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To investigate the relationship between serum phospholipid omega-3 polyunsaturated fatty acids (ω-3 PUFAs) and insulin resistance (IR) in patients with type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD).51 patients with T2DM and NAFLD (T2DM+NAFLD group), 50 with T2DM alone (T2DM group), 45 with NAFLD alone (NAFLD group), and 42 healthy control subjects (NC group) were studied. Serum ω-3 PUFA profiles were analyzed by gas chromatography, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), and serum lipid concentrations were measured. Insulin resistance was assessed by the homeostasis model assessment method (HOMA-IR).HOMA-IR levels were higher in the T2DM+NAFLD group than in the T2DM, NAFLD and NC groups (p0.05), as were ALT, AST, GGT, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) concentrations (p0.05). Conversely, serum ω-3 PUFA levels were significantly lower in the T2DM+NAFLD group than in the other groups (p0.05). The ω-3 PUFA level was negatively correlated with HOMA-IR, TC, LDL-C and TG.Serum phospholipid ω-3 PUFA levels were significantly decreased in patients with T2DM and NAFLD, and were negatively related with insulin resistance. Thus, reduced ω-3 PUFAs may play an important role in the development of T2DM and NAFLD.

Activin, a member of the TGF-beta superfamily, inhibits the proliferation of breast cancer cells. Activin interacts with its type I and type II receptors to induce phosphorylation of intracellular signaling molecules known as Smads. Previous studies showed that mouse ARIP2 can reduce activin signaling by interacting with activin type II receptors (ActRIIs); however, the activity of ARIP2 in breast cancer is still unclear. In this study, we used RT-PCR to obtain a human homologue of mouse ARIP2, human activin receptor-interacting protein 2 (hARIP2). Like murine ARIP2, hARIP2 has a PDZ domain in its NH2-terminal region and can interact specifically with ActRIIs. Overexpression of hARIP2 reduced activin-induced transcriptional activity and enhanced cell proliferation and colony formation in human breast adenocarcinoma MCF-7 cells and MDA-MB-231 cells. However, down-regulation of hARIP2 expression by RNAi enhanced activin-induced transcriptional activity and reduced cell proliferation and colony formation. Immunohistochemistry revealed that hARIP2 was expressed more frequently and much more intensely in malignant breast tissues such as simple carcinoma, invasive ductal carcinoma and mucinous adenocarcinoma than in benign hyperplasia or fibroadenoma cases. These results suggest that hARIP2 is a putative growth-promoting factor involved in breast tumorigenesis and tumor development.

Studies have shown that SCC-S2 can be detected in cancer cells, but its relation with thyroid cancer remains uncertain. In the current study, we investigated SCC-S2 expression in thyroid cancer from the immune cell perspective and tumor tissue perspective. Levels of SCC-S2 in CD4+ T cells, CD8+ T cells, monocytes, natural killer (NK) T cells, tumor tissues, and adjacent noncancerous thyroid tissues were tested by real-time reverse transcription PCR and Western blot. Results revealed that mRNA and protein levels of SCC-S2 were significantly increased in peripheral CD4+ (mRNA, 1.90-fold; protein, 1.55-fold) and CD8+ T cells (mRNA, 2.37-fold; protein, 1.72-fold) but not monocytes and NKT cells in patients than in healthy donors. Further elevated mRNA level but not protein expression was observed in tumor-infiltrating CD4+ T cells, whereas both mRNA level and protein expression were further increased in tumor-infiltrating CD8+ T cells. Also, mRNA and protein levels of SCC-S2 in thyroid tissues were significantly elevated than those in adjacent noncancerous thyroid tissues. Moreover, patients with cervical lymph node metastasis presented clearly higher mRNA and protein expression of SCC-S2 compared to those without cervical lymph node metastasis (p

