Emerging data indicated that HCV subverts the antiviral activity of interferon (IF); however,whether HCV core protein contributes to the process remains controversial. In the present study, we examined the effect of HCV core protein on interferon-induced antiviral gene expression and whether the effect is involved in the activation and negative regulation of the Jak/STAT signaling pathway. Our results showed that, following treatment with IFN-α, the transcription of PKR, MxA and 2'-5'OAS were down-regulated in HepG2 cells expressing the core protein. In the presence of HCV core protein,ISRE-dependent luciferase activity also decreased. Further study indicated that the core protein could inhibit the tyrosine phosphorylation of STAT1, whereas the level of STAT1 expression was unchanged.Accordingly, SOCS3, the negative regulator of the Jak/STAT pathway, was induced by HCV core protein. These results suggests that HCV core protein may interfere with the expression of some interferon-induced antiviral genes by inhibiting STAT1 phosphorylation and induction of SOCS3.

It is held by some of the researches that the "16 collaterals" is composed of the "15 collaterals" and "the major collateral of stomach". And it is included into the textbook that Xuli, the major collateral of stomach, is the pulsation point at the cardiac region. Xuli is often explained as the empty portion of the human body by many researches. Through analysis and summarization of the related theory of the major collateral of stomach, the above mentioned opinion is discussed. And the understanding on the major collateral of stomach is deepened. As a result, it is concluded that count the major collateral of stomach into the 16 collaterals together with the 15 collaterals is inadvisable. The real pulsation point at the cardiac region locates under the left breast. And the real meaning of Xuli is "extending in all directions".
Acupuncture ; history ; China ; Collateral Circulation ; History, Ancient ; Humans ; Medicine in Literature ; Meridians ; Stomach ; blood supply

Adolescent ; Adult ; Automobile Driving ; China ; Electrocardiography ; Female ; Heart ; physiopathology ; Humans ; Male ; Middle Aged ; Noise, Occupational ; adverse effects ; Occupational Exposure ; adverse effects ; Stress, Psychological ; etiology ; physiopathology ; Vibration ; adverse effects

OBJECTIVETo study the effect of Ganoderma lucidum polysaccharides on oxidative stress of hyperlipidemic fatty liver in rats.

METHODSeventy-two SD rats were randomly divided into six groups, namely the normal control group (NG), the model group (MG), the G. lucidum polysaccharides groups of low, middle and high dose (GLPs-LG, GLPs-MG, GLPs-HG) and the Simvastatin group (SV). The rats were fed with high fat diet to establish the model of hyperlipidemic fatty liver in rats. After administration for 12 weeks, rats in each group were tested with the following indexes: total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) in serum as well as the contents of SOD, MDA, GSH-Px and T-AOC in hepatic tissues. Histopathological changes of hepatic tissues were observed under light glass.

RESULTSThe contents of TC, TG and LDL-C were significantly increased in the model group (P < 0.01). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in TC, TG and LDL-C (P < 0.05 or P < 0.01), while the GLPs-H group showed a notable increase in HDL-C (P < 0.05). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in MDA (P < 0.05 or P < 0.01) and notable increases in SOD, GSH-Px, T-AOC (P < 0.05 or P < 0.01). The GLPs-M group and the GLPs-H group proved a remarkable alleviation in fatty degeneration of hepatic cells.

CONCLUSIONG. lucidum polysaccharides can significantly reduce the blood fat level of hyperlipidemic fatty liver in rats and effectively inhibit oxidant stress, showing the effect on preventing and treating hyperlipidemic fatty liver in rats to some extent.

Animals ; Antioxidants ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Fatty Liver ; drug therapy ; metabolism ; Glutathione Peroxidase ; metabolism ; Humans ; Male ; Malondialdehyde ; blood ; Oxidative Stress ; drug effects ; Polysaccharides ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Reishi ; chemistry ; Triglycerides ; blood

OBJECTIVETo observe the effects of subchronic benzo[a]pyrene (B[a]P) exposure on the neurobehavior and hippocampal acetylcholine (Ach) level, acetylcholinesterase (AChE) activity, and mRNA and protein expression of nicotinic acetylcholine receptor α7 subtype (nAChR α7) in rats, and to investigate the neurotoxic mechanism of B[a]P.

METHODSSixty healthy male SD rats were randomly divided into blank control group, solvent control group, and B [a]P exposure groups. Each rat in the exposure groups was intraperitoneally injected with B[a]P at 1.0, 2.5, or 6.25 mg/kg once every other day for 90 days. The learning and memory ability of the rats was examined by Morris water maze test and step-down test; the hippocampal Ach level was measured by alkaline hydroxylamine method; the AChE activity was measured by DNTB method; the mRNA and protein expression levels of hippocampal nAChR α7 were measured by quantitative PCR and Western blot.

RESULTSThe 2.5 and 6.25 mg/kg B[a]P exposure groups showed significantly lower learning and memory abilities than the blank control group and solvent control group (P < 0.05); also, the two groups had significantly lower hippocampal Ach levels than the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group (P < 0.05). The 6.25 mg/kg B[a]P exposure group showed significantly lower hippocampal AChE activity than the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group (P < 0.05). There were no significant differences in the mRNA and protein expression levels of nAChR α7 among all groups (P > 0.05). The hippocampal Ach level was negatively correlated with the mean escape latency period and total distance travelled (r = -0.567, P < 0.01; r = -0.503, P < 0.01) but positively correlated with the time in platform quadrant (r = 0.800, P < 0.01).

CONCLUSIONSubchronic B[a]P exposure may impair the learning and memory ability in rats, which is related to the downregulation of hippocampal Ach level.

Acetylcholine ; metabolism ; Acetylcholinesterase ; metabolism ; Animals ; Benzo(a)pyrene ; toxicity ; Hippocampus ; drug effects ; metabolism ; Male ; Maze Learning ; drug effects ; Memory ; drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholinergic ; metabolism ; Toxicity Tests, Subchronic ; alpha7 Nicotinic Acetylcholine Receptor ; metabolism

OBJECTIVETo evaluate the effects of asthma and inhaled corticosteroids (ICS) in children on the final adult height.

METHODSA search was performed to collect studies evaluating the relationship between asthma and ICS in children and the final adult height in PubMed, BCI, EMbase, Web of Science, CNKI and Wanfang databases, then a systemic review and Meta analysis were conducted.

RESULTSSix studies evaluating the relationship between childhood asthma and the final adult height were enrolled. Three of them indicated that the final adult height was not influenced by childhood asthma. Two of them suggested a mild effect, and the effect was correlated with severity of childhood asthma. One of them indicated that a lower final adult height related to childhhod asthma was found only in black females without a high school education. Four studies evaluating the relationship between ICS and the final adult height were included. Compared with the non-ICS treatment group, healthy control group and the target height, ICS treatment had no effects on the final adult height.

CONCLUSIONSChildhood asthma does not or only mildly decrease the final adult height. ICS treatment does not significantly affect the final adult height.

Administration, Inhalation ; Adrenal Cortex Hormones ; adverse effects ; Adult ; Asthma ; drug therapy ; Body Height ; drug effects ; Child ; Humans

This paper analyses the defects of bubble oxygen inhalators currently used, and investigates into their solutions for improvement.
Oxygen Inhalation Therapy ; instrumentation ; methods ; Oxygenators ; standards

Objective To detect the disease-causing mutations in Duchenne muscular dystrophy (DMD) gene of DMD or Becher's muscular dystrophy (BMD) patients or carriers. Methods Multiplex ligation-dependent probe amplification (MLPA) and denaturing high performance liquid chromatography (DHPLC) were coupled to analyze the disease-causing mutations in DMD gene. Results Ten patients were detected to have deletions in different exons; 1 patient was caused by duplication of exon 50 using DHPLC analysis, and 4 patients were found to be caused by non-sense point mutations. However, the disease-causing mutations of other 5 patients remained to be determined. Conclusion MLPA coupled with DHPLC analysis can be used to detect the disease-causing mutations of DMD or BMD systematically, and provide valuable information for the affected families in preventing from recurrence of DMD or BMD.

OBJECTIVETo explore the toxic effect of fluoride on the human thyroid cells (Nthy-ori 3-1) and its mechanism.

METHODSNthy-ori 3-1 cells were exposed to 0.0, 0.1, 1.0, 3.0 mmol/L of sodium fluoride (NaF) in vitro. After 24 hours incubation, 3 (4,5-Dimethylthiazol-z-yl)-3, 5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) assay were used to measure cell viability and the LDH leakage rate. Reactive oxygen species (ROS) level, constituent ratio of the cell cycle, and apoptosis rate were measured by flow cytometry.

RESULTSComparing to viability of control group (set as 100.00%), the cell viability of the 1.0, 3.0 mmol/L fluoride-treated groups (76.64 +/- 9.13)%, (64.04 +/- 6.32)% were significantly decreased (all P values <0.01). LDH leakage rate and ROS level of the 3.0 mmol/L fluoride-treated group ((48.66 +/-7.15)%, (29993.50 +/- 1786. 86) FI) were significantly increased (all P values <0.01) compared to control group ((35.24 +/- 3.02)%, (13021.33 +/- 1067.55) FI). The G0/G1 phase cells of the 1.0 mmol/L fluoride-treated group ((40.76 +/- 5.65)%) were lower than control group (60.09 +/- 1.76)% (P < 0.01), yet the percentage of cells in S phase ((54.05 +/- 4.59)%) were higher than the control group (32.59 +/- 2.43) % (P < 0.01). Comparing to control group ((9.64 +/- 3.44)%), the percentage of apoptosis cells increased in the 3.0 mmol/L fluoride-treated group ((20.09 +/- 3.22)%) (P < 0.01).

CONCLUSIONTo Nthy-ori 3-1 cells, fluoride under experimental concentrations decreases cell viability, improve the LDH leakage rate, and ROS level. It blocks the cells in S phase and induce cell apoptosis.

Apoptosis ; drug effects ; Cell Cycle ; Cell Division ; Cell Line ; Fluorides ; toxicity ; Humans ; Reactive Oxygen Species ; analysis ; Thyroid Gland ; cytology ; drug effects

To study the effect of HCV core protein on the interferon-induced antiviral genes expression and its mechanisms. Methods HepG2 cells were transiently transfected with HCV core protein expression plasmid and the blank plasmid respectively. RT-PCR was used to analyze the effect of HCV core protein on PKR and 2'-5'OAS expression. The effect of HCV core protein on ISRE-medicated gene expression was detected by luciferase activity assay. Western-blot assay was performed to observe the change of mRNA and protein levels of SOCS3, STAT1 and p-STAT1 following HCV core expression. In the presence of HCV core protein, the transcription of PKR and 2'-5' OAS are down-regulated. ISRE-medicated reporter gene expression and STAT1 phosphorylation were inhibited. The transcription and expression of SOCS3 were induced compared with blank plasmid-transfected group. In HepG2 cells, HCV core protein can down-regulate the expression of some interferon-induced antiviral genes, which involves the induction of SOCS3 and the inhibition of STAT1 phosphorylation.
2',5'-Oligoadenylate Synthetase ; genetics ; metabolism ; Carcinoma, Hepatocellular ; pathology ; Down-Regulation ; Hepacivirus ; genetics ; metabolism ; Humans ; Interferon-Stimulated Gene Factor 3 ; genetics ; metabolism ; Interferon-alpha ; genetics ; immunology ; Liver Neoplasms ; pathology ; Protein Kinases ; genetics ; metabolism ; STAT1 Transcription Factor ; genetics ; metabolism ; STAT2 Transcription Factor ; genetics ; metabolism ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Viral Core Proteins ; genetics ; metabolism ; physiology