Systemic effects of ethanolamine oleate in analbuminemic rats

BACKGROUND/AIMS: The present study was an attempt to clarify whether only serum albumin inactivates ethanolamine oleate (EO) in vivo and whether EO has an adverse effect on the lung, kidney, and liver in the presence of analbuminemia. METHODOLOGY: Fifty-five female Nagase Analbuminemia Rats (NAR) and 55 female Sprague-Dawley Rats (SDR) were injected with 5% EO in the left femoral vein. Changes in respiratory, renal, and hepatic function and the extent of hemolysis following the injection of the EO were examined. RESULTS: In both groups, a transient but significant increase was seen in serum hemoglobin at up to 1 hour after injection of EO. No significant changes in PaO2, PaCO2, blood urea nitrogen, or serum creatinine following injection of EO were seen in either group. The total bilirubin significantly increased within 30 min in the SDR group, but this increase was prolonged for 5 days in the NAR group. Glutamic pyruvic transaminase (GPT) increased for 12 hours in the NAR group, while no change was seen in the SDR group. CONCLUSIONS: These observations suggest that EO may have hepatotoxic effects, that serum albumin may afford protection, and that other humoral substances which inactivate EO, including serum globulin, may be present.     

Development of the dental CAD/CAM system

Studies have been undertaken to apply CAD/CAM system to Dentistry and to make prosthetic appliances with this system automatically. Specimens are 4 times large plaster models. For the inside of the crown, the plaster model of prepared tooth is measured with laser displacement meter then the numerical data is obtained. After modification of this data for the concave cutting, the modeling machine works with this numerical data. For the outside of the crown, the typical colonal figure data (= CAD Data Base) is prepared. And this data is modified with computer to fit the prepared tooth margin and proximal or antagonical tooth (= CAD). This CAD Data Base was obtained with 3 dimensional point digitizer (3DPD). Because this measuring method with 3DPD is to be able to select points, the CAD Data Base could be consists of characteristic points. When this data base is really used, it is interpolated with s-spline. Spline interpolation is indispensable to the CAD/CAM system. Further understanding of this system, explanation is divided into three parts which are 3D measurement, CAD and CAM. (3D measurement) Two types of 3D measurement is dealed with this system. One is for the CAD data base and another is for the prepared tooth model. 3D measurement of the prepared tooth model is equivalent of the impression takings in the routine method. For the clear marginal line and for the uniform distribution of measuring points, the prepared tooth model is tilted and rotated on the working table when it is measured with laser. (CAD) The CAD Data Base can be extended, contracted, parallel translated and rotated with the Affine transformation. For putting the individual margin data on the CAD Data Base, the prepared tooth margin is re-digitized with 3DPD. Occlusal data is taken from F.G.P. core. (CAM) The application of the spline interpolation to the tool offset theory, which is effective at the groove especially, makes easy to calculate the tool path. When the prepared tooth model is manufactured, it is tilted and rotated on the table like the measurement with laser-scan.     

Defective mitogen-activated protein kinase (ERK2) signaling in gastric mucosa of portal hypertensive rats: potential therapeutic implications.

Portal hypertensive (PHT) gastropathy is a frequent, serious complication of liver cirrhosis. PHT gastric mucosa has numerous abnormalities such as reduced mucosal potential differences, reduced surface oxygenation, and increased susceptibility to injury caused by alcohol, aspirin, and other noxious factors. Because such mucosal injury is initially mediated by oxygen free radicals, and because mitogen-activated protein (MAP) kinase (ERK2) protects against cellular stress and induces cell proliferation, we postulated that oxidative stress-induced ERK2 activation is defective in PHT gastric mucosa. Here we show that in PHT gastric mucosa, ERK2 activation by oxidative stress is impaired. This impairment is mediated by overexpression of MAP kinase phosphatase-1 (MKP-1), which results from the underlying and continual oxidative state associated with portal hypertension, and is ameliorated by inhibiting MKP-1. Furthermore, we found that supplementing vitamin E, a free radical scavenger, reduces the oxidative state in PHT gastric mucosa, normalizes MKP-1 expression, and thereby reverses impairment of oxidative stress-induced ERK2 activation. Finally, we show that orally administered vitamin E completely reverses the increased susceptibility of PHT gastric mucosa to alcohol injury. Our findings point to a new molecular and mechanistic basis for PHT gastropathy and provide a new therapeutic modality for protection of PHT gastric mucosa.     

