Objective] To discuss the effect of timely infection evaluation and intervention on reducing infection to low-body mass incubator infants of primary hospitals. [Method] Select 98 cases of low-body mass incubator infants of 1210~2000g as control group(routine prevention used), and another 95 cases of 1200~2010g as observation group(taking timely infection evaluation, giving pointing intervention to infants with various infective risk factors). Compare their infection and in-hospital period. [Result]In control group 98 cases, 45 cases(45.92%) had infection; in observation group 95 cases, 11 (11.58%) had infection; the infective rate of observation group was lower than control group, the difference had statistical meaning( P<0.05). [Conclusion] To take timely infection evaluation and preventive intervention can definitely reduce infection.

Objective To study the relationship between the expression of EBV lytic genes and systemic lupus erythematosus (SLE). Methods The blood samples from 44 SLE patients and 43 matched normal controls were tested for BamHⅠ-W, the specific DNA fragment of EBV, by polymerase chain reaction(PCR)-Southern analysis. RT-PCR and Southern blotting were used to detect the EBV lytic genes (including immediate early genes BZLF1 and BRLF1, early genes BARF1, late genes BcLF1 and BLLF1) in EBV DNA-positive SLE patients. Results The EBV DNA was positive in 32 SLE patients and 3 controls. There was significant difference between the SLE patients and controls in the EBV DNA expression ( ?2 = 39.18, P 0.05). In the EBV DNA-positive SLE patients, 2 (both with active SLE) were positive for BARF1 mRNA; 14 (11 with active SLE and 3 with inactive SLE) were positive for BcLF1 mRNA; none was positive for BZLF1,BRLF1 or BLLF1 mRNA. No lytic genes were expressed in any of the 3 EBV DNA-positive controls. Conclusion EBV infection may be related to the development of SLE. EBV lytic infection exists in some SLE patients. EBV is at a low level of lytic activity in patients with SLE.

Objective To investigate the role of human cytomegalovirus (CMV) in the occurrence of drug eruptions.Methods Peripheral blood samples were collected from 44 patients with drug eruptions (including 13 severe cases) and 50 healthy human controls.Taqman fluorescent real-time quantitative PCR (RT-PCR) was performed to determine the positive rate and load of CMV DNA in peripheral blood mononuclear cells (PBMCs).Enzyme-linked immunosorbent assay (ELISA) was conducted to detect anti-CMV IgM antibodies in sera.Results The positive rate of CMV DNA was significantly higher in the patients than in the controls (65.91％ (29/44) vs.28.00 ％ (14/50),x2 =13.552,P ＜ 0.05),significantly different among patients with severe drug eruptions (11/13),patients with mild drug eruptions (58.06％ (18/31)) and the controls (x2 =16.153,P ＜ 0.05).In addition,patients with severe drug eruptions showed a higher positive rate of CMV DNA compared with patients with mild drug eruptions (x2 =13.817,P ＜ 0.05) and the controls (x2 =7.237,P ＜ 0.05).CMV DNA load was significantly higher in the patients than in the controls ((28 183.829 ± 19 527.654) vs.(3 019.952 ± 1 760.952) copies,t' =8.517,P ＜ 0.05).No significant difference was found in CMV DNA load between patients with severe drug eruptions ((554 813.389 ± 722 642.498) copies),patients with mild drug eruptions ((13 290.558 ± 14 082.356) copies)) and the controls (P ＞ 0.05).The positive rate of anti-CMV IgM antibodies was similar between the patients and controls (13.64％ (6/44) vs.6.00％ (3/50),P ＞ 0.05),but significantly different among patients with severe drug eruptions (4/13),patients with mild drug eruptions (6.45％,2/31) and the controls (x2 =7.832,P ＜ 0.05),and significantly higher in patients with severe drug eruptions than in the controls (x2 =6.409,P ＜ 0.05).Conclusions CMV infection exists in patients with drug eruptions,and might be a factor associated with the initiation and aggravation of drug eruptions.

