for early surgical intervention. We review 5 cases with evaluation, treatment and followup. Delays in treatment lead to long-term complications, such as erectile dysfunction and penile curvature.     

Reduction of bacterial adherence to catheter surface with heparin

Despite many advances in catheter design and use, the most common cause of hospital-acquired infections is catheterization of the urinary tract. In the present investigation the adherence of bacteria to catheters coated with heparin was studied. Since heparin itself does not coat the plastic catheter surface, a complex of heparin with tridodecylmethylammonium chloride (TDMAC) was used which results in hydrophobic association of hydrocarbon chains of the TDMAC with the catheter leaving the quaternary ammonium moiety of TDMAC exposed to the surface forming ionic bonds with the highly anionic sulfate groups of heparin. Coating latex catheter material with TDMAC without heparin resulted in 3.6-fold higher adherence whereas coating with the TDMAC-heparin complex reduced adherence to less than 10% of control untreated latex. TDMAC-heparin also significantly reduced bacterial adherence to teflon coated latex (Bardex) and vinyl catheter material. Less than 30% of the original heparin was removed after wash periods of up to one week. These results indicate that TDMAC-heparin coating of urethral catheters reduces bacterial adherence and thereby may delay the acquisition of catheter associated urinary tract infection.     

Nitrofurantoin not surface active agent in rabbit urinary bladder

It has been recently suggested that nitrofurantoin may induce symptoms of interstitial cystitis by acting as a surface active agent that destroys glycosaminoglycan (GAG) on the bladder surface. Evidence accumulated over the past decade has demonstrated that the bladder surface GAG prevents bacterial adherence. In this experiment, exposure of the bladder lumen to nitrofurantoin at more than twice the therapeutic concentration did not destroy the bladder GAG layer (as evidenced by periodic acid-Schiff histochemistry) nor increase bacterial adherence as did a true surface active agent (Triton X-100). Acid treatment as well as all tested organic solvents except 50% dimethyl sulfoxide (DMSO) also removed the bladder GAG layer and increased bacterial adherence. These results indicate that neither nitrofurantoin nor 50% DMSO has adverse effects on the bladder surface and thus is unlikely to initiate the interstitial cystitis symptom complex by means of surfactant activity.     

Effect of serotonin re-uptake inhibition by fluoxetine on body weight and spontaneous food choice in obesity.

The effect of fluoxetine on body weight and spontaneous food choice was studied in twenty-three healthy, non-depressed, obese females on an outpatient basis. After a one week placebo run-in period, subjects were randomized to receive either fluoxetine (FXT) 60 mg daily (n = 11) or placebo (P) (n = 12) for 6 weeks in a double blind study design. BMI (35.2 +/- 0.8 vs 36.4 +/- 1.3 kg/m2, mean +/- s.e.m.) and age (38.1 +/- 239 vs 37.3 +/- 2.7 years) were not different in either group. No specific diet was prescribed. On four separate days per 14 days food records were collected. Data were analysed with the use of food composition tables. Statistical analysis was performed using Student's t test for independent samples for data on body weight and calorie intake. Macro-nutrient composition of the diet was analysed using multivariate analysis of variance and post hoc Student's t test for independent samples. All subjects lost weight during fluoxetine treatment. Mean (+/- s.e.m.) weight loss in the fluoxetine treated group was 3.6 +/- 0.5 kg, compared to a mean weight gain of 0.3 +/- 0.5 kg in the placebo treated group (P less than 0.001). In all patients food intake was reduced during fluoxetine treatment and this reduction could fully account for the observed weight loss. The mean total caloric intake per day was significantly lower during fluoxetine treatment compared with placebo (FXT 1123 +/- 118 kcal vs P 1845 +/- 87 kcal, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Construction and validation of a Parkinson's disease mutation genotyping array for the Parkin gene.

Parkin mutations account for the majority of familial and sporadic early onset Parkinson's disease (EOPD) cases with a known genetic association. More than 100 mutations have been described in the Parkin gene that includes homozygous, compound heterozygous, and single heterozygous mutations. We have designed a Parkin mutation genotyping array (gene chip) that includes published Parkin sequence variants and allows their simultaneous detection. The chip was validated by screening 85 PD cases and 47 controls previously tested for Parkin mutations. Similar genotyping microarrays have been developed for other genetically heterogeneous diseases including age-related macular degeneration. Here, we show the utility of a genotyping array for Parkinson's disease by analysis of 60 subjects from the Genetic Epidemiology of Parkinson Disease (GEPD) study that includes 15 early-onset PD case probands and 45 relatives.     

