Objective To explore the role of Epstein-Barr virus (EBV) infection in the etiology of drug eruption. Methods PCR-Southern blot was used to detect EBV-specific DNA fragment BamH I -W in peripheral blood mononuclear cells of 32 patients with drug eruption and 30 age- and sex-matched normal controls. The mRNA expression of EBV lyric gene BZLF1 in EBV DNA-positive samples was measured by RT-PCR and Southern blot. ELISA was performed to detect EBV virus capsule antigen (VCA)-specific IgM. Results The positivity rate of EBV DNA was significantly higher in patients with drug eruption than in normal controls (78.13% (25/32) vs 10.00% (3/30), P < 0.01), while no significant difference was noted between patients with severe and mild drug eruption (P > 0.05). The expression of BZLF1 mRNA was detected in 3 out of 25 EBV DNA-positive patients; of the 3 patients, 1 suffered from mild drug eruption, and 2 from severe drug eruption. EBV VCA-specific IgM was observed in 6 of 32 patients with drug eruption, but not in any normal controls. No significant difference in the positivity rate of EBV VCA-specific lgM existed between patients with severe and mild drug eruption (P > 0.05). Conclusions There is an active infection of EBV in patients with drug eruption. EBV infection is probably an environmental factor affecting the development of drug eruption.

Objective To evaluate the effects of problem-based learning (PBL) teaching mode and lecture-based learning (LBL) teaching mode applied in clinical teaching of dermatology in China.Methods All studies on PBL teaching mode and LBL teaching mode applied in clinical teaching of dermatology in China published from 1990 to 2015 were identified by searching in CNKI,VIP database,Wanfang data and so on.Meta-analysis was performed by RevMan 5.3 software.Results Six random controlled trials on 710 clinical students qualified for the meta-analysis according to our criteria.The students in PBL group got significant higher scores than those of the students in LBL group in theoretical scores [WMD=3.75,95％CI=2.58-4.92,P＜0.05],clinical skills tests [WMD=5.27,95％CI=4.60-5.94,P＜0.05] and total scores [WMD=7.93,95％CI=6.49-9.37,P＜0.05].Conclusion PBL teaching mode is an effective mode on teaching of dermatology in China,particularly for theoretical scores and clinical skills,compared with LBL mode.

ObjectiveTo assess the relationship between Candida adhesivity and biofilm formation. MethodsEight Candida strains belonging to 8 species and 1 Saccharomyces cerevisiae strain were cultured in yeast peptone dextrose (YPD) fluid and agar medium respectively. The flocculation and adhesion of Candida were observed. Candida biofilm models were developed in 96-well microculture plates. The kinetics of biofilm formation was measured. ResultsAll the 9 fungal strains had flocculation capability and could adhere to the surface of the yeast peptone dextrose agar medium. After mild shaking of the fluid medium, it is difficult for C. albicans, C. kefyr, C. glabrata and C. tropicalis to resuspend, but easy for Saccharomyces cerevisiae. The adhesivity of C. albicans, C. kefyr, C. glabrata and C. tropicalis was stronger than that of the other Candida strains. Common pathogenic Candida strains could form biofilm, and the metabolic activity of Candida cells in the biofilm increased over time. A significant increment was observed in the ability of C. albicans and C. kefyr to form biofilm compared with the other species(all P ＜ 0.05), and in that of C. tropicalis and C. glabrata compared with C. krusei, C. parapsilosis and C. gulliermondii (all P ＜ 0.05). The nonpathogenic Saccharomyces cerevisiae could not form biofilm. ConclusionsCandida has the ability to adhere and form biofilm,and the ability varies with Candida species. Moreover, the ability to form biofilm positively correlates with the adhesivity of Candida.

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 characterize the natural history of psoriasis vulgaris.Methods A retrospective study was carried out.Totally,245 patients admitted to hospitals within three months after the first episode of psoriasis vulgaris were selected from 1136 patients with psoriasis vulgaris who had been followed up for more than 20 years.Changes in disease severity during the long-term follow-up were traced,and information on the shape and distribution of skin lesions,family history,use of anticancer drugs,vitamins and traditional Chinese medicines was collected and analyzed.SPSS13.0 software package was utilized to assess factors associated with the evolution of psoriasis vulgaris.Results The natural course of psoriasis vulgaris could be classified into six types:immediate healing,slow healing,intermittent relapse,frequent mild relapse,frequent moderate relapse,and frequent severe relapse.The immediate healing type and slow healing type amounted to 30％ of these patients,and the frequent severe relapse type to less than 10％.Statistical analysis revealed that the clinical severity of psoriasis was associated with the age of onset and family history,and was negatively correlated with the use of anticancer drugs.Conclusions The long-term follow-up study reveals the natural course of psoriasis vulgaris,which may be helpful in guiding the prediction of prognosis,prevention of recurrence and selection of treatment.

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 investigate the role of human herpesvirus type 7 (HHV-7) in the development of drug eruptions.Methods Venous blood samples were collected from 35 patients with mild drug eruptions at acute stage,15 patients with severe drug eruptions at both acute stage and remission stage,as well as 50 healthy human controls.PCR was performed to detect HHV-7 DNA in peripheral blood mononuclear cells (PBMCs),and enzymelinked immunosorbent assay (ELISA) to determine the titer of anti-HHV-7 IgM antibody in serum.Statistical analysis was carried out by t test,one way analysis of variance,Chi-square test and q test.Results The detection rate of HHV-7 DNA was significantly higher in these patients with drug eruptions than in the healthy controls (82.00％ (41/50) vs.62.00％ (31/50),x2 =4.96,P ＜ 0.05),different among patients with severe drug eruptions (93.33％ (14/15)),patients with mild drug eruptions (77.14％ (27/35)) and the healthy controls (x2 =6.32,P ＜ 0.05),higher in the patients with severe drug eruptions than in the healthy controls (q =3.50,P ＜ 0.05),but not significantly different between the patients with severe drug eruptions at acute stage and those at remission stage (73.33％(11/15),P ＞ 0.05).The anti-HHV-7 IgM antibody titer was significantly increased in the patients with drug eruptions compared with the healthy controls ((69.319 0 ± 25.289 7) ng/L vs.(59.785 3 ± 22.438 2) ng/L,t =1.99,P ＜ 0.05),but no significant difference was observed among the patients with severe drug eruptions (74.340 7 ±31.411 2) ng/L),patients with mild drug eruptions ((65.479 1 ± 21.326 1) ng/L) and healthy controls (P ＞ 0.05) or between HHV-7 DNA-positive patients ((63.748 1 ± 27.239 1) ng/L) and-negative patients ((65.580 2 ± 36.258 4) ng/L,P ＞ 0.05).Conclusions Active HHV-7 infection exists in patients with drug eruptions,and may be associated with the development and aggravation of this entity.

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 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 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.