ObjectiveTo clone the full-length cDNA of Microsporum canis membrane protein PQ-loop repeat protein(PQ-LRP) gene,so as to investigate the roles of PQ-LRP in the pathogenesis of tinea capitis.MethodsA Microsporum canis strain(A518) from a patient with tinea capitis served as the experimental strain.Rapid cDNA end amplification(RACE) was performed to clone the full length cDNA sequence of PQLRP gene.Bioinformatics methods were used to make a preliminary functional analysis of the gene.Results The cDNA of PQ-LRP gene was obtained with a full length of 1522 bp,including the 5' untranslated region (49 bp),coding region(1080 bp) and 3' untranslated region(393 bp).The coding region encoded a protein precursor including 359 amino acid residues.The cloned cDNA of PQ-LRP gene shared an 81％ nucleotide identity with that of Trichophyton tonsurans and a 79％ nucleotide identity with that of Trichophyton rubrum.Conclusions The full-lengthcDNA of Microsporumcanis membraneproteinPQ-LRP gene hasbeen successfully cloned,which will provide an important basis for further researches into the roles of PQ-LRP in Microsporum canis-associated diseases.

Objective To study the change of the level of plasma D-dimer(DD) in patients with coronary heart disease(CHD)and its significance.Methods 96 CHD patients were divided into various groups according to coronary angiography and clinical manifestation: 26 patients with simple lesions,47 patients with complex lesions,12 patienty with acute myocardial in-farction(AMI),42 patienty with unstable angina pectoris(UAP),19 patienty with stable angina pectoris(SAP)and 23 patienty with normal healthy control subjects.The level of plasma DD was detected.Results Plasma concentrations of DD were higher in patients with complex lesion((0.501?0.209)mg/L)than in those with simple lesions((0.328?0.1)mg/L)(P

Objective To explore the significance of FSH1 in the pathogenicity of M. canis. Methods Thirty M. cam's strains from tinea capitis lesions and 30 M. canis strains from tinea corporis lesions were cultured, passaged, and induced by medium containing skin tissue of scalp or foreskin from children. Semi-quantitative reverse transcription (RT)-PCR was carried out to detect the expression of FSH1 mRNA in the firstand fifth-generation M. canis strains, as well as M. canis strains induced by the skin tissues. Results The mRNA expression of FSH1 was higher in M. canis strains derived from tinea capitis lesions than in those from tinea corporis lesions (P < 0.01), but there was no significant difference between the first-generation and fifthgeneration M. canis strains (P> 0.05). The skin tissue from scalp and foreskin induced a significant elevation in the mRNA expression of FSH1 in these M. canis strains (F = 2025.713, 1833.139, both P< 0.01), and the inductive effect of the scalp tissue was different from that of the foreskin tissue (P < 0.01). Conclusions The FSH1 mRNA expression is different in M. canis isolated from different body sites. Local skin tissue has an inductive effect on the expression of FSH1 mRNA, and the inductive effect of scalp tissue is more apparent than that of foreskin tissue.

Background Genetic mutation remains to be the most common cause of congenital cataract.Whole exon sequencing technology is an ideal method to detect the pathogenic gene mutations.Objective This study was to identify the pathogenic gene in a Chinese autosomal dominant congenital cataract (ADCC) family by whole-exome sequencing.Methods This study complied with Helsinki Declaration and the protocol was approved by Ethic Committee of Peking University Third Hospital.Informed consent was obtained from each subject before any medical examination.A cross-sectional study was designed.A Chinese ADCC family with 4 generations and 48 members were enrolled in Peking University Third Hospital,of which Ⅰ1 and Ⅰ2 died.The periphery blood of 8-10 ml was collected from each member of Ⅱ,Ⅲ and Ⅳ generations for the high throughput sequencing of genes using whole exon trapping and new sequencing technology,and the sequencing results were compared with the data of human HA PMAP8,dbSNP130 and 1000 Genome Project database.The synonymous mutation was filtered after reported common variants,and the false positive results of explicit sequencing were finally excluded by Sanger sequencing and then the candidate genes were identified.The mutation genes were screened to determine the pathogenic gene of this ADCC family.Results Eleven ADCC patients were found in this family,and the patients distributed in each generation with an equal chance for involvement in male and female subjects,which conformed to an autosomal dominant inheritance pattern.All the patients were nuclear cataract.Genome-wide whole-exome sequencing found that major intrinsic protein (MIP) gene was known genes of ADCC in initially identified candidate genes,so the Sanger was used to verify the MIP gene.The heterozygous mutation of MIP gene (chr12:56845250 C ＞ T) appeared to be the pathogenic cause of this ADCC family.The mutation occurred in the splice sites of the gene,resulting in the fourth exon coded-61 amino acids are replaced by leucine,histidine and serine,which lead to the abnormal truncated proteins.Conclusions The heterozygous mutation of MIP gene is the molecular pathogenesis of this Chinese ADCC family.

