Objective To investigate cognitive status and influencing factors for hand hygiene(HH)among health care workers(HCWs),and provide basis for scientific management of HH.Methods In April 2013,HCWs in a general hospital were selected by randomly sampling method,questionnaires were used to survey the implementation of HH in recent one month and HCWs’cognition on knowledge about HH.Results A total of 750 HCWs were in-vestigated,652 available questionnaires were collected.The frequency of hand washing and hand disinfection per day among most HCWs were 10 - 19 times,accounting for 46.62% and 47.85% respectively;30.52% of HCWs washed their hands for ≥30 seconds each time,60.58% of HCWs dried hands with paper towel after washing hands,57.21 % of HCWs abided by six-step hand washing method.The overall correct rate of cognition on ten op-portunities that requiring HH in clinical practice was 68.68%.The main factors influencing the implementation of HH were as follows:skin irritation of hand sanitizer and hand disinfectant subjectively considered by HCWs (63.34%),inadequate hand washing facilities(41 .10%);high cost of hand sanitizer ,hand disinfectant,and dry paper towel (38.96%),et al.Conclusion In addition to intensifying education on HH,installing rational HH facili-ties and improving HH standard are key points in strengthening HH in general hospital.

Objective To evaluate the accuracy of the delay time after contrast media administration in intracranial CTA study during brain CT perfusion study.Methods 14 patients with history of episodes of typical transient ischemic attack(TIA)or ischemic cerebrovascular disease were included.After cerebral CT perfusion study,the CTA study of Willis circle was performed with the delay time by measuring the different value between the time to peak(TTP)and beginning scan time of anterior cerebral artery in CT perfusion.The quality of the CTA images were evaluated.Results All the CTA images of the Willis circle were satisfactory.Conclusion It's a satisfactory method based on successful cerebral CTA study to take the time to peak in CT perfusion as the delay time.

Objective: To study the gene expression characteristics of steroid- and catecholamine-synthesizing enzymes in adrenal gland of spontaneously hypertensive rats (SHRs), Goto-Kakizaki (GK) rats and normal Wistar rats with the same traditional Chinese medicine syndromes. Methods: Sixteen-week-old Wistar rats, SHRs and GK rats were used. By the quantitative four diagnosis and syndrome differentiation methods and GeneChip Mouse Exon 1.0 ST Array, we observed adrenal gland gene expressions in normal Wistar rats, qi deficiency Wistar rats, SHRs with qi deficiency and qi excess, GK rats with qi deficiency and qi excess. Differentially expressed genes of steroid- and catecholamine-synthesizing enzymes and their regulatory factors were analyzed. Results: Thirty-one genes were differentially expressed among all syndromes. Hsd3b6 was down-regulated significantly 6.0-fold in GK rats with qi deficiency syndrome and qi excess syndrome, and Cyp11b2 was up-regulated 1.5 times in GK rats with qi deficiency syndrome. Por, Hsd11b2, and Nr2f6 were up-regulated in all syndromes, and Cyp2c23, Cyp4a3, Cyp4a8 and Cyp2e1 were down-regulated. However, Srd5a1 and Nr4a1 were up-regulated only in GK rats, and Lss was down-regulated only in SHRs. Th was up-regulated 1.5 times in SHRs with qi deficiency syndrome, GK rats with qi deficiency syndrome and GK rats with qi excess syndrome. Ddc was up-regulated 1.5 times in GK rats with qi excess syndrome. Dbh was up-regulated 3.0 times in GK rats with qi deficiency syndrome and qi excess syndrome. However, Comt was down-regulated 1.5 times in GK rats with qi deficiency syndrome and qi excess syndrome, and Mao was up-regulated 1.5 times in SHRs with qi deficiency syndrome and qi excess syndrome. Conclusion: Some genes associated with steroid- and catecholamine-synthesizing pathways were differentially expressed in SHRs and GK rats, and the differentially expressed genes may be related to the development of traditional Chinese medicine syndromes.

ObjectiveTo observe gene transcription characteristic of AC-cAMP signal pathway in thyroid of H22 tumor-bearing mice with different syndromes.MethodsThe quantitative four diagnosis and syndrome differentiation methods and Affymetrix Gene Chip Mouse Exon 1.0 ST Array were used,thyroid gene expression of normal mice,qi-deficiency syndromes (QDS) and poisonous pathogenic factors syndrome (PPFS) in early stage of H22 tumor-bearing mice were detected.Genes of AC-cAMP signal pathway in gene chips,which related with thyroid hormone synthesis and secretion were selected,and then analyzed their expressive characteristic.Results ①In key genes,TG and Pax8 were down-regulated in early stage,TSHr down-regulated in PPFS while contrary in QDS.②the transcription level of most genes in QDS were slightly higher than in PPFS,Nis,Tpo,AC,Ttf1,Titf2 and Prkaca were included.()Slight changes showed in other genes in this pathway.ConclusionIn AC-cAMP pathway of H22 tumor-bearing mice with different symptoms,some key genes showed similar characteristics including TSHr,AC,Pax8,Ttf1,Tiff2,TG,Nis and Tpo.This suggested that the thyroid is inhibited in mice with PPFS.

