33 research outputs found

    Atmospheric environment and severe acute respiratory infections in Nanjing, China, 2018–2019

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    The annual burden of severe acute respiratory infection (SARI) is enormous, and environmental factors may have a vital role in respiratory infections. This study aimed to investigate the potential effects of the atmospheric environment on SARI. A time-series analysis was performed on the relationship between atmospheric environment and 136,989 SARI cases by distributed lag non-linear model. Wind speed, PM10, PM2.5, O3, and CO exhibited differential effects at a range of lag times or exposure ranges. Air pressure, temperature, and diurnal temperature range showed risk effects in the full range. The lag effect of high pollution was stronger, appeared earlier, and lasted longer than that of low pollution. Most environmental factors had a certain non-linear lag relationship with SARI. Low wind speed and high air pollution may be increasing risk factors for SARI.</p

    Image1_Folic Acid Alleviates High Glucose and Fat-Induced Pyroptosis via Inhibition of the Hippo Signal Pathway on H9C2 Cells.TIF

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    Diabetic cardiomyopathy (DCM) is the leading cause of death in diabetic patients. Folic acid has a protective effect on diabetes-induced cardiomyocyte damage. The aim of this study was to explore the effects of folic acid on cardiomyocytes cultured under high glucose and fat (HGF) conditions and type 2 diabetes mellitus (T2DM) mice, and elucidate the underlying mechanisms. Bioinformatics analysis was used to identify the potential drugs through the Drug-Gene Interaction database. H9C2 cardiomyocytes were cultured with 30 mM glucose and 500 nM palmitic acid in the presence or absence of folic acid or YAP1 inhibitor (verteporfin) or YAP1 siRNA. The cell viability and lactate dehydrogenase (LDH) release were measured using specific assay kits. Pyroptosis was detected by flow cytometry. The concentrations of IL-1β and IL-18 in the supernatants were measured by ELISA. The NLRP3, ASC and caspase-1 mRNA levels were detected by qRT-PCR and that the proteins expression of NLRP3, ASC, cleaved caspase-1 (p10), caspase-1, YAP1, p-YAP1, LATS1 and P-LATS1 were detected by Western blotting. C57BL/6 mice were fed with high fat diet (HFD) combined with streptozotocin (STZ) intraperitoneally to establish a T2DM model, folic acid or PBS treatment for 8 weeks by oral gavage, blood glucose and body weight were measured every 4 weeks, mouse heart tissue was used to detect pyroptosis and hippo signaling pathway related protein expression. We identified 427 differentially expressed genes in the cardiac tissues of high fat diet + streptozotocin mice, among the 30 most significantly DEGs, folic acid was predicted to be the most likely therapeutic drug. Folic acid alleviated HGF-induced cell damage in vitro and in vivo by decreasing activation of the Hippo pathway, as indicated by lower LDH release and increased cell viability, and decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1β, IL-18, p-YAP and p-LATS. Verteporfin or YAP1 siRNA neutralized the protective effect of folic acid by reversing YAP1-induced pyroptosis. Folic acid reduced NLRP3 inflammasome-mediated pyroptosis by down-regulating the Hippo signaling pathway, thereby effectively reducing T2DM-induced damage in H9C2 cells and animals.</p

    Image2_Folic Acid Alleviates High Glucose and Fat-Induced Pyroptosis via Inhibition of the Hippo Signal Pathway on H9C2 Cells.TIF

    No full text
    Diabetic cardiomyopathy (DCM) is the leading cause of death in diabetic patients. Folic acid has a protective effect on diabetes-induced cardiomyocyte damage. The aim of this study was to explore the effects of folic acid on cardiomyocytes cultured under high glucose and fat (HGF) conditions and type 2 diabetes mellitus (T2DM) mice, and elucidate the underlying mechanisms. Bioinformatics analysis was used to identify the potential drugs through the Drug-Gene Interaction database. H9C2 cardiomyocytes were cultured with 30 mM glucose and 500 nM palmitic acid in the presence or absence of folic acid or YAP1 inhibitor (verteporfin) or YAP1 siRNA. The cell viability and lactate dehydrogenase (LDH) release were measured using specific assay kits. Pyroptosis was detected by flow cytometry. The concentrations of IL-1β and IL-18 in the supernatants were measured by ELISA. The NLRP3, ASC and caspase-1 mRNA levels were detected by qRT-PCR and that the proteins expression of NLRP3, ASC, cleaved caspase-1 (p10), caspase-1, YAP1, p-YAP1, LATS1 and P-LATS1 were detected by Western blotting. C57BL/6 mice were fed with high fat diet (HFD) combined with streptozotocin (STZ) intraperitoneally to establish a T2DM model, folic acid or PBS treatment for 8 weeks by oral gavage, blood glucose and body weight were measured every 4 weeks, mouse heart tissue was used to detect pyroptosis and hippo signaling pathway related protein expression. We identified 427 differentially expressed genes in the cardiac tissues of high fat diet + streptozotocin mice, among the 30 most significantly DEGs, folic acid was predicted to be the most likely therapeutic drug. Folic acid alleviated HGF-induced cell damage in vitro and in vivo by decreasing activation of the Hippo pathway, as indicated by lower LDH release and increased cell viability, and decreased expression of NLRP3, ASC, cleaved caspase-1, IL-1β, IL-18, p-YAP and p-LATS. Verteporfin or YAP1 siRNA neutralized the protective effect of folic acid by reversing YAP1-induced pyