Drug-induced lupus (DIL) is a lupus-like illness that has been recognized as a side effect of over 80 drugs since its first description in association with sulfadiazine in 1945. The epidemiology and clinical course of idiopathic systemic lupus erythematosus and DIL differ markedly, and prognosis is generally favorable in the latter although occasional life-threatening cases have been reported in the literature. Constant pharmacovigilance is crucial for prompt diagnosis and cessation of offending therapy, hence achieving the best outcome. This review discusses the clinical presentation, diagnosis and treatment of DIL so as to call for vigilance of medical workers.

Objective To evaluate the actual mismatch risk for KIR genes,KIR ligand HLA-C gene and KIR ligand HLA-Bw4I80 related genes in kidney transplant recipients and their donors.Method KIR genes,KIR ligand HLA-C gene and KIR ligand HLA-Bw4I80 related genes were analyzed in 322 recipients and their donors who received kidney transplantation.The effect of mismatches on acute rejection after transplantation was studied as well.Result In 322 cases of recipients and their donors,average mismatch risk for KIR-L gene was 4.73％,9.10％ for KIR-S gene and 1.95％ for KIR ligand HLA-C gene respectively.There were 245 cases (76.09％) of KIR ligand HLA-Bw4I80 related genes mismatch and 77 cases (23.91 ％) of match resepctively.There was no statistically significant difference in AR rate between KIR ligand HLA-Bw4I80 related genes mismatch group and match group (8.16％ in 245 vs.7.79％ in 77) (P＞0.05).AR reversal rate in mismatch group and match group was 95.0％ and 66.7％ (P＞0.05).Conclusion The mismatch risk for KIR ligand HLA-Bw4I80 related genes was even common between kidney transplant recipients and their donors,and this specific mismatch may be of benefit to patients who undergo actuate rejection.Further study is still required.

Objective To investigate sexual function in male kidney transplant recipients and their offsprings health condition.Methods We studied 60 male kidney transplant recipients who had a normal sex life before kidney failure and had good renal graft function after transplant.The questionnaire was used to investigate the time of first spermatorrhea,viability of sex activities,frequency and sexual intercourse satisfaction of sex activities,procreation status,growth and intelligence status of the offspring.Semen routine tests before and after the transplantation were done.Results Hyposexuality or declined sexual function was found in all over 60 cases of recipients.And after surgery,sexual function of the recipients was improved obviously following the graft function gradually regained.Fifty-four patients had spermatorrhea in the first 1-3 months post-transplantation,and rest 6 cases had no spermatorrhea because of sexual life.After operation 56 male patients began to have sex life in 2-4 months with satisfaction rate of 86.7％ (52/60),except the other 4 cases who refused sex life due to worrying about graft damage by sex life.Sixty-eight children were born by 56 recipients after operation,and the growth and intelligence status had no significant difference from the children of the same age.No transplant graft failure or rejection was found after the recipients had children.Conclusion After kidney transplantation,the sexual function of male recipients could return to the normal status and the growth and intelligence status of the offspring is normal.

Objective To investigate the clinical and electrophysiology features of infantile spinal muscular atrophy,and explore the clinical significance of genetic diagnosis. Methods The clinical data of 13 infants suffering from infantile spinal muscular atrophy were analysed.The serum creatine phosphokinase was examined,and nerve conduction velocity was tested in median nerve,ulnar nerve,tibial nerve and peroneal nerve.The parameters such as distal motor latency,motor nerve conduction velocity and amplitude of compound motor active potential were analysed.Electromyography was performed in no less than four muscles,and the insertion potential,spontaneous potential and motor unit action potential were observed.Deletion of exon 7 in SMN1 gene was detected by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). Results All these infants were characterized by progressive flaccid paralysis in limbs.In all cases,amplitude of muscle response was significantly decreased,with prolonged distal latency and slowed conduction velocity.Electromyography demonstrated motoneuron degeneration.Deletion of exon 7 in SMN1 gene was detected in all 13 infants. Conclusion There are unique clinical and electrophysiology features for infantile spinal muscular atrophy,and electromyography may play an important role in the diagnosis.Prenatal genetic diagnosis may help to avoid the birth of this kind of infants.

Objective To investigate the clinical value of tissue polypeptide specific antigen(TPS),neuron-specific enolase(NSE),carcinoembryonie antigen(CEA)and CA125 in serum of small cell lung cancer(SCLC)patients and its significance in diagnosis and disease monitoring.Methods Serum leveh of TPS was detected using ELISA and serum levels of NSE,CA125 and CEA was detected using ECLin 27 1 SCLC patients.80 pulmonary benign disease patients and 224 normal healthy people.Diagnostic values of these tumor markers were analyzed by receiver operative characteristic(ROC)curve.Results The levels of TPS,NSE,CA125 and CEA iu the serum of SCLC group were signifieanfly higher than those in pulmonary benign disease and healthy group(Z＞1.90,P＜0.01).The levels of TPS and NSE in the serum of extensive stage small cell lung cancer(ESCLC)patients were significantly higher than those in limited stage small cell lung cancer(LSCLC)(Z=2.69,2.27,P=0.009,0.02 respectively).,The level of TPS and NSE showed statistical significance among SCLC patients with different prognosis after therapy(Z=4.06,3.11.P=0.001,0.007 respectively).The TPS+NSE showed the highest sensitivity of 86.7%,and the specificity,PPV and NPV were 75.0%,81.0% and 82.2%,respectively.Conclusions Serum levels of TPS,NSE,CA125 and CEA are useful for SCLC diagnosis.TPS+NSE shows the highest clinical values in SCLC diagnosis and prognosis.

