Network meta-analysis of migraine disorder treatment by NSAIDs and triptans

Node splitting of direct and indirect comparisons according to type of interventions for rescue medication and recurrence. (EPS 1963 kb

Wounding triggers MIRO-1 dependent mitochondrial fragmentation that accelerates epidermal wound closure through oxidative signaling.

Organisms respond to tissue damage through the upregulation of protective responses which restore tissue structure and metabolic function. Mitochondria are key sources of intracellular oxidative metabolic signals that maintain cellular homeostasis. Here we report that tissue and cellular wounding triggers rapid and reversible mitochondrial fragmentation. Elevated mitochondrial fragmentation either in fzo-1 fusion-defective mutants or after acute drug treatment accelerates actin-based wound closure. Wounding triggered mitochondrial fragmentation is independent of the GTPase DRP-1 but acts via the mitochondrial Rho GTPase MIRO-1 and cytosolic Ca2+. The fragmented mitochondria and accelerated wound closure of fzo-1 mutants are dependent on MIRO-1 function. Genetic and transcriptomic analyzes show that enhanced mitochondrial fragmentation accelerates wound closure via the upregulation of mtROS and Cytochrome P450. Our results reveal how mitochondrial dynamics respond to cellular and tissue injury and promote tissue repair

Differential Gene Transcription in Honeybee (Apis cerana) Larvae Challenged by Chinese Sacbrood Virus (CSBV)

Honey bees are economically important social insect. They are suffering from all kinds of pathogens, especially the virus. In response to pathogens, different immune pathways such as Toll, Imd, Jak-Stat and RNAi are involved. In the present study, the transcription analysis of 32 immune-related genes from Apis cerana challenged by Chinese sacbrood virus (CSBV), the most widely distributed virus in A. cerana, was carried out by qRT-PCR to provide cues for the antiviral mechanism and the effective control of bee viruses. The expression level of 22 genes were statistically changed, including 11 up-regulated genes (catus-2, lys-2, vir, s3a, mta1, faa, vhdl, co-1-iv, ago-1, ago-3, aub) in which 3 (ago-1, ago-3, aub) were related to RNAi pathway, and 11 down-regulated genes (kenny, pgrp-lc, pgrp-s2, abaecin, lys-1, lys-3, domeless, tepa, mlc, dscam, rpl8) related to Toll, Imd, and Jak-Stat pathways. The results indicated CSBV infection in A. cerana may activate a RNA-based antiviral immunity system. This work constituted the first report, under laboratory conditions, about induction of immune related genes in response to CSBV

Association of FokI, TaqI, BsmI and ApaI polymorphisms with diabetic retinopathy: a pooled analysis of case-control studies

Background: To assess synthetically the association between polymorphisms in the vitamin D receptor (VDR) gene (FokI, BsmI, ApaI, and TaqI) and diabetic retinopathy (DR).Methods: Pubmed, Embase, ISI Web of Science, Google-scholar and CBMDisc, CNKI and Chongqing VIP databases were searched. A meta-analysis was performed.Results: Six studies with 636 cases and 1,035 controls were included in this meta-analysis. The outcomes showed that the FokI polymorphism (F allele) of VDR gene had no statistical protective relationship with DR in overall studies. Interestingly, stratification analysis showed that the FokI polymorphism (Fallele) was significantly associated with decreased DR risk in the Chinese population, among included studies without publication bias, during a comparison analysis between normal subjects and DR patients, and among articles published after 2010. However, the TaqI, BsmI and ApaI polymorphisms of VDR gene had no significant association with the risk of DR.Conclusion: This meta-analysis of case-control studies revealed that the VDR-FokI polymorphism (F allele) decreased the risk of DR in Chinese people, among included studies without publication bias, during a comparison analysis between normal subjects and DR patients, and among articles published after 2010. Further rigorous and prospective studies with large sample size are needed to confirm our findings.Keywords: Diabetic retinopathy; polymorphism; Vitamin D receptor

The nonequilibrium evolution near the phase boundary

We study the nonequilibrium evolution near the phase boundary of the 3D Ising model, and find that the average of relaxation time (RT) near the first-order phase transition line (1st-PTL) is significantly larger than that near the critical point (CP). As the system size increases, the average of RT near the 1st-PTL increases at a higher power compared to that near the CP. We further show that RT near the 1st-PTL is not only non-self-averaging, but actually self-diverging: relative variance of RT increases with system size. The presence of coexisting and metastable states results in a substantial increase in randomness near the 1st-PTL, making it difficult to achieve equilibrium.Comment: 6 pages, 3 figure

Investigations into the characteristics and influences of nonequilibrium evolution

In order to estimate qualitatively the influence of nonequilibrium evolution in relativistic heavy ion collisions, we use the three dimensional Ising model with Metropolis algorithm to study the evolution from nonequilibrium to equilibrium on the phase boundary. The evolution of order parameter approaches its equilibrium value exponentially, the same as that given by Langevin equation. The average relaxation time is defined which is demonstrated to well represent the relaxation time in dynamical equations. It is shown that the average relaxation time at critical temperature diverges as the zth power of system size. The third and the fourth cumulants of order parameter during the nonequilibrium evolution could be either positive or negative, depending on the observation time, consistent with dynamical models at T > Tc. It is found that the nonequilibrium evolution at T > Tc lasts very short, and the influence is weaker than that at T < Tc. Those qualitative features are instructive to determine experimentally the critical point and the phase boundary of QCD.Comment: 8 pages, 5 figures; add fig.3 and up date the eq.(9-10), and content

Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and α

Peroxisome proliferator activated receptor-γ (PPARγ) is a ligand-activated transcription factor of the nuclear hormone receptor superfamily. The decreased phosphorylation of PPARγ due to rosiglitazone (ROS) is the main reason for the increased insulin sensitivity caused by this antidiabetic drug. However, there is no clear evidence whether the nuclear translocation of p-PPARγ stimulated by ROS is related to fluid retention. It is also unclear whether the translocation of p-PPARγ is associated with the change of aquaporin-2 (AQP2) and epithelial sodium channel α subunit (αENaC) in membranes, cytoplasm, and nucleus. Our experiments indicate that ROS significantly downregulates nuclear p-PPARγ and increases membrane AQP2 and αENaC; however, SR1664 (a nonagonist PPARγ ligand) reduces p-PPARγ and has no effect on AQP2 and αENaC. Therefore, we conclude that in vitro the fluid retention caused by ROS is associated with the increases in membrane αENaC and AQP2 but has little relevance to the phosphorylation of PPARγ