Objective To investigate the relationship between dietarytherapy compliance of diabetes mellitus patients with pulmonary tuberculosis and glycemic control.Methods According to the three levels (good,medial and bad) of dietary therapy compliance,136 diabetesmellituspatients with pulnonary tuberculosis were divided into three groups signed by group 1 (good compliance),2 (medial compliance) and 3 (bad compliance).Questionnaire survey was appliedto respectively investigate the blood glucose level,body mass index,the sputum negative conversion rate and loci absorption rate of the patients in those groups.Results Of the 136 patients,group 1 had 32 (23.5％) patients,while group 2 had 62 (45.6％)patients,group 3 had 42 (30.9％) patients.Among these three groups,the fasting blood glucose (FBG) was (8.36±1.62) mmol/L,the postprandial 2h blood glucose (PBG) was (10.43±1.69) mmol/L,the HbAlc was (8.15±0.99)％,the body mass index (BMI) was (20.46±1.68) kg/m2,the sputum negative conversion rate was 55.9％ (76/136),foci absorption rate was 46.3％ (63/136).The comparisons of the three groups on FBG (F=34.01,P＜ 0.01),PBG (F=30.77,P＜ 0.01),HbA1c (F=32.35,P＜ 0.01),BMI (F=16.29,P＜0.01),the sputum negative conversion rate(x2=10.49,P ＜ 0.05),foci absorption rate(x2=7.47,P ＜ 0.05) had statistical significance.Thecourse of diabetes (x2=18.14,P＜ 0.01) and patients' literacy (x2=21.04,P＜ 0.01) were both influence factors of dietarytherapy compliance.Conclusions Dietarytherapy compliance of diabetes mellitus patients with pulmonary tuberculosis is low and the glycemic control of those patients is poor.The situation of glycemic control and the therapeutic effect,the education about health to patients should be enhanced to make the dietarytherapy compliance better.

BACKGROUND: It has been demonstrated that amyloid-beta 42 protein (Aβ42) immunization in transgenic mouse models of Alzheimer disease(AD)can induce specific Aβ42 antibody, clear Aβ from the brain, and thereby improve spatial learning and memory. It has been a promising treatment strategy for AD.OBJECTIVE: To explore the effect of Aβ42 and its subunit vaccines immunization on spatial learning and memory of APPSWE transgenic mice.DESIGN: A randomized controlled experiment with mice as subjects.SETTING: The brain research laboratory of the anatomy department in a the medical college of a univeristy.MATERIALS: The experiment was conducted in the Experimental Animal Center and the Anatomy Department of Sun Yat-sen University from April 2003 to February 2004. Thirty-two APPSWE transgenic mice of 5 months old were bought from Taconic Company, USA. The second generation of mice were successfully reproduced in the Anatomy Department. These mice were randomly assigned into four groups: control group, Aβ42 group, Aβ1-15group, and Aβ36-42 group. Each group contained 8 in each group.INTERVENTIONS: Aβ42 and its subunits combined with MF59 adjuvant were subcutaneously injected for fundamental immunity and then applied in nasal mucosa for intensified immunization. The immunization period was 8 months. Y-maze was used for behavior test before immunization and Morris water maze was used after immunization.MAIN OUTCOME MEASURES: Spatial learning and memory, mean escape latency, times of passing through the platform point, swimming distance percentage of the first quadrant, and swimming distance percentage of the 20% marginal area.RESULTS: The correct reaction times in Y-maze behavior test were 7.50 ±0. 81, 7.06 ±0.71, 7.19 ±0.91, and 7.50 ±0.86 respectively in the control, Aβ42, Aβ1-15, Aβ36-42 groups and there was no significant difference ( P ＞ 0. 05) . After immunization, the mean escape latencies in 8 units of localized navigation test were(67.3 ±2. 8) s, (23.6 ± 1.6) s, (26.4 ±2.0) s,and (36.5 ± 2.2) s. The results in three experiment groups were different from that in control group and there was no difference between the three experiment groups ( P ＞ 0. 05 ) . The mean times of passing through the platform point in the 4 groups were 0.71 ±0.29, 8.14 ± 1.37, 7.28 ± 1.34,and 3.29 ± 0. 67. Swimming distance percentage of the first quadrant in the4 groups were(24.3 ±2.9)%, (50.6±11.6)%, (49.9±9.3) %,and(35.4±7.0)% and the swimming distance percentages of 20%marginal area were (46.4 ± 7.3 ) %, ( 11.6 ± 3.9) %, ( 14.4 ± 2. 6) %, and (25.8 ± 3.3)%. The mice in three experiment groups showed increase in the times of passing through platform point, swimming distance percentage of the first quadrant, and decrease in distance percentage of 20% marginal area compared with control group. The results in three experiment groups were no significantly different( P ＜ 0. 05).CONCLUSION: Immunization with A342 and its subunits can effectively ameliorate impairment of spatial learning and memory in APPSWE transgenic mice.

