Evidence from Mendelian randomization: increased risk of miscarriage in patients with asthma.

OBJECTIVE: Several observational studies have revealed a possible association between asthma and miscarriage. However, inferring causal relationships from observational studies may be fraught with problems like bias, reverse causation, and residual confounding. Therefore, to assess the possible causal effect of asthma on miscarriage, we performed a two-sample Mendelian randomization (MR) analysis. MATERIALS AND METHODS: Asthma (56,167 cases and 352,255 controls) and miscarriage (9,113 cases and 89,340 controls) data from two GWAS of European ancestry were evaluated. Single nucleotide polymorphisms (SNPs) were used as instrumental variables (IVs). The random effect inverse-variance weighted (IVW) Mendelian randomization approach was used as the primary method, and MR-Egger, weighted-median, and MR-PRESSO approaches were replenished as sensitivity analysis to test the robustness of the results. RESULTS: In total, 70 SNPs were obtained using the SNP criteria. Additionally, the MR study found substantial evidence of the causality between asthma and miscarriage [IVW, OR=1.092; 95% CI=1.017-1.174; p<0.05]. The sensitivity analysis demonstrated the reliability of the MR findings [horizontal pleiotropy (MR-Egger, intercept=-0.0002; Standard error of mean, se=0.006; p=0.975)]. CONCLUSIONS: Asthma is a causal risk factor for miscarriage in European populations, according to MR evidence. Our results emphasize the significance of asthma management in reducing the risk of miscarriage in individuals with asthma.

Inhibition of microRNA-543 alleviates sepsis-induced acute kidney injury via targeting Bcl-2.

OBJECTIVE: Sepsis has a high morbidity and mortality and is prone to cause acute kidney injury (AKI). Here, we aimed to demonstrate the function and molecular mechanism of microRNA-543 (miR-543) in septic AKI. MATERIALS AND METHODS: MiR-543 inhibitor or NC was transfected into LPS-treated HK-2 cells to observe lipopolysaccharide (LPS)-induced inflammation and apoptosis. The detection of inflammation and apoptosis of HK-2 cells relies on Western blot, quantitative Reverse-Transcription Polymerase Chain Reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining. RESULTS: MiR-543 expression was increased in LPS-treated HK-2 cells. By transfecting miR-543 inhibitor into HK-2 cells, miR-543 expression was dramatically reduced. The downregulation of miR-543 remarkably inhibited the inflammation and apoptosis, which was manifested by the reduction of inflammatory cytokines (TNF-α, IL-6, IL-1ß), the reversal of apoptosis-related proteins expression (Bcl-1, Bax), the increase of cell viability and the decrease of the proportion of apoptotic cells. The result of Luciferase activity assay demonstrated that miR-543 directly targets Bcl-2. CONCLUSIONS: MiR-543 expression was increased in LPS-treated HK-2 cells, and silencing miR-543 could inhibit LPS-induced inflammation and apoptosis in HK-2 cells via targeting Bcl-2.

MiR-298 suppresses the malignant progression of osteosarcoma by targeting JMJD6.

OBJECTIVE: To explore the role of microRNA-298 (miR-298) in affecting biological characteristics of osteosarcoma cells, and the possible molecular mechanism. PATIENTS AND METHODS: Fifty clinical cases of osteosarcoma were collected for detecting differential expressions of miR-298 using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and its level in osteosarcoma cell lines was determined as well. Proliferative and migratory changes in MG63 and U2OS cells overexpressing miR-298 were assessed by Cell Counting Kit-8 (CCK-8), transwell and wound healing assay. Candidate targets of miR-298 were predicted using online databases, and JMJD6, the most optimal target, was specifically analyzed by Dual-Luciferase reporter assay and rescue experiments. RESULTS: MiR-298 was both expressed in osteosarcoma and healthy bone tissues, which was lowly expressed in the former tissues. It was downregulated in osteosarcoma cell lines as well. Low level of miR-298 predicted higher incidences of lymphatic metastasis, distant metastasis, and lower overall survival and progression-free survival in osteosarcoma. Overexpression of miR-298 weakened proliferative and migratory changes in MG63 and U2OS cells. JMJD6 was confirmed as the target gene binding miR-298, and negatively correlated to miR-298 level in osteosarcoma tissues. Overexpression of JMJD6 reversed the effect of overexpressed miR-298 on alleviating the malignant progression of osteosarcoma. CONCLUSIONS: MiR-298 is less abundant in osteosarcoma samples, which is correlated to metastasis and prognosis of osteosarcoma. MiR-298, serving as a tumor suppressor, weakens proliferative and migratory abilities of osteosarcoma cells.

