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.

Objective To investigate the relationship between nasal colonization of Staphylococcus aureus(SA) and nosocomial infection in intensive care unit(ICU), and observe the therapeutic effect of Anerdian III in nasal decolonizaion. Methods Bacterial cultures were made by means of nasal swabs among inpatients whom the occurrence of nosocomial infection were observed.Patients with SA colonization were randomly divided into two groups:control and treatment.Control group were given regular treatment, and treatment group were administered Anerdian III in addition to regular treatment.Then the clearance rate of SA and the occurrence of nosocomial infection of two groups were observed. Results A total of 751 patients were enrolled, of whom 108(14.4%) were with nosocomial infection and 85(11.3%) with SA nasal colonization. Methicillin resistant Staphylococcus aureus ( MRSA ) was detected in 33 patients (4.4%).The nosocomial infection rate of patients with MRSA colonization was 51.5%, which was significantly higher than those in patients with other bacterial colonization(P<0.05).The SA clearance rate in treatment group was significantly higher than that in control group(81.4% vs.42.8%,P<0.05).The nosocomial infection rate in treatment group was significantly lower than that in control group ( 16 .3% vs. 40.5%,P <0.05).After decolonization treatment,the nosocomial infection rate of patients with MRSA colonization was significantly lower than that in control group(25.0% vs.76.5%,P <0.05). Conclusion The incidence rate of nosocomial infection in patients with MRSA nasal colonization is markedly increased in ICU, and the decolonization treatment by Anerdian III increases the clearance rate of nasal SA and decreases the incidence rate of nosocomial infection.

Objective To observe the clinical efficacy of electroacupuncture (EA) in treating knee osteoarthritis (KOA).Method Sixty KOA patients were randomized into a treatment group and a control group by using random number table, 30 cases each. The control group was intervened by oral administration of Celecoxib capsules, while the treatment group was given EA, 14 d as a treatment course. The changes of relevant cytokines [apelin, tumor necrosis factor (TNF)-α, TNF soluble receptor (TNFsR)-Ⅰ, TNFsR-Ⅱ, interleukin (IL)-1β, and IL-6] in serum of the two groups were observed.Result The intra-group comparisons of the total score, and the scores of pain, stiffness and dysfunction of the Western Ontario and McMaster Universities (WOMAC) osteoarthritis index showed significant differences in both groups (P<0.05); there were significant between-group differences in comparing the total score, and the scores of pain, stiffness and dysfunction of the WOMAC index after the treatment (P<0.05). The Visual Analogue Scale (VAS) scores were changed significantly after the intervention in both groups (P<0.05); there was nosignificant difference in comparing the VAS score between the two groups after the treatment (P>0.05). The levels of IL-6, TNF-α and TNFsR-Ⅰ were significantly changed after the treatment in both groups (P<0.05); the level of IL-1β was markedly changed after the intervention in the control group (P<0.05); there was a significant change in the level of apelin after the intervention in the treatment group (P<0.05), and there was a significant difference in comparing the level of apelin between the two groups after the treatment (P<0.05).Conclusion EA can produce a satisfactory efficacy in treating KOA; it can significantly improve the symptoms and signs, and mitigate pain and symptoms through regulating the expressions of cytokines.

Objective To explore clinical features and imaging diagnosis of colonic stenosis in infants. Methods Seven patients with congenital and acquired colonic stenosis proved by surgery were included in this study. The clinical features, erect abdominal plain radiograph and barium enema were analyzed. Results Of the 7 patients, 4 were congenital colonic stenosis with progressive abdominal distention and vomiting. The erect abdominal plain radiograph showed that intestinal inflation in 3 patients, low-set mechanical intestinal obstruction in 1 patient. In the remaining 3 patients who underwent ileostomy after neonatal necrotizing enterocolitis (NEC). Barium enema showed colonic stenosis in 5 patients and 2 were missed diagnosed who underwent contrast examination in the small intestine, and which showed stenosis in ascending colon near the ileocecus. Seven patients were all proved by surgery. The stenosis sites were located in sigmoid colon in 2 cases, in descending colon in 2 cases, in ascending colon in 2 cases and in transverse colon in 1 case. In 4 cases of congenital colonic stenosis, 2 cases underwent surgical staging, 1 case was followed up for half a year, showing normal defecation and well development, the other 1 case was lost visit after hospital discharge. The other 2 cases received end-to-end ileum and colon anastomosis, the abdominal distension was relieved in outpatient review, showing well-developed. Three cases with NEC and secondary colonic stenosis underwent staged surgery. Two patients were followed up in outpatient 2 weeks after operation. They were followed up for half a year, showing normal defecation and well-developed. The other 1 case was lost visit after hospital discharge. Conclusion Clinical features of colonic stenosis are very different and depend on the stenosis degree. NEC is the main cause of acquired colonic stenosis and it can be diagnosed by barium enema.

OBJECTIVETo investigate the intervention effect of thalidomide on paraquat-induced acute lung injury in mice and its mechanism.

