Superficial Radial Nerve and Cephalic Vein: An Anatomic Study by Cadaver Dissection

OBJECTIVE: To acquire normal anatomy of superficial radial nerve and cephalic vein and identify the optimal site for venipuncture of cephalic vein at wrist to decrease the damage of superficial radial nerve. METHOD: We examined anatomic relationships of the superficial radial nerve, cephalic vein, and styloid process of radius in 14 hands from 10 cadavers. The distances were measured from the styloid process of radius to the point at which the superficial radial nerve pierced fascia, and to the crossing point of superficial radial nerve with cephalic vein. RESULTS: The mean distance from the styloid process of radius to the point at which the superficial radial nerve pierced fascia was 79.9+/-9.84 (60~93) mm and from the styloid process of radius to the crossing point of superficial radial nerve with cephalic vein was 29.5+/-15.24 (13~55) mm. CONCLUSION: The most optimal injection site for venipuncture of cephalic vein at wrist was located 55 mm more proximal area from styloid process.

A Case of Conversion Disorder Presenting Hemiplegia

Patients with conversion disorder are often presented with critical symptoms or signs which could suggest severe organic disorders. Hysterical hemiparesis is a relatively rare presentation and it is difficult to diagnose because it is displayed as a unilateral motor weakness with or without sensory deficits. A previously healthy 23-years-old woman developed sudden onset of hemiplegia and hemianesthesia with loss of anal tone. Before the onset, she had a traffic accident. A through medical workup including X-rays, MRI, CT scans, EMG, and brain SPECT revealed no organic causes for such neurologic deficits. She gradually regained neurologic function over 2 months from the onset. Conversion disorder should be considered when symptom- related anatomic or physiologic abnormalities could not be proven with appropriate workup. Medical evaluation must be performed in advance to the diagnosis of conversion disorder to avoid misdiagnosis.

Thyrotropin Suppresses INF-r Mediated Gene Expression by Inhibiting Signal Transducer and Activation of Transcription 1(STAT1) Activity in FRTL-5 Cells / 대한내분비학회지

BACKGROUND: The proinflammatory cytokine, IFN-y has been shown to exert pleiotropic effects in a variety of pathophysiologic conditions in autoimmune thyroid disease. The thyrocyte response to IFN-y is mediated two distinct classes of proteins, Janus kinases(Jakl and Jak2) and Signal Transducers and Activation of Transcription(STATl). The activation of STAT 1 is involved in the regulation of many interferon stimulated genes, such as MHC class II, intercellular adhesion molecules-1(ICAM-1) and MHC class II transactivator(CIITA) after the binding to the GASgFN- pactivated site) of the gene promoters. Recently we found TSH/forskolin inhibits IFN-y stimulated maximal expression of ICAM-1 in FRTL-5 cell. IFN-y action is localized between -175 bp and -97 bp from the start of translation of ICAM-1 gene which contains regulatory elements known to be involved in IFN-y action in other eukaryotic cells, palindromic IFN-y activated site(GAS)(5-TTTCCGGGAAA-3) which could bind STAT1, STAT3, STAT5, STAT6. Furthermore, the addition of TSH and forskolin causes a decrease in ICAM-1 promoter activity and its action was localized in GAS. These findings suggested TSH/cAMP signaling pathways downregulate IFN-y activated Janus kinase-STAT signaling path. We wanted to explore the possible involvement of elevated cAMP in the negative regulation of IFN-y induced STAT1 activation in thyroid cells. METHOD: We made several 5-deletion constructs of rat ICAM-1 promoter and analyzed the promoter activities by measuring the luciferase activity after tranfection into FRTL-5 cells. The protein/DNA complex was measured by electrophoretic mobility shift analysis using labeled oligonucleotide. We checked the level of total and phosphorylated STATl protein by immunoblot analysis using specific antibodies. RESULTS: Stimulation of IFN-y in FRTL-5 cells resulted in rapid activation of STATl/DNA binding activity, which was apparent after several minute of stimulation, maintains its activity until 48 h. Incubation of cells with TSH result in suppression of IFN-p mediated STAT1/DNA binding activity throughout the time course of activation by IFN-y. Addition of TSH into 5H maintained FRTL-5 cells did not change the total amount of latent STAT1 amount and also not affect IFN-y mediated production of total STAT1 until 4 h. IFN-y(100 U/mL) rapidly induced phosphorylation of STAT1 within 30 min. and maintained its level without significant change until 48 hours. Cells treated with TSH dramatically lowered the level of IFN-y induced production and phosphorylation of STAT1 after 12 h, 24 h, 36 h, and 48 h but TSH had no effect on the level of phosphorylated STATl within 4 h after IFN-y stimulation. The proteasome inhibitor, MG132 and phosphatase inhibitor, sodium orthovanadate did not block the TSH or forskolin mediated downregulation of phosphorylated STAT1. CONCLUSION: These results indicate a regulatory mechanism which TSH signaling can modulate the prolonged activation of Jak/Stat by IFN-y. We identified one of mechanisms related to TSH mediated negative suppression of the ICAM-1 gene; TSH/cAMP signaling pathways downregulate the cytokine activated Janus kinase-STAT signaling path.