The potential roles of RNA N6-methyladenosine in atherosclerosis.

OBJECTIVE: Atherosclerosis, characterized by endothelial injury, multicellular involvement, chronic inflammation, and lipid deposition, can lead to acute cardiovascular events. N6-methyladenosine (m6A) is the most abundant, prevalent RNA modification in mammalian cells. m6A, a reversible modification, can be catalyzed by m6A methyltransferase complexes (writers), reverted by demethylases (erasers), and recognized by m6A-binding proteins (readers). Emerging evidence suggests that m6A modification plays a significant role in regulating many biological and cellular processes in atherosclerosis. In this review, we highlight the biological function of m6A modification and give a brief perspective on its future applications in atherosclerosis. MATERIALS AND METHODS: This is a narrative review. The literature search strategy for indexed Scopus articles was performed randomly using PubMed and MEDLINE as the primary sources. No specific term was used. RESULTS: As the mechanism of the relationship between inflammatory response and atherosclerosis, m6A has become a new focus in the study of clinical treatment strategies for atherosclerosis. METTL14-dependent m6A modification may be a target for atherosclerosis therapy. A variety of m6A regulatory factors promote the progression of atherosclerosis by regulating polarization and inflammation of macrophages. WTAP and METTL14 can affect the phenotypic modulation of VSMCs through m6A modification. CONCLUSIONS: The existence of m6A in cardiovascular transcripts is necessary to maintain cardiac function, and the level of m6A modification is increased in a variety of atherosclerotic vascular cells, indicating that m6A modification is involved in the pathophysiological process of atherosclerosis. m6A modification plays an important character in atherosclerosis.

Inhibition of microRNA-495 inhibits hypoxia-induced apoptosis in H9c2 cells via targeting NFIB.

OBJECTIVE: Acute myocardial infarction (AMI) is a serious cardiovascular disease that threatens human life. MicroRNA is considered to be an important participant in the pathophysiology of AMI. This article focused on the role of microRNA-495 (miR-495) in regulating apoptosis after myocardial infarction (MI) and its underlying mechanisms. MATERIALS AND METHODS: H9c2 cells were cultured in an incubator containing 1% O2 to establish a cell model of MI. Quantitative reverse-transcription polymerase chain reaction (RT-PCR) was utilized to detect miR-495 expression in H9c2 cells. The effects of miR-495 and NFIB on hypoxia-treated H9c2 cells were observed by Western blot, lactate dehydrogenase (LDH) detection, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, flow cytometry, and terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling (TUNEL) staining. Luciferase reporter gene experiment was used to prove the regulatory relationship between miR-495 and NFIB. RESULTS: Hypoxia induced injury to H9c2 cells, which was manifested by decreased cell viability, increased LDH release, increased pro-apoptotic proteins (Bax, Cleaved Caspase-3) expression, decreased anti-apoptotic protein (Bcl-2) expression, and increased in the rate of apoptosis and TUNEL positive cells. MiR-495 expression was remarkably increased in H9c2 cells treated with hypoxia. Inhibiting miR-495 expression markedly alleviated the hypoxia-induced injury in H9c2 cells, while silencing NFIB aggravated the hypoxia-induced damage. In addition, NFIB was confirmed to be the target of miR-495. CONCLUSIONS: MiR-495 expression was increased in hypoxia-treated H9c2 cells. Silencing miR-495 could significantly inhibit hypoxia-induced apoptosis of H9c2 cells by targeting NFIB.

Effect of ß-casomorphin-7 on myocardial hypertrophy in hyperthyroidism-induced cardiomyopathy.