Objective To detect the mutations of COL7A1 gene in three cases of dystrophic epidermolysis bullosa pruriginosa (DEBP). Methods Clinical data were collected from 3 patients with DEBP. Skin lesions were obtained from these patients and subjected to transmission electron microscopy. DNA was extracted from the peripheral blood of the 3 patients, their 16 relatives, and 150 unrelated normal human controls, and PCR was performed to amplify all the exons and flanking sequences of COL7A1 gene followed by sequencing.Results The patient 1 and 2 had family history, whereas the case 3 was sporadic. Transmission electron microscopy showed tissue cleavage beneath lamina densa in case 1 and slightly decreased anchoring fibrils in some areas of the lesions in case 1 and 3. Three heterozygous mutations of COL7A1 gene, i.e., c. G6734T, c.G6859A and c. G5318T, which leaded to three amino acid mutations, i.e., p. G2245V, p. G1773V and p. G2287R, were found in patient 1, 2 and 3 respectively. Of them, p. G2245V and p. G1773V were novel mutations. The mutations strictly cosegregated with the phenotype in the patients of family 1 and 2. No mutation was detected in the unaffected parents of patient 3 or the 150 unrelated healthy controls. Conclusions The p. G2245V, p. G2287Rand p. G1773V mutations of COL7A1 gene may be responsible for the phenotype of DEBP in the three cases,and of them, p. G2245V and p. G1773V have never been reported.

Objective To identify allergens in portunus trituberculatus responsible for atopic dermatitis (AD) in children.Methods Totally,145 child outpatients with AD were enrolled in this study from September 2013 to July 2014,and underwent the skin prick test (SPT) with crab proteins or crab-specific IgE determination assay.Then,the children with positive SPT or elevated IgE levels underwent an oral challenge with portunus trituberculatus.Serum samples were collected from 33 children with a positive oral food challenge (test group) and from 30 health check-up child examinees (control group).Total proteins were extracted from fresh portunus trituberculatus.Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot were conducted to identify the protein fragments of portunus trituberculatus responsible for AD among these children.Results The SDS-PAGE of crude protein extracts from portunus trituberculatus yielded 11 protein bands with relative molecular masses of 94 000,70 000,58 000,49 000,36 000,34 000,32 000,27 000,21 000,19 000 and 17 000 respectively.Of the 11 protein bands,only 4 with relative molecular masses of 70 000,58 000,49 000 and 36 000 respectively reacted with sera from the patients by Western blot,with the reaction rate being 93.9％,45.4％,39.4％ and 100％ respectively.None of these protein bands reacted with sera from the control group by Western blot.There were significant differences between the test group and control group in the reaction rates of the four proteins with relative molecular masses of 70 000,58 000,49 000 and 36 000 respectively to sera (x2 =55.483,17.898,14.891,63.000,all P ＜ 0.05).Conclusion The two proteins with relative molecular masses of 70 000 and 36 000 respectively are major allergens in portunus trituberculatus responsible for AD among children.

Objective To explore the role of viral infection in the development of drug eruption in patients with HIV infection, and to evaluate the efficacy of antiviral treatment. Methods This study enrolled 87 HIV-positive patients, including 11 with and 76 without drug eruption, all of whom received highly active antiretroviral therapy(HAART). Clinical data on, baseline CD4+ and CD8+ T cell counts and CD4/CD8 ratio in these subjects were retrospectively analyzed. Results The severity of drug eruption was mild in the 11 HIV-positive patients, with a mean latency period of (14.00 ± 8.10)(range, 8 - 34)days. Of the 11 patients with drug eruption, 7 had liver function impairment, which was not in accordance with the severity of skin lesions. Drug eruption was controlled in all the 11 patients after anti-anaphylactic treatment without withdrawal of antiviral drugs. Compared with 75 HIV-positive patients without drug eruption, the 11 HIV-positive patients with drug eruption showed significantly increased baseline CD4 + T cell counts (493.00 ± 245.68 (range, 42 - 810)/μl vs. 347.81 ± 167.00 (range, 11 - 814)/μl, t = 647.50, P < 0.05), but decreased proportion of patients with baseline CD4+ T cell counts below the lower limit of normal(3/11 vs. 48/75(64.00%), X2 = 3.95, P < 0.05). There were no significant differences between 10 patients with drug eruption and 69 patients without drug eruption in the baseline CD8+ T cell count(1472.30 ± 858.55/μl vs. 1356.59 ± 684.06/μl, P > 0.05), CD4/CD8 ratio(0.40 ± 0.27 vs. 0.29 ± 0.16, P > 0.05), or percentage of patients with a CD4/CD8 ratio below the lower limit of normal (9/10 vs. 68/69 (98.55%), P >0.05). Conclusions The latency period of drug eruption seems to be long in HIV-positive patients receiving HAART, and mild drug eruption can be complicated by liver function impairment in the patients. Relatively high CD4 + counts may be a risk factor for the development and aggravation of drug eruption in HIV-positive patients.

