An unenveloped single-stranded DNA virus (TTV) has been reported in association with posttransfusion and acute and chronic hepatitis of unknown etiology. DNA of TTV was tested for by polymerase chain reaction with heminested primers in 127 patients with chronic liver disease and 105 healthy blood donors in Thailand. TTV DNA was detected in 23 (59%) of the 39 patients without hepatitis B surface antigen or RNA of hepatitis C virus, at a frequency significantly higher than the detection in 21 (36%) of the 59 patients with HBsAg (P < 0.05) or in 38 (36%) of the 105 blood donors (P< 0.05). Among patients with chronic liver disease, TTV DNA occurred in those with liver cirrhosis and hepatocellular carcinoma more frequently than in those with chronic hepatitis (35 of 65 or 54% vs. 20 of 62 or 32%, P< 0.05). There were no differences in age, sex, or markers of infection with hepatitis B, C and GBV-C/HGV viruses, indicating a mode of transmission of TTV different from those of the other hepatitis viruses. Phylogenetic analysis indicated three different genotypes of TTV with six distinct subtypes in Thailand. Based on these results, TTV would have a role in the development of chronic liver disease of unknown etiology in Thailand.
Periodical nutritional management improved MHE and QOL. Improving the patient's nutritional condition may be one approach to treating MHE.
BACKGROUND AND PURPOSE:MetS is a cluster of risk factors associated with significant cardiovascular morbidity and mortality and diminished cognitive function. Given that little is known about the early signs of brain vulnerability related to persistent metabolic dysfunction, we set out to determine whether cognitively healthy middle-aged individuals with MetS exhibit an altered cerebrovascular response to a cognitive challenge relative to those without MetS. MATERIALS AND METHODS: Forty neurologically healthy adults aged 40 -60 years (19 with MetS and 21 healthy controls) performed a 2-back verbal working memory task during fMRI. We compared BOLD responses between the 2 groups in 8 a priori regions of interest previously shown to be associated with the 2-back in patients with cardiovascular disease.
The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.
Smooth muscle contraction is regulated by the phosphorylation of myosin. It is well known that tonic smooth muscles can maintain force with low energy consumption (latch state); however, the molecular mechanism underlying this phenomenon is unresolved. Here we show that single-head phosphorylated smooth myosin (SHPMII) exhibits fast (ϳ24 s ؊1 ) and slow prolonged (ϳ1 s ؊1 ) actin interactions, whereas double-head phosphorylated myosin (DHPMII) predominantly exhibits the fast (ϳ29 s ؊1 ) interaction, suggesting that the phosphorylated head of SHPMII is mechanically as active as that of DHPMII. Both the fast and the slow actin interactions of SHPMII support the positive net mechanical displacement of actin. The actin translocating velocity of SHPMII was much slower than that of DHPMII, which is consistent with the slow actin interaction of SHPMII. We propose that the "latch state" can be explained by the motor characteristics of SHPMII that is present during the sustained phase of contraction.Smooth muscle is distributed in a variety of tissues such as airways, vasculature, digestive tract, bladder, and uterus. Some smooth muscle cells, such as found in digestive tract, ileum, bladder, and uterus, are mainly relaxed and show phasic contractions upon stimulations. These smooth muscles (often referred to as "phasic smooth muscles") contract and relax rapidly, and their phasic responses are advantageous to the physiological functions such as peristalsis. On the other hand, other smooth muscle cells, such as the smooth muscle cells in airways and vasculature, show sustained contractions, and thus they are often referred to as "tonic smooth muscles." Tonic smooth muscles contract slowly, and very importantly, they can maintain force with very low energy consumption (1, 2). This state of tonic contraction is referred to as the "latch state," and the tone of the contraction plays critical roles in the change in dimension of the hollow organs for regulating airflow, blood flow, organ perfusion, filtration rate of glomeruli, and so forth. Dysregulation of these smooth muscles causes a variety of pathophysiological states such as asthma and hypertension.Contractions of both phasic and tonic smooth muscles are regulated by the phosphorylation of the regulatory light chain (RLC) 3 of smooth muscle myosin (3-8), and the muscle shortening velocity is closely correlated with the extent of the phosphorylation. Upon agonist stimulations, both phasic and tonic smooth muscles show a transient increase in force that is closely correlated with the transient increment of myoplasmic Ca 2ϩ concentration and the concomitant RLC phosphorylation. In a phasic contraction, the force returns quickly to the basal level because of the reduction of the myoplasmic Ca 2ϩ concentration (thus the phosphorylation level of RLC) to the basal level. In a tonic contraction, however, although the level of myosin phosphorylation declines after the transient increment of the myoplasmic Ca 2ϩ concentration, it does not completely return to the basal level, an...
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