Abstract: Methodology of syndrome differentiation and syndrome-based treatment in rats and mice has professional characteristics and caters to the research and development of traditional Chinese medicine (TCM). In this paper, the authors introduced their systematic research in five aspects. 1) Rats and mice can be used to simulate TCM clinical practice. Diagnosis and syndrome differentiation can be done to the rats and mice, and information collected by the four diagnostic methods from the experimental animals meets the requirements of treatment based on syndrome differentiation. 2) Standardized and quantified four diagnostic methods and syndrome differentiation for rats and mice can be established, and are operational and applicable for general use. 3) There exists constitution and syndrome diversity in normal rats and mice. A spontaneous syndrome can develop in diseased rats and mice, and it can be accompanied by or even change to another syndrome, similar to that in human beings. 4) There is a complicated material base for syndromes inferred from the different gene expressions and splices in neuroendocrine-immune network. 5) Individualized treatment based on syndrome differentiation, as well as quantified evaluation and comparison of the treatment efficacy can be done in the rat and mouse models of syndromes. The established methodology and criteria for syndrome differentiation and syndrome-based treatment in rats and mice can be used in the following four research fields: 1) syndrome identification on rat or mouse models; 2) research on the basic theories of TCM, such as the research on the viscera manifestation theory, the material base of syndromes, function mechanisms of the treatment based on syndrome differentiation, and the diagnostics of TCM; 3) study in clinical subject of TCM, such as evaluation and comparison of the efficacy of treatment based on syndrome differentiation, protocol optimization of syndrome differentiation and treatment, and preventive treatment of diseases; 4) study in traditional Chinese drugs, such as the research on properties of Chinese herbal drugs, and pharmacological research on Chinese herbal medicines and formulas.

Objective To study the expression features of hydrolase genes related to the secretion of thyroid hormone of H22 hepatoma mice with different symptoms in early stage. Methods Firstly, The quantitative diagnosis and syndrome differentiation methods were used in H22 tumor-bearing mice in early stage, the expression profile of Tg and related hydrolase genes in poisonous pathogenic factors syndrome group (PPFS) and qi-deficiency syndromes (QDS) were got, and the major differential expression were selected. Secondly, the experiment was repeated and ELISA were used to detect T3 and T4 in serum, RT-PCR were applied to detect gene transcription level of genes including Tg, Ctsb, Ctsd, Ctsl, Napsa and Tpp1. Results ① Based on gene chip, the expression of Tg, Ctsb, Ctsd, Ctsl, Napsa and Tpp1were decreased in the first batch of experiment, the exactly ratio was Tg(0.77 in PPFS;0.84 in QDS), Ctsb(0.83 in PPFS, 0.91 in QDS), Ctsd(0.79 in PPFS;no notable change in QDS), Ctsl(no notable change in PPFS; 0.65 in QDS), Napsa(0.78 in PPFS; no notable change in QDS), and Tpp1 (0.75 in PPFS; no notable change in QDS), respectively. ② T3 and T4 downregulated in PPFS (the T3 value was 1.519±0.162ng/ml, T4 value was 2.194±0.305mg/dl) and in QDS (the T4 value is 4.366±0.727μg/dl) in early stage (P<0.01), especially in PPFS, which was in accordance with the change of Tg in both batches. ③the same trend happened in the validation of Tg(0.22 in PPFS;0.38 in QDS), Ctsb(0.31 in PPFS;0.55 in QDS), Ctsd(0.36 in PPFS;0.78 in QDS) and Napsa(0.24 in PPFS;0.59 in QDS) ,while ctsl(1.24 in PPFS;2.11 in QDS) and Tpp1 (2.85 in PPFS;0.85 in QDS)werethe opposite;even this, the total trend of the expression in QDS was still higher than that in PPFS. Conclusion All the results showed that the thyroid function of H22 hepatoma mice was inhibited in early stage especially in PPFS.