Human Herpesvirus 6 in Bronchalveolar Lavage Fluid after Lung Transplantation: A Risk Factor for Bronchiolitis Obliterans Syndrome?

Bronchiolitis obliterans syndrome (BOS) is the limiting factor to long-term survival after lung transplantation. Previous studies suggested respiratory viral tract infections are associated with the development of BOS. To identify the impact of virus detection in bronchoalveolar lavage (BAL) fluid, we analyzed BAL samples from 87 consecutive lung transplant recipients for human herpesvirus (HHV)-6, Epstein-Barr virus, Herpes simplex virus 1/2, Cytomegalovirus, respiratory syncytical virus and adenovirus by PCR. Acute rejection, BOS and death were recorded for a mean follow-up time of 3.27 +/- 0.47 years. Results of PCR analysis and other potential risk factors were entered into a Cox regression analysis of BOS predictors and death. Only acute rejection was a distinct risk factor for BOS of all stages, death and death from BOS. HHV-6 was detected in 20 patients. Univariate and multivariate analysis revealed that HHV-6 was associated with an increased risk to develop BOS > orb = stage 1 and death, separate from the risk attributable to acute rejection. Identification of HHV-6 DNA in BAL fluid is a potential risk factor for BOS. Our results warrant further studies to elucidate a possible causal link between HHV-6 and BOS.     

Loss of Anticoagulant Effect of Heparin During Circulation of Human Blood In Vitro

Device-induced thrombogenesis was studied in an in vitro model using human blood circulated through an artificial ventricle. A new constant pressure filtration technique was used to detect circulating microemboli, the activated partial thromboplastin time (APTT) test was used to monitor the blood for the presence of anticoagulant activity of heparin, and hemolysis was quantified by measuring the plasma free hemoglobin level. Circulation of blood through a 20-ml stroke volume pneumatically driven ventricle for 6-9 h resulted in a significant reduction of APTT, indicating the loss of the anticoagulant effect of heparin. Microemboli concentration was minimal until the APTT decreased below 125 s, at which time the microemboli concentration increased rapidly. This was presumed to be due to the formation of thrombi following a decrease in heparin activity. A significant increase in hemolysis was also noted when blood was pumped. None of these changes was noted in the nonpumped control blood. Spontaneous loss of heparin activity in blood circulated by a pneumatically driven pump may have clinical implications and may help understanding of the problems associated with device-induced thrombogenesis.     

Aspergillus peritonitis in peritoneal dialysis: case report and a review of the literature

Aspergillus peritonitis is a rare complication of continuousambulatory peritoneal dialysis. The case is described of a 68-year-oldman in whom Aspergillus fumigatus was isolated from the peritonealdialysate after recurrent peritonitis with Gram-negative rodsin association with diverticulosis. Treatment consisting ofremoval of the catheter and intravenous administration of amphotericinB followed by oral itraconazole was successful. A review of the sparse literature (12 cases) displays uncertaintiesregarding diagnostic awareness, culture diagnosis, and therapeuticmanagement. Next to institution of appropriate antifungal therapy,early removal the peritoneal dialysis catheter is recommended,as delayed removal of the catheter appears to be associatedwith increased mortality and morbidity.     

Macrophage colony-stimulating factor gene transfer into tumor cells induces macrophage infiltration but not tumor suppression

In order to analyze the effect of a high local concentration of macrophage colony-stimulating factor (M-CSF; CSF-1) on tumor growth, the plasmacytoma cell line J558L was transfected with the human M-CSF gene and injected into syngeneic BALB/c mice. In contrast to the parental tumors, M-CSF transfectants were heavily infiltrated by macrophages as evidenced by immunohistochemistry with antibodies to Mac-1 and Mac-3 and by isolation of the macrophages from the tumor. Nevertheless, tumor growth was only slightly affected by M-CSF and M-CSF-producing cells grew as tumor in all cases. The growth retardation of M-CSF-producing cells varied depending on the experiment and seemed to be due to an indirect effect because the growth rate of the cells in vitro had not changed upon gene transfer. Attempts to activate the tumor-infiltrating macrophages for tumor suppression by systemic application of interferon-γ and/or lipopolysaccharide were not successful. Altogether, our results suggest that M-CSF is a potent chemoattractant for macrophages in vivo but alone is not sufficient to activate these macrophages for tumoricidal activity.