富氧对海拔3700m高原人体运动心力储备的影响

目的　探讨富氧对高原人体运动心力储备方面的影响。方法　对海拔 3 70 0m高原的 1 2名健康青年富氧 (氧浓度为 2 4%～ 2 5 %)前后分别进行踏阶运动 ,采用心力监护仪采集和记录心动周期和心力信息 ,把完成规定运动量运动后第一心音 (S1 )幅值对安静时S1 幅值增加的相应倍数评估心肌收缩能力储备指数 (CCRI) ;利用舒张期和收缩期时限数据计算舒张期 /收缩期比值 (D/S比 )。结果　运动后较安静时HR ,D/S ,S1 幅值均增高 ,有非常显著性差异 (P <0 .0 1 ) ;富氧运动较未富氧运动CCRI,D/S ,S1 幅值增高 ,有显著性差异 (P <0 .0 5 ) ,HR无统计学意义 (P >0 .0 5 )。结论　高原低氧环境下心脏储备主要是心肌收缩能力储备而不是心率储备。富氧对增强机体心力储备具有重要作用     

Enhancement of hepatic hemangiomas with levovist on coded harmonic angiographic ultrasonography.

OBJECTIVE: To evaluate the pattern of contrast enhancement with Levovist on coded harmonic angiographic ultrasonography of hepatic hemangiomas. METHODS: Twenty hemangiomas were evaluated with coded harmonic angiographic ultrasonography and a microbubble contrast agent. Verification of the diagnosis of a hemangioma was made by means of dynamic computed tomography (n = 8), dynamic magnetic resonance imaging (n = 1), radionuclide scanning (n = 6), or follow-up ultrasonography (n = 5). Ultrasonographic images were obtained before contrast agent administration and with a bolus injection of 2.5 g of a microbubble contrast agent (300 mg/mL Levovist; Schering AG, Berlin, Germany) every 10 to 15 seconds for 5 minutes. The contrast enhancement patterns of the 20 hemangiomas were assessed. RESULTS: The tumor diameters as measured on ultrasonography were 7 to 97 mm (mean, 26.7 mm). Of the 20 hemangiomas, peripheral globular enhancement with progressive centripetal fill-in was shown in 15 (75%), rimlike enhancement with progressive centripetal fill-in was shown in 2 (10%), and homogeneous enhancement was shown in 1 (5%). In the remaining 2 lesions (10%), the enhancement patterns could not be seen, because they were not found on coded harmonic angiographic ultrasonography. CONCLUSIONS: Coded harmonic angiographic ultrasonography with a microbubble contrast agent can depict the typical enhancement pattern in most hepatic hemangiomas.     

Copy-milled all-ceramic restorations: case reports.

When all-ceramic systems are used, a respect for biocompatibility, an understanding of the patient's esthetic demands, and a justifiable reliance on the strength of the selected system are integral to success. Severely damaged molar teeth in two patients were restored with all-ceramic onlays that were prepared with a copy-milling system for ceramics. The onlay patterns were fabricated directly in the mouth with autopolymerizing resin. For these patients, the use of biologic, all-ceramic, copy-milled restorations resulted in clinical success as well as recovered function and esthetics.     

Umbilical portion of recipient's left portal vein: a useful vascular conduit in dual living donor liver transplantation for the thrombosed portal vein.

We considered performing living donor liver transplantation (LDLT) in a larger-size recipient. When the recipient was large-sized, or when the donor liver was severely steatotic or had a right-to-left volume discrepancy. We devised dual living donor liver transplantation (DLDLT) to make up for graft size insufficiency and to secure the donor's safety. However, portal vein thrombosis (PVT) presented a challenge for DLDLT because of the need for intact right and left portal veins for the implantation of both liver grafts. Our 52-year-old male patient with hepatitis B cirrhosis had suffered from repeated esophageal and gastric variceal bleeding and underwent 2 trials of a transjugular intrahepatic portosystemic shunt (TIPS). He developed TIPS occlusion and PVT involving the area just above the spleno-mesenteric confluence to the right and left PV. Also, the right PV orifice was destructed and difficult to isolate because of severe periportal inflammation and neointima growth in the TIPS mesh. The patient's two sons were inadequate for donation because of right-to-left volume discrepancy. Therefore, DLDLT using 2 left lobes was necessary to compensate for graft-size insufficiency and to secure donor safety, and we substituted an intact umbilical portion of recipient's left PV for the destroyed right PV. The patient recovered well, and liver function has been normal for more than a year. In conclusion, the umbilical portion of recipient's left PV can be a useful vascular substitute for the reconstruction of a thrombosed main portal branch in DLDLT.     

