No abstract available.
Muscular Dystrophy, Duchenne*

No abstract available.
Moyamoya Disease*

Dysplasia Epiphysealis Hemimelica is a rare developmental disorder of epiphyseal growth characterized by asymmetrical cartilagenous overgrowth. This disorder was first described with the “la tarsomegalie” by Mouchet and Belot in 1926 but this name, Dysolasia Epiphysealis Hemimelica, was first proposed by Fairbank in 1956. This disorder is usually limited to either the medial or lateral half of a single extremity in childhood. It is asymptomatic until the protruding epiphyseal mass interferes joint function. The character istic abnormalities are deformities, restricted motion and pain. The most frequent finding at the initial examination is an irregular, often multicentric radiopacity, and when the lesion is matured it looks irregular, and frequently there is a lobulated osseous mass protruding from the epiphysis of tarsal and carpal bones. Diagnosis by the roentgenogram requires primarily knowledge of this condition. The lesion is often microscopically indistinguishable from an osteochondroma. A case of Dysplasia Epiphysealis Hemimelica in a 17 year old male, showing typical roentgenographic appearances, is reported together with a brief review of literature in this paper.
Carpal Bones ; Congenital Abnormalities ; Diagnosis ; Epiphyses ; Extremities ; Humans ; Joints ; Male ; Osteochondroma

No abstract available in English.
Spondylolisthesis

No abstract available.
Hypertension ; Leigh Disease*

No abstract available.
Animals ; Intercellular Signaling Peptides and Proteins* ; Rats* ; Urinary Bladder Neck Obstruction* ; Urinary Bladder*

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.
Acute Kidney Injury* ; Carbon Monoxide* ; Carbon* ; Rhabdomyolysis*

No abstract available.
Intercellular Signaling Peptides and Proteins*

No abstract available.
Humans ; Biomarkers, Tumor* ; Uterine Cervical Neoplasms*