Objective To study the chemical constituents of Dioscorea zingiberensis.Methods The fresh rhizome of D.zingiberensis was extracted three times,3 h once with EtOH-H2O at 80 ℃.The EtOH was evaporated under reduced pressure to give a residue which was suspended in water and then was exacted with petroleum ether,ethyl acetate,and n-butanol fraction.The water fraction was isolated by the reversed-phase ODS column chromatography.The chemical structures were elucidated by means of 1H-NMR,13C-NMR,135DEPT,HMQC,and HMBC spectroscopic analyses.Results Three steroidal saponins were isolated from the fresh rhizome of D.zingiberensis.The compounds were identified as:diosgenin-3-O-?-D-glucopyranosyl(1→3)-?-D-glucopyranosyl(1→4)-[?-L-rhamnopyranosyl(1→2)]-?-D-glucopyranoside(Ⅰ),(25R)-26-O-?-D-glucopyranosyl-furost-5-en-3?,22?-diol-3-O-?-D-glucopyranosyl(1→3)-?-D-glucopyranosyl(1→4)-[?-L-rhamnopyranosyl(1→2)]-?-D-glucopyranoside(Ⅱ),and(25R)-26-O-?-D-glucopyranosyl-furost-5-en-3?,22?-diol-7-carbonyl-3-O-?-D-glucopyranosyl(1→3)-?-D-glucopyranosyl(1→4)-[?-L-rhamnopyranosyl(1→2)]-?-D-glucopyranoside(Ⅲ).Conclusion Compound Ⅲ is a novel compound named as zingiberenin H.

AIMTo analyze the characteristics of publications of Chinese Journal of Applied Physiology between 2000 and 2006, evaluate the academic level and the popularity of the issues, and supplying an evidence for the journal reform.

METHODSWith CNKI and manpower search, by use of literature metrology, a comprehensive analysis of the publications of Chinese Journal of Applied Physiology between 2000 and 2006 was made.

RESULTSThe number of articles published form 2000 to 2006 in Chinese Journal of Applied Physiology was 968, The average number of each issue is 34.57, the average page of each article is 3.11, in the columns, the article about original articles was top of rank (66.22% of the total). In the quotation, the quotation increase year by year (100% in 2004-2006), the number of English quotation is very more (76.52% in average). In the time lag, the longest is 510 days, the shortest if 60 days, the average is 196.51 days. In the fund support, the level is increase by fund support, the article number by fund support is increase too, It is 97 in 2005. In the authors' professional positions and academic degrees, the authors' level is more and more higher. In the authors column, Beijing's author is the top of rank, has 162 persons (16.74% of the total).

CONCLUSIONThe Chinese Journal of Applied Physiology has published high quality articles. It is the one of the most important information resource for the physiological research and the most important medical journal.

