[The construction of reporter plasmid of ULBP1 and preliminary studying on the influence of NS3/4A on transcription of ULBP1].

Aim: To construct a report vector of ULBP1 promoter gene and preliminary study on the influence of NS3/4A on transcription of ULBP1.

Methods: ULBP1 core promoter sequence was amplified by PCR, and inserted into pGL3-enhance vector, constructing ULBP1 reporter plasmid pGL3-ULBP1; The HCV protease NS3/4A gene was subcloned into pcDNA3-Flag vector (pcDNA3-Flag-NS3/4A), and the expression of this plasmid was demonstrated by Western blot. The influence of inhibition by NS3/4A on the level of ULBP1 transcription was tested by assaying the Luciferase activity in cells transfected with pGL3-ULBP1 with Luminometer.

[Comparison of pragmatic clinical trials and explanatory clinical trials].

Clinical trials are often designed as either pragmatic or explanatory. The pragmatic clinical trials are generally used for measuring the effectiveness of a treatment in common clinical practice, while the explanatory trial for measuring the efficacy of a treatment under ideal conditions. Since the methods concerning pragmatic clinical trials are less introduced in China, its archetypal features, advantages and limitations were introduced in this paper.

Fabrication of graded TiN coatings on nitinol occluders and effects on in vivo nickel release.

A nano-structured TiN/Ti coating with a total thickness of 0.9 mum was deposited on nitinol cardiac occluders using the filtered multi-arc vacuum ion plating technique at less than 300 degrees C. The coating was composed of laminated TiN/Ti layers with thickness of about 100 nm.

Proliferating cell nuclear antigen destabilizes c-Abl tyrosine kinase and regulates cell apoptosis in response to DNA damage.

The tyrosine kinase, c-Abl, plays important roles in many aspects of cellular function. The activity of c-Abl is tightly controlled, but the underlying mechanism is unclear. Recent studies suggest that c-Abl function is regulated by distinct lipids in different cell types.

Hepatitis C virus infection downregulates the ligands of the activating receptor NKG2D.

Natural killer (NK) cells are a major component of the host innate immune defense against various pathogens. Several viruses, including hepatitis C virus (HCV), have developed strategies to evade the NK-cell response. In our study, we found HCV infection could trigger DNA damage response by both ataxia telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) pathways.

[Patient-reported outcomes: advances in research and practical application].

Clinical evaluation proceedings from patient-reported outcomes (PRO) are being concerned increasingly. Based on the concept of PRO, the report discusses the findings in the research recently made at home and abroad. PRO from apoplexy patients with spastic paralysis was taken as an example in the exploration of how to evaluate the curative effects in clinical practice on the basis of PRO.

Ataxia telangiectasia-mutated-Rad3-related DNA damage checkpoint signaling pathway triggered by hepatitis B virus infection.

Aim: To explore whether acute cellular DNA damage response is induced upon hepatitis B virus (HBV) infection and the effects of the HBV infection.

Methods: We incubated HL7702 hepatocytes with HBV-positive serum, mimicking a natural HBV infection process. We used immunoblotting to evaluate protein expression levels in HBV-infected cells or in non-infected cells; immunofluorescence to show ATR foci ands Chk1 phosphorylation foci formation; flow cytometry to analyze the cell cycle and apoptosis; ultraviolet (UV) radiation and ionizing radiation (IR)-treated cells to mimic DNA damage; and Trypan blue staining to count the viable cells.

[Characterization of pyrolysis of waste printed circuit boards by high-resolution pyrolysis gas chromatography-mass spectrometry].

Thermal degradation of pyrolysis of waste circuit boards was investigated by high-resolution pyrolysis gas chromatography-mass spectrometry (PyGC-MS) and thermogravimetry (TG). In helium atmosphere, the products of FR-4 waste printed circuit board were pyrolyzed at 350, 450, 550, 650, and 750 degrees degrees C, separately, and the pyrolysis products were identified by online MS. The results indicated that the pyrolysis products of the FR-4 waste circuit board were three kinds of substances, such as the low boiling point products, phenol, bisphenol and their related products.

[HBV infection downregulated Mre11 expression and induced genome instability].

