True epiphrenic diverticulum of esophagus secondary to tubercular adenitis.

Ephiphrenic esophageal diverticulum is rare and usually is a pulsion-type pseudodiverticulum that occurs in association with motility disorders of the esophagus. We report a 35-year-old man with tubercular lymphadenitis causing true traction type of epiphrenic diverticulum. Esophageal diverticulectomy and esophagomyotomy was done; he is doing well on antitubercular drugs.     

External duodenal fistula following closure of duodenal perforation.

AIM: Retrospective analysis of experience with management of external duodenal fistula (EDF) without using total parenteral nutrition (TPN). METHOD: Medical records of 31 patients with EDF following closure of duodenal ulcer perforation, treated over a 7-year period (1994-2001), were studied. Twenty-one patients (68%) had evidence of sepsis at presentation or during the course of treatment. None could afford TPN for optimum time. All patients received hospital-based enteral nutrition through nasojejunal tube, besides supportive medical treatment and/or surgery. Peritonitis or failure to insert nasojejunal tube for enteric alimentation led to early surgery. RESULTS: Two patients died of septicemia and multi-organ failure within 48 hours of admission. Fourteen patients (48.3%) initially received conservative treatment (Group I); six of them later required surgery. Fifteen patients (51.7%) underwent early surgery due to peritonitis (n=9) or failure to establish enteral feeding (n=6) (Group II); wound infection, intra-abdominal abscess and septicemia were more common in these patients than those in Group I. Survival rate was higher in Group I than in Group II (86% versus 40%; p< 0.05). Septicemia and gastrectomy were the independent factors associated with high mortality. CONCLUSIONS: EDF can be satisfactorily managed without TPN. Successful placement of enteral feeding line, supportive treatment and delayed surgery can achieve survival in 85% of patients. Minimum intervention is recommended when early surgery is performed in peritonitis or to establish enteral feeding line.     

Modification of apomorphine-induced behaviour following chronic swim exercise in rats.

Four week swim exercise schedule (45 min day-1, 6 days each week) in rats led to a significant adaptive change in functional responsiveness of dopamine receptors (auto-receptors) in the nigrostriatal and mesolimbic system that was evident from the modification of behavioural responses elicited by a low dose of apomorphine, a direct acting dopamine receptor agonist. Thus, a remarkable increase in yawning response, development of full blown stereotypy, as well as profound attenuation of locomotory and hypothermic response was observed in exercise-trained rats as compared with the non-exercise group (control), following intraperitoneal administration of 0.3 mg kg-1 of apomorphine.     

Acute polymyositis associated with W. bancrofti

Two cases of acute polymyosotis associated with W. bancrofti , presented with generalised painful swelling and weakness of the muscles. These patients had elevated muscle enzymes, a myopathic EMG pattern, inflammatory myopathy on biopsy and W. bancrofti in the peripheral blood smear. The clinical, improvement of the disorder and total clearance of microfilariae was obtained with the combination therapy of steroid and diethyl-carbamazine in comparison with steroid alone.     

Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.     

The effect of TNFa on bradykinin receptor binding, phosphatidylinositol turnover and cell growth in human A431 epidermoid carcinoma cells.

In this study, we examined the effect of TNFa on bradykinin (BK) B2 receptor binding and function in human A431 epidermoid carcinoma cells. [3H]BK binds to a single class of receptors on A431 cells in a saturable and reversible manner. A binding affinity (KD) of 3.0 +/- 0.3 nM (n = 4) and a Bmax of 151 +/- 14 fmols/10(6) cells, representing approximately 90,000 BK receptors per cell, was observed. The rank order of potency for BK agonist peptides indicates that the A431 BK receptor appears to be of the B2 subtype. When A431 cells were incubated with TNFa (10 ng/ml) for 48 h prior to BK binding, a significant decrease in the number of BK receptors compared to control was observed. TNFa did not influence the affinity of BK binding to A431 cells and direct addition of TNFa to the binding assay did not effect BK binding. BK-stimulated IP1 formation appeared to be increased in TNFa treated cells compared to control whereas histamine-stimulated IP1 formation was not influenced. Both control and TNFa treated cells were greater than 95% viable. However, TNFa treated cells were blocked in the G1 phase of the cell cycle resulting in a decrease in DNA synthesis. This may be one mechanism for the TNFa-induced decrease in BK receptors in A431 cells.