OBJECTIVE: The purpose of this study was to investigate the effect of ß-casomorphin-7 (ß-CM-7) on myocardial hypertrophy (MH) in hyperthyroidism-induced cardiomyopathy in vivo and in vitro. MATERIALS AND METHODS: Thirty C56BL/6 mice were randomly divided into three groups: control group, hyperthyroidism group, and ß-CM-7 treatment group. An animal model of cardiac hypertrophy of hyperthyroid heart disease (HHD) was constructed by continuous intraperitoneal injection of 100 µg of L-thyroxine (L-Thy) for 28 days, and the serum TT3 and TT4 concentrations were measured. After that, myocardial specimens were collected to measure left and right ventricular MH index, and the myocardial cell structure was observed under hematoxylin and eosin (HE) staining. Thereafter, Masson staining was adopted to determine collagen volume fraction, and hydroxylamine method was used to measure superoxide dismutase (SOD) activity, Meanwhile, DTNB direct method was applied to measure GSH-Px activity, thio-malonylurea method was utilized to measure malondialdehyde (MDA) content, and the level of reactive oxygen species (ROS) was detected by flow cytometry. Finally, the expressions of oxidative stress (OS) and inflammation-related factors in vivo and the nuclear factor-κB (NF-κB) pathway in vitro were detected by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: Compared with those in control group, TT3 and TT4 were remarkably increased, the structure of myocardial cells was disordered, the interstitial fibrosis and the ventricular MH index were significantly increased, the OS and inflammatory responses were increased, and the NF-κB pathway was activated in the Hyperthyroidism group. In the ß-CM-7 group, the content of TT3 and TT4 was decreased, the myocardial cell structure was slightly disturbed, the fibrosis and the ventricular MH index were reduced, OS and inflammatory response were reduced, and the NF-κB pathway was inhibited. CONCLUSIONS: ß-CM-7 can prevent and treat MH in mice with L-Thy-induced HHD probably through regulating the NF-κB signaling pathway.

The effect of single nucleotide polymorphisms of STAT3 on epilepsy in children.

OBJECTIVE: To investigate the effect of single nucleotide polymorphisms (SNPs) of signal transducer and activator of transcription 3 (STAT3) on epilepsy in children. PATIENTS AND METHODS: A total of 169 children suffering from epilepsy admitted in No. 1 People's Hospital of Jining from July 2015 to December 2016 were enrolled as the research subjects. Immunohistochemistry and real time-PCR were used for analysis of the expression of STAT3 and p-STAT3 in epilepsy patients. The genotypes and alleles of rs1053005 and re744166 were analyzed through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Statistical analysis was conducted to explore the correlation between the polymorphism of STAT3 and the incidence of epilepsy in children, and the polymorphism of STAT3 in the drug-resistant and non-resistant patients was compared. RESULTS: Both the STAT3 and p-STAT3 were over-expressed in epilepsy patients. The GG genotype of rs1053005 was significantly lower in epilepsy patients than that of health control, p<0.05. By contrast, no significant difference was found in genotypes of rs744166 between epilepsy and healthy children. When comparing the genotypes of drug-resistant patients and that of non-resistant patients, the distribution of rs1053005 genotypes in the two groups showed a significant difference, p<0.05. No statistical difference was observed in rs744166 genotypes. CONCLUSIONS: STAT3 polymorphism was associated with the risk of epilepsy and drug resistance to epilepsy. This study may provide a better understanding of STAT3 in epilepsy patients and provide new targets for the treatment of epilepsy patients.

Correlation of lipid peroxidation and ATP enzyme on erythrocyte membrane with fetal distress in the uterus in patients with intrahepatic cholestasis of pregnancy.

OBJECTIVE: This paper aims to investigate the correlation of lipid peroxide in erythrocytes and ATP (Adenosine Triphosphate) enzyme activity of erythrocyte membrane with fetal distress in patients with intrahepatic cholestasis of pregnancy (ICP). PATIENTS AND METHODS: Forty-three patients with ICP treated at Jining No. 1 People's Hospital were enrolled as a study group, and another forty healthy parturient women in the same period were enrolled as a control group, to extract their elbow venous blood and fetal umbilical cord blood. Thiobarbituric acid (TBA) was used to detect superoxide dismutase (SOD) activity of erythrocytes, malondialdehyde (MDA) activity in plasma, Na+-K+-ATP enzyme activity and Ca2+-Mg2+-ATP enzyme activity of erythrocytes, which were compared between the study and control groups. The correlation of MDA, Na+-K+-ATP enzyme and Ca2+-Mg2+-ATP enzyme activities with fetal distress in the study group was analyzed, and the correlation of MDA with Na+-K+-ATP enzyme activity was investigated. RESULTS: SOD and MDA activities of erythrocytes in maternal blood of the study group were significantly higher than those in the control group (p<0.05, p<0.001, respectively), but MDA activity in umbilical cord blood of the study group was markedly higher than that in the control group (p<0.001). Na+-K+-ATP enzyme and Ca2+-Mg2+-ATP enzyme activities of maternal and fetal erythrocytes of the study group were remarkably lower than those of the control group (p<0.001). MDA in the fetal distress group was significantly higher than that in the no fetal distress group in the study group (p<0.001). Na+-K+-ATP enzyme activity was negatively correlated with MDA concentration in maternal and fetal erythrocytes of patients with ICP (both p<0.001). CONCLUSIONS: Lipid peroxidation in patients with ICP will affect ATP enzyme activity of erythrocyte membrane, and the down-regulation of ATP enzyme activity in umbilical cord blood of patients with ICP may cause fetal distress in the uterus.

