No abstract available.
Neck* ; Retreatment*

No abstract available.
Pregnancy* ; Pyelonephritis*

No abstract available.
Slipped Capital Femoral Epiphyses*

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

No abstract available.

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

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

Genomic instability, which occurs through both genetic mechanisms (underlying inheritable phenotypic variations caused by DNA sequence-dependent alterations, such as mutation, deletion, insertion, inversion, translocation, and chromosomal aneuploidy) and epigenomic aberrations (underlying inheritable phenotypic variations caused by DNA sequence-independent alterations caused by a change of chromatin structure, such as DNA methylation and histone modifications), is known to promote tumorigenesis and tumor progression. Mechanisms involve both genomic instability and epigenomic aberrations that lose or gain the function of genes that impinge on tumor suppression/prevention or oncogenesis. Growing evidence points to an epigenome-wide disruption that involves large-scale DNA hypomethylation but specific hypermethylation of tumor suppressor genes, large blocks of aberrant histone modifications, and abnormal miRNA expression profile. Emerging molecular details regarding the modulation of these epigenetic events in cancer are used to illustrate the alterations of epigenetic molecules, and their consequent malfunctions could contribute to cancer biology. More recently, intriguing evidence supporting that genetic and epigenetic mechanisms are not separate events in cancer has been emerging; they intertwine and take advantage of each other during tumorigenesis. In addition, we discuss the collusion between epigenetics and genetics mediated by heterochromatin protein 1, a major component of heterochromatin, in order to maintain genome integrity.
Biology ; Carcinogenesis ; Chromatin ; DNA ; DNA Methylation ; Epigenomics* ; Genes, Tumor Suppressor ; Genetics* ; Genome ; Genomic Instability ; Heterochromatin ; Histones ; MicroRNAs ; Sequence Deletion