Animals ; Apoptosis ; Carcinoma, Hepatocellular ; pathology ; virology ; Cell Line, Tumor ; Cell Proliferation ; Hepatitis B virus ; Hepatocytes ; pathology ; virology ; Humans ; Liver Neoplasms ; pathology ; virology ; Trans-Activators ; genetics ; metabolism ; physiology

Animals ; Apoptosis ; Cell Cycle ; Cell Cycle Proteins ; genetics ; metabolism ; physiology ; DNA Repair ; Homeodomain Proteins ; genetics ; metabolism ; physiology ; Humans ; Inhibitor of Growth Protein 1 ; Intracellular Signaling Peptides and Proteins ; genetics ; metabolism ; physiology ; Neoplasm Metastasis ; Neoplasms ; metabolism ; pathology ; Neovascularization, Pathologic ; pathology ; Nuclear Proteins ; genetics ; metabolism ; physiology ; Prognosis ; Receptors, Cytoplasmic and Nuclear ; genetics ; metabolism ; physiology ; Signal Transduction ; Transcription Factors ; genetics ; metabolism ; physiology ; Tumor Suppressor Protein p53 ; metabolism ; Tumor Suppressor Proteins ; chemistry ; genetics ; metabolism ; physiology

Cardiovascular System ; metabolism ; Humans ; Risk Assessment

Heparanase(HPA) is an endo-beta-D-glucuronidase that degrades heparan sulfate proteoglycans side chains.Recently data suggested a role of HPA in several proteinuric diseases and an increased glomerular basement membrane.The research advanced of the molecular properties,the role in proteinuric diseases and the specific inhibitor of the human HPA were described.

Fluorodeoxyglucose F18 ; Humans ; Lymphoma ; diagnostic imaging ; Positron-Emission Tomography ; methods ; Tomography, X-Ray Computed ; methods

Adult ; Desmin ; metabolism ; Diagnosis, Differential ; Female ; Heart Neoplasms ; pathology ; Humans ; Myxoma ; pathology ; Ovarian Neoplasms ; secondary ; surgery ; Pulmonary Veins ; Sarcoma ; diagnostic imaging ; metabolism ; pathology ; secondary ; surgery ; Tomography, X-Ray Computed ; Vascular Neoplasms ; diagnostic imaging ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

Child ; Female ; Hearing Loss, Bilateral ; etiology ; Humans ; Mumps ; complications

AIM: To observe the effect of cannabinoid receptor (CB1R) agonist WIN55-212-2 on the expression of brain-derived neurotrophic factor (BDNF), c-Fos and protein kinase A beta-catalytic subunit (PKAC-β) in cerebrum cortex after intracerebral hemorrhage (ICH) in rats. METHODS: The intracerebral hemorrhage model of rat was made by the injection of collagenase Ⅶ, and WIN55-212-2 was intraperitoneally (ip) injected 30 min later. The rats were killed for sampling the brain tissues as specimens 24 h after ICH. The methods of immunohistochemical analysis and Western blotting were adopted to detect the expression of PKAC-β and BDNF. The mRNA expression of PKAC-β, c-Fos and BDNF was determined by RT-PCR. RESULTS: WIN55-212-2 obviously improved some nervous deficit symptoms and increased the expression of BDNF at mRNA and protein levels with upregulating the mRNA expression of c-Fos and downregulating the expression of PKA at mRNA and protein levels in the ipsilateral cerebral cortex. The proteins of PKAC-β, c-Fos and BDNF were expressed on the membrane or nucleus of the neuron or in the cytoplasm of glial cells, respectively. CONCLUSION: The expression of BDNF is induced not only by upregulation of c-Fos, but also by downregulation of PKA in WIN55-212-2 treated rats.

Humans ; Metabolic Syndrome ; prevention & control

Microglia is the most important immune cell in the central nervous system.It plays a key role in mediating the immune response in the central nervous system.Sterile inflammation is the key factor in the pathophysiological process following ischemic stroke.Microglia is activated and induces a series of inflammatory signals through binding of injuring related ligands to their corresponding receptors.This article introduces the activation of microglia and inflammatory response after ischemic stroke from Toll-like receptors,inflammasome,cytokine receptors,Notch signaling and other signaling pathways.