No abstract available.
Neck* ; Retreatment*

No abstract available.
Pregnancy* ; Pyelonephritis*

No abstract available.
Carcinoma, Squamous Cell* ; Ear Canal*

No abstract available.
Slipped Capital Femoral Epiphyses*

No abstract available.
Carcinoma, Squamous Cell* ; Head* ; Neck* ; Neoplasm Metastasis*

No abstract available.

p73, a first p53 relative, has been identified at chromosome 1p36, a region that is deleted in variety of human cancers. This protein shares strong homology with p53 protein, suggesting functional similarities with p53. Indeed, p73 can activate p53 downstream genes inducing apoptosis or growth arrest in tumor cells lacking p53. This phenomenon leads us to investigate the function of p73 in ovarian cancer because aberrant p53 was very frequently found in this cancer. We hypothesize that DNA damaging agents trigger p53 dependent apoptotic pathway through p73 instead of p53 in ovarian cancer having aberrant p53. We selected SKOV3 ovarian cancer cell line having no p53 gene and treated this cell line with cisplatin. After the treatment, we examined the transcriptional level of p73 and p21. Moreover, to identify whether the status of p53 influence to the function of p73, we performed same experiment after inserting adenovirus mediated p53(Avp53) into cell line. We detected significantly increased transcripts of p73 whcn treated with cisplatin. But treated with Avp53 or combined treatment with cisplatin, the transcriptional levels were not changed. These data suggest that overexpression of p73 may be important to trigger apoptotic pathway when the p53 gene is lost, but not so important in cells having normal p53.
Adenoviridae ; Apoptosis ; Cell Line* ; Cisplatin ; DNA ; Genes, p53 ; Genes, Tumor Suppressor ; Humans ; Ovarian Neoplasms*

No abstract available.
Cerebral Palsy* ; Equinus Deformity* ; Heel* ; Muscle Spasticity*

A 69-year-old man was admitted to the hospital because of flu-like symptoms and fatigue for 2 weeks. Computed tomography revealed ground glass opacity and consolidation in both the lungs as well as pleural effusion. The patient was diagnosed with pneumonia and was hospitalized. At the time of hospitalization, he complained of shortness of breath and coughed-up blood-tinged sputum. Two days after admission, he died suddenly. An autopsy was performed; cardiomegaly was noted, and further examination revealed that the aortic valve had been destroyed by multiple, irregular vegetations. Herein, we report an autopsy case of infective endocarditis with a review of the relevant literatures.
Aged ; Aortic Valve ; Autopsy* ; Cardiomegaly ; Dyspnea ; Endocarditis* ; Fatigue ; Glass ; Hospitalization ; Humans ; Lung ; Pleural Effusion ; Pneumonia ; Sputum

The kidney and balances of fluid and volume are the basic components of bloocl pressure control, and the kidney is the primary site that initiates the hypertensive process and is affected by hypertensive vascular disease. In the kidney, the dopamine is a potent natriuretic and vasodilating agent, participat- ing in renal sodium excretion and maintenance of cardiovascular homeostasis. And the dopamine receptors in central nervous system and peripheral organs were identified by physiological, biochernical and radioligand binding techniques. Rut previous morphological and biochemical studies have been unable to characterize or determine the tissue distribution of the dopamine receptor subtypes because no selective ligands are available yet. Furthermore, the cellular distribution of the dopamine receptor subtypes in the rat kidney is not demonstrated well. In the SHR, the ability of exogenous and endogenous renal dopamine to engender a natriuresis is impaired. Since renal dopamine levels in genetic models of hypertension are not lower than their normotensive controls, the impaired intrarenal paracrine effect of dopamine in these animal models of hypertension appears to be receptor or postreceptor mediated. And renal dopamine derives mainly from renal tubular dopamine production and to a lesser extent from dopaminergic nerves. The present study utilizes imrnunohistochemistry with specific antibodies to characterize the renal distribution of dopamine receptor subtypes and recognize the role of dopamine receptor defect in the pathogenesis of hypertension in 14-week-old WKY (mean HP 108+/-5mmHg) and SHR (mean RP 174+/-7 mmHg) kidneys. Also it utilizes antibody of tyrosine hyclroxylase (TH) to recognize the site of the dopamine production mediated by TH using light microscopic immunohistochemistry. In the immunohistochemistry of the WKY kidney, dopamine D1 receptor protein is localized to glomerulus, proximal tubule, distal tubule, renal vessels, cortical and medullary collecting duct. And in the SHR kidney, dopamine D1 receptor protein is localized to glomerulus, distal tubule, renal vessels, cortical and medullary collecting duct, and juxtaglomerular apparatus (JGA). But there is no demonstrable positive reaction in the proximal tubule and weakly positive reactions in the renal arterioles of SHR compared with WKY kidney. In the immunohisto-chemistry of the WKY kidney, dopamine D1 receptor protein is localized to glomerulus, proxirnal tubule, distal tubule, renal vessels, cortical and rnedullary collecting duct. And in the SHR kidney, dopamine D2 receptor protein is localized to glomerulus, distal tubule, renal vessels, cortical and medullary collecting duct, and JGA. So, there is no demonstrable positive reaction in the proximal tubule of SHR compared with WKY. In the glomerulus of the WKY and SHR kidneys, both dopamine D1 and D2 receptors are localized. In the in situ hybridization of the WKY and SHR kidneys, dopamine D and D receptors are only demonstrated at the renal vessels. The positive reaction to TH immunohistochemistry of the WKY and SHR kidneys is only observed in the renal medulla compared with negative reaction on the renal cortex. Considering the excretion of sodium up to 65-70% with volume expansion may be mediated by dopamine D1-like receptors in the proximal tubule, our immunohistochemistry findings for the dopamine receptors may support the failure of natriuretic response in the SHR due to an abnormal dopamine receptor. Also our results rnay mean that the glornerular filtration rate is mediated by both dopamine D1 and Dz receptors comparing with the previous studies that the glomerular filtration rate was mediated by dopamine D2 receptor. I'here are some differences in the receptors expressing sites on the previous radioligand binding and pharmacologic studies, but our results suggest that at least some of the renal dopamine DA and DAz receptors correspond structurally to the central dopamine D1 and D2 receptors. Finally the result of TH immunohisto-chemistry suggests that the production of dopamine in the proximal tubule is not mediated by TH.
Animals ; Antibodies ; Arterioles ; Central Nervous System ; Dopamine* ; Filtration ; Glomerular Filtration Rate ; Homeostasis ; Hypertension ; Immunohistochemistry* ; In Situ Hybridization ; Juxtaglomerular Apparatus ; Kidney* ; Ligands ; Models, Animal ; Models, Genetic ; Natriuresis ; Rats* ; Rats, Inbred SHR* ; Receptors, Dopamine ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Sodium ; Tissue Distribution ; Tyrosine ; Vascular Diseases