No abstract available.

No abstract available.
Chickenpox ; Polymerase Chain Reaction ; Pregnancy

No abstract available.
Porokeratosis*

No abstract available.
Acneiform Eruptions ; Bevacizumab

BACKGROUND: Although postmenopausal estrogen replacement therapy is known to reduce cardiovascular mortality, the mechanism is not clear yet. Furthermore, the effect of estrogen on vascular tonus is reportedly variable according to the animal models, vascular beds and agonists used. MATERIALS AND METHOD: Bilateral ovariectomies were performed in 12 week-old, 18 spontaneously hypertensive rats (SHR) and 18 normotensive Wistar-Kyoto rats (WKY). Rats were divided into three groups according to the dose of 17beta-estradiol (E 2 ) pellets implanted subcutaneously two weeks after ovariectomy: control (no implantation), low-dose (0.5 mg) and high-dose (5 mg) E 2 replacement group. Two weeks after pellet implantation, organ bath experiments were performed using descending thoracic aortae. For endothelium-dependent relaxation, acetylcholine (10(-9) -3x10(-6) M) was cumulatively added into the vessels precontracted with 10(-7) M norepinephrine (NE). For vasoconstrictor responses, cumulative concentration-contraction curves were constructed in quiescent vessels using NE (10(-9) -10(-5) M), U46619 (10(-9) -3x10(-6) M), endothelin-1 (10(-10) -10(-7) M). In addition, contraction to angiotensin II (10(-7) M) was also obtained. Serum 17beta-estradiol levels were measured by radioimmunoassay. Blood pressure was measured by tail-cuff method in some SHRs before ovariectomy and after placebo/E 2 replacement. RESULTS: Endothelium-dependent relaxation to acetylcholine was impaired in WKY treated with 5 mg E 2 (pIC 50 : control vs 5mg E 2 : 7.75+/-0.13 vs 7.27+/-0.16: n=6: p<0.05). No significant effect was noted in SHR. Contraction to angiotensin II was inhibited by low-dose E 2 in WKY and high-dose E 2 in SHR (% of the contraction to 60 mM KCl: WKY: control vs 0.5 mg E 2 : 39+/-5 vs 25+/-2: SHR: control vs 5 mg E 2 : 34+/-4 vs 22+/-2: n=6 and p<0.05 in WKY and SHR). In contrast, NE-induced contraction was enhanced by E 2 replacement (both low- and high-dose) in WKY and SHR (WKY: control vs 0.5 mg E 2 vs 5 mg E 2 : AUC: 280+/-24 vs 387+/-26 vs 374+/-25: maximal contraction: 137+/-8 vs 166+/-8 vs 162+/-3: pD 2 : 7.63+/-0.11 vs 8.17+/-0.13 vs 8.13+/-0.13: SHR: control vs 0.5 mg E 2 vs 5 mg E 2 : AUC: 265+/-17 vs 349+/-16 vs 406+/-19: maximal contraction: 152+/-6 vs 181+/-9 vs 203+/-16: pD 2 : 7.45+/-0.13 vs 7.91+/-0.08 vs 8.04+/-0.04: n=6 and p<0.05 between control and treated groups in WKY and SHR for all parameters). Contraction to U46619 was enhanced by E 2 replacement in SHR (control vs 0.5 mg E 2 : AUC: 478+/-30 vs 574+/-23: maximal contraction: 181+/-9 vs 230+/-10: n=6: p<0.05 for both parameters). Maximal contractile response to endothelin-1 was also enhanced in SHR (control vs 0.5 mg E 2 vs 5 mg E 2 : maximal contraction: 165+/-7 vs 189+/-7 vs 199+/-8: n=6 and p<0.05 between control and treated groups) but not in WKY. Blood pressure was not different between placebo and E 2- treated SHR (171+/-2 vs 174+/-4 mmHg). CONCLUSION: In WKY, chronic high-dose estrogen replacement impairs endothelium-dependent relaxation to acetylcholine.: low-dose estrogen replacement does not affect endothelium-dependent relaxation in SHR and WKY. Estrogen replacement enhances the contraction to most of the contractile agonists tested except angiotensin II in both WKY and SHR. These results suggest that estrogen replacement affect the vascular tonus differently according to the vasoactive substances and/or hormones without significant effect on blood pressure.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ; Acetylcholine ; Angiotensin II ; Animals ; Aorta, Thoracic ; Area Under Curve ; Baths ; Blood Pressure ; Endothelin-1 ; Estrogen Replacement Therapy* ; Estrogens* ; Female ; Models, Animal ; Mortality ; Norepinephrine ; Ovariectomy ; Radioimmunoassay ; Rats ; Rats, Inbred SHR* ; Relaxation

No abstract available.
Neurofibromatoses* ; Peripheral Nerves*

No abstract available.
Histiocytosis*

No abstract available.
Cyclosporine* ; Humans ; Vitiligo*

PURPOSE: The purpose of this study was to compare the retention of the two denture adhesives with a silicone edentulous model and a resin denture base in vitro study. MATERIAL AND METHODS: The experimental groups were used two denture adhesives and classified into 5 subgroups each. Subgroups were divided by the number of times the saliva sprayed. The control group was used synthetic saliva only. Dislodging tensile strengths were applied to the resin denture base using Instron in 3 directions : vertical, lateral, and anterior-posterior. RESULTS: The retention of two denture adhesives was increased significantly than saliva alone (P < .05). In each denture adhesives, the retention of saliva sprayed first was decreased than denture adhesive alone, but it didn't have significant differences. Whenever saliva sprayed repeated, the retention was decreased significantly than saliva sprayed first (P < .05). In each denture adhesives, vertical retentive force was highest than lateral and anterior-posterior retentive forces, and anterior-posterior retentive force was higher than lateral retentive force. This results were significantly different (P < .05). Significant differences of the retentive ability among two denture adhesives were not observed. CONCLUSION: From the results, use of the denture adhesives resulted in improved retentive ability of denture. Especially retentive force was highest in vertical direction.
Adhesives ; Denture Bases ; Denture, Complete ; Dentures ; Retention (Psychology) ; Saliva ; Silicones ; Tensile Strength

OBJECTIVE: The present study aimed to determine the intracellular action of the antidepressant, venlafaxine, in C6 glioma cells using heat shock protein 70 (HSP70) immunocytochemistry and HSP70 Western blots; HSP70 is known to be associated with stress and depression. METHODS: The extent of HSP70 expression was measured after rat C6 glioma cells were treated with 1) dexamethasone only, 2) venlafaxine only, 3) simultaneous venlafaxine and dexamethasone, or 4) dexamethasone after venlafaxine pretreatment. Dexamethasone (10 microM, 6 hours) did not affect the level of HSP70 expression relative to control. RESULTS: Short-term (1 hour) venlafaxine treatment significantly increased the level of HSP 70 expression. Simultaneous long-term (72 hours) venlafaxine and dexamethasone treatment significantly reduced the level of HSP70 expression. Dexamethasone treatment administered following long-term (24 and 72 hours) pretreatment with venlafaxine also significantly reduced the level of HSP70 expression. CONCLUSION: Short-term treatment with venlafaxine increases the expression of HSP70, but prolonged treatment with dexamethasone suppresses the venlafaxine-induced expression of HSP70. These findings suggest that HSP70 and dexamethasone play a significant role in the pathophysiology of depression.
Animals ; Cyclohexanols ; Depression ; Dexamethasone ; Glioma ; Heat-Shock Proteins ; HSP70 Heat-Shock Proteins ; Immunohistochemistry ; Rats ; Venlafaxine Hydrochloride