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We analyzed the primary tumors, sonographic findings, clinical manifestations, and prognosis in five cases of isolated splenic metastases to determine in what situations these rare metastases should be suspected. The metastases were detected by ultrasonography in all five patients, and the primary tumors were colonic cancer in four patients and renal cancer in one patient. Splenectomy was performed and the postoperative course was uneventful in all patients. We conclude that preoperative and follow-up examinations must be performed with special attention given to the spleen in colonic or renal cancer patients.

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PURPOSE: The purpose of this study is to establish a simple technique to evaluate anorectal motility and the dynamics of defecation. METHODS: Pressure fluctuations in the rectum and anal canal during 500 ml of saline infusion in the rectum and then a saline evacuation curve were recorded using manometer and uroflowmeter. RESULTS: This study consisted of 37 patients with a mean age of 49.6 years. All patients without problems with defecation showed periodic relaxation of the anal canal, which was synchronized with rectal contractions during saline infusion. The saline evacuation curves of these patients were characterized by short evacuation time and high-peak flow. Of the 13 patients with constipation, 9 showed no rectoanal synchronization and had segmental evacuation curves. The patients with incontinence tended to have poor ability for holding saline in the rectum, resulting in low-peaked evacuation curves. CONCLUSIONS: This simple and noninvasive technique for recording anorectal pressure fluctuations and dynamics of saline evacuation from the rectum enables quantitative and qualitative evaluation of the ability to defecate.

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A 24-week study was conducted to evaluate the effects of the dihydropyridine calcium channel blocker nilvadipine on urinary albumin excretion in eight microalbuminuric hypertensive patients with non-insulin-dependent (type II) diabetes mellitus. Blood pressure and urinary albumin excretion measurements before the administration of nilvadipine (8 mg) were compared with those after 4, 8, 12 and 24 weeks of treatment. No significant changes were observed in the mean values of haemoglobin A1C. Systolic blood pressure was significantly reduced from 174 +/- 23 mmHg before treatment to 144 +/- 13 mmHg after 24 weeks of treatment (P < 0.02). Diastolic blood pressure was significantly reduced from 93 +/- 11 mmHg at baseline to 79 +/- 8 mmHg after 24 weeks of treatment (P < 0.05). Urinary albumin excretion was significantly reduced from 65.4 +/- 37.4 mg/g creatinine at baseline to 51.6 +/- 41.1 mg/g creatinine (P < 0.05) after 4 weeks, and to 39.1 +/- 26.9 mg/g creatinine (P < 0.02) after 24 weeks of treatment. These data suggest that in hypertensive microalbuminuric patients with non-insulin-dependent diabetes mellitus, treatment of hypertension with the calcium blocker nilvadipine may slow the progression of diabetic nephropathy.

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A 12-year-old girl with massive hemoperitoneum caused by a ruptured hemorrhagic ovarian cyst (HOC) is described. Although HOC is not common in early adolescence, it should be included in the differential diagnosis of any adnexal mass or lower abdominal pain in a girl.

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Although it has been firmly established that D-glucose inhibits glucagon secretion from pancreatic A cells, the regulatory mechanism of glucagon secretion by D-glucose has not been elucidated. To study this regulatory mechanism by D-glucose, the effects of hexoses and their derivatives on glucagon secretion from the A cells of isolated perfused rat pancreas were investigated. When these cells were perfused with D-glucose, D-fructose, D-sorbitol, D-galactose, 2-deoxy-D-glucose, D-gluconic acid sodium salt and D-glucosamine HCl salt, glucagon secretion was significantly inhibited. None of the hexoses or their derivatives tested were found to stimulate glucagon secretion. The effects of these sugars on glucagon secretion were independent of their metabolism in the cells. From the findings that the sugars both metabolized and unmetabolized in the cells demonstrated comparable inhibition of glucagon secretion from the isolated perfused rat pancreas, it is speculated that the recognition system for these sugars may be probably present on the A cell membrane and responsible for mediating these inhibitory effects of glucagon secretion.

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The objective of this study was to develop an easy and simple experimental rat model of total hepatectomy, hepatic ischemia and extrahepatic portal obstruction. The first operation involved transposing the spleen with its scarified capsule in a subcutaneous pouch to produce portasystemic anastomosis. Total hepatectomy was easily performed in a lobe-by-lobe fashion 2 weeks following the first stage operation. Anhepatic rats receiving a glucose infusion survived for about 10 hours and all died of acute hepatic failure. Hepatic support systems can be accurately evaluated in this anhepatic rat model because of its uniformity. Sixty minutes of hepatic ischemia was able to be performed in rats with a transposed spleen for a portasystemic shunt and no complicated or technically involved procedure was required for the ischemic model. No rats died due to technical difficulties, suggesting the reliability and reproducibility of this ischemic model. An animal model resembling extrahepatic portal vein obstruction was also obtained by ligation of the portal vein; a simple maneuver which was able to produce collateral veins to the liver and cavernous transformation, as similarly seen in clinical patients with extrahepatic portal obstruction. Because these 3 animal models were so easily achieved in the rat, and since the changes in hepatic function and formation of the collaterals to the liver after portal vein occlusion are still poorly understood, this model should prove valuable for future study.

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Obstructive jaundice model was created using rats by the ligation of bile duct. One, 2, 3 weeks later, the respiratory function and morphology of the hepatic mitochondria were comparatively evaluated between mitochondria directly fractionated from liver tissue and mitochondria from isolated hepatocytes. Respiratory function of the former deteriorated with the duration of jaundice. ATP synthesis decreased to 75% of the control at 1 and 2 weeks, and 58% at 3 weeks after ligation. On the contrary, it was 97%, 88% and 87% of the control. On the contrary, it was 97%, 88% and 87% of the control at 1, 2 and 3 weeks in the latter. By electron microscopic examination, the size of mitochondria of the jaundiced liver is inconsistent and smaller in general than the control. These data suggest that the deterioration of mitochondrial function in the jaundiced liver is not caused mainly by the disturbance of mitochondria themselves, but caused by the respiratory inhibitory factors which exist around the mitochondria.

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