Datasheet1_Study on the relationship between intrapartum group B streptococcus prophylaxis and food allergy in children.pdf

ObjectiveTo investigate the associations between intrapartum antibiotic prophylaxis of group B streptococcus (GBS) in pregnant women and the risk of food allergy in Chinese childrenDesignRetrospective cohort study of 2,909 mother-child pairs.SettingTaixing People's Hospital in Eastern China.ParticipantsTerm infants born 2018–2019, followed longitudinally from birth to 3 years.ExposuresThe GBS-IAP was defined as therapy with intravenous penicillin G or ampicillin or cefazolin ≥4 h prior to delivery to the mother. Reference infants were defined as born without or with other intrapartum antibiotic exposure.MethodsTo investigate the incidence information of food allergy in children aged 18 months and three years old. Kaplan-Meier survival analysis and log-rank tests were used to evaluate the cumulative incidence in the group with GBS-IAP and the group without GBS-IAP. Cox proportional hazards models were conducted to determine the univariate and multivariate association between maternal GBS-IAP and incident food allergy after various covariates were adjusted.ResultsThe cumulative incidence of food allergy in the group with GBS-IAP was higher than that in the group without GBS-IAP in children under 18 months old (8.1% vs. 4.5%, P = 0.005, log-rank test), but no significant differences were observed in children under three years old (9.2% vs. 7.0%, P = 0.146, log-rank test). The univariate cox proportional hazards model in children under 18 months old revealed that children in the GBS-IAP group had faster food allergy development when compared with children in the group without GBS-IAP (HR.: 1.887,95% CI: 1.207–2.950, P = 0.005), so was the multivariate model (HR.: 1.906,95% CI: 1.158–3.137, P = 0.011). However, both univariate (HR: 1.343, 95% CI: 0.891∼2.026, P = 0.159) and multivariate (HR: 1.253, 95%CI: 0.796∼1.972, P = 0.329) cox proportional hazards model in children under three years old showed no significant differences between children in the group with GBS-IAP and group without GBS-IAP.ConclusionIntrapartum antibiotic prophylaxis of group B streptococcus may increase the cumulative incidence and risk of food allergy in children under 18 months old, but it had no significant effect on children under three years old.</p

Interplay of Proximal Flow Confluence and Distal Flow Divergence in Patient-Specific Vertebrobasilar System - Fig 7

<p>(A-F) TAWSS and (G-L) OSI near vertebrobasilar flow divergence with BA bifurcating into LSCA, RSCA, LPCA and RPCA.</p

Anatomy of the vertebrobasilar system in human subjects A-F.

<p>Anatomy of the vertebrobasilar system in human subjects A-F.</p

Statistics for SAR-TAWSS and SAR-OSI in each vessel of the vertebrobasilar system of human subjects A-F.

<p>Statistics for SAR-TAWSS and SAR-OSI in each vessel of the vertebrobasilar system of human subjects A-F.</p

Demographics of the study population.

<p>Demographics of the study population.</p

Interplay of Proximal Flow Confluence and Distal Flow Divergence in Patient-Specific Vertebrobasilar System - Fig 4

<p>(A-F) OSI (left: anterior view; right: posterior view) in the vertebrobasilar system corresponding to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0159836#pone.0159836.g003" target="_blank">Fig 3A–3F</a>.</p

Interplay of Proximal Flow Confluence and Distal Flow Divergence in Patient-Specific Vertebrobasilar System - Fig 3

<p>(A-F) TAWSS (left: anterior view; right: posterior view) in the vertebrobasilar system corresponding to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0159836#pone.0159836.g001" target="_blank">Fig 1A–1F</a>.</p

Statistics for junctional surface area, SAR-TAWSS, and SAR-OSI at vertebrobasilar flow convergence and divergence.

<p>Statistics for junctional surface area, SAR-TAWSS, and SAR-OSI at vertebrobasilar flow convergence and divergence.</p

Additional file 3: Figure S3. of Thrombin-induced, TNFR-dependent miR-181c downregulation promotes MLL1 and NF-κB target gene expression in human microglia

Schematic overview of thrombin’s effects upon miR-181c and MLL1 in human microglia. Thrombin (via PAR4) induces TNF-α secretion from human microglia [21]. Thrombin-induced TNF-α (via TNFR) suppresses miR-181c levels. This suppression of the inhibitory miR-181c promotes MLL1 expression, increases NF-κB activity, and upregulates downstream NF-κB target gene expression in human microglia. (JPG 456 kb

Additional file 2: Figure S2. of Thrombin-induced, TNFR-dependent miR-181c downregulation promotes MLL1 and NF-κB target gene expression in human microglia

Thrombin’s proteolytic activity contributed to its effects upon miR-181c and MLL1 expression in human microglia. (A) Validation of the thrombin-specific proteolytic inhibitor PPACK’s inhibition of thrombin activity. Thrombin’s proteolytic activity was measured via a chromogenic assay following pre-incubation in the absence or presence of various concentrations of PPACK. Heat-inactivated (boiled) thrombin was applied as a negative control. *p < 0.05 versus control, †p < 0.05 versus boiled thrombin, ‡p < 0.05 versus thrombin. (B) Pre-incubating with PPACK significantly inhibited thrombin’s effects upon miR-181c and MLL1 expression. *p < 0.05 versus control, †p < 0.05 versus thrombin. (TIF 598 kb