Objective:To investigate the association between pulse pressure(PP) and new-onset diabetes in overweight and obese people.Methods:A prospective cohort study was conducted in overweight or obese participants selected from Kailuan Study who underwent 2006-2007 annual checkup and met the inclusion and exclusion criteria. PP was calculated by blood pressure and participants were divided into 4 groups according to PP quartile. The cumulative incidence of new-onset diabetes of different PP groups was calculated by Kaplan- Meier method and compare by Log- Rank test. The multivariate Cox proportional hazards model was used to analyze the association between different PP groups and new-onset diabetes. Results:During an average follow-up of 8.45 years, 8 922 diabetes was identified. The cumulative incidence rate of the Q1, Q2, Q3, and Q4 groups were 22.12%, 24.48%, 27.97%, and 33.44% respectively, which were statistically different( χ2=368.16, P<0.01). Cox proportional hazards regression analysis showed that after adjusting for multiple confounding factors, compared with Q1 group, the hazard ratio for diabetes in Q2, Q3, and Q4 groups were 1.07(1.00-1.14), 1.13(1.05-1.21), and 1.17(1.09-1.27) respectively. And the HR of diabetes event in pulse pressure(per 1 SD increase) was 1.04(1.02-1.07). Similar results were found in participants who were over-weight, obese, with normal blood pressure or hypertensive without drugs use. Conclusion:PP is positively correlated with the new-onset diabetes. High PP is one of the risk factors for developing diabetes in overweight and obese people.

Objective:To observe the presence or absence of necroptosis in PC12 cells after radiation injury, and to detect the expression of receptor-interacting protein 3(RIP3) and evaluate its regulatory effect on necroptosis.Methods:PC12 cells were treated with different doses of irradiation and their necroptosis was detected by lactate dehydrogenase (LDH) release at different time points. After pretreatment with necroptosis inhibitor Necrostatin-1(Nec-1), the changes of cell necroptosis were detected by LDH. The expression level of RIP3 after irradiation intervention was detected by Western blot (WB). After pretreatment with the RIP3-specific inhibitor GSK′872, the changes of cell necroptosis were detected by LDH. The best transfection sequence of RIP3 knockout was screened by WB. The cells were divided into the control group, irradiation group, solvent control group, no-load control group and pretreatment group. WB, immunofluorescence staining, MTT, LDH and Annex V-fluorescein Isothiocyanate/Propidium Iodide (AnnexV-FITC/PI) flow cytometry were used for detection and analysis.Results:After 4 Gy irradiation, the degree of cell necrosis was the highest after 3 hours of culture, and the expression level of RIP3 protein was up-regulated. The cell necrosis was decreased after Nec-1, GSK′872 and RIP3 gene knockdown pretreatment.Conclusions:The radiation injury of 4 Gy can induce the necroptosis of PC12 cells, and the most significant effect can be observed when cultured for 3 hours after irradiation. RIP3 is involved in the process of necroptosis of PC12 cells induced by radiation injury, and plays a pivotal positive regulatory role.