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Objective To measure serum levels of 25-hydroxyvitamin D (25HVD) in patients with chronic urticaria (CU),and to explore its role in the occurrence of CU.Methods Peripheral blood samples were obtained from 50 patients with CU and 40 healthy controls.The urticaria activity score (UAS) was used to assess the severity of CU and to group the patients with CU.Enzyme-linked immunosorbent assay (ELISA) was performed to measure the serum levels of 25HVD,interferon-γ (IFN-γ),interleukin-4 (IL-4) and immunoglobulin E (IgE).Statistical analysis was carried out by t test,rank sum test and linear correlation analysis.Results The serum level of 25HVD was significantly lower in the patients with CU than in the healthy controls (15.20 ± 7.72 vs.21.54 ± 8.31 μg/L,t =3.75,P < 0.05).Moreover,there was a significant difference in the distribution of serum 25HVD levels between the patients and healthy controls (H =17.9,P < 0.05).However,no significant difference was observed in the serum level of 25HVD between severe and mild CU groups (15.57 ± 7.38 vs.14.86 ± 6.28 μg/L,t =0.37,P > 0.05).Compared with the control group,the patient group showed significantly decreased serum levels of IFN-γ (t =15.34,P < 0.05),but increased serum levels of IL-4 and IgE (t =6.54,4.88,respectively,both P < 0.05).Among the patients with CU,the serum level of 25HVD was positively correlated with that of IFN-γ(r =0.738,P < 0.05),but negatively correlated with that of IL-4 (r =-0.689,P < 0.05),and uncorrelated with that of IgE (r =-0.271,P > 0.05).Conclusion The serum level of 25HVD evidently decreased in patients with CU,and it may participate in the occurrence of CU by mediating the Th 1/Th2 imbalance.
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Objective To evaluate the effect of total glucosides of paeony (TGP) on the expression of interleukin-18 (IL-18) in human HaCaT keratinocytes,and to explore the roles of extracelluar signal-regulated protein kinase1/2 (ERK1/2) and c-Jun N-terminal kinase 1/2 (JNK1/2) signaling pathways in the effect.Methods Some cultured human HaCaT keratinocytes were classified into three groups:control group treated with dimethyl sulfoxide (0.031%),TGP groups treated with 6 different concentrations (0.5,2.5,12.5,62.5,125.0 and 312.5 mg/L) of TGP respectively,inhibitor groups treated with TGP of 125 mg/L after 2-hour pretreatment with PD98059 (an ERK1/2 inhibitor) and SP600125 (a JNK1/2 inhibitor) of 10 μmol/L respectively.After additional culture for 48 hours,reverse transcription (RT)-PCR was performed to measure the mRNA expression level of IL-18,and enzymelinked immunosorbent assay (ELISA) to determine the level of IL-18 protein in the culture supematant of HaCaT cells.Some HaCaT keratinocytes were classified into two groups to be treated with TGP of 125 mg/L for 15,30 and 60 minutes with or without the pretreatment with PD98059 and SP600125 of 10 μmol/L; then,Western blot was carried out to determine the phosphorylation levels of ERK1/2 and JNK1/2 in HaCaT cells.Results The levels of IL-18 mRNA and protein in culture supernatant were significantly increased by TGP of 0.5 and 2.5 mg/L,but decreased by TGP of 62.5 and 125.0 mg/L,and TGP of 125.0 mg/L showed the strongest inhibitory effect.After treatment with TGP of 125.0 mg/L,the level of phosphorylated ERK1/2 in HaCaT cells peaked at 15 minutes (0.448 ± 0.018),decreased to 0.213 ± 0.005 at 30 minutes and 0.217 ± 0.005 at 60 minutes,with significant differences between TGP-treated and untreated cells at 15 minutes (0.448 ± 0.018 vs.0.204 ± 0.005,P< 0.05) but not at 30 or 60 minutes (both P > 0.05).The phosphorylation level of ERK1/2 was 0.237 ± 0.010 in HaCaT cells pretreated with PD98059 prior to the treatment with TGP,significantly different from that in HaCaT cells treated with TGP only (P <0.01).TGP of 125.0 mg/L had no obvious effect on JNK phosphorylation,and there was no significant difference in the level of phosphorylated JNK1/2 between HaCaT cells untreated and those treated with TGP of 125.0 mg/L for different durations (all P > 0.05).Conclusions TGP can inhibit the expression of IL-18 mRNA and protein in HaCaT cells,likely through the ERK1/2 signaling pathway.
