A 24-year-old man presented with a 1.5 × 0.5 cm-sized erythematous nodule with central crust on the forehead since 5 years ago. There was no history of trauma or previous skin disorders. Histopathologic examination showed a typical picture of osteoma cutis. In addition, transepidermal elimination of bony material was observed: red linear plate-like calcified lamella structures had extruded to the skin surface through the perforated epidermis. The perforating type of osteoma cutis was discussed.
Epidermis ; Forehead ; Humans ; Osteoma* ; Skin ; Young Adult

BACKGROUND: Although hypoxic pulmonary vasoconstriction (HPC) and hypoxic coronary vasodilatation (HCD) have been recognized by many researchers, the precise mechanism remains unknown. As isolated arteries will constrict or relax in vitro in response to hypoxia, the oxygen sensor/transduction mechanism must reside in the arterial smooth muscle, the endothelium, or both. Unfortunately, much of the current evidence is conflicting, especially concerning to the dependency of HPC and HCD on the endothelium and the role of the K+ channel. Therefore, this experiment was attempted to clarify the dependency of HPC and HCD on the endothelium and the role of the K+ channel on HPC and HCD. METHODS: HPC was investigated in isolated main pulmonary arteries precontracted with norepinephrine (NE). HCD was investigated in isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit solution. Hypoxia was induced by gassing the chamber with 95% N2 +5% CO2, which was maintained for 15 - 25 min. RESULTS: 1)Hypoxia elicited a vasoconstriction in NE-precontracted pulmonary arteries with endothelium, but a vasodilatation in PGF 2 alpha-precontracted coronary arteries with and without endothelium. There was no difference between the amplitude of the HPC and HCD induced by two consecutive hypoxic challenges and the effect of normoxic and hyperoxic control Krebs-Henseleit solution on subsequent response to hypoxia. 2)Inhibition of NO synthesis by the treatment with Nw-nitro-L-arginine reduced HPC in pulmonary arteries, but inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HPC and HCD, respectively. 3)Blockades of the TEA-sensitive K+ channel abolished HPC and HCD. 4)Apamin, a small conductance Ca2+/-activated K+ (KCa) channel blocker, and iberiotoxin, a large conductance KCa channel blocker, had no effect on the HCD. 5)Glibenclamide, an ATP-sensitive K+ (KATP) channel blocker, reduced HCD. 6)Cromakalim, an K(ATP) channel opener, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia and glibenclamide reduced both hypoxia- and cromakalim-induced vasodilations. 7)Verapamil, a Ca2+ entry blocker, caffeine, a Ca2+ emptying drug; and ryanodine, an inhibitor of Ca2+ release from SR, reduced HPC, respectively. CONCLUSION: HPC is dependent on the endothelium and is considered to be induced by inhibition of the mechanisms of NO-dependent vasodilation while HCD is independent of the endothelium and is considered to be induced by activation of the K(ATP) channel.
Anoxia ; Arteries ; Caffeine ; Coronary Vessels ; Cromakalim ; Dinoprost ; Endothelium ; Glyburide ; Indomethacin ; Muscle, Smooth ; Norepinephrine ; Oxygen ; Prostaglandin-Endoperoxide Synthases ; Prostaglandins F ; Pulmonary Artery ; Relaxation ; Ryanodine ; Vasoconstriction* ; Vasodilation*

No abstract available.
Chloroform*

Pelvic Bones* ; Sex Differentiation*

No abstract available.
Calcium* ; Erythrocytes* ; Sodium* ; Spherocytes

No abstract available.
Macrophages, Peritoneal* ; Nitric Oxide ; Nitric Oxide Synthase* ; Shock* ; Tumor Necrosis Factor-alpha

The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic ; Cell Membrane ; Endothelial Cells ; Indomethacin ; Lanthanum ; Muscle, Smooth, Vascular* ; Ouabain ; Ryanodine ; Sarcoplasmic Reticulum ; Sodium* ; Vanadates* ; Verapamil

No abstract available.
Leukemia*

No abstract available.
Antipsychotic Agents* ; Biomarkers*

BACKGROUND: Electroconvulsive therapy (ECT) that works by electrically inducing grand mal seizure is an effective therapy for patients with major psychosis and affective disorders. But ECT may produce intense stimulation of the central nervous system resulting in hypertension and tachycardia. Such an acute hyperdynamic state may be undesirable because of possible cardiovascular complications. We compared the ability of different bolus doses of esmolol to blunt the hemodynamic effects of ECT. METHODS: Twenty ASA physical status 1~2 patients were enrolled in a crossover design study to determine the effects of two standard esmolol bolus doses (0.5 mg/kg and 1.0 mg/kg) on the hemodynamic response and seizure duration during ECT. In each patients receiving esmolol or placebo, arterial pressure, heart rate, seizure duration and peripheral oxygen saturation (SpO2) were recorded. RESULTS: The seizure duration with placebo was 43 +/- 9 sec, esmolol 0.5 mg/kg bolus dose was 39 +/- 14 sec and esmolol 1.0 mg/kg bolus dose was 39 +/- 12 sec, but it was not significant. Compared with esmolol 0.5 mg/kg bolus dose, esmolol 1.0 mg/kg bolus dose decreased blood pressure and heart rate during ECT more effectively. CONCLUSIONS: Esmolol 1.0 mg/kg bolus dose was considered to be the better dose in blunting the hyperdynamic response during ECT without shortening of seizure duration.
Arterial Pressure ; Blood Pressure* ; Central Nervous System ; Cross-Over Studies ; Electroconvulsive Therapy* ; Heart Rate* ; Heart* ; Hemodynamics ; Humans ; Hypertension ; Mood Disorders ; Oxygen ; Psychotic Disorders ; Seizures ; Tachycardia