Esophageal cancer is a unique malignant disease in China. A fundamental difference exists between the Chinese population and the western population on esophageal cancer in terms of epidemiology, histogenesis, and carcinogenic risk factors. Therefore, ap-plying the western academic achievements to Chinese is difficult. Thus, Chinese scientists have the responsibility to conquer esopha-geal cancer in China. This article reviews the progress of esophageal cancer focused on the molecular mechanism for interactions of ge-netic and environmental risk factors and human esophageal multistage carcinogenesis.

Objective To investigate the effect of plasma homocysteine (Hcy) levels and cognitive dysfunction on patients with type 2 diabetes and explore the other factors that affect cognitive function.Methods 80 patients with type 2 diabetes were selected as our subjects and they were divided into cognitive impairment group (38 cases),cognitive normal group (42 cases) according to a simple mental state scale(MMSE) score.The plasma Hcy,glycosylated hemoglobin,blood lipid,uric acid,24 h urine trace albumin were measured.Results Plasma Hcy concentration in diabetic cognitive dysfunction,non cognitive impairment group and normal control group respectively were(19.56 ± 5.23),(16.21 ± 3.27),(14.67 ± 4.27) tmol/L,and there was statistically significant difference(F =3.76,P ＜0.05).The plasma Hcy levels in diabetic cognitive impairment group was higher than that non-cognitive impairment group(P ＜ 0.05) and normal control group (P ＜ 0.01),The factors impaired cognitive function in patients with other factors included age,glycosylated hemoglobin,body mass index,diabetes duration and plasma Hcy levels,and there were negative correlation with MMSE score (r =-0.336,-0.285,-0.226,-0.392,-0.312 ; all P values were less than 0.05).Conclusion Patient's age,duration of diabetes,glycosylated hemoglobin and BMI can affect cognitive function in patients.Higher Hcy levels in patients with type 2 diabetes is a risk factor for cognitive impairment.

Objective To explore the effect of clinical pathway in surgical treatment for patients with mandibular fracture.Methods 80 patients with mandibular fracture were randomly divided into the conventional therapy group(the control group) (n =40） and the clinical pathway therapy group (CP group) (n =40).The hospitalization time,medical expenses,satisfaction for the treatment,health awareness,and incidence of complications were compared between two groups.Results The results of hospitalization time,medical expenses,satisfaction for the treatment,and health awareness of the CP group were (11.86 ± 3.05) d,(9 115.43 ± 1 689.84) yuan,(91.19 ± 1.02) ％,(95.18 ±4.11)points,respectively,which were significantly better than those of the control group [(17.53 ± 2.98)d,(12 066.75 ±2 513.22)yuan,(89.39 ±1.35)％,(82.83 ± 6.56) points] (t =8.41,6.16,6.73,10.01,all P ＜0.05).The complication rate of the two groups was 2.5％,7.5％,respectively,which had no significant differences (χ2 =0.26,P ＞ 0.05).Concltsion The clinical pathway for mandibular fracture surgery is worthy of promotion.

Objective To investigate 4 variants single nucleotide polymorphisms (SNPs) of 5-lipoxygenase-activating protein(ALOX5AP) in lipoxygenase pathway and in cytochrome P450 pathway as susceptibility genes for stroke in a southeastern Chinese population,and evaluate the associations between susceptibility genes and cerebral infarction,to find whether gene-gene interactions increase the risk of cerebral infarction.Methods By case-control study,two hundred and ninety-two patients with cerebral infarction and 259 healthy control subjects were included.Eight variants in 5 candidate genes were examined for stroke risk,including the SG13S32 (rs9551963),SG13S42 (rs4769060),SG13S89 (rs4769874),and SG13Sl14 (rs10507391) variants of the ALOX5AP gene,the G860A (rs751141) variant of the soluble epoxide hydrolase (EPHX2) gene,the A1075C (rs1057910) variant of the CYP2C9 *2 gene,the C430T (rs1799853) variant of the CYP2C9* 3 gene,and the A6986G (rs776746) variant of the CYP3A5 gene.Gene-gene interactions were explored using generalized multifactor dimensionality reduction (GMDR)methods.Results There were no statistically significant differences in the frequencies of the genotypes of the 8 candidate genes.The GMDR analysis showed a significant gene-gene interaction between SG13S114 and A6986G,with scores of 10 for cross-validation consistency and 9 for the sign test (P =0.011).These genegene interactions predicted a significantly higher risk of cerebral infarction (adjusted for age,hypertension,and diabetes mellitus;OR =1.804,95％ CI 1.180-2.759,P =0.006).Conclusions A two-loci gene interaction confers significantly higher risk for cerebral infarction.The combinational analysis used in this study may be helpful in the elucidation of genetic risk factors for common and complex diseases.

MTM1 gene is essential for SOD2 activity and normal mitochondrial function. MTM1 deletion results in decreased SOD2 activity, impaired mitochondrial function and growth defect on nonfermentable carbon source. A yeast genomic library was transformed into mtm1 deletion mutant to screen for suppressor genes of MTM1. The damage caused by MTM1 deletion is irreversible and even overexpression of MTM1 can not rescue the growth defect of mtm1 deletion mutant. Another screening strategy was adopted: a plasmid overexpressing MTM1 was transformed into wild type before the MTM1 gene on chromosome was deleted. The resulting strain, designated YES2MTM1, was transformed with a yeast genomic library. Transformants lost the plasmid overexpressing MTM1 after 5-FOA treatment. Yeast strains able to grow on nonfermentable carbon source with MTM1 deletion and overexpression of some DNA fragments were picked up and candidate suppressor genes were identified. Overexpression of five genes were identified to be able to rescue the growth defect on nonfermentable carbon source. The study will provide reference for MTM1 gene function and screening for suppressor of genes whose deletion result in irreversible damage.