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Objective To study the mutation of STK11 gene in a Chinese family and a sporadic patient with Peutz-Jeghers syndrome (PJS),and to provide a basis for genetic diagnosis and counseling.Methods One sporadic patient and two patients from a family with PJS were collected,all of whom had typical mucosal pigmentation and gastrointestinal polyposis.Blood samples were obtained from the two patients and six unaffected relatives in this family,the sporadic patient,and 100 healthy controls.DNA was extracted,and PCR was performed to amplify nine exons and their adjacent introns in the STK11 gene followed by direct sequencing.The sequencing results were aligned to the published sequence of STK11 gene from Genbank.Results No mutation was found in the STK11 gene of any of the patients,unaffected relatives,or healthy controls.Conclusions Genetic heterogeneity exists in Peutz-Jeghers syndrome,hinting that there may be other causative genes or sites for this entity.
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Objective To detect the expression of Livin,an apoptosis-inhibiting protein,and Smac,an apoptosis-promoting protein,in basal cell carcinoma (BCC) lesions.Methods Skin specimens were obtained from the lesions of 80 patients with BCC and normal skin of 30 human controls.Immunohistochemical SP method was used to detect the pmtein expression of Livin and Smac in these specimens.Chi-square test was conducted to compare the expression rate of Livin and Smac protein between the lesional and control specimens.The relationship between the protein expression of Livin and Smac in BCC was analyzed by Spearman correlation coefficients.Results The expression rate of Livin protein was significandy higher (77.50% vs.3.33%,x2 =49.04,P < 0.001),while that of Smac protein was statistically lower (46.25% vs.100%,x2 =26.47,P < 0.001),in BCC than in the control specimens.No significant difference was observed in the expression rate of Livin or Smac protein between nodular ulcerative and pigmented BCC specimens (75.41% vs.80.00%,x2 =0.001,P > 0.05; 47.54% vs.40.00%,x2 =0.28,P> 0.05) or between nodulocystic and pigmented BCC specimens (73.58% vs.80.00%,x2 =0.03,P > 0.05; 45.28% vs.40.00%,x2 =0.13,P > 0.05).There was a negative relationship between the protein expression of Livin and Smac in BCC lesions (r =-0.432,P < 0.01).Conclusion The upregulated expression of Livin and downregulated expression of Smac may be invoved in the occurrence and development of BCC.
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Objective To detect Ureaplasma urealyticum (Uu) and Mycoplasma hominis (Mh) in urogenital tract of healthy elementary and high school students,and to determine the biovars and serotypes of Uu isolates.Methods Urine specimens were collected from 957 healthy school children,including 404 elementary school students,260 junior high school students and 293 senior high school students,and submitted for Uu and Mh culture in selective liquid medium.Thc specimens positive for Uu and (or) Mh culture were subsequently subjected to PCR.The biovars and serotypes of Uu were determined.Results Uu was detected in 4.81% (46/957) of the school children.Among the 46 Uu positive specimens,32 (69.57%) harbored Ureaplasma Parvum (biovar 1 ),14 (30.43%) Ureaplasma urealytieum (biovar 2); 12 (2.97%) were from elementary school students,including 9(75.00%) cases of Ureaplasma Parvum and 3(25.00%) Ureaplasma urealytieum,8(3.08%) were from junior high school students,including 5 cases of Ureaplasma Parvum and 3 Ureaplasma urealytieum,26 (8.87%) were from senior high school students,including 18 (69.23%) cases of Ureaplasma Parvum and 8 (30.77%)Ureaplasma urealytieum.Mh was positive in 9 (0.94%) school students,including 1 elementary school student,1 junior school student and 7 senior high school students.The detection rate of Uu was significantly higher in females than in males in all the 3 groups (elementary school,junior and senior high school) of students.Conclusions Mh and Uu are commensals in urogenital tract of elementary and high school students without symptoms.Ureaplasma Parvum is the predominant biovar in this population,though Ureaplasma urealytieum accounts for a significant proportion,which implies that Uu is commensal in healthy elementary and high school students,and females are more liable to be colonized than males.
