Marcussenkahn1415

low tertile, OR for asthma = 1.25; 95% CI (1.02-1.54); p = 0.035]. Traditional and Prudent dietary patterns were not associated with the prevalence of asthma.

The fast food/sweet dietary pattern was directly associated with the prevalence of asthma among adults in Qatar. Reducing the fast foods and sugary-rich foods may be beneficial for respiratory health.

The fast food/sweet dietary pattern was directly associated with the prevalence of asthma among adults in Qatar. Reducing the fast foods and sugary-rich foods may be beneficial for respiratory health.Epithelial-mesenchymal transition (EMT)-a fundamental process in embryogenesis and wound healing-promotes tumor metastasis and resistance to chemotherapy. While studies have identified signaling components and transcriptional factors responsible in the TGF-β-dependent EMT, whether and how intracellular metabolism is integrated with EMT remains to be fully elucidated. Here, we showed that TGF-β induces reprogramming of intracellular amino acid metabolism, which is necessary to promote EMT in non-small cell lung cancer cells. Combined metabolome and transcriptome analysis identified prolyl 4-hydroxylase α3 (P4HA3), an enzyme implicated in cancer metabolism, to be upregulated during TGF-β stimulation. Further, knockdown of P4HA3 diminished TGF-β-dependent changes in amino acids, EMT, and tumor metastasis. Conversely, manipulation of extracellular amino acids induced EMT-like responses without TGF-β stimulation. These results suggest a previously unappreciated requirement for the reprogramming of amino acid metabolism via P4HA3 for TGF-β-dependent EMT and implicate a P4HA3 inhibitor as a potential therapeutic agent for cancer.Epithelial-mesenchymal transition (EMT) plays a crucial role in the development of pulmonary fibrosis. This study aims to investigate the effects of valproic acid (VPA) on EMT in vitro and in vivo. In vitro, EMT was induced by the administration of transforming growth factor-β1 (TGF-β1) in a human alveolar epithelial cell line (A549). The dose effects of VPA (0.1-3 mM) on EMT were subsequently evaluated at different timepoints. VPA (1 mM) was applied prior to the administration of TGF-β1 and the expression of E-cadherin, vimentin, p-Smad2/3 and p-Akt was assessed. In addition, the effects of a TGF-β type I receptor inhibitor (A8301) and PI3K-Akt inhibitor (LY294002) on EMT were evaluated. In vivo, the effects of VPA on bleomycin-induced lung fibrosis were evaluated by assessing variables such as survival rate, body weight and histopathological changes, whilst the expression of E-cadherin and vimentin in lung tissue was also evaluated. A8301 and LY294002 were used to ascertain the cellular signaling pathways involved in this model. The administration of VPA prior to TGF-β1 in A549 cells prevented EMT in both a time- and concentration-dependent manner. Pretreatment with VPA downregulated the expression of both p-Smad2/3 and p-Akt. A8301 administration increased the expression of E-cadherin and reduced the expression of vimentin. Thapsigargin LY294002 inhibited Akt phosphorylation induced by TGF-β1 but failed to prevent EMT. Pretreatment with VPA both increased the survival rate and prevented the loss of body weight in mice with pulmonary fibrosis. Interestingly, both VPA and A8301 prevented EMT and facilitated an improvement in lung structure. Overall, pretreatment with VPA attenuated the development of pulmonary fibrosis by inhibiting EMT in mice, which was associated with Smad2/3 deactivation but without Akt cellular signal involvement.

To correlate arterial umbilical cord gas (aUCG) and infant blood gas with severity of neurological injury.

Retrospective single-site study of infants evaluated for therapeutic hypothermia. Clinical neurological examination and a validated MRI scoring system were used to assess injury severity.

Sixty-eight infants were included. aUCG base deficit (BD) and lactate correlated with infant blood gas counterparts (r = 0.43 and r = 0.56, respectively). aUCG and infant pH did not correlate. Infant blood gas lactate (R



 = 0.40), infant BD (R



 = 0.26), infant pH (R



 = 0.17), aUCG base deficit (R



 = 0.08), and aUCG lactate (R



 = 0.11) were associated with clinical neurological examination severity. aUCG and infant blood gas measures were not correlated with MRI score.

Metabolic measures from initial infant blood gases were most associated with the clinical neurological examination severity and can be used to evaluate hypoxic-ischemic cerebral injury risk.

Metabolic measures from initial infant blood gases were most associated with the clinical neurological examination severity and can be used to evaluate hypoxic-ischemic cerebral injury risk.

To evaluate acute stress disorder (ASD) symptoms and their predictors in Neonatal Intensive Care Unit (NICU) mothers.

In this cross-sectional study, 119 mothers (~72% Medicaid) completed surveys during the first month of their infants' hospitalizations. Correlations and structural equation models (SEMs) evaluated relations among mothers' childhood trauma history, infant health appraisals, objective infant health, and ASD.

ASD symptoms (~55%) and childhood trauma (~33%) were prevalent. ASD was correlated with childhood trauma, infant health, and infant health appraisals. All SEMs had good fit, indicating that (a) infant health appraisals partially mediated relations between childhood trauma and ASD, and (b) infant health appraisals fully mediated relations between objective infant health and ASD.

ASD symptoms are prevalent among NICU mothers regardless of infant health severity. Recognition of childhood trauma history and appraisals of infant health is critical for trauma-informed care.

ASD symptoms are prevalent among NICU mothers regardless of infant health severity. Recognition of childhood trauma history and appraisals of infant health is critical for trauma-informed care.Suicide is a significant public health concern with complex etiology. Although the genetic component of suicide is well established, the scope of gene networks and biological mechanisms underlying suicide has yet to be defined. Previously, we reported genome-wide evidence that neurexin 1 (NRXN1), a key synapse organizing molecule, is associated with familial suicide risk. Here we present new evidence for two non-synonymous variants (rs78540316; P469S and rs199784139; H885Y) associated with increased familial risk of suicide death. We tested the impact of these variants on binding interactions with known partners and assessed functionality in a hemi-synapse formation assay. Although the formation of hemi-synapses was not altered with the P469S variant relative to wild-type, both variants increased binding to the postsynaptic binding partner, leucine-rich repeat transmembrane neuronal 2 (LRRTM2) in vitro. Our findings indicate that variants in NRXN1 and related synaptic genes warrant further study as risk factors for suicide death.