METHODSMale ICR mice were randomly allocated to negative control group (n = 30), thalidomide control group (n = 30), paraquat poisoning group (n = 30), 50 mg/kg thalidomide treatment group (n = 30), 100 mg/kg thalidomide treatment group (n = 30), and 150 mg/kg thalidomide treatment group (n = 30). The negative control group was intraperitoneally injected with the same volume of saline; the thalidomide control group was intraperitoneally injected with thalidomide (150 mg/kg); the paraquat poisoning group was intraperitoneally injected with diluted paraquat solution (22 mg/kg); each thalidomide treatment group was intraperitoneally injected with the same volume of paraquat solution (22 mg/kg) and was injected with thalidomide (50, 100, or 150 mg/kg) 1 h later. All mice were anesthetized and sacrificed at 1, 3, or 7 d after paraquat poisoning, and their lung tissue was collected. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in lung tissue were measured by double-antibody sandwich ELISA; the mRNA expression of nuclear factor-kappa B (NF-κB) was measured by RT-PCR; the protein expression of nuclear NF-kgr;B p65 was measured by Western blot. The pathological changes of lung tissue were observed under light microscope; the wet/dry ratio of the lung was calculated.

RESULTSCompared with the negative control group, the paraquat poisoning group had significantly increased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratio of the lung (P < 0.05). Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratios of the lung (P < 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65. The observation of pathological changes showed that the paraquat poisoning group had the most marked lung tissue damage at 3 d after poisoning, and the lung tissue damage was lessened in the thalidomide treatment groups.

CONCLUSIONThalidomide can reduce paraquat-induced acute lung injury and lung edema. The mechanism may include inhibition of NF-κB activation and expression and downregulation of TNF-α, IL-1β, and IL-6.

Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Cytokines ; metabolism ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred ICR ; NF-kappa B p50 Subunit ; metabolism ; Paraquat ; poisoning ; Thalidomide ; pharmacology ; Transcription Factor RelA ; metabolism

UNLABELLED: OBJECTIVE To investigate the time-dependent expression of c-jun during the healing of incised wound in mice skin. METHODS: The expression of c-jun in different stages after the incised wound were detected by immunohistochemistry and Western blot. RESULTS: There was a low level expression of c-jun in normal mice skin. Expression of c-jun was mainly detected in neutrophils from 3 h to 12h after injury. The c-jun positive cells were almost mononuclear cells (MNCs) and fibroblasts between 1 d and 5 d after injury. The c-jun positive cells were mostly fibroblasts between 7 d and 14 d after injury. The ratio of the c-jun positive cells increased in the wound specimens from 3 h to 12 h, peaked at 12 h, declined partially from 1 d to 5 d, and reached the peak secondly at 7 d, then decreased from 10 d to 14 d. The expression of c-jun was observed throughout the wound healing stages by Western blot with two peaks occurring at 12 h and 7 d after injury. CONCLUSION The c-jun may play a potential role in inducing apoptosis of neutrophils, MNCs and fibroblasts during skin wound healing, and it may be used as the marker for wound age determination.
Animals ; Apoptosis ; Blotting, Western ; Disease Models, Animal ; Female ; Fibroblasts/metabolism* ; Immunohistochemistry ; Male ; Mice ; Neutrophils/metabolism* ; Proto-Oncogene Proteins c-jun/metabolism* ; Random Allocation ; Skin/metabolism* ; Time Factors ; Wound Healing ; Wounds and Injuries/metabolism*

Objective] To discuss comprehensive intervention effect on the control of hospital in-fections in the intensive care unit ( ICU ) of a hospital by monitoring Staphylococcus aureus infections and their drug resistance . [ Methods] Comparative analysis was done retrospectively in separation results of Staphylococcus aureus between 2011 and 2012 in ICU patients of a hospital . [ Results] Between 2011 and 2012, there was no obvious difference found in relevance ratio of Staphylococcus aureus(P>0.05), but that of methicillin resistant Staphylococcus aureus was on the decline significantly (P<0.05).The drug re-sistance rates of Staphylococcus aureus to oxacillin, ciprofloxacin, levofloxacin were on the decline signifi-cantly(P <0.05).The drug susceptibility rates of Staphylococcus aureus to vancomycin, teicoplanin, linezolid , nitrofurantoin and primaquine slave tianeptine/dafoe tianeptine were the highest , reaching up to 100.00%. [ Conclusion] By comprehensive intervention , Staphylococcus aureus infections in ICU have been improved and drug resistance rates on the decline as a whole .

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

Adult ; Eosinophilic Granuloma ; diagnosis ; Female ; Hodgkin Disease ; diagnosis ; Humans ; Male ; Spinal Diseases ; diagnosis

OBJECTIVETo identify gene mutations involved in five cases of inherited factor V (FV) deficiency.

METHODSActivity of FV was determined by one-stage clotting assay using FV-deficiency plasma, and FV antigen by an ELISA assay. All the exons and exon-intron boundaries of FV gene were amplified by PCR and then DNA sequencing. Restriction enzyme analysis was used to analyze the probands, their family members and healthy volunteers.

RESULTSBoth activity and antigen of FV in the 5 patients were extremely lower compared with that of normal mixed plasma. Six mutations were identified in these 5 patients, G69969T (G2079V), C45533T (R712Ter), C46796T (R1133Ter), G45366A (C656Y), C46253T (R952C) and G16088C (D68H), the latter three were novel mutations reported for the first time and the C46253T (R952C) was the first missense mutation reported in B domain. The result of sequencing or restriction enzyme analysis showed that the three novel missense mutations were not caused by single nucleotide polymorphisms.

CONCLUSIONGene mutations in 5 type I inherited FV deficiency of patients including 2 nonsense mutations and 4 missense mutations identified which led to the instability of FV protein and the reducing of FV: Ag in the plasma.

Adolescent ; Adult ; Child ; DNA Mutational Analysis ; Exons ; genetics ; Factor V ; genetics ; metabolism ; Factor V Deficiency ; blood ; genetics ; Female ; Humans ; Male ; Mutation ; Pedigree ; Phenotype ; Young Adult