Objective To assess and compare the Beck Depression Inventory-II ( BDI-Ⅱ) , Hospital Anxiety and Depression Scale-Depression Subscale ( HADS-D) and Center for Epidemiologic Studies Depression Scale ( CES-D) as screening instruments for depression in patients with epilepsy .Methods One hundred and seventeen patients diagnosed with epilepsy were evaluated by BDI-Ⅱ, HADS-D and CES-D, the performance of BDI-Ⅱ, HADS-D and CES-D was evaluated by ROC curve .Results There were 33 epileptics with depression .The sensitivity and specificity of BDI-Ⅱfor the diagnosis of depression was around 90% for critical value 16, the sensitivity of CES-D was more than 80%for critical value 15, and specificity was 72.6%.The sensitivity and specificity of HADS-D was more than 80%for critical value 9, and the sensitivity of HADS-D was 91.3% for critical value 7, and specificity was 76.8%.Three instruments showed a negative predictive value of over 90%.Comparisons of the areas under the ROC curve for these instrument were not statistically significant difference (all P>0.05).Conclusion HADS-D is a brief efficient screening instruments to identify depression in patients with epilepsy .

Objective To investigate whether glucosyltransfernse(GTF) and open reading frame 4 (ORF4) coded by fap1-orf4 gene locus of Streptococcus parasanguis was involved in the regulation of Fap1 glycosylation, and mature and to determine whether there was interaction between GTF and ORF4. Methods A gene replacement strategy was adapted to construct gtf and orf4 allele replace mutant of S. Parasanguis. Complementation assay and Western blot were used to test fap1 expression levels. Yeast two-hybrid analysis and GST pull down assays were adapted to determine the interaction between GTF and ORF4. Results (1) Compared with wild S. Parasanguis, mature Fapl (Mr about 220×103) disappeared and were substituted with high molecular weight Fapl (Mr about 360×103) in gtf or orf4 alleie replace mutants of S. Parasan-guis. Complementation assay showed that pVPT-GFP-gtf and pVPT-GFP-orf4 restored mature fap1 expression in gtf or orf4 alleie replace mutants, respectively. (2) With Yeast two-hybrid analysis, the eotransformants, AH109/pAD-Gtf+pBD-orf4 and AHlOg/pAD-orf4+pBD-gtf growed on SD-LTHA selective ngar plate after streaked, reversely, the eotransformants, AH109/pAD+pBD-orf4,AH109/pAD+pBD-gtf、AH109/pBD+ pAD-orf4、AH109/pBD+pAD-gtf did not grow on SD-LTHA selective agar plate, furthermore, the cotrans-formants, AH109/pAD+pBD-orf4 and AH109/pAD-orf4+pBD-gtfshowed blue during X-α-gal assay. (3) GST pull down assay confirmed the direct interaction between GTF and ORF4. Conclusion There is inter-action between GTF and ORF4 coded byfapl-orf4 gene locus of S. Parasangnis and the formation of the GTF and ORF4 complex was required for the glycosylation and mature of Fapl in S. Parasanguis.

Objective To study whether ORF3 coded by fap1-orf4 gene locus of Streptococcus pa-rasanguis is involved in the regulation of Fap1 glycosylation and maturation and to investigate whether ORF3 influences Streptococcus parasanguis adhesion. Methods A gene replacement strategy was adapted to con-struct orf3 alleic replace mutant of Streptococcus parasanguis. Complementation assay and Western blot were used to test Fap1 expression levels. Whole saliva-coated hydroxyapatite (SHA) adhesion assay was adapted to determine Streptococcus parasanguis adhension. Results (1) Non-polar was found in strain VT1774, the orf3 alleic replace mutant of Streptococcus parasanguis. (2) Western blot showed that mature Fapl (Mr about 220 × 103) disappeared and were substituted with high molecular weight Fapl (Mr about 470 × 103) in strain VT1774, furthermore, complementation assay showed VT1775, the complementation strain of VT1774, re-stored mature Fapl expression. (3) The binding ability reduced significantly in strain VT1774. Conclusion ORF3 coded byfapl-orf4 gone locus was required for Fap1 glycosylation and maturation in Streptococcus pa-rasanguis, orf3 alleic replacment resulted in Fap1 glycosylation and mature disorder and decreasing of adhen-sion ability of Streptococcus parasanguis.