Secondary Metabolites from Streptomyces sp CSDX076 for the First Time / Metabolitos secundarios de Streptomyces SP CSDX076 por primera vez

ABSTRACT Objective: To investigate the secondary metabolites from the cultures of Streptomyces sp CSDX076. Methods: The compounds were isolated using column chromatography and RP-18 medium-pressure liquid chromatography. Their structures were elucidated by one-dimensional and two-dimensional nuclear magnetic resonance spectroscopic methods in combination with mass spectrometry experiments. Results: Four compounds were isolated from the cultures of Streptomyces sp CSDX076 and identified as aurantiamide benzoate, deoxytryptoquivaline, 2-acetyl-3,5-dihydroxyl-benzene acetic acid, and 2-acetyl-3,5-dihydroxyl-benzene ester. Conclusion: It was the first time that the four isolated compounds were obtained from the Streptomyces genus.

RESUMEN Objetivo: Investigar los metabolitos secundarios de los cultivos de Streptomyces sp CSDX076. Métodos: Los compuestos fueron aislados usando la cromatografía de columna y cromatografía líquida RP-18 de presión media. Sus estructuras fueron dilucidadas mediante métodos espectroscópicos de resonancia magnética nuclear unidimensional y bidimensional, combinados con experimentos de espectrometría de masa. Resultados: Cuatro compuestos de culturas de Streptomyces sp CSDX076 fueron aislados e identificados como benzoato de aurantiamida, deoxitriptoquivalina, ácido acético 2-acetil-3,5-dihidroxil-benzeno, y éster 2-acetil-3,5-dihidroxil-benzeno. Conclusión: Fue la primera vez que los cuatro compuestos aislados se obtuvieron del género Streptomyces.

Dynamic and contrast enhanced CT imaging of lung carcinoma, pulmonary tuberculoma, and inflammatory pseudotumor.

OBJECTIVE: Our main aim was to investigate the effect of dynamic and contrast enhanced CT imaging on differential diagnosis of lung carcinoma, pulmonary tuberculoma, inflammatory pseudotumor, and coexisting pulmonary tuberculosis and lung cancer. PATIENTS AND METHODS: About, 144 patients with pulmonary sarcoidosis as the study subjects were chosen which included: 36 patients with lung carcinoma, 36 patients with pulmonary tuberculoma, 36 patients with inflammatory pseudotumor, 36 patients with coexisting pulmonary tuberculosis and lung cancer. CT imaging scan was carried out on all of these 144 patients. RESULTS: CT scan value of lung carcinoma was different from other conditions such as pulmonary tuberculoma, inflammatory pseudotumor, and coexisting pulmonary tuberculosis and lung cancer (p < 0.01). Similarly, the peak of enhancement of lung carcinoma was different from others including inflammatory pseudotumor, and coexisting pulmonary tuberculosis and lung cancer (p < 0.01). Both, the intensive added values and S/A values of lung carcinoma, inflammatory pseudotumor, and coexisting pulmonary tuberculosis and lung cancer differed between them (p < 0.01). CONCLUSIONS: Helical incremental dynamic CT is helpful in differential diagnoses of lung carcinoma, pulmonary tuberculoma, inflammatory pseudotumor, and coexisting pulmonary tuberculosis and lung cancer.

Genetic variants in FH are associated with renal histopathologic subtypes of lupus nephritis: a large cohort study from China.

Objective Genetic variants in FH (complement factor H) were reported to associate with susceptibility to systemic lupus erythematosus (SLE). This study proposed that the genetic defects of FH in the susceptibility and in the development of lupus nephritis might be different. Methods This study enrolled 334 lupus nephritis patients, 269 SLE patients without clinical renal involvement and 350 controls. Two-step genotyping was performed. First, all the exons of the FH gene were fully sequenced in 100 lupus nephritis patients and 100 healthy controls. Second, genotyping of three common variants reported to be functional, rs1061170, rs800292 and rs6677604, was conducted in all the recruited individuals. Further, analysis of their associations with SLE/lupus nephritis susceptibility and the clinico-pathological parameters in the lupus nephritis group was performed. Results No significant differences were observed in allele and genotype frequencies of the three single nucleotide polymorphisms between lupus patients and controls. There was a significantly higher ratio of CC/CT genotypes of rs1061170 in lupus nephritis patients with class III than in the other two classes (class III vs. class IV vs. class V: 21.0% vs. 9.7% vs. 9.4%; P = .044). The rs6677604-GG genotype was observed to be associated with the absence of anti-ds DNA antibody ( P = .021), and the rs800292-TT genotype was associated with a higher level of circulating C3 ( P = 0.20) in lupus nephritis. Conclusion In an independent cohort, this is the first genetic association analysis focusing on FH genetic variants in Chinese lupus nephritis patients. It was found that the variants in the FH gene might affect the histopathologic subtypes and some clinical features of the disease.