Objective To explore the function of ERCC2/XPD polymorphisms in the repair of DNA damage induced by UVC. Methods Plas?mids stably expressing ERCC2/XPD rs13181 AA(Lys751)and ERCC2/XPD rs13181 CC(Gln751)were transfected into Chinese hamster ovary cells,and the stable ERCC2 transfected cell lines were obtained. MTT assay was used to compare the inhibitory rates of the transfected cells treated with UVC at different irradiation intensity. The DNA damage repair ability of the transfected cells treated with UVC for 1,3,6 and 24 h was detected by modified comet assay. Results Compared with UV5ERCC2(CC),UV5ERCC2(CC) was more sensitive to UVC with decreased cell viability. DNA damage level of UV5ERCC2(CC) cells was more serious than UV5ERCC2(CC). Conclusion DNA repair capacity of ERCC2/XPD rs13181A allelic is lower than its wild?type,suggesting that ERCC2/XPDpolymorphisms play a critical role in UVC?induced DNA damage repair.

Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite. In addition, the potentials of migration and invasion for SMMC-7721 cells were increased significantly at the same time. Furthermore, sodium nitrite exposure displayed an increase of stress fibers, lamellipodum and perinuclear mitochondrial distribution by cell staining with Actin-Tracker Green and Mito-Tracker Red, which was reversed by N-acetylcysteine (NAC, a reactive oxygen scavenger). DCFH-DA staining with fluorescent microscopy showed that the intracellular level of ROS concentration was increased by the sodium nitrite treatment. LC3 immunostaining and Western blot results showed that sodium nitrite enhanced cell autophagy flux. Under the transmission electron microscopy (TEM), more autolysosomes formed after sodium nitrite treatment and NAC could prevent autophagosome degradation. RT-PCR results indicated that the expression levels of COX I and COXIV mRNA were decreased significantly after sodium nitrite treatment. Meanwhile, laser scanning confocal microscopy showed that sodium nitrite significantly reduced mitochondrial mass detected by Mito-Tracker Green staining. The expression levels of HIF-1α, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC. Our results demonstrated that sodium nitrite (16 mg x L(-1)) increased the potentials of invasion and migration of hepatic cancer SMMC-7721 cells through induction of ROS and HIF-1α mediated mitophagy.
Acetylcysteine ; pharmacology ; Autophagy ; Carcinoma, Hepatocellular ; pathology ; Cell Line, Tumor ; Cell Movement ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Liver Neoplasms ; pathology ; Mitochondrial Degradation ; Neoplasm Invasiveness ; Nitrites ; metabolism ; Reactive Oxygen Species ; metabolism ; Sodium Nitrite ; pharmacology

Guanylate binding protein-1(GBP-1) is an interferon-induced protein. To observe its antiviral effect against Hepatitis B virus (HBV) and Coxsackie virus B3 (CVB3), we constructed an eukaryotic expression vector of human GBP-1(hGBP-1). Full-length encoding sequence of hGBP-1 was amplified by long chain RT-PCR and inserted into a pCR2.1 vector, then subcloned into a pCDNA3.1(-) vector. Recombinant hGBP-1 plasmids and pHBV1.3 carrying 1.3-fold genome of HBV were contransfected into HepG2 cells, and inhibition effect of hGBP-1 against HBV replication was observed. Hela cells transfected with recombinant hGBP-1 plasmids were challenged with CVB3, and viral yield in cultures were detected. The results indicated that recombinant eukaryotic expression plasmid of hGBP-1 was constructed successfully and the hGBP-1 gene carried in this plasmid could be efficiently expressed in HepG2 cells and Hela cells. hGBP-1 inhibit CVB3 but not HBV replication in vitro. These results demonstrate that hGBP-1 mediates an antiviral effect against CVB3 but not HBV and perhaps plays an important role in the interferon-mediated antiviral response against CVB3.

To establish a replication cellular model of hepatitis B virus (HBV) and determine its application in antiviral drug evaluation,we constructed an expression plasmid which contained 1.3 copies of the HBV genome,and measured the level of viral replication after transient transfection in Huh7 cells.We then observed the effect of antiviral drug administration.1.3 fold of the HBV(ayw) gene fragment was cloned into pCR2.1 by PCR and restriction endonuclease digestion.The recombinant plasmid was trans ient transfected into Huh7 cells,HBsAg,HBeAg and HBV DNA in supernatant of Huh7 cells were measured by ELISA and real-time PCR respectively; intracellular HBV replicative intermediates and intracellular HBV transcripts were detected by Southern blot and Northern blot respectively.The antiviral effect of adefovir,a novel anti-HBV nucleotide analogue,was evaluated in this cellular model system.The results indicated that a recombinant plasmid of HBV replicon was constructed successfully; the HBV genome carried in plasmid pHBV1.3 could efficiently replicate and be expressed in Huh 7 cells,adefovir could inhibit HBV replication in this cellular model,and the inhibition was dosage-dependent.The conclusion is HBV replicon,which can initiate viral replication efficiently in hepatoma cells,may be a useful tool in the study of HBV replication and antiviral drug.