Subtypes of the Gc gene (vitamin D binding protein) in the Polish population

Gc subtypes were analyzed by isoelectric focusing on thin-layer polyacrylamide gel. In the sample of the Polish population including 278 persons, six Gc phenotypes were encountered: 1S, 1F-1S, 1F, 2-1S, 2-1F, 2 with the following frequencies: 0.342, 0.151, 0.014, 0.360, 0.072 and 0.061. Frequency of Gc1S was 0.597, Gc1F - 0.126 and Gc2 - 0.277. It was shown that a group system of the Gc protein in the Polish population was in good agreement with Hardy Weinberg equilibrium.     

Chronic verapamil administration lowers portal pressure and improves hepatic function in rats with liver cirrhosis

The effects of verapamil on portal pressure, microsomal liver function and extravascular albumin space were investigated in rats rendered cirrhotic by chronic exposure to phenobarbital and carbon tetrachloride. Verapamil significantly decreased splenic pulp pressure by 28% (P less than 0.05). In cirrhotic animals it improved liver function, measured by the aminopyrine and caffeine breath tests, by 36% (P less than 0.025) and 53% (P less than 0.05), respectively. The extravascular albumin space, an important determinant of drug clearance, was measured by a multiple indicator dilution technique. It was significantly larger in verapamil treated than in untreated cirrhotics (4.41 +/- 1.06 vs 2.73 +/- 0.79 ml/g; P less than 0.01). We conclude that verapamil has significant potential as a portal antihypertensive agent and its value in treating cirrhosis in man should be explored by controlled studies.     

The behaviour of activity of selected enzymes in urine and in serum in experimental intoxication of animals with sublimate (mercury chloride). Part I. Acute intoxication

In the work the behaviour of activity of selected enzymes in urine and in serum of experimental animals, which were intoxicated in an acute way, is presented. In the investigations there was observed the increase of activity of alkaline phosphatase in urine, simultaneous with its decrease in serum, the increase of GGTP in urine and shift in the composition of LDH isoenzymes in direction of slow migrating fractions.     

Murine CD9 is the receptor for pregnancy-specific glycoprotein 17.

Pregnancy-specific glycoproteins (PSGs) are a family of highly similar secreted proteins produced by the placenta. PSG homologs have been identified in primates and rodents. Members of the human and murine PSG family induce secretion of antiinflammatory cytokines in mononuclear phagocytes. For the purpose of cloning the receptor, we screened a RAW 264.7 cell cDNA expression library. The PSG17 receptor was identified as the tetraspanin, CD9. We confirmed binding of PSG17 to CD9 by ELISA, flow cytometry, alkaline phosphatase binding assays, and in situ rosetting. Anti-CD9 monoclonal antibody inhibited binding of PSG17 to CD9-transfected cells and RAW 264.7 cells. Moreover, PSG17 binding to macrophages from CD9-deficient mice was significantly reduced. We then tested whether PSG17 binds to other members of the murine tetraspanin family. PSG17 did not bind to cells transfected with CD53, CD63, CD81, CD82, or CD151, suggesting that PSG17-CD9 binding is a specific interaction. We have identified the first receptor for a murine PSG as well as the first natural ligand for a member of the tetraspanin superfamily.     

<Emphasis Type="Italic">p</Emphasis>-Glycoprotein ABCB5 and YB-1 expression plays a role in increased heterogeneity of breast cancer cells: correlations with cell fusion and doxorubicin resistance

Background  

Cancer cells recurrently develop into acquired resistance to the administered drugs. The iatrogenic mechanisms of induced chemotherapy-resistance remain elusive and the degree of drug resistance did not exclusively correlate with reductions of drug accumulation, suggesting that drug resistance may involve additional mechanisms. Our aim is to define the potential targets, that makes drug-sensitive MCF-7 breast cancer cells turn to drug-resistant, for the anti-cancer drug development against drug resistant breast cancer cells.