Isomerization of the osmium-tellurium cluster Os3(µ-TeR)2(CO)10: a kinetic and computational study.

The kinetics for the isomerization of the 50e cluster Os3(µ-TeTol-p)2(CO)10 (), where the tellurides bridge two different Os-Os edges, to one in which the tellurides bridge the same open OsOs edge () have been measured experimentally by (1)H NMR spectroscopy. The determined activation parameters are ΔH(‡) = 77 ± 9 kJ mol(-1) and ΔS(‡) = -12 ± 28 J mol(-1) K. The conversion of to has been computationally investigated by electronic structure calculations using the model compound Os3(µ-TeMe)2(CO)10. The computed isomerization pathway is consistent with the kinetic data and the thermodynamic preference for the product stereoisomer that possesses a slipped, eclipsed conformation for the two p-tolyl groups.

Association of angiopoietin-1, angiopoietin-2 and caspase-5 polymorphisms with psoriasis vulgaris.

BACKGROUND: Psoriasis involves a multifaceted interplay of keratinocytes, blood vessels, immune system mediators and expressed genes. AIM: To determine whether genetic polymorphisms in the angiopoietin-1 (ANGPT1), angiopoietin-2 (ANGPT2) and caspase-5 (CASP5) genes are associated with an increased risk of developing psoriasis vulgaris (PV) in a Han population in northeastern China. METHODS: We analysed single nucleotide polymorphisms of ANGPT1 (rs2507800, rs1954727 and rs1010824), ANGPT2 (rs3739390, rs2442598 and rs1868554) and caspase-5 (rs507879, rs518604 and rs523104) in 343 patients with PV and 347 healthy controls (HCs) by the SNaPshot method, and evaluated the risk for psoriasis conferred by the individual polymorphisms and haplotypes. RESULTS: The rs2442598 polymorphism of ANGPT2 was significantly associated with PV. The CT+TT genotype was present at an increased frequency in patients with PV (adjusted OR = 1.45, 95% CI 1.04-2.03, P = 0.03). However, the distribution of the other genotypes (rs2507800, rs1954727 and rs1010824 of ANGPT1; rs3739390 and rs1868554 of ANGPT2; and rs507879, rs518604 and rs523104 of caspase-5) was not significantly different between patients with PV and the HCs. Furthermore, none of the genes in the haplotype-based analysis showed any association with psoriasis risk. CONCLUSIONS: Our data suggest that ANGPT2 variants may be involved in PV risk in a Han population in northeastern China.

Measurement of serum estrogen and estrogen metabolites in pre- and postmenopausal women with osteoarthritis using high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry

Although 17β-estradiol (E2) deficiency has been linked to the development of osteoarthritis (OA) in middle-aged women, there are few studies relating other estrogens and estrogen metabolites (EMs) to this condition. We developed a high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (HPLC-ESI-MS/MS) method to measure the levels of six EMs (i.e., estrone, E2, estriol, 2-hydroxyestrone, 2-hydroxyestradiol, and 16a-hydroxyestrone) in healthy pre- and postmenopausal women and women with OA. This method had a precision ranging from 1.1 to 3.1% and a detection limit ranging from 10 to 15 pg. Compared to healthy women, serum-free E2 was lower in the luteal and postmenopausal phases in women with OA, and total serum E2 was lower in postmenopausal women with OA. Moreover, compared to healthy women, total serum 2-hydroxyestradiol was higher in postmenopausal women with OA and total serum 2-hydroxyestrone was lower in both the luteal and follicular phases in women with OA. In conclusion, our HPLC-ESI-MS/MS method allowed the measurement of multiple biochemical targets in a single assay, and, given its increased cost-effectiveness, simplicity, and speed relative to previous methods, this method is suitable for clinical studies.

