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Opportunistic infection of the upper gastrointestinal tract by cytomegalovirus (CMV) or invasive fungal infection was studied in 219 consecutive kidney and kidney/pancreas transplant recipients with regard to incidence, presentation, and clinical outcome. Prompt upper endoscopy was done in all patients with these symptoms: dyspepsia, dysphagia, or bleeding. Multiple biopsies were obtained for fungal culture, CMV culture, CMV assay, and histologic examination for fungal invasion. Between April 1991 and July 1993, 57/219 (26%) transplant patients developed upper gastrointestinal symptoms. At endoscopy, gross mucosal abnormality was evident in 48/57 (84%). Opportunistic infection was found in 21/48 (44%); however, CMV infection was also detected in 2/9 (22%) who had a normal study. Overall, CMV was present in 15/57 (26%) and invasive fungal infection in 8/57 (14%). All 23 infections were successfully eradicated. Opportunistic infection occurred in 12/31 (39%) with dyspepsia, 9/14 (64%) with dysphagia, and 2/12 (17%) with bleeding. Graft loss occurred in 5/23 (22%) with opportunistic infection vs 23/196 (12%) other recipients. Upper gastrointestinal symptoms are indicative of serious opportunistic infection in a significant number of transplant recipients. As opportunistic infection may jeopardize allograft function, all patients with upper gastrointestinal tract symptoms require prompt endoscopy and biopsy to effect appropriate therapy. Random biopsy is also recommended in the face of a normal endoscopic examination. [ABSTRACT FROM AUTHOR]

Background: Laparoscopic donor nephrectomy (LDN) has been shown to be a safe and effective option for renal procurement. Studies comparing open nephrectomy and hand-assisted laparoscopy have emphasized decreased warm ischemia time when compared with “pure” laparoscopic retrieval. However, no data exist that define exactly what constitutes a prolonged warm ischemia time in terms of recipient graft function. The aim of this study was to use a large, single-institution experience with LDN to determine if warm ischemia time correlates with recipient graft function as measured by serum creatinine levels. Methods: A total of 640 LDNs were performed from March 1996 to August 2001. Warm ischemia times were prospectively collected and were defined as the time from renal artery occlusion to immersion in iced saline. Serial recipient creatinine levels were measured at 1 week and 1, 3, 6, and 12 months (when possible) from the transplant. Data were analyzed using Pearson correlation analysis at a confidence interval of 95%. Results: Mean warm ischemia time was 151 s with a standard error of 3.4 s and ranged from 35 to 720 s. Recipient creatinine mean at 1 week was 1.94 mg/dl with a standard error of 0.06 mg/dl and ranged from 0.5 to 10.5 mg/dl. Recipient creatinine mean at 1 month was 1.68 mg/dl with a standard error of 0.06 mg/dl and ranged from 0.6 to 8.5 mg/dl. Recipient creatinine mean at 3 months was 1.60 mg/dl with a standard error of 0.04 mg/dl and ranged from 0.6 to 8.8 mg/dl. Recipient creatinine mean at 6 months was 1.63 mg/dl with a standard error of 0.06 mg/dl and ranged from 0.7 to 13.5 mg/dl. Recipient creatinine mean at 12 months was 1.70 mg/dl with a standard error of 0.07 mg/dl and ranged from 0.5 to 14.5 mg/dl. No correlation was found between warm ischemia time and recipient creatinine levels at 1 week (p = 0.4737), 1 month (p = 0.9180), 3 months (p = 0.6227), 6 months (p = 0.8349), or 12 months (p = 0.2835). Conclusions: Warm ischemia time does not correlate with recipient graft function in LDN within the range of times studied. Shorter warm ischemia time associated with open donor nephrectomy and hand-assisted LDN does not necessarily offer a measurable advantage in recipient graft function. During extraction of the kidney, expediency to minimize warm ischemia time should not supersede controlled and safe maneuvers in renal vessel division and extraction of the kidney. [ABSTRACT FROM AUTHOR]