The cell-free plasma DNA (cfpDNA) has been suggested as a useful tumor marker for its quantitative and qualitative tumor-specific alterations that reflect the biological characteristics and the progression and outcomes of tumors.Therefore,it has been used as liquid biopsy to detect cfpDNA in peripheral blood for the diagnosis,monitoring of clinical effects,and prognosis of malignancies

Objective To investigate the relationship between arsenic in drinking water and skin lesions in endemic arsenism area in Shanyin County of Shanxi Province,in order to provide epidemiologic data for further arsenism research.Methods One hundred and eighty-nine endemic arsenism patients and 59 controls were randomly selected in 17 endemic amenism countries in Shanyin County of Shanxi Province.The content of arsenic in drinking water which wa8 collected indoom was half-quantitatively screened by a kit made by Chinese Center for Disease Control and Prevention,then quantitatively determined by HPLC-ICP-MS.Patients of endemic arsenism were diagnosed by "The Standard of Diagnosis for Endemic Amenism"(WS/T 211-2001).Results There were 64.9% (87/134)samples above the arsenic level(50μg/L)of drinking water and the median value of arsenic in drinking water was 91.43 μg/L in 134 water samples.The OR(95%CI)value between arsenic in drinking water and hyperkeratosis,hyperpigmentation,depigmentation was 2.46(1.22-4.94),3.34(1.50～7.44)and 2.86(1.50-5.46),respectively.The prevalence of hyperkeratosis,hyperpigmentation and depigmentation increased,as the arsenic in drinking water increased(≤10,≤50,≤200,＞200μg/L),especially in＞200μg/L group(OR=6.15,13.96,11.41,P＜0.05).The arsenic level in drinking water of Ⅲ degree of depigmentation patients(318.300μg/L)was higher(P＜0.05)than that of 0,Ⅰ and Ⅱ degree groups(86.670,131.800,1 10.590μg/L,P＜0.05).Conclusions Shanyin County is a medial arsenic pollution area. Arsenic in drinking water is considered as a risk factor of skin lesion. The degree of skin lesions increased,as the arsenic in drinking water increased.

OBJECTIVETo observe the inhibitory effect of gefitineb on the proliferation and its inducing effect on the apoptosis of mouse I-10 Leydig testicular cancer cells in vitro.

METHODSWe treated I-10 Leydig testicular cancer cells of mice with gefitineb at 0, 1.25, 2.5, 5, 10, 20, and 40 µmol/L. Then we determined the inhibitory effect of gefitineb on the growth of the cells by MTT, detected their early and late apoptosis by Annexin V-FITC/propidium iodide double staining and Hoechst 33258 nuclear staining, respectively, and observed the expressions of apoptosis-related proteins Bcl-2, Bax and caspase 3/9 by Western blot.

RESULTSCompared with the blank control group, gefitineb significantly inhibited the proliferation of the I-10 cells at 10 and 20 µmol/L (P < 0.05). The survival rate of the cells was (32.4 ± 2.8)% (P < 0.01) and their early and late apoptosis rates were (26.7 ± 4.2)% and (59.33 ± 10.2)% in the 40 µmol/L group, significantly different from those in the control (P < 0.05 and P <0.01). In comparison with the blank control group, gefitineb at 10, 20, and 40 µmol/L increased the expression of pro-apoptotic protein Bax by (41.9 ± 7.1), (60.1 ± 9.8), and (69.0 ± 11.3)% (all P < 0.05), decreased that of apoptosis-inhibitory protein Bcl-2 by (50.3 ± 8.9), (63.9 ± 6.9), and (88.7 ± 13.9)% (all P < 0.05), and elevated that of the cleft proteins caspase-3 by (69.0 ± 6.9)% (P < 0.05), (71.5 ± 8.1)% (P < 0.05), and (110.9 ± 14.2)% (P < 0.01) and caspase-9 by (51.8 ± 4.9), (54.7 ± 6.7), and (43.8 ± 11.8)% (all P < 0.05).

CONCLUSIONGefitineb can increase the cytotoxicity of I-10 Leydig testicular cancer cells of mice and induce their apoptosis via the mitochondria-mediated apoptosis signaling pathway.

Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Apoptosis Regulatory Proteins ; metabolism ; Caspase 3 ; metabolism ; Caspase 9 ; metabolism ; Cell Proliferation ; drug effects ; Cell Survival ; Leydig Cell Tumor ; drug therapy ; metabolism ; pathology ; Male ; Mice ; Neoplasm Proteins ; metabolism ; Neoplasms, Germ Cell and Embryonal ; drug therapy ; metabolism ; pathology ; Quinazolines ; pharmacology ; Testicular Neoplasms ; drug therapy ; metabolism ; pathology ; bcl-2-Associated X Protein ; metabolism

Gindenosides are the active ingredients of Panax ginseng. 20 (S) -protopanaxadiolocotillol type epimers are the main metabolites of 20 (S) -protopanaxadiol. The previous studies showed that there are stereoselectivity difference in pharmacodynamics and pharmacokinetics between 24R-epimer and 24S-epimer. The purpose of this study was to explore the excretion of the epimers in bile, feces and urine of rat. Liquid chromatography tandem mass spectrometry method has been performed for determination of 24R-epimer and 24S-epimer in bile, feces and urine. 24R-epimer or 24S-epimer was intragastric administered to rats at a single dose of 10 mg x kg(-1). Results showed that after administration the recovery of 24R-epimer and 24S-epimer in feces was 17.69% and 17.09%, respectively, while both of the two epimers were hardly detected in urine. The 48 h cumulative biliary excretion rate of 24R-epimer was 8.01% after administration, while only 1.47% for 24S-epimer. It indicated that there are stereoselectivity in biliary excretion of the epimers with intragastric administration.
Animals ; Bile ; chemistry ; metabolism ; Drugs, Chinese Herbal ; chemistry ; pharmacokinetics ; Feces ; chemistry ; Ginsenosides ; chemistry ; pharmacokinetics ; Male ; Mass Spectrometry ; Panax ; chemistry ; Rats ; Rats, Sprague-Dawley ; Stereoisomerism ; Urine ; chemistry

Objective To investigate the altered expression of muscarinic receptor 2 (M_2 receptor) in the pedunculopontine nucleus (PPN) of Parkinson's disease (PD) model rat by immunocytochemical technique and explore the role of M_2 receptor in etiopathogenesis and pathophysiological changes of PD. Methods Sixteen healthy SD rats were divided randomly into two groups. Rat monoclonal antibody against the M_2 receptor was used. Then we used positive cell counting and optical density as indicators to analyze the altered expression of M_2 receptor in PPN of PD model rats. Results The counting of M_2 receptor positive cells in the PPN was not obviously changed in normal rats and the unlesioned side of PD rats (P>0.05), whereas a significant decrease was observed when compared to that in normal rats and the lesioned side of PD rats, respectively (P<0.05). However, the positive intensity in the three groups did not differ significantly. Conclusion The results indicate that there was a degenerative death or receptor loss of M_2 receptor positive cells in the lesioned PPN of PD rats. The expression intensity of M_2 receptor positive cells without degenrative death or receptor loss was not affected. It was also found that the factor affecting the change of M_2 receptor positive cells in the PPN involved only one side.

To investigate the high-risk factors for newborn hearing loss and to provide information for preventing the development of hearing loss and delaying its progression, from May 2003 to June 2006, neonates who failed to pass the universal newborn hearing screening (UNHS) were referred to Jinan Newborn Hearing Screening and Rehabilitation Center from 7 newborn hearing screening centers in seven cities of Shandong province. One-to-one pair-matched case-control method was employed for statistical analysis of the basic features of definitely identified cases. High-risk factors relating to the bilateral hearing loss were evaluated by univariate and multivariate Logistic regression analysis. Our results revealed that 721 transferred newborns who didn't pass the hearing screening received audiological and medical evaluation and 367 were confirmed to have hearing loss. Of them, 177 neonates with hearing loss who met the matching requirements were included in the study as subjects. Univariate analysis showed that high-risk factors related to hearing loss incuded age of father, education backgrounds of parents, parity, birth weight, gestational weeks, craniofacial deformity, history of receiving treatment in neonatal intensive care unit (NICU), neonatal disease, family history of otopathy and family history of congenital hearing loss. Multivariate Logistic regression analysis revealed that 4 independent risk factors were related to bilateral hearing loss, including parity (OR=16.285, 95% CI 3.379-78.481), neonatal disease (OR=34.968, 95% CI 2.720-449.534), family history of congenital hearing loss (OR=69.488, 95% CI 4.417-1093.300) and birth weight (OR=0.241, 95% CI 0.090-0.648). It is concluded that parity, neonatal disease and family history of hearing loss are the promoting factors of bilateral hearing loss in neonates and appropriate intervention measures should be taken to deal with the risk factors.