No abstract available.
Animals ; Gonadotropins* ; Mice* ; Oocytes*

No abstract available.
Hepacivirus* ; Hepatitis C* ; Hepatitis* ; Prevalence*

No abstract available.
Factor VIII* ; Prevalence*

No abstract available.
Disasters*

BACKGROUND: The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action
Animals ; Apoptosis ; Cricetinae ; Cricetulus ; DNA ; Female ; Glucose ; Humans ; Insulin ; Ovary ; p38 Mitogen-Activated Protein Kinases ; Phosphotransferases* ; Protein Isoforms ; Protein-Tyrosine Kinases ; Receptor, Insulin ; RNA, Messenger ; Vanadates

BACKGROUND: The p38 mitogen-activated protein kinases (p38Map kinases) are a family of prolinedirected serine/threonine kinases. At least four isoforms of p38Map kinases have been identified; however, their physiological significances remain to be understood. Recently, the role of p38Map kinase in insulin-stimulated glucose uptake has been suggested. The present study aimed to investigate which isoform(s) were responsive to insulin stimulation. In addition, the activities of p38 Map kinase isoforms that may participate in the insulin's antiapoptotic function in CHO-IR cells were also determined. METHODS: Chinese hamster ovary cells, expressing wild- or mutated human insulin receptors (CHO-IR cells), were used to investigate whether insulin can stimulate any of the isoform(s) of the p38Map kinases. The p38Map kinase activity was determined by measuring the degree of 32P-labelling of ATF-2 protein, a specific substrate of p38Map kinase. A DNA laddering assay was performed to examine the degree of apoptosis and a RT-PCR analysis to determine which isoform(s) of the p38Map kinases were expressed in response to insulin. RESULTS: p38Map kinase activation by insulin was sharply suppressed in only the CHO-IR/A1018K cells, which lack the intrinsic tyrosine kinase activity of insulin receptors. Insulin stimulation of p38Map kinase was insensitive to SB203580, an inhibitor of the alpha(alpha)-and beta(beta)-isoforms of p38Map kinases. Moreover, orthovanadate, known as a specific stimulator of the gamma(gamma)-and delta(delta-) isoforms, stimulated the p38Map kinase activity in CHO-IR cells. Insulin increased the degree of mRNA expression of the delta-isoform, but not that of the alpha-isoform p38Map kinase. Interestingly, PD98059, an inhibitor of ERK, suppressed p38Map kinase stimulation, as well as the antiapoptotic protection of cells by insulin. As insulin was found to still protect ERK-lacking cells (CHO-IR/ SOS) from apoptosis, any substantial role(s) of ERK might be excluded. CONCLUSION: Our data suggest that insulin may stimulate the activity and expression of the-isoform of p38Map kinase in a MEK1/2-dependent manner. The involvement of the delta-isoform of p38Map kinase in insulin's antiapoptotic protection was also suggested, but remains to be investigated further to clarify the nature of its mechanism of action
Animals ; Apoptosis ; Cricetinae ; Cricetulus ; DNA ; Female ; Glucose ; Humans ; Insulin ; Ovary ; p38 Mitogen-Activated Protein Kinases ; Phosphotransferases* ; Protein Isoforms ; Protein-Tyrosine Kinases ; Receptor, Insulin ; RNA, Messenger ; Vanadates

BACKGROUND: The basal ganglia plays a major role in regulating motor, cognitive and emotional functions. In addition, it has been proposed that the functions of the basal ganglia is also related to control of sensory discrimination and sensorimotor integration. One possible way to test this hypothesis would be to investigate sensory functions in patients with various diseases affecting basal ganglia functions. Since idiopathic Parkinson's disease (IPD) is caused by selective impairment of basal ganglia functions, it could be a good model for this purpose. METHODS: We measured the grating resolution threshold (GRT) using the JVP (Johnson-Van Boven-Phillips) dome in 52 patients with IPD and 25 age-matched healthy controls. Statistical analysis employed unpaired t-test, paired t-test and simple regression analysis. P-values less than 0.05 were considered as significant. RESULTS: Patients showed significantly higher GRT than controls (3.07 +/- 0.74 vs 2.03 +/- 0.80; p<0.05). In patients, the mean GRT was not different between symptomatically dominant and non-dominant hands (3.10 +/- 0.95 vs 2.93 +/- 0.82). In the patients with hemiparkinsonism, GRT was also significantly higher in asymptomatic hands compared with controls (3.00 +/- 0.71 vs 2.03 +/- 0.80; p<0.05). The severity of sensory dysfunction in patients was not correlated with symptom duration or to symptom severity, measured by the modified Columbia rating scale (MCRS). CONCLUSIONS: The present results demonstrate that spatial discrimination is impaired in IPD, suggesting the basal ganglia plays a role in sensory regulation.
Basal Ganglia ; Discrimination (Psychology)* ; Dopamine ; Hand ; Humans ; Parkinson Disease* ; Regression Analysis ; Sensation

No abstract available.
Asthma*

No abstract available.
Lymphohistiocytosis, Hemophagocytic*

BACKGROUND: Many studies have demonstrated that nitrous oxide diffuses into the cuffs of endotracheal tubes and increases cuff volumes and pressures. Such increments of cuff pressure maybe result in damage to the trachea. We evaluated the increase of intracuff pressure, volume and the statistical significance was analyzed with personal computer. METHODS: Fourty-nine patients ranging in age 37+/-15 years, in ASA physical status class 1~2 , they were 26 males and 23 females. They divided into two groups, group I(n=25) were anesthesia with nitrous oxide : oxygen (2 L/min : 2 L/min), group II were(n=24) anesthesia with nitrous oxide : oxygen (4 L/min : 2 L/min). The cuff pressure was measured every 30 minutes and compared with each others and group I and II. RESULTS: Our results suggest that a significant intracuff volume and pressure changes developed between two groups (p<0.05), more significant intracuff pressure changes occured at group II than group I (p=0.001) and significant increment changes according to time and different concentration of nitrous oxide between two groups (p<0.05). CONCLUSIONS: This study was conducted to determine the degree of intracuff pressure and volume changes during general inhalation anesthesia with different concentration of nitrous oxide. These results suggest that a nitrous oxide significantly increases cuff pressure and volume in a concentration and time related fashion.
Anesthesia ; Anesthesia, Inhalation* ; Female ; Humans ; Inhalation* ; Male ; Microcomputers ; Nitrous Oxide* ; Oxygen ; Trachea