MicroRNAs (miRNAs) control gene expression by destabilizing target transcripts and inhibiting their translation. Aberrant expression of miRNAs has been described in many human diseases, including schizophrenia. However, the effects on miRNA expression in response to antipsychotic treatment in peripheral circulation have not been thoroughly examined.Using quantitative real-time PCR (qRT-PCR), We quantified the expression of seven candidate miRNAs in plasma samples of 40 first-episode schizophrenics before and after antipsychotic treatment. The patients were all treated with risperidone and achieved remission in 1 year.Compared with the baseline, the expression levels of miR-365 and miR-520c-3p were significantly down-regulated after 1 year of risperidone treatment (P0.001). There were no significant correlations between the clinical symptoms and the expression levels of these two miRNAs (P0.05).This study analyzed possible circulating miRNAs in response to antipsychotic monotherapy for schizophrenia, the further mechanism need to be confirmed.

Nucleophosmin plays a critical role in embryonic development. This study aimed to examine the expression pattern of nucleophosmin in glandular epithelium of human endometrium during the menstrual cycle.Endometrial tissues used for this study were obtained from 46 non-pregnant patients who underwent hysterectomy which had been performed to treat benign diseases. Nucleophosmin expression was assessed by in situ hybridization and immunohistochemistry.At the early-, mid- and late-proliferative phase, nucleophosmin mRNA was highly expressed in glandular epithelium of human endometrium. At the secretory phase, the expression of nucleophosmin mRNA was reduced in glandular epithelium in early-secretory phase, and the expression in mid- and late-secretory phases was not detected. Similarly, nucleophosmin protein was strongly expressed in endometrial glands throughout the proliferative phase, but was gradually reduced during secretory phase.Nucleophosmin mRNA and protein are expressed in glandular epithelium of human endometrium throughout the menstrual cycle.

To investigate the relationship between serum omega-3 polyunsaturated fatty acid (omega-3PUFA) and insulin resistance (IR) in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease (NAFLD).This trial involved 51 patients of type 2 diabetes mellitus with NAFLD (G4 group), 50 patients of type 2 diabetes alone (G3 group), 45 patients of NAFLD alone (G2 group) and 42 healthy control subjects (G1 group). Serum omega-3PUFA profile was analyzed with capillary gas chromatography. Insulin resistance was assessed by homeostasis model assessment (HOMA-IR). ALT, AST, gamma-glutamyltransferase (GGT) and serum lipids were measured.The levels of HOMA-IR were higher in G4 group than those in G3, G2 and G1 group (4.90 + or - 2.54 vs 2.38 + or - 1.23, 2.20 + or - 1.15, 1.13 + or - 0.42; P0.05). The level of ALT, AST, GGT, TC, TG, LDL-C were higher in G4 group than those in G3, G2 and G1 group (P0.05). The level of omega-3PUFA was significantly lower in G4 group than those in G3, G2 and G1 group (5.68 + or - 2.02 vs 7.17 + or - 2.38, 6.97 + or - 2.32, 10.08 + or - 2.76; P0.05). omega-3PUFA concentration was negatively correlated with HOMA-IR, TC, TG and LDL-C (r = -0.491, -0.376, -0.462, -0.408, P0.05).Serum omega-3PUFA is significantly decreased in patients with type 2 diabetes mellitus and NAFLD. Serum omega-3PUFA is negatively correlated with insulin resistance. omega-3PUFA plays a very important role in the development of diabetes mellitus and NAFLD.