AML1-ETO targets and suppresses cathepsin G, a serine protease, which is able to degrade AML1-ETO in t(8;21) acute myeloid leukemia.

Although the significance of cathepsin G (CTSG) in host defense has been intensively investigated, little is known about its potential roles in granulopoiesis or leukemogenesis. We report here that CTSG is directly targeted and suppressed by AML1-ETO in t(8;21) acute myeloid leukemia (AML). Luciferase assays demonstrate that the CTSG promoter is strongly transactivated by AML1 and the AML1-dependent transactivation is suppressed by AML1-ETO. We also define a novel regulatory mechanism by which AML1-ETO-mediated transrepression requires both AML1-ETO and AML1 binding at adjacent sites, instead of the replacement of AML1 by AML1-ETO, and wild-type AML1 binding is a prerequisite for the repressive effect caused by AML1-ETO. Further evidence shows that CTSG, as a hematopoietic serine protease, can degrade AML1-ETO both in vitro and in vivo. Restoration of CTSG induces partial differentiation, growth inhibition and apoptosis in AML1-ETO-positive cells. In addition to t(8;21) AML, CTSG downregulation is observed in AML patients with other cytogenetic/genetic abnormalities that potentially interrupt normal AML1 function, that is, inv(16) and EVI1 overexpression. Thus, the targeting and suppression of CTSG by AML1-ETO in t(8;21) AML may provide a mechanism for leukemia cells to escape from the intracellular surveillance system by preventing degradation of foreign proteins.

Association study of C1qA polymorphisms with systemic lupus erythematosus in a Han population.

OBJECTIVE: The aim of this study was to evaluate the association of single nucleotide polymorphisms (SNPs) in the C1qA gene region with systemic lupus erythematosus (SLE) in a Chinese Han population. METHODS: Chinese SLE patients (n = 748) and ethnically- and geographically-matched healthy controls (n = 750) were genotyped for the C1qA region SNPs, rs172378 and rs665691, by using the Sequenom MassArray system. RESULTS: The Chinese Han SLE patients and controls had statistically similar frequencies of alleles, genotypes, and haplotypes of C1qA polymorphisms. Moreover, no association signal was detected on different genetic models (additive, dominant, and recessive) or in SLE subgroups stratified by various clinical manifestations. CONCLUSIONS: The C1qA SNPs, rs172378 and rs665691, confer no genetic predisposition to SLE in a Chinese Han population.

Association of the PTPN22 gene (-1123G > C) polymorphism with rheumatoid arthritis in Chinese patients.

This study aimed at examining the association of the single nucleotide polymorphism (SNP) in the protein tyrosine phosphatase gene (PTPN22) with the risk of rheumatoid arthritis (RA) in a Chinese population. A total of 200 RA patients and age and gender-matched healthy controls were recruited. Their genotypes and allelic frequency were determined by the TaqMan-MGB probe-based polymerase chain reaction (PCR). The frequencies of the CC genotype and C allele in RA patient group were significantly higher than that of controls (P < 0.01 or P < 0.05) with an odds ratio of 1.67, respectively. These data suggest, the CC genotype and C allele of the -1123G > C in the PTPN22 gene are associated with an increased risk for RA in Chinese population. Therefore, the CC genotype and C allele of the -1123G > C in the PTPN22 gene may be used as a genetic marker for the predisposition of RA in Chinese.

Changes of serum brain-derived neurotrophic factor in children with obstructive sleep apnoea-hypopnoea syndrome following adenotonsillectomy.

Children with obstructive sleep apnoea syndrome (OSAS) have substantial cognitive functional morbidity. Brain-derived neurotrophic factor (BDNF) is a key mediator of memory and cognition, but its regulation in OSAS is unknown. Circulating BDNF, transforming growth factor-ß(1) and 5-hydroxytryptamine levels, cognitive ability and overnight polysomnography were evaluated in 44 children with newly-diagnosed OSAS and in 26 healthy children. All parameters were monitored pre-operatively and at 3, 6 and 12 months after adenotonsillectomy. Pre-operative cognitive ability and sleep parameters were significantly poorer in children with OSAS compared with controls, but BDNF levels were similar. At 3 months post-operation, serum BDNF concentrations decreased, but cognitive ability and sleep parameters remained deficient. At 6 months post-operation, serum BDNF levels, sleep parameters and cognitive ability had improved and, by 12 months, there were no differences between the two groups. It is concluded that adenotonsillectomy can rapidly normalize sleep parameters and improve the cognitive ability of children with OSAS, by regulating the circulating level of BDNF.