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

Intracranial tuberculoma may imitate, both clinically and radiologically, the more commonly observed intracranial tumors. A 16 year old female patient was admitted due to exophthalmus(o.d) and headache. Neurologically papilledema was noted on the both fundus and exophthalmometry revealed that exophthalmus(17mm, 13mm). CT brain scan showed slightly high density lesion with surrounding low density in right frontotemporal area, attached to the sphenoid bone. And also hyperostosis was noted at the right sphenoid bone and dense homogeneous enhancement of mass after contrast infusion was seen. This case reports outlines the development of such a lesion masquerading as a typical meningioma of the sphenoid ridge. Discussion of intracranial tuberculoma follows, with special reference to clinical and radiological findings.
Adolescent ; Brain ; Female ; Headache ; Humans ; Hyperostosis ; Intracranial Pressure ; Meningioma* ; Papilledema ; Sphenoid Bone ; Tuberculoma* ; Tuberculoma, Intracranial

No abstract available.
Asthma*

PURPOSE: To investigate the influence of 2 phases of short interval intracortical inhibition (SICI) on the cortical silent period (SP). MATERIALS AND METHODS: Single- and paired-pulse transcranial magnetic stimulations (TMSs) at 1 and 2.5ms interstimulus intervals (ISIs) were applied to the left motor cortex in 12 healthy subjects while their right hand muscles were moderately activated. Conditioning stimulation intensity was 90% of the active motor threshold (AMT). Test stimulation intensities were 120, 140, 160, 180, 200, 220, 240, 260% of the AMT and at 100% of the maximal stimulator output, the order of which was arranged randomly. The rectified electromyography area of motor evoked potential (MEP) and duration of the SP were measured off-line using a computerized program. RESULTS: At high-test stimulation intensities, MEP areas were saturated in both single- and paired-pulse stimulations, except that saturated MEPs were smaller for the paired-pulse TMS at 1ms ISI than for the other conditions. As the test stimulation intensity increased, SP was progressively prolonged in both single- and paired-pulse stimulations but was shorter in paired-pulse than single-pulse TMS. Overall, the ratio of SP duration/MEP area was comparable between single- and paired-pulse TMS except for the paired-pulse TMS at 1 ms ISI with a test stimulation intensity at 140-180% of the AMT, in which the ratio was significantly higher than in the single pulse TMS. CONCLUSION: These results suggest that 2 phases of SICI modulate MEP saturation and SP duration differently and provide additional evidence supporting the view that 2 phases of SICI are mediated by different inhibitory mechanisms.
Adult ; Evoked Potentials, Motor/*physiology ; Female ; Humans ; Male ; Motor Cortex/*physiology ; Transcranial Magnetic Stimulation

BACKGROUND: Although post operative pain has been reduced significantly since the advent of laparoscopic surgery, many patients still complain of moderate abdominal and shoulder pain after surgery. METHOD: Patients scheduled for elective laparoscopic cholecystectomy were assigned to three groups by simple randomization(12 patients per group). Group I patients(control) had no specific treatment, group II patients had 10 ml of normal saline instillation, and group III patients had 10 ml of 0.5% bupivacaine instillation. Instillation was made directly into the gallbladder bed and right subdiaphragmatic space under direct vision by the surgeon at the end of the procedure and before evacuating the pneumoperitoneum. RESULT: Compared to that of the group I, VAS of group II and III did not show any statistically significant difference. Compared to the group I, group II & III showed no significant difference in numbers of requests of Tiaprofenic acid during the 36hours after the surgery. CONCLUSION: Topical instillation of 0.5% bupivacaine 10 ml to the gallbladder bed and right subdiaphragmatic space after laparoscopic cholecystectomy is not effective for the post operative pain control.
Bupivacaine* ; Cholecystectomy, Laparoscopic* ; Gallbladder ; Humans ; Laparoscopy ; Pain, Postoperative* ; Pneumoperitoneum ; Shoulder Pain