Activin is a growth factor belong to the transforming growth factor-? superfamily.Recently,experimental studies have shown that activin and activin A expressed higher in various brain injury models and activin have beneficial roles to neuronal protection.The high correlation of activin and activin A with clinical and biochemical signs of brain injury lead us to suggest that activin and activin A are new possible indicators to predict and treat brain injury.

It have been known that many epigenetic alterations palyed an important role in development of myelodysplastic syndromes (MDS). In contrast to genetic alterations, epigenetic alterations could be in principle pharmacologically reversed. Application of epigenetic drugs can reactivate inactivated suppressor genes. Epigenetic drugs mainly include demethylating agents and histone deacylase (HDAC) inhibitors, which are available in treatment. 5-AZA and decitabine as DNA demethylation agents have been approved by FDAof treatment in intermediate or high risk MDS, especially those old patients who are resistant to chemotherapy.HDAC inhibitors such as valproic acid are mostly employed in phase I trial, probably effective in treating low risk MDS, but treatment schedules and curative effects still have to be evaluated. The combination of demethylation agents and HDAC inhibitors may result in synergistic activity, but its therapeutic effect seems not to be superior to monotherapy of demethylation agents in current clinical trials, and it still need new clinical trials containing more cases and rational treatment schedules to identify safety and effect of combination.

Antimicrobial susceptibility testing (AST) is an important means to clinical microbiology. At present, there are no standard AST methods for aquatic pathogens comparing with human and veterinary pathogens. We reviewed the recent research progress on establishing these methods and discussed the key factors in AST of aquatic pathogens. Furthermore the defect of AST of aquatic pathogens in China was profiled and prospect for further research was put forward.

Animals ; Genes, p53 ; Genetic Therapy ; Humans ; Neoplasms ; genetics ; metabolism ; therapy ; Proto-Oncogene Proteins c-mdm2 ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

Objective To evaluate the clinical parameter, diagnosis and operative mode of parathyroid tumor. Methods The clinical symptoms, examination methods and the mode of operation in 15 operated patients with parathyroid tumor from May 1979 to October 2001 were retrospectively analyzed. Results 15 patients with parathyroid tumors, including 10 adenomas, 3 carcinoma and 2 cysts, all revealed the symptom of hyperparathyroidism except 2 cases of cyst. The accuracy of B-US and CT in preoperative diagnosis on location was 86 7% and 91 7% respectively, and their accuracy in preoperative diagnosis on quality was 26 7% and 75 0% respectively. All patients were treated by surgery. Among them, 12 patients were cured, 1 died, and 2 relapsed. Conclusion If a patient has the symptoms of bone pain, nephrolith and the mass in neck, we should consider whether he suffers from parathyroid tumor. B-US is the first choice in preoperative diagnosis on tumor location, and CT was the good examination method for tumor location also. The diagnosis on tumor quality dependeds on pathological examination mostly. Surgery remains to be the most important. The only unilateral exploration for the benign parathyroid tumor is performed and the operative range of parathyroid carcinoma should include both the mass and thyroid.

Aim: To study the distribution and excretion of baicalein and baicalin in rats. Methods: An LC/MS method was applied. Chromatographic separation was performed on a C_(18) column( 150 mm ×6.0 mm, 5 μm) with methanol-10 mmol/L ammonium acetate (containing 0. 5% formic acid) as the mobile phase. A trip-quadrupole tandem mass spectrometer was set in positive selected reaction monitoring mode. The sample was extracted with methanol-acetonitrile( 1:1) after the addition of phosphoric buffer solution and luteolin, which acted as the internal standard. The supernatant was evaporated to dryness, and the residual was reconstituted with mobile phase and analyzed. Results: The distribution profiles of the parent drug and its main metabolite showed two peaks between 20-40 min and 8-10 h after oral administration of baicalein, which fit the plasma concentration-time profile of baicalein in rats. At 20 min after the dosing, the concentration levels of baicalein were significantly higher than those of baicalin in stomach, liver and intestines, the converse result occurred in kidney. The excretion results showed that baicalin was the predominant excretion form in bile and urine, while baicalein was the negligible excretion form. There was more baicalein than baicalin in rat feces. Conclusion: Baicalein was absorbed and distributed quickly to various tissues and easily transformed to its metabolite at the same time.

Objective To identify the mediators of CDC42 signaling pathway involved in hepatitis B virus X protein (HBx)-mediated cellular transformation.Methods The mass defect-based pseudo-isobaric dimethyl labeling method (pIDL)was used to detect the differentially expressed proteins with a deficiency of CDC42.Furthermore,we conducted a gene ontology (GO)of differentially expressed proteins.Results and Conclusion We totally qualified 3409 proteins and found 220 differentially expressed proteins.Palladin,formin-like 1 (FMNL1)and keratin-19,which were implicated in cytoskeleton organization,were down-regulated with the deficiency of CDC42.Our results have provided candidate genes and proteins that may play an important role in HBx-mediated cellular transformation.

Cell division cycle 42 (CDC42)is a member of Rho guanosine triphosphatase (GTPase) family,which plays an important role in cell proliferation , cell migration and cell transformation .The activity of CDC42 can be regulated by guanine nucleotide exchange factors (GEFs),GTPase activating proteins (GAPs) and guanine nucleotide-dissociation inhib-itors (GDIs).Recently,CDC42 has been reported as abnormally expressed in many human cancers ,suggesting that CDC42 performs complex functions in tumorigenesis .Therefore,this paper aims to shed light on the functions of CDC 42 in cancers in terms of the alteration of CDC42 activity,CDC42 regulators,as well as its effectors.

Objective To investigate the protective effect and it's possible mechanism of Tanshinone ⅡA in radiation-induced pulmonary fibrosis.Methods Having the right hemithorax of female Wistar rats irradiated(30?Gy) in 10 fractions within 14 days by 6 ?MV photons,the radiation-induced pulmonary fibrosis animal model was established.In the treatment group,sodium Tanshinone ⅡA sulfonate(15?mg/kg) was given by intraperitoneal injection 1 hour before each fraction of irradiation.Five months after irradiation,the difference of the histopathological changes,the hydroxyproline content and expression of TGF-?1 between the radiation alone group,tanshinone plus radiation and control group were analyzed by HE stain,Massion stain,immunohistochemical methor and reverse transcriptase polymerase chain reaction(RT-PCR) method.Results The histopathological comparison revealed the protective effect of Tanshinone ⅡA.The content of hydroxyproline was(21.99?3.96),((38.25?)(7.18)),(28.94?4.29)??g/g in the control group,radiation alone group and radiation plus Tanshinone ⅡA.The expression of TGF-?1(mRNA and protein) was reduced by Tanshinone ⅡA.Pathological changes of the pulmonary fibrosis was reduced by Tanshinone ⅡA yet.Conclusions Our study shows that Tanshinone ⅡA can inhibit radiation-induced pulmonary fibrosis,and the possible mechanism of its may be made possible through down-regulating the expression of TGF-?1 in the irritated lung tissue.