ABSTRACT
Objective: To evaluate the relative safety of different ventilation methods regarding mortality and rates of complication, on neonatal respiratory distress syndrome (NRDS). Methods: Network Meta-analysis was used to collect data on randomized controlled trials of pulmonary ventilation strategies in preterm infants with a mean gestational age of less than 32 weeks. Diagnostic criteria on NRDS were published in the PubMed, Cochrane, Web of Science, EBSCO, and Springer Link databases from January 1986 to June 2018. Revman 5.3 software was used to evaluate the quality of studies, based on the Cochrane quality assessment tool. Data were analyzed by Bayesian and frequency methods, using both Win BUGS 1.4.3 and STATA 13.0 software. Safety of different ventilation strategies for NRDS mortality and complications would include intraventricular hemorrhage (IVH), patent ductus arteriosus (PDA) and retinopathy of prematurity (ROP) and were evaluated. Counted data was displayed by OR and 95%CI. Results: A total of 31 RCTs were included in this paper, including 5 827 preterm infants and 11 ventilation strategies. There were no statistically significant differences appearing in 11 ventilation strategies on mortality, PDA or ROP. IVH results were reported in 28 studies. Compared with nasal intermittent positive pressure ventilation (NIPPV), both high- frequency oscillation ventilation (HFOV) (OR=3.33, 95%CI: 1.08-16.67, P<0.05) and synchronized intermittent mechanical ventilation (SIMV) (OR=8.22, 95%CI: 1.25-29.44, P<0.05) schemes seemed to have increased the risk of IVH in preterm infants with NRDS. NIPPV appeared the optimal ventilation strategy in the rankings of cumulative probability. Results on clustering showed that NIPPV was probably the best ventilation strategy for children with NRDS after considering the orders of IVH, PDA and ROP on mortality, respectively. However, HFOV, IMV, and SIMV did not seem to be the ideal ventilated strategies. Conclusions: Most of the clinical decision makers might prefer using NIPPV in the treatment of children with NRDS through mechanical ventilation systems to reduce both the incidence and death caused by IVH, PDA and ROP. It was not recommended to use HFOV, SIMV and IMV in treating NRDS with gestational less than 32 weeks. We suggested that larger numbers of multi-center RCTs ba carried out to make the above conclusions more convincing.
Subject(s)
Respiration, Artificial/adverse effects , Respiration, Artificial/methods , Respiratory Distress Syndrome, Newborn/therapy , Bayes Theorem , Humans , Infant, Newborn , Infant, Premature , Intermittent Positive-Pressure Ventilation/adverse effects , Intermittent Positive-Pressure Ventilation/methods , Network Meta-Analysis , Randomized Controlled Trials as Topic , Treatment OutcomeABSTRACT
Objective: To detect the alterations of telomerase activity and the expression for oxidative stress responsive genes related with senescence during cellular replicative senescence and hydrogen peroxide-induced premature senescence in human embryonic lung fibroblasts (HELFs) in vitro. Methods: The HELFs were divided into young cells (22 population doubling levels, 22PDL) , mid-aged cells (35PDL) and replicative senes-cent cells (49PDL) and premature senescent cells induced by H(2)O(2)(premature senescence, PS). The telomerase activity was detected by ELISA assay during cellular replicative and premature senescence. The mRNA level of oxidative stress responsive genes related with senescence for Foxo1, Foxo3, Pdx1, apoA-I and MMP1 was per-formed by RT-Q-PCR separately. Results: The mRNA level for Foxo1, Foxo3, apoA-I and Pdx1 was decreased separately during cellular replicative senescence compared to that in the young-stage cells with statistical signifi-cance (P<0.05). The expression of MMP1 was up-regulated 5.1-fold obviously (P<0.05). In premature senes-cence, the mRNA level was only decreased for Foxo1, Foxo3 and apoA-I, but up-regulated 2.3-fold and 6.2-fold for Pdx1 and MMP1 respcetively vs 22PDL significantly (P<0.05). The telomerase activity in young cells was not detected, and it increased in mid-aged cells and replicative senescence stages during cellular replicative se-nescence as compared to 22PDL with statistical significance (P<0.05). The telomerase activity in premature se-nescence was highly active. Conclusion: The expression for genes related with senescence has differences be-tween replicative and premature senescence and hydrogen peroxide modifies their expression levels. The telomer-ase activity has been going up with increased PDLs.
