Carcinoma in Situ ; epidemiology ; etiology ; pathology ; Carcinoma, Squamous Cell ; pathology ; surgery ; Disease Progression ; Female ; Humans ; Lichen Sclerosus et Atrophicus ; epidemiology ; etiology ; pathology ; Prevalence ; Vulvar Neoplasms ; epidemiology ; etiology ; pathology

Biomedical Research ; Histones ; Humans ; Neoplasms

Aged ; Humans ; Lung ; pathology ; Male ; Middle Aged ; Pneumoconiosis ; complications ; diagnosis ; pathology ; Reference Standards

Breast Neoplasms ; metabolism ; pathology ; Cell Proliferation ; Female ; Humans ; Neoplasm Proteins ; metabolism

Adenocarcinoma, Clear Cell ; pathology ; Humans ; Salivary Gland Neoplasms ; pathology ; Salivary Glands ; pathology

Female ; Humans ; Male ; Mouth ; injuries ; Mouth Diseases ; chemically induced ; nursing ; Paraquat ; poisoning ; Patient Care ; standards

Objective It is known that free radicals are involved in neurodegeneration and cognitive dysfunction, as seen in Alzheimer' s disease (AD) and aging. The present study examines the protective effects of aniracetam against H2O2-induced toxicity to neuron viability, mitochondria potential and hippocampal long-term potentiation (LTP). Methods Tetrazolium salt 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) was used to detect neuronal viability. MitoTracker Red (CMX Ros), a fluorescent stain for mitochondria, was used to measure mitochondria potential. Electrophysiological technique was carried out to record hippocampal LTP. Results H2O2 exposure impaired the viability of neurons, reduced mitochondria potential, and decreased LTP in the CA1 region of hippocampus. These deficient effects were significantly rescued by pre-treatment with aniracetam (10-100 mu mol/L). Conclusion These results indicate that aniracetam has a strong neuroprotective effect against H2O2-induced toxicity, which could partly explain the mechanism of its clinical application in neurodegenerative diseases.

OBJECTIVEElectron microscopical study of infected cells to identify the pathogenic agent of SARS.

METHODSVero E6 cells infected with lung autopsy samples or nasopharyngeal swabs from SARS patients of Beijing and Guangzhou were inoculated. The supernatant and cultured cells exhibiting identifiable cytopathic effect (CPE) were prepared for electron microscopic study.

RESULTSExamination of CPE cells on thin-section revealed characteristic coronavirus particles within the cisternae of endoplasmic reticulum, Golgi apparatus, vesicles and extracellular space. They were mainly spherical or oval in shape, annular or dense, about 80 nm in diameter. Negative-stain electron microscopy identified coronavirus particles in culture supernatant, 80 - 120 nm in diameter, with club-shaped surface projections. Elongated, rod-, kidney- or other irregular shaped virons with the size of 100 - 200 nm by 60 - 90 nm were also found in the cultured cells infected with the lung samples from the Guangdong patients. Infectious virons entered cells by endocytosis or membrane fusion and released through a budding process.

CONCLUSIONThese data indicate a novel coronavirus as the causative agent of SARS. Most viral particles showed typical characteristics of coronavirus. The potential role of special shape viruses is expected to be further investigated.

Animals ; Cercopithecus aethiops ; Humans ; Microscopy, Electron ; SARS Virus ; ultrastructure ; Severe Acute Respiratory Syndrome ; virology ; Vero Cells

BACKGROUNDIgA nephropathy is the major cause of end-stage renal failure in patients with primary glomerular diseases. Tumor suppressor cylindromatosis (CYLD), the recently identified member of the deubiquitinating enzymes, has been actively involved in regulation of inflammation. This study was undertaken to investigate the CYLD expression profile in IgA nephropathy and identify factors associated with CYLD expression.

METHODSForty-one cases of IgA nephropathy were selected. CYLD expression in the kidney biopsy tissue was measured by immunohistochemical staining. Relevant clinical and pathological data were analyzed, and Logistic regression analysis was carried out to identify factors associated with CYLD expression.

RESULTSCYLD was specifically expressed in renal tubular epithelial cells in 70% of the studied patients with IgA nephropathy. All patients with positive CYLD staining had proteinuria, while only 72.7% of patients with negative CYLD had proteinuria (P = 0.003). Among studied proteinuric patients, those with positive CYLD had significantly less tubulo-interstitial lesions and higher estimated glomerular filtration rate (eGFR) levels when compared with those patients showed negative CYLD results. Logistic regression analysis indicated that the urinary protein excretion and eGFR were identified as predictors for the CYLD expression.

CONCLUSIONCYLD is expressed in renal tubular epithelial cells and appears to be associated negatively with tubulointerstitial lesions, however, its exact functional role remains to be clarified in further experiments.

Deubiquitinating Enzyme CYLD ; Glomerular Filtration Rate ; Glomerulonephritis, IGA ; metabolism ; Humans ; Immunohistochemistry ; Kidney Diseases ; metabolism ; Logistic Models ; Proteinuria ; metabolism ; Tumor Suppressor Proteins ; metabolism

OBJECTIVETo explore the effects of silencing HERC4 on the proliferation, apoptosis, and migration of cervical cancer cell line Hela and the possible molecular mechanisms.

METHODSThree HERC4-specific small interfering RNAs (siRNAs) were transfected into Hela cells, and HERC4 expression in the cells was examined with Western blotting. CCK-8 assay, annexin V-FITC/PI assay, and wound healing assay were used to assess the effect of HERC4 silencing on the proliferation, apoptosis and migration ability of Hela cells. The expression levels of cyclin D1 and Bcl-2 in the cells were detected using Western blotting.

RESULTSTransfection of siRNA-3 resulted in significantly decreased HERC4 protein expression (P<0.01). HERC4 silencing by siRNA-3 markedly suppressed the proliferation and migration of Hela cells, increased the apoptosis rate (P<0.01) and reduced the expression levels of cyclin D1 and Bcl-2 (P<0.01).

CONCLUSIONSilencing of HERC4 efficiently inhibits the proliferation, migration, and invasion of Hela cells in vitro, and the underlying mechanisms may involve the down-regulation of cyclin D1 and Bcl-2.

Apoptosis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin D1 ; metabolism ; Down-Regulation ; Female ; HeLa Cells ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; RNA Interference ; RNA, Small Interfering ; genetics ; Transfection ; Ubiquitin-Protein Ligases ; genetics ; metabolism ; Uterine Cervical Neoplasms ; pathology