Objective: Prolonged infection with Hepatitis B virus (HBV) has been recognized as a major factor for hepatocellular carcinoma (HCC). In this study, we studied the host protein Mrel11 fluctuations after HBV infection which might be eventually contributed to cell transformation.

Methods: Western Blot was monitored to detect the expression of Mre11, and RNA interference was used to downregulate protein expression.

Syntaxin 6, a regulator of the protein trafficking machinery and a target of the p53 family, is required for cell adhesion and survival.

The p53 family consists of p53, p63, and p73. It has been well characterized that all of the p53 family proteins are transcription factors and capable of regulating cell cycle and apoptosis. To determine whether the p53 family exerts tumor suppression by other mechanisms, we set to identify novel p53 family target genes.

Cellular DNA repair cofactors affecting hepatitis B virus infection and replication.

Aim: To investigate whether hepatitis B virus (HBV) infection activates DNA damage response and DNA repair cofactors inhibit HBV infection and replication.

Methods: Human hepatocyte cell line HL7702 was studied. Immunoblotting was performed to test the expression of ataxia telangiectasia-mutated (ATM)-Rad3-related protein (ATR), p21 and the level of phosphorylation of Chk1, p53, H2AX, ATM in HBV-infected or non-infected-cells.

Structural and biochemical characterization of the therapeutic Anabaena variabilis phenylalanine ammonia lyase.

We have recently observed promising success in a mouse model for treating the metabolic disorder phenylketonuria with phenylalanine ammonia lyase (PAL) from Rhodosporidium toruloides and Anabaena variabilis. Both molecules, however, required further optimization in order to overcome problems with protease susceptibility, thermal stability, and aggregation. Previously, we optimized PAL from R.

Acoustic characteristics of English lexical stress produced by native Mandarin speakers.

Native speakers of Mandarin Chinese have difficulty producing native-like English stress contrasts. Acoustically, English lexical stress is multidimensional, involving manipulation of fundamental frequency (F0), duration, intensity and vowel quality. Errors in any or all of these correlates could interfere with perception of the stress contrast, but it is unknown which correlates are most problematic for Mandarin speakers.

Protective effects of apocynin and allopurinol on ischemia/reperfusion-induced liver injury in mice.

Aim: To determine the effects of allopurinol, an inhibitor of xanthine oxidase, and apocynin, an inhibitor of NADPH oxidase, on oxidant stress and liver injury caused by hepatic ischemia/reperfusion (I/R) procedure in mice.

Methods: Mice were pretreated with a xanthine oxidase inhibitor, allopurinol, or NADPH oxidase (NOX) inhibitor, apocynin before the hepatic I/R procedure. Then treated or untreated mice underwent the hepatic I/R procedure.

[Study on the mechanism of DDP-resistance mediated by phosphate JNK in gastric cancer].

Objective: To investigate the mechanism of DDP-resistance in gastric cancer cell line SGC7901/DDP mediated by phosphate(p)-JNK.

Methods: The p-JNK expression was blocked by the JNK inhibitor SP600125. The drug sensitivity was detected by MTT.

Inhibition of CCN6 (Wnt-1-induced signaling protein 3) down-regulates E-cadherin in the breast epithelium through induction of snail and ZEB1.

The cysteine-rich protein CCN6 [or Wnt-1-induced signaling protein 3 (WISP3)] exerts tumor-suppressive effects in aggressive inflammatory breast cancer. Loss of CCN6 is associated with poorly differentiated phenotypes and increased invasion. Here, we show that reduction of CCN6 expression occurs in 60% of invasive breast carcinomas and is associated with axillary lymph node metastases.

Effects of high dietary vitamin A supplementation on tibial dyschondroplasia, skin pigmentation and growth performance in avian broilers.

An experiment was conducted to study high dietary vitamin A on tibial dyschondroplasia, growth performance and skin pigmentation in broilers. One hundred and twenty Avian commercial broilers were randomly allotted to three treatments: group C (control group), in which broilers were fed basic diet containing vitamin A 5512IU/kg diet; group A, in which broilers were fed basic diet with addition vitamin A 35512IU/kg; group B, broilers were fed basic diet with supplement vitamin A 65512IU/kg. The experiment lasted 35d and at the end of the trial, broilers were killed and the right proximal tibiotarsi were dissected in longitudinal section for the assessment of TD incidence and TD index, skin from the same area of breast and tibia in broilers were collected to determine pigmentation.