To investigate the association of 5-HT(2A) receptor gene (HTR2A)-1438A/G, Catechol-O-methyltransferase (COMT) gene Val158Met, Monoamine oxidase A ( MAOA ) gene 30 bp-VNTR(MAOA-uVNTR)polymorphisms, and the educational attainment level of the parents with the intelligence of attention deficit hyperactivity disorder (ADHD) in China.A total of 485 DSM-IV ADHD children of Chinese Han descent were included, both complete IQ evaluation, HTR2A-1438A/G, COMT gene Val158Met, and MAOA-uVNTR genotyping results were obtained. The quantitative traits of psychometric IQ were calculated by using the Chinese Wechsler Intelligence Scale for Children (C-WISC). The multifactor linear regression analysis was used to test the associated factors on intelligence.Analyses revealed that ADHD children with low enzymatic activity (3R for males, 3R3R for females) of MAOA-uVNTR performed better on Full Scale IQ (FIQ) than did patients with high enzymatic activity (4R for males, 3R4R/4R4R for females) [(102.6+/-12.4) vs (100.3+/-11.7), P=0.078]. The patients with high-enzymatic activity (ValVal) of COMT gene Val158Met performed significantly better on FIQ than did patients with mid-low enzymatic activity (ValMet and MetMet)[(103.5+/-13.6) vs (100.5+/-11.5), P=0.036]. ADHD children with GG genotype of HTR2A-1438A/G performed significantly better on some aspects of C-WISC test (Full Scale IQ and Verbal Scale IQ) than did children with GA and AA genotypes [FIQ :(106.9+/-10.7) vs (100.7+/-12.3) vs (101.7+/-12.9), P=0.003; VIQ: (110.1+/-10.6) vs (103.5+/-12.1) vs (105.1+/-13.2), P=0.001]. The educational attainment level of the parents was associated with all the aspects of C-WISC test (Full Scale IQ, Verbal Scale IQ, and Performance Scale IQ). The multiple linear regression analysis showed that the genotype of HTR2A-1438A/G had significant correlation with FIQ, VIQ and PIQ; while the educational attainment level of the mother had significant correlation with FIQ and VIQ.The HTR2A-1438A/G polymorphism and the educational attainment level of the mother were associated with the intelligence of ADHD children in China.

To explore the inhibiting effect of human papillomavirus 16 E6-specific small interfering RNA (siRNA) on cervical cancer transplanted in nude mice.CaSki cells transfected with HPV16 E6 siRNA were transplanted into nude mice. HPV16 E6 siRNA was injected into the tumor, and the control group was treated with NS. Tumor growth was monitored once every other day. Terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) was performed to detect apoptosis. The expression of E6 and p53 protein was assessed by immunohistochemistry. The contents of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured and the liver and kidney were examined by histopathology.Inhibition of tumor growth was demounstrated after treatment with HPV16 E6 siRNA. The volume and weight of tumors were significantly decreased in comparison with those of control group (P0.05). Apoptosis occurred more frequently in the experiment group than in the control. The expression of E6 and p53 was down-regulated. The contents of ALT and AST underwent no significant changes, and the histopathology of liver and kidney showed no abnormal changes.The growth ability of human cervical cancer xenograft tumors in nude mice can be inhibited by HPV16 E6-specific siRNA, with no toxic side effect on the liver. It may provide an useful method of gene-therapy against cervical cancer.

To observe whether human papillomavirus 16 (HPV16) E6-specific small interfering RNAs (siRNAs) can be employed to inhibit the growth of cervical cancer cell line, and to investigate the associated mechanism.RNAi was performed using synthetic small interfering RNAs transferred into CaSki cell line by lipofectamine. The cell growth curves, live cell ratio and inhibition ratio of cells were measured by using cell counting. At various time points of post-transfection, the distributions of cell cycle, the expression levels of HPV16 E6, p53, p21 mRNA and proteins were detected by using flow cytometry (FCM) and real-time quantitative reverse transcription-polymerase chain reaction (real-time RT-PCR).The growth inhibition of E6 siRNA to CaSki cells was demonstrated after cells treated with E6 siRNA. No substantial G1 arrest was observed by FCM analysis. For 24 hours after cell transfection, the level of E6 mRNA was decreased by 20. 11 folds compared with control (P0.05). However, p53 and p21 mRNA levels appeared unaffected. 48 hours after cell transfection, the expression level of E6 protein was efficiently decreased, but the P53 and P21 protein levels increased in comparison.The inhibitory effect of HPV16 E6 siRNA to CaSki cell maybe due to specially and efficiently silence E6 mRNA expression, decrease the degradation of wild type P53 protein, and then recover the function activity of P53 protein.

