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Interfacial electrical tree (IET) is easily initiated by a high electric field near the triple point (TP) in the power modules, propagating along the packaging material and ceramic substrate interface until electrical breakdown occurs. To assess the degree of IET degradation, this study fabricates the silicone elastomer (SE) packaging modules without IET and with three levels of IET degradation. Then, a novel diagnostic indicator is derived from the charge measurement results by the direct current integrated charge [DCIC- Q(t)] equipment. This indicator can effectively, nondestructively, and quantitatively distinguish different levels of IET degradation based on the charge ratio values within the voltage range of 250–2000 V at 150 °C. Notably, the charge ratio value of the IET-degraded modules exhibits significant voltage dependency at low voltages and high temperatures due to the interfacial space charge accumulation effect. The diagnostic indicator increases with the IET degradation degree, indicating a higher accumulation of interfacial space charges in the IET channels, consistent with theoretical analyses. It is expected that the proposed diagnostic indicator may help to diagnose the degradation levels in other electrical equipment as well.

Bile salts regulate the subselection ofphosphatidylcholine species secreted into bile andthereby modulate bile metastability. The aim of thisstudy was to determine whether bile salts alterphosphatidylcholine species of the canalicular membrane, and ifthey do, to clarify whether the cytoprotective action ofhydrophilic bile salts is associated with modulation ofphosphatidylcholine composition in cell membrane bilayers. Bile salt-pool-depleted rats wereinfused intravenously with sodium taurocholate at aconstant rate (200 nmol/min/100 g body wt) for 2 hr,followed by infusion of either sodiumtauroursodeoxycholate, sodium tauroalphamuricholate, or sodiumtaurobetamuricholate (200 nmol/min/100 g) for 2 hr.Biliary outputs of cholesterol and phosphatidylcholineand phosphatidylcholine hydrophobicity in bile andsubcellular fractions were determined. The cytoprotectiveaction of hydrophilic bile salts was determined by therelease of canalicular membrane-localizing enzymes(alkaline phosphatase, leucine aminopeptidase) into bile. Tauroursodeoxycholate,taurobetamuricholate, and tauroalphamuricholatedecreased the release of these enzymes when compared tovalues under taurocholate infusion. Bilephosphatidylcholine hydrophobicity was also decreased by the bile salts, whereasthe cholesterol/phosphatidylcholine ratio was increased.In contrast, phosphatidylcholine hydrophobicity in thecanalicular membrane was increased by these three bile salts. In conclusion, hydrophilicbile salts promote biliary secretion of relativelyhydrophilic phosphatidylcholine secretion into bile, andconsequently phosphatidylcholine hydrophobicity in canalicular membranes increased. Such analteration in phosphatidylcholine species withincanalicular membrane enhances its lateral packingdensity with less fluidity, and this may account, inpart, for the cytoprotective action of hydrophilic bilesalts against hydrophobic bile salts.

Although bile salts play an important role inthe secretion of biliary lipid, little is known aboutthe relationship between bile salt hydrophobicity andthe selection of lecithin species to be secreted into bile. We therefore investigated whetherbile salts modulate the selection of biliary lecithinsubspecies. Rats that were depleted of the bile saltpool were infused with taurocholate (50, 100, 200, and 400 nmol/min/100 g body weight),taurochenodeoxycholate (25, 50, 100, and 200nmol/min/100 g body weight), tauroursodeoxycholate (100,200, 400, and 800 nmol/min/100 g body weight), ortaurobetamuricholate (100, 200, 400, and 800 nmol/min/100 g bodyweight). Bile was collected to analyze bile flow, bileacid output, cholesterol levels, and lecithin levels.The hydrophobic-hydrophilic balance of the bile salts and biliary lecithin species was assessedby determining the retention times during reverse-phasehigh-performance liquid chromatography. Biliary lecithinsecretion rates correlated with the hydrophobicity index of the biliary bile salts administered.Thus, biliary lecithin hydrophobicity increased withincreasing bile salt hydrophobicity, whereas the molarcholesterollecithin ratio in the bile decreased. In conclusion, bile salt hydrophobicityregulates the selection of biliary lecithin subspeciesduring biliary secretion and thereby modulates, at leastin part, bile cholesterol metastability. Thus, bile salt hydrophobicity accounts for thephysicochemical conditions determining bile lipidmetastability.

A novel fat absorption test to clarify the malabsorption syndrome was developed using a micronephelometric technique and compared with the classic conventional technique using 131I‐triolein. An integrity of time‐sequential light scattered from chylomicron‐related turbidity in serum was determined between 0 and 300 min after butter fat load, being expressed in terms of the light scattering intensity (LSI). A good correlation was obtained between LSI and the serum level of chylomicron‐triglyceride determined by an ultracentrifugation technique (r=0.819, P< 0.001). The maximal LSI was consistently observed at 180 min after administration of a test meal in the normal group (n= 39), whereas the malabsorption syndrome group (n= 35) was distinctly different and could be further classified according to four patterns of LSI changes. In addition, an inverse correlation was found between this fat absorption test and the 131I‐triolein absorption test. It was concluded that the micronephelometric technique which does not use a radionuclide is advantageous in its simple and safe evaluation of fat malabsorption syndrome.

A molybdenum(IV) aqua ion with sulfur bridges, Mo3OS34+, has been prepared and characterized. An X-ray structure analysis of the iminodiacetato complex prepared from the aqua ion has revealed the core structure of Mo3(μ-O)(μ-S)2(μ3-S).

Inhibitors of 3-hydroxy,3-methylglutaryl coenzyme A (HMG-CoA) reductase have been reported to decrease the cholesterol saturation index (CSI) in duodenal bile in humans and to prevent formation of cholesterol gallstones in animal studies. We performed a prospective study to evaluate the role of HMG-CoA reductase inhibitors as gallstone-dissolving agents. Fifty patients with radiolucent gallstones in a gallbladder opacifying at drip infusion cholecystography were treated with either 10 mg/day simvastatin plus 600 mg/day ursodeoxycholic acid (group 1, n = 26) or 600 mg/day ursodeoxycholic acid alone (group 2, n = 24) for 12 months. The ratio of solitary to multiple gallstone cases was 21:29. Plasma lipid levels were assessed and ultrasonographic examination of the gallbladder was performed at baseline and at 3-month intervals during treatment. Duodenal bile sampling was performed in five patients in each group at baseline and after 12 months of treatment. Plasma cholesterol decreased significantly in group 1 but not in group 2. In solitary gallstone cases, no significant difference in dissolution rates was observed between groups 1 (3 of 9, 33%) and 2 (4 of 12, 33%). In contrast, the dissolution rate in multiple gallstone cases was significantly higher in group 1 (12 of 17, 71%) than in group 2 (3 of 12, 25%) (p < 0.01). Bile cholesterol saturation index was significantly decreased (p < 0.01) but did not significantly differ between the two groups. These results suggest that combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than ursodeoxycholic acid monotherapy in patients with multiple gallstones.