Characterization of pyrazines in some Chinese liquors and their approximate concentrations.

Pyrazines are very important impact aroma compounds in Chinese liquors. The identification of pyrazine derivatives was carried out by liquid-liquid extraction (LLE). The liquor sample was adjusted to the H(+) concentration of 1 N with 12 N HCl and then concentrated by rotatory evaporator under vacuum condition.

Role of MAPK phosphatase-1 in sustained activation of JNK during ethanol-induced apoptosis in hepatocyte-like VL-17A cells.

Ethanol metabolism plays a central role in activating the mitogen-activated protein kinase (MAPK) cascade leading to inflammation and apoptosis. Sustained activation of c-Jun N-terminal kinase (JNK), one of the MAPKs, has been shown to induce apoptosis in hepatocytes. MAPK phosphatase-1 (MKP-1) has been shown to dephosphorylate MAPKs in several cells.

Ethanol induces apoptosis in hepatocytes by a pathway involving novel protein kinase C isoforms.

Unlabelled: Ethanol abuse is one of the major etiologies of cirrhosis. Ethanol has been shown to induce apoptosis via activation of oxidative stress, mitogen-activated protein kinases (MAPK), and tyrosine kinases. However, there is a paucity of data that examine the interplay among these molecules.

[Study on the drug-resistant genes associated with beta-lactams and aminoglycosides in clinically isolated Pseudomonas aeruginosa].

Objective: To investigate drug-resistant genes associated with beta-lactams and aminoglycosides in clinically isolated Pseudomonas aeruginosa.

Methods: Twenty strains of Pseudomonas aeruginosa were isolated from wound excretion of hospitalized burn patients. The strains resistant to 14 antibiotics were selected for detection of 16 kind of drug-resistant genes (TEM, SHV, OXA-10 cluster, PER, VEB, GES, CARB, CTX-M- I, IMP, VIM, SPM, GIM, DHA, MOX, FOX, oprD2) and 6 kind of aminoglycoside modification genes (aac(3)- I, aac(3)-II, aac(6')-I, aac(6')-II, ant (3")- I , ant(2")- I) in them by PCR.

Combination of ZD55-MnSOD therapy with 5-FU enhances antitumor efficacy in colorectal cancer.

Purpose: ZD55-MnSOD is an E1B 55 kDa-deleted replication-competent adenovirus and armed with the therapeutic gene MnSOD. The expression of the therapeutic gene MnSOD increases with the selective replication of the oncolytic adenovirus (ZD55) so that ZD55-MnSOD has more significant activity than the replicate defective adenovirus Ad-MnSOD in vitro and in vivo. The tumor cannot be completely eradicated only with ZD55-MnSOD, although ZD55-MnSOD has obvious antitumor activity.

CCN6 (WISP3) as a new regulator of the epithelial phenotype in breast cancer.

CCN6 (WISP3) is a cysteine-rich secreted protein that belongs to the CCN (Cyr61, CTGF, Nov) family of genes. We found that CCN6 mRNA is reduced in 80% of cases of the most lethal form of locally advanced breast cancer, inflammatory breast cancer. CCN6 contains four highly conserved motifs with sequence similarities to insulin-like growth factor binding proteins, von Willebrand type C, thrombospondin 1, and a carboxyl-terminal domain putatively involved in dimerization.

Short hairpin RNA causes the methylation of transforming growth factor-beta receptor II promoter and silencing of the target gene in rat hepatic stellate cells.

Small interfering RNA (siRNA) induces transcriptional gene silencing (TGS) in plant and animal cells. RNA dependent DNA methylation (RdDM) accounts for TGS in plants, but it is unclear whether siRNA induces RdDM in mammalian cells. To determine whether stable expression of short hairpin siRNA (shRNA) induces DNA methylation in mammalian cells, we transduced rat hepatic stellate SBC10 cells with lentiviral vectors which encode an U6 promoter-driven shRNA expression cassette homologous to the transforming growth factor-beta receptor (TGFbetaRII) promoter region.