To observe the effect of HPV16E7 specific expression vector on cell proliferation in cervical carcinoma SiHa cells.The HPV16E7 siRNA expression vector and empty expression vector were transfected into SiHa cells by liposome. The effects on E7 mRNA and E7 protein expression, cell cycle phase and cell growth rate were examined respectively by real-time RT-PCR, FCM and MTT assay.The HPV16E7 siRNA expression vector significantly inhibited the expression levels of E7 mRNA and E7 protein, the inhibition rates being 92.15% and 84.30% respectively. It also inhibited the transition from G, phase to S phase and the growth of SiHa cell line.HPV16E7 specific siRNA expression vector could specifically and efficiently inhibit the expression of E7 gene and hence it could regulate cell cycle and inhibit cell proliferation in cervical carcinoma SiHa cells. siRNA expression vector

To study age distribution of attention deficit hyperactivity disorder (ADHD) comorbidities in a relatively large sample, and exam the hypothesis of bad prognosis for ADHD.Using semi-structured clinical diagnosis interview scale, we investigated comorbidities of 1,002 ADHD children and adolescents from psychiatric out-patient clinic, and compared comorbidity frequency in 4 age groups.The comorbidity frequencies of disruptive behavior disorder (DBD), mood disorder, tics disorder and learning disorder (LD) in different age groups of ADHD patients differed significantly (P0.01). DBD and mood disorder in the age group of 12-14 years (124 cases,51.5%;18 cases,7.5%, respectively) were more than those in the 6-8 years group (160 cases,41.7%;9 cases,2.3%, respectively; P0.05). And the comorbidity frequencies of the 15-17 years group were significantly higher than those in other age groups (P0.05). Tics disorder in the 12-14 years group (50 cases,20.8%)was more than those in the two age groups of less than 12 years group (for the 6-8 years group, 51 cases,13.4%;for the 9-11 years group , 42 cases,12.5%; P0.05).The comorbidity frequency of learning disorder grew up with age. The comorbidity frequency of the 9-11 years group (106 cases,31.5%) was significantly higher than that of the 6-8 years group (80 cases,20.9%; P0.01); and those of both age groups more than 12 years (for the 12-14 years group, 164 cases,68.0%;for the 15-17 years group, 28 cases,70.0%) were higher than those of the two age groups of less than 12 years (P0.01). ADHD patients without any comorbidities in the two age groups more than 12 years (for the 12-14 years group, 29 cases,12.0%;for the 15-17 years group, 4 cases,10.0%)were less than those in the two age groups of less than 12 years (for the 6-8 years group, 126 cases,32.8%;for the 9-11 years group, 110 cases,32.6%; P0.01). These characteristics maintained in boys.Many comorbid psychiatric disorders increase as the ADHD children become adolescents. The situation is severer in late adolescence. Therefore, ADHD children should accept appropriate treatment as early as possible, and adopt the second degree prevention actively.

To examine the role of dopamine D4 receptor gene (DRD4) in attention deficit hyperactivity disorder (ADHD) with/without disruptive behavior disorder (DBD) by focusing on a-521C/T SNP within the promoter region of this gene.A total of 401 DSM-IV ADHD children (including 284 trios) of Chinese Han descent were genotyped. Chi-square test and the transmission disequilibrium test (TDT) were used to test for associations in ADHD with and without DBD respectively.In the comparison of ADHD with (n=143) and without (n=258) DBD, the -521T allele ( chi(2) = 6.778, P= 0.009, OR= 1.485) and the TT genotype (chi(2) = 6.292,P=0.012,OR=1.729) showed higher frequency in children with ADHD and DBD simultaneously. For family based analysis, T allele of the -521C/T polymorphism was preferentially transmitted to ADHD children with comorbid DBD (n=100, chi(2) = 3.868,P=0.049), whereas no significant distortion was found in the transmission of the tested variant for ADHD without DBD (n=184, chi(2) = 0.223, P=0.637).Our findings suggest that the -521C/T SNP of DRD4 may contribute to the predisposition to ADHD with comorbid DBD. This study supports for the hypothesis that ADHD with comorbid DBD may be influenced by greater genetic effect compared to ADHD alone.