Prognostic Significance of Hepatic Vein Waveform by Doppler Ultrasonography in Cirrhotic Patients with Portal Hypertension

Objective: We prospectively evaluated the prognostic value of the flat hepatic vein waveform, measured by Doppler ultrasound, in cirrhotic patients with portal hypertension.
Methods: The Doppler pattern of right and left hepatic veins in a series of 120 consecutive cirrhotic patients with portal hypertension but without hepatocellular carcinoma was examined, together with clinical and biochemical parameters.
Results: Flat waveform of the right hepatic vein was recognized in nine patients and that of the left hepatic vein was seen in 13. After a mean follow-up of 13.6 ± 9.7 months, 17 patients died, all from liver failure. In the univariate analysis, variables significantly associated with the duration of survival were age, etiology of the liver cirrhosis, upper gastrointestinal bleeding after start of the study, Child-Pugh score, ascites, encephalopathy, prothrombin index, bilirubin, albumin, and flat Doppler waveform in the right and left hepatic veins. Multivariate analysis showed that flat Doppler waveform in the right hepatic vein, bilirubin, and prothrombin index were independently related to survival.
Conclusions: The prognostic accuracy in cases of cirrhosis with portal hypertension is significantly improved with acquistion of information obtained from hepatic vein waveform by Doppler ultrasound.     

Hepatitis B: Who should be treated?-managing patients with chronic hepatitis B during the immune-tolerant and immunoactive phases

New hepatitis B virus (HBV) infections are decreasing owing to improved antiviral therapy and increased HBV vaccination worldwide; however, the number of HBV infections remains a major cause of liver carcinogenesis. HBV triggers cytotoxic immunity to eliminate HBV-infected cells. Therefore, the HBV pathophysiology changes in persistently infected individuals depending on host immune responses and HBV DNA proliferation state. To prevent liver cirrhosis and carcinogenesis caused by HBV, it is important to treat HBV infection at an early stage. Active treatment is recommended for the immunoactive hepatitis B surface-antigen-positive and -negative phase, but not during the immune-inactive phase or immune-tolerant phase; instead, follow-up is recommended. However, these patients should be monitored through regular blood tests to accurately diagnose the immune-inactive or -tolerant phases. The treatment regimen should be determined based on the age, sex, family history of liver cancer, and liver fibrosis status of patients. Early treatment is often recommended due to various problems during the immune-tolerant phase. This review compares the four major international practice guidelines, including those from the Japanese Society of Hepatology, and discusses strategies for chronic hepatitis B treatment during the immune-tolerant, immune-inactive, and resolved phases. Finally, recommended hepatitis B antiviral therapy and follow-up protocols are discussed.     

Portal vein thrombosis in liver cirrhosis简

Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.     

Cystic and alveolar echinococcosis: an epidemiological survey in a Tibetan population in southeast Qinghai, China

An epidemiological investigation on echinococcosis was made in Jiuzhi County of Qinghai Province, western China. Ultrasonography and an indirect hemagglutination test revealed a morbidity of 8.0% (124/1,549) and a seroprevalence of 25.8% (287/1,113), respectively, in the Tibetan population. The morbidity in herdsmen (16.6%) and Buddhist priests (15%) was significantly higher than that in other occupation groups (3.2%), and it was higher in females (9.8%) than in males (6.2%). The ultrasound images showed a coexistence of cystic echinococcosis (CE) and alveolar echinococcosis (AE), occupying 69 and 31% of the cases, respectively. An Echinococcus Western blot assay was performed as a serological backup test for differentiating CE and AE. The assay revealed that serum samples from most cases with a positive AE image showed a specific antibody against antigen bands at 16/18 kDa. Autopsy proved that 9 out of 12 stray dogs were infected with Echinococcus granulosus (n = 8) and E. multilocularis (n = 1). Inspection at the abattoirs demonstrated a hydatid rate of 78.5% in yaks and 82.6% in sheep. The data indicate that Jiuzhi County is an important endemic area for both CE and AE, in both human and animal populations.     

Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

BACKGROUND AND AIMS: Portal hypertensive gastropathy (PHG) is now recognized to be a distinct entity. Recently, angiogenesis has been noticed as a key factor in clarifying the pathophysiology of various diseases. Angiogenesis in the PHT of explored gastric mucosa has yet to be explored. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor. The aim of the present study was thus to investigate whether the hypoxic state exists in PHG, and whether VEGF appears more strongly in PHG than in normal gastric mucosa and, if so, what exactly is the role of the hypoxic state and VEGF in PHG. METHODS: At 1, 3, 7 and 14 days after either a portal ligation or sham operation, the portal venous pressure, the gastric mucosal blood flow volume and the blood gas were measured and, the expression of VEGF and antiproliferating cell nuclear antigen (PCNA) in gastric mucosal specimens was immunohistochemically assessed. RESULTS: The portal pressure (PP) and the gastric mucosal blood flow (GMBF) in the PHT rats were significantly greater than in the control (CTR). Both the SaO2 and PaO2 of the arterial blood gas were lower in the PHT rats than in the control rats. The percentage of VEGF expression in the PHG was found to be higher than that in the control gastric mucosa. The percentage of PCNA expression in the PHG was higher than that in the control gastric mucosa. CONCLUSION: The levels of SaO2 and PaO2 were lower in the PHT rats. There is a possibility that a kind of portal hypertensive gastric change may trigger an enhanced histochemical expression of VEGF. The increased activity of VEGF may have a possibility of the hypoxic gastric mucosal state caused by the presence of active congestion. This damaged mucosal state 'PHG' may thus facilitate the fragility in PHG and such lesions may be slow and insidious, which may therefore lead to sudden and severe anemia, thus causing massive and sometimes fatal hemorrhaging.     

An increase in murine skeletal muscle peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) mRNA in response to exercise is mediated by beta-adrenergic receptor activation

A single bout of exercise increases expression of peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha mRNA, which may promote mitochondrial biogenesis in skeletal muscle. In brown adipose tissue, cold exposure up-regulates PGC-1alpha expression via adrenergic receptor (AR) activation. Because exercise also activates the sympathetic nervous system, we examined whether exercise-induced increase in PGC-1alpha mRNA expression in skeletal muscle was mediated via AR activation. In C57BL/6J mice, injection of the beta2-AR agonist clenbuterol, but not alpha-, beta1-, or beta3-AR agonists, increased PGC-1alpha mRNA expression more than 30-fold in skeletal muscle. The clenbuterol-induced increase in PGC-1alpha mRNA expression in mice was inhibited by pretreatment with the beta-AR antagonist propranolol. In ex vivo experiments, direct exposure of rat epitrochlearis to beta2-AR agonist, but not alpha-, beta1-, and beta3-AR agonist, led to an increase in levels of PGC-1alpha mRNA. Injection of beta2-AR agonist did not increase PGC-1alpha mRNA expression in beta1-, beta2-, and beta3-AR knockout mice (beta-less mice). PGC-1alpha mRNA in gastrocnemius was increased 3.5-fold in response to running on a treadmill for 45 min. The exercise-induced increase in PGC-1alpha mRNA was inhibited by approximately 70% by propranolol or the beta2-AR-specific inhibitor ICI 118,551. The exercise-induced increase in PGC-1alpha mRNA in beta-less mice was also 36% lower than that in wild-type mice. These data indicate that up-regulation of PGC-1alpha expression in skeletal muscle by exercise is mediated, at least in part, by beta-ARs activation. Among ARs, beta2-AR may mediate an increase in PGC-1alpha by exercise.