Objective To observe the therapeutic efficacy of intravitreal ranibizumab combined with laser photocoagulation for the treatment of macular edema associated with ischemic branch retinal vein occlusion (BRVO).Methods Together 60 patients (60 eyes) with BRVO in Anshan City Central Hospital were included and divided into three groups,20 patients with intravitreal ranibizumab treatment as A group,20patients with retinal laser photocoagulation treatment as B group,and another 20 patients with intravitreal ranibizumab combined with retinal laser photocoagulation therapy as C group,followed by the preoperative observation of the best corrected visual acuity (BCVA),slit lamp,fundus and intraocular pressure examination,fundus fluorescein angiography (FFA),optical coherence tomography (OCT).One day after the surgery,BCVA,slit lamp and intraocular pressure examination were conducted,and 1 month,2months,3 months after the surgery,observation of BCVA,slit lamp,fundus and intraocular pressure examination were performed.Then,OCT was used to determine the status of macular edema.And finally,BCVA and central macular thickness (CMT) in the three groups were statistically analyzed by observing the above indicators.Results The BCVA at 1 month,2 months,and 3 months after treatment was higher than before treatment in all three groups,and the differences were statistically significant (all P ＜ 0.05).The BCVA of A group was 0.26 ±0.14 and 0.26 ±0.14 at 2 and 3 months after treatment,respectively,which was significantly better than that of B group (0.39 ±0.10 and 0.40 ±0.10) (all P ＜0.05).At 3 months after treatment,the BCVA in C group was 0.14 ±0.11,which was significantly higher than that in A group (0.26 ±0.14) (P＜0.05).The BCVA of C group was 0.30 ±0.13,0.20 ±0.12,0.14 ± 0.11 at 1 month,2 months and 3months after treatment,respectively,which was better than that of B group (0.43 ±0.10,0.39 ± 0.10,0.40 ± 0.10),and the differences were statistically significant (all P ＜0.05).The postoperative CMT was significantly reduced when compared with preoperation in all three groups (all P ＜ 0.05).The CMT at 1 month,2 months and 3 months after treatment in C group was (318.85 ± 71.48)μm,(287.15 ± 56.71) μm and (255.05 ± 60.90)μm,respectively,which was better than that in A group [(347.00 ± 67.59) μm (305.10 ± 47.44) μm and (282.40 ± 36.26) μm],and B group [(417.05 ± 63.94) μm,(394.80 ±57.18) μm,and (375.90 ± 55.10) μm],with significant differences (all P ＜ 0.05).At 2 months and 3 months after treatment,CMT in A group was better than that in B group,and the difference was statistically significant (P ＜ 0.05).Conclusion The efficacy of retinal laser photocoagulation combined with intravitreal ranibizumab in the treatment of BRVO macular edema is better than simple retinal laser photocoagulation and simple intravitreal ranibizumab.

Infantile neuroaxonal dystrophy (INAD) is a rare autosome-recessive disease characterized by progressive motor and cognitive regression.The PLA2G6 gene is its causative gene,which encodes calcium-independent phospholipase A2 enzyme (iPLA2-VIA).The diagnosis of INAD is difficult because of its clinical heterogeneity,and the rate of misdiagnosis is high.The purpose of this study is to describe the clinical characteristics,molecular genetics,treatment and prognosis of INAD to improve the acknowledgement of INAD in medical workers and to help make an early diagnosis of INAD.

Objective:To study the interaction between cisplatin and bovine serum albumin ( BSA) under the simulated human physiological condition. Methods:The interaction mechanism of BSA and cisplatin was investigated by fluorescent spectrometry; the binding constant, binding site and interaction force were studied, and the interaction effects on the conformation change of BSA were investigated as well. Results:The results of fluorescent spectrometry showed that a ground state complex was formed between cisplatin and BSA, and the mechanism of fluorescence quenching was static quenching. The binding parameters of cisplatin and BSA were as follows:the binding constant was 1. 36 × 104 L·mol-1 , the binding site was 0. 991, and the interaction was mainly driven by hydrogen bonds and Van Der Waals forces. The results of synchronous fluorescent spectrometry demonstrated that the interaction influenced the micro-environments of amide acid residues. Conclusion:Cisplatin can interact with BSA and change the conformation of BSA.