Objective To explore the relationship between interleukin-8 (IL-8) gene 1633C/T polymorphism and late-onset Alzheimer's disease in order to provide genetic reference data for late-onset Alzheimer's disease.Methods Polymorphism distribution of IL-8 gene 1633C/T in 80 LOAD and 80 normal controls were detected by polymerase chain reaction-restriction fragment length polymorphism(PCRRFLP) analysis.The alleles and gene frequencies type were calculated by the direct counting.Type of gene was proceeded with the Hardy-Weinberg balance estimate.The other statistical analyses were carried out with SPSS13.0 software.The genotype frequencies and allele frequencies were compared with the Chisquare test (x2 test).Results For IL-8 gene1633 C/T,the genotype frequencies (CC,20.0％ ; CT,41.2％ ; TT,38.8％) in the LOAD group were not significantly different from those (CC,11.3％ ; CT,40.0％ ; TT,48.7％) in the control group (P ＞ 0.05).Conclusions IL-8 gene 1633 C/T polymorphism is probably not related to the genetic susceptibility of late-onset Alzheimer's disease.

Objective To study the relation between IL-8 gene-251A/T polymorphism and delayed Alzheimer's disease (AD)in Xinjiang Han people .Methods Eighty delayed AD patients served as a delayed AD group and 80 subjects undergoing physical examination served as a control group in this study .Distribution of IL-8 gene-251A/T polymorphism in two groups was detected by PCR-RFLP .Results The distribution of genotypes and alleles was different in two groups (P=0 .023 , P= 0 .010) .Further stratified analysis showed that the frequency of A allele was significantly higher in delayed AD group than in control group (OR= 1 .851 ,95% CI:1 .159 -2 .957 ,P=0.010) ,indicating that A allele is the risk factor for delayed AD .The frequency of AA genotype was significantly higher in delayed AD group than in control group (OR=3 .370 ,95% CI:1 .143-9.939 ,P=0 .023) ,indicating that the risk of delayed AD was 3 .370-fold higher in subjects with AA genotype than in those with TT genotype .The AT genotype was not related with the risk of delayed AD (OR=1 .944 ,95% CI:0 .994-3 .803 ,P=0 .051) .Conclusion IL-8 gene-251A/T pol-ymorphism is related with the risk of delayed AD .

The self-designed experiments of extract preparations is practiced in pharmacy teach-ing. Students work in groups, first consulting literature material, selecting the prescription and devis-ing a plan. Then, if the plan has carried on the feasible proof, students begin to purchase raw materi-als, complete the extraction and separation of effective components, the preparation of molding and the analysis of experimental results and finally form their self-evaluation. This experiment can strengthen students' experiment skill and promote their comprehensive application ability of all the subjects in the pharmacy field. At the same time it can also play an important role in the improvement of the students' social practice ability and the cultivation of students' creative thinking.

AIM: HLCDG1 is a novel gene cloned recently, and its expression inhibits significantly the growth of A549 cells and tumorigenesis of A549 cells transplanted in nude mice. In this study, our aim was to construct HLCDG1 gene short/small interference double-strand RNA (siRNAs) expression vector and to observe its influence on cell cycle and proliferation of A549 cells. METHODS: Using RNA interference (RNAi) techniques, a DNA vector-driven siRNAs expression vector was constructed, and a lung carcinoma cell line stably expressing siRNAs was also selected. Sequentially, using flow cytometry analysis and MTT assay, the changes of cell cycle and cell proliferation in this cell line were observed. RESULTS: Four site-match and one site-mismatch plasmids were constructed, which were named pHL-si-1, pHL-si-2, pHL-si-3, pHL-si-4 and pHL-si-c. These plasmids were co-transfected with a pcDNA3.1(+)/HLCDG1 plasmid into A549 cells, respectively. Among five co-transfected A549 cell lines, a A549 cell line co-transfected by the pcDNA3.1(+)/HLCDG1 and pHL-si-1 plasmids, namely A549-HLCDG1-si-1, showed nearly complete inhibition of HLCDG1 expression. MTT assay and flow cytometry analysis indicated that A549-HLCDG1-si-1 cells, namely the HLCDG1 gene-silencing cells, got a faster growth compared with other HLCDG1 expression cell lines, and that HLCDG1 gene-silencing induced A549-HLCDG1-si-1 cells into S phase and G_2+M phase significantly. CONCLUSION: These results suggest that the HLCDG1 gene is proved to have a markedly inhibitory effect on growth in A549 lung carcinoma cells. This study might provide some understanding of the biological function and molecular mechanism of HLCDG1 gene.

Objective Rheumatoid arthritis (RA) is a systemic autoimmune disease, which mainly involves joints across the body, resulting in joint stiffness and loss of daily activity. Recent evidence suggests that numerous self-reacting T cells, including Th1 and Th17, infiltrate the synovium in RA patients, accompanied by functionally-compromised Treg. Iguratimod, a new small molecule with anti-inflammatory and immunomodulatory effects, has shown curative effects in animal models of arthritis. In this study, we aimed to test the clinical effects of Iguratimodˊs on RA patients and its role in immunoregulation. Methods We examined the clinical effects of iguratimod on RA patients in a random controlled clinical trials and analyzed its effects on Th1, Th17 and Treg as well as their associated cytokines and transcription factors by flow cytometry and real-time polymerase chain reaction (PCR). Then t-test, chi-square test and rank sum test were used to conduct statistical analysis. Results Our results revealed that iguratimod therapy provided significantly greater clinical benefit [ACR20, ACR50, ACR70 reached 50%, 20%, 15% respectively in iguratimod treatment group, Z=-2.216,P=0.027] than placebo group with the reduction of Th1 and Th17 but increment of Treg after iguratimod treatment [Th1: week 0 (26.5 ±8.0)%, week 24 (14.2 ±7.3)%, P<0.01; Th17:week 0 (1.7±0.7)%, week 24 (1.3±0.4)%, P<0.05;Treg:week 0 (6.8±1.6)%, week 24 (8.9±2.9)%, P<0.05], which was statistically significant. Conclusion Our results provide theoretical and clinical based evidence for the impact of iguratimod on immunomodulation of RA.

We report a case of cushing's syndrome caused by ectopic adreocortical adenoma. The patient is a 37 years old woman, she was admitted to our hospital for " 2 years history of hypertension and weakness in both lower extremities for 2 months". Physical examination revealed: blood pressure 160/116 mmHg(1 mmHg＝0.133 kPa), body mass index 27.47 kg/m2, moon-face, increased fat in the neck and back, purple marks on abdominal skin, withⅡdegree edema of both lower extremities. Laboratory examination revealed that serum cortisol levels were elevated, loss of normal circadian rhythm, and serum adrenocorticotropic hormone (ACTH) was suppressed, the level of cortisol could not be suppressed in low dose desamethasone suppression test. Adrenal computed tomography ( CT) revealed a nodule in the right retroperitoneum, compression of the renal hilum, no bilateral adrenal adenoma and hyperplasia were found. This patient was diagnosed as corticotropin-independent Cushing's syndrome unequivocally. The clinical symptoms were relieved after successful laparoscopic retroperitoneum resection of the nodule. Pathological exam confirmed adrenocortical adenoma in ectopic adrenal tissue. Thus, we should consider the ectopic corticosteroid-secreting tumor in the context of corticotropin-independent Cushing's syndrome, especially when the imaging studies of adrenal revealed bilateral adrenal glands were normal or atrophic, which helped to make an appropriate strategy treatment.