OBJECTIVE To study the gene chip joint pyrosequencing technology in the newborn genetic deafness gene mutation screening, and provide a theoretical basis for the early diagnosis and prevention of genetic deafness. METHODS 2000 Neonatal EDTA umbilical cord blood was collected and genomic DNA (gDNA) was extracted. Microarray chip was used to detect four deafness gene at 9 mutation sites. And the positive result of gene chip detection was verified by pyrosequencing.RESULTS Among the GJB2 mutations, there were 1 case of 35delG mutation type, 3 cases of 176 del16 mutation type, 57 cases of 235del C mutation type, 9 cases of 299 del AT mutation type, 6 cases of GJB3 gene 538C>T mutation type. There were 5 cases of 1555A>G mutations and 1 case of 1494C>T mutations in mitochondrial 12S rRNA. There were 6 cases of 2168A>G mutation type and 23 cases of IVS7-2A>G mutations in SLC26A4. 103 cases of newborns carry the mutated gene in 2,000, the gene mutation rate is 5.15%. CONCLUSION All the four genes mutation at nine mutation sites are found in newborns with family history of non-hereditary deafness, and GJB2 gene mutation is common. The screening of genetic deafness in newborns is very important for early diagnosis and prevention of hereditary hearing loss. In particular, the diagnosis of mitochondrial 12S rRNA gene mutation can prevent the occurrence of deafness caused by drug use, for the genetic mutation of these carriers' health is of great significance.

Aim To investigate the protective effects of beraprost sodium on cerebral cortical neuron injury in chronic aluminum-overload rats and its effects on PGIS-IP signaling pathway. Methods 75 SD rats were randomized into five groups: normal control group, chronic aluminum-overload group ( model group) and beraprost sodium groups-low dose (6 μg· kg-1 ), medium dose ( 12 μg · kg-1 ) and high dose (24 μg·kg-1). Aluminum gluconate (Al3+ 200 mg ·kg-1 d-1, once a day, 5d a week, for 20 weeks, p. o. ) was administered to rats of cerebral damage model. The rats of experimental groups were concomi-tantly treated with beraprost sodium ( p. o. ) daily for 20 weeks. After the model was built successfully, the spatial learning and memory( SLM) function was done by Morris water maze. The cortical neurons damage was detected by HE staining, SOD activities and MDA contents. The 6-k-PGF1α levels in cortex were meas-ured by ELISA. The expressions of PGIS, IP mRNA and IP protein were also studied. Results Compared with the rats of normal control group, the SLM function was significantly impaired ( P<0. 01 ) and considera-ble karyopycnosis was observed in model group rats. The SOD activities were weakened ( P <0. 01 ), the MDA contents increased ( P<0. 05 ) and the levels of 6-k-PGF1α raised significantly ( P <0. 01). The ex-pressions of PGIS and IP mRNA in the rats cortex obvi-ously increased ( P<0. 01 ), so did the expression of IP protein(P<0. 05). Compared with the rats of mod-el group, the SLM function of rats in experimental groups decreased significantly ( P<0. 01 ) and damage of cortical neurons reduced remarkably. The SOD ac-tivities increased ( P <0. 01 ) and the MDA contents decreased ( P <0. 01). Besides, the content of 6-k-PGF1α, the expressions of PGIS mRNA and IP protein in the rats cortex decreased significantly ( P<0. 05 ) as well as IP mRNA ( P<0. 01). Conclusion Our re-sults demonstrate that in cerebral cortical neuron of chronic aluminum-overload rats, beraprost sodium has notably protective effects and the mechanism might be related to PGIS-IP signaling pathway.

OBJECTIVE: To assess the association of single nucleotide polymorphisms (SNPs) of microRNA-146a (miR-146a) with clinical features of rheumatoid arthritis (RA). METHODS: In 126 patients with RA and 102 matched healthy controls, SNPs of miR-146a rs2910164 locus were determined with a high-resolution melting method. The association of such polymorphisms with disease activity score in 28 joints (DAS28) and clinical features of RA was assessed. RESULTS: The distribution of SNPs of miR-146a rs2910164 among RA patients did not differ from that of the control group. No significant association was found between miR-146a rs2910164 polymorphism with DAS28. However, RA patients with a GG genotype had a greater chance to develop extra-articular manifestations (P<0.01). CONCLUSION Polymorphisms of miR-146a rs2910164 locus is not an independent risk factor for RA, though its GG genotype may be associated with extra-articular manifestations of RA.
Arthritis, Rheumatoid ; genetics ; Case-Control Studies ; Genetic Predisposition to Disease ; Genotype ; Humans ; MicroRNAs ; genetics ; Polymorphism, Single Nucleotide