Subject(s)
Aging/genetics , Cellular Senescence/drug effects , Fibroblasts/drug effects , Hydrogen Peroxide/pharmacology , Telomerase/genetics , Cell Proliferation/drug effects , Cells, Cultured , Cellular Senescence/genetics , DNA (Cytosine-5-)-Methyltransferases/metabolism , Embryo, Mammalian , Gene Expression/drug effects , HumansABSTRACT
miR-137, a brain-enriched microRNA, is involved in the control of neuronal proliferation, differentiation, and dendritic arborization, all of which are important for proper neurogenesis and relevant to schizophrenia. miR-137 is also known to regulate many genes implicated in schizophrenia risk. Although reports have associated the miR-137 polymorphism rs1625579 with this disease, their results have been inconsistent. The aim of this meta-analysis was to evaluate the relationship between rs1625579 and schizophrenia. Data were obtained from an electronic database, and pooled odds ratios (ORs) with 95% confidence intervals (95%CI) were used to test the association using the RevMan 5.3 software. Twelve case-control studies comprising 11,583 cases and 14,315 controls were included. An estimated lambda value of 0.46 was recorded, suggesting that a codominant model of inheritance was most likely. A statistically significant association was established under allelic (T vs G: OR = 1.15, 95%CI = 1.10-1.21, P < 0.001) and homogeneous codominant models (TT vs GG: OR = 1.32, 95%CI = 1.13-1.54, P < 0.001), but no such relationship was detected using the heterogeneous codominant model (GT vs GG: OR = 1.14, 95%CI = 0.97-1.34, P = 0.11). This meta-analysis demonstrates that the rs1625579 miR-137 genetic variant significantly increases schizophrenia risk.
Subject(s)
Genetic Association Studies , Genetic Predisposition to Disease , MicroRNAs/genetics , Schizophrenia/genetics , Alleles , Genotype , Humans , Risk Factors , Schizophrenia/pathologyABSTRACT
Celiac disease (CD) is a common autoimmune disorder characterized by heightened immunological response to ingested gluten. Certain gene polymorphisms of IL2/IL21 (rs6822844 and rs6840978) and SH2B3 (rs3184504) may influence susceptibility to CD, although the effects remain unclear. We performed a meta-analysis of the associations between rs6822844, rs6840978, and rs3184504 polymorphisms and CD risk. PubMed, EMBASE, and the China National Knowledge Infrastructure were searched. ORs and 95%CIs of each single nucleotide polymorphism (SNP) were estimated using the fixed-effect model if I(2) < 50% in the test of heterogeneity; otherwise, the random-effect model was used. Our meta-analysis included 12,986 CD cases and 28,733 controls from 16 independent samples, and the analysis of each SNP contained a subset of the total. We found that the minor allele T of both rs6822844 (T vs G, OR = 0.72, 95%CI = 0.67-0.78, P < 0.001) and rs6840978 (T vs C, OR = 0.76, 95%CI = 0.71-0.83, P < 0.001) in IL2/IL21 significantly decreased the risk of CD. However, the minor allele A of rs3184504 (A vs G, OR = 1.18, 95%CI = 1.12-1.24, P < 0.001) in SH2B3 significantly increased CD susceptibility. The estimated lambda values were 0.49, 0.50, and 0.53 for rs6822844, rs6840978, and rs3184504, respectively, suggesting that a co-dominant model of genotype effect was most appropriate for the three SNPs. Our results support associations between the three SNPs and CD and provide a strong argument for further research.
Subject(s)
Celiac Disease/genetics , Genetic Predisposition to Disease , Interleukin-2/genetics , Interleukins/genetics , Polymorphism, Single Nucleotide , Proteins/genetics , Adaptor Proteins, Signal Transducing , Alleles , Case-Control Studies , Celiac Disease/epidemiology , Gene Frequency , Genotype , Humans , Intracellular Signaling Peptides and Proteins , Odds Ratio , Publication Bias , RiskABSTRACT
Toll-like receptors (TLRs), the triggers of the innate and adaptive immune responses, are involved in the pathogenesis of type 2 diabetes mellitus (T2DM). Several studies have investigated the effects of genetic polymorphisms in TLR4 and TLR2, but they have yielded limited results. We investigated whether non-missense genetic polymorphisms in the regulatory regions of TLR4 and TLR2 were related to T2DM in a southern Chinese population. Single nucleotide polymorphisms (SNPs) in TLR4 (rs1927911, rs11536889, rs1927907, rs1927906, rs1927914, rs7873784, and rs2149356) and TLR2 (rs1898830, rs3804099, rs4696480, and rs3804100) were genotyped in 552 T2DM and 552 unrelated age- and gender-matched controls by SNaPShot Multiplex assay. Genotypes GG (OR = 0.09, 95%CI = 0.01- 0.83, P = 0.03) and CG (OR = 0.08, 95%CI = 0.01-0.74, P = 0.03) of the 3'-untranslated region (UTR) SNP rs7873784 in TLR4, and genotype AG (OR = 0.67, 95%CI = 0.46-0.97, P = 0.04) and allele G (OR = 0.88, 95%CI = 0.79-0.97, P = 0.01) of the intron SNP rs1898830 in TLR2 were identified as protective against the development of T2DM in southern Chinese people. In contrast, a meta-analysis of rs1927911 and rs1927914 showed no association. Haplotypes AGTT (OR = 0.34, 95%CI = 0.15-0.77, P = 0.01) and AATT (OR = 1.20, 95%CI = 1.01- 1.44, P = 0.05) in TLR2 were significantly associated with susceptibility to T2DM. Our results suggest that the effects of non-missense polymorphisms located in the regulatory regions of TLR4 and TLR2 should not be neglected in T2DM association analysis.