Background: Although rare, visceral and vascular injuries related to the insertion of conventional laparoscopic trocars may have disastrous consequences. Most of these injuries are due to the high puncture force applied to the trocar. We present the results of an animal laboratory evaluation of a newly developed ultrasonically activated trocar. Methods: A total of 40 punctures were made in four pigs with an average weight of 53 kg. An 11-mmHg pneumoperitoneum was created through a Veress needle. A 10-mm diameter trocar was inserted in the midline for a laparoscope. A series of five trocars were then inserted on each lateral wall under laparoscopic control. Twenty punctures were made with a conventional reusable 11-mm trocar (CT) whose tip was sharp and conical. Twenty punctures were made with an 11-mm ultrasonically activated trocar (UT), whose fequency was 23.5 KHz and amplitude 150 mm. The cutaneous incision was made large enough so that the skin did not interfere with the trocar insertion. The force applied to the trocar was measured with a push-pull gauge connected to a computer. The following data were recorded: maximal force applied to the trocar to obtain insertion of the tip through the abdominal wall, maximum abdominal pressure increase during trocar insertion, and time for abdominal penetration. Results: The average time needed for trocar penetration was 12.8 s with CT and 4.5 s with UT (p < 0.001). The average maximal force was 6.8 kgF with CT and 0.4 kgF with UT (p < 0.001). The average abdominal pressure increase was 7.6 mmHg with CT and 0.8 mmHg with UT (p < 0.001). At 30 days, no necrosis was found. Pathological findings were similar in both groups. Conclusion: Ultrasonically activated trocars required less time and much less force to be inserted. This may be a breakthrough in the safety of trocar insertion. [ABSTRACT FROM AUTHOR]

Fludarabine is active but not curative in the treatment of chronic lymphocytic leukemia (B-CLL). Nitric oxide (NO) supplied from exogenous, NO-donating pro-drugs can also induce apoptosis and death of acute leukemia cells. This study investigated combinations of fludarabine with NO-donating pro-drugs for their cytotoxicity against freshly isolated B-CLL lymphocytes following a 72 h exposure in vitro. The median IC(50)for fludarabine was 2.2 microM (n = 85). The nitric oxide donors DETA-NO, PAPA-NO, and MAHMA-NO were also cytotoxic, and their effects were inversely related to rates of NO release. Neither DETA-NO depleted of NO nor DETA itself was effective, indicating that NO was required for cytotoxicity. Drug interactions were evaluated by a modified combination index method. Synergy was observed in combinations of fludarabine or nelarabine (506U78) with DETA-NO in 52% and 88% of samples, respectively. Interestingly, the combination of fludarabine and DETA-NO was more cytotoxic in B-CLL cells less sensitive to fludarabine. DETA-NO did not enhance the activity of other DNA anti-metabolites, topoisomerase I and II inhibitors, or alkylating agents. Finally, the anti-leukemic activity of fludarabine alone or in combination with DETA-NO was found to correlate with inhibition of cellular RNA synthesis. These results indicate that NO donors could enhance fludarabine therapy for B-CLL. [ABSTRACT FROM AUTHOR]

Assesses the degree of concordance between genetic groups and W.K. Fisher's taxa within the Leptasterias subgenus Hexasterias. Morphological and statistical analysis conducted on the sea star genus Leptasterias; Status of the L. aleutica/L. camtschatica complex; Minimum evolution tree obtained for mitochondrial DNA haplotypes.

A patient with a previous vagotomy and pyloroplasty was evaluated for symptoms of gastric outlet obstruction. Endoscopy revealed a thick, fibrous bridge that created a dual-channel pylorus. Symptomatic improvement was not achieved with balloon dilatation. Surgery was avoided by dividing the tissue bridge endoscopically with a sphincterotome. Since reestablishing a normal pyloric aperture, the patient's symptoms have been alleviated. This is the first description of this minimally invasive technique in the management of a symptomatic double-channel pylorus. [ABSTRACT FROM AUTHOR]