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Objective To evaluate the effects of total glucosides of paeony (TCP) on cell proliferation of and expression of VECF and IL-23 in human HaCaT keratinocytes and their potential mechanisms. Methods MTT assay was performed to detect the cell proliferation of HaCaT cells incubated with various concentrations (0.5 to 312.5 mg/L) of TGP. HaCaT cells were classified into 8 groups, control group without any treatment, TGP groups treated with 6 different concentrations of TGP, SB203580 group treated with TGP of 125 mg/L after 2-hour pretreatment with SB203580 of 10 μmol/L After additional culture, reverse transcription (RT)- PCR and enzyme linked immunosorbent assay (ELISA) were conducted to determine the expression levels of VEGF and IL-23 mRNA and protein, Western blot to test the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in these cells. Results The proliferation of HaCaT cells was promoted by TGP of low concentrations (0.5 and 2.5 mg/L), but inhibited by TGP of equal to or more than 12.5 mg/L, and peaked at the concentration of 125 mg/L. TGP of 0.5 and 2.5 mg/L enhanced the mRNA and protein expressions of VEGF and IL-23, while TGP of 12.5 to 125 mg/L suppressed the expression of VEGF mRNA and protein, and TGP of 62.5 to 125 mg/L downregulated the expression of IL-23 mRNA and protein. The phosphorylation of p38 protein kinase in HaCaT cells was induced by TGP of 125 mg/L in a time-dependant manner. Concretely, the level of phosphorylated p38 kinase in HaCaT cells was 0.3314 ± 0.0245 (peak) at 5 minutes, decreased to 0.2173 ± 0.0189 at 10 minutes (still statistically higher than untreated HaCaT cells) and 0.1664 ± 0.0201 at 30 minutes after treatment with TGP of 125 mg/L. SB203580 attenuated the effect of TGP on p38 phosphorylation, and the level of phosphorylated p38 kinase was 0.1529 ±0.0147 in HaCaT cells pretreated with SB203580 prior to the treatment with TGP. Conclusion TGP can inhibit the cell proliferation of and expressions of VEGF and IL-23 mRNA and protein in HaCaT cells, likely mediated by the p38 MAPK signaling pathway.
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Objective To study the relationship of age and high risk behaviors (HRBs) related to HIV/AIDS among men who have sex with men (MSM) in China. Methods One thousand one hundred and nine anonymous questionnaires were collected from MSM in 1999. Univariate analyses were applied to clarify the relation of the age and HRBs. Results The numbers of accumulative partners and oral intercourse behavior were higher in 35 ~ 44 age group (P
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ObjectiveTomonitorthehighriskbehaviorsandotherAIDS/STIrelatedfactorsamongmenwhohavesexwithmen(MSM),especiallymalehomosexualsinmainlandChina.MethodsSelf-administratedanonymousmailsurveyswerecarriedoutin2001,andanalyzedwithSPSS.ResultsOnethousandonehundredandnineeffectivequestionnaireswerecollectedfrom30provincesandcities.MostofMSMlivedinbigormedi-um-sizedcities,havinggoodeducation,andbeingyounger.Thenumbersofsamegendersexpartnersweremorethanone.Theyoftenhadcasualsexpartnersandunprotectedintercourse.Inthelastyear,11.45%reportedhavingbeendiagnosedSTI.AmongMSMwhohavebeentestedforHIVantibody,5.45%oftestswerepositive.ConclusionsWhileSTIratehasbeenreachingahighlevel,MSMwithSTIalsohavebeeninfectedwithHIVintheMSMofmainlandChina.OthergroupshavingsexwithMSMareatgreaterriskofSTI/HIVinfection.ItisinurgentneedtopreventandcontrolSTI/AIDSinMSM.
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Objective To investigate the role of the expression of p27 and cyclin E in the pathogenesis of Bowen's disease and squamous cell carcinoma (SCC). Methods The expression of p27 and cyclin E was assessed by immunohistochemical method in 16 patients with Bowen's disease, 53 patients with SCC and 25 normal controls. Results The expression of p27 was lower in Bowen's disease and SCC compared to that in the normal skin, and the expression level decreased with a decline in the differentiation of tumors, i.e. the lowest expression was observed in poorly differentiated SCC, followed by highly differentiated SCC and Bowen's disease. The expression of cyclin E was higher in Bowen's disease and SCC than that in the normal skin, and the expression level increased with a decline in the differentiation of tumors. The expression of p27 was inversely correlated with that of cyclin E among all the cases of Bowen's disease and SCC. Conclusion The abnormal expression of p27 and cyclin E may contribute to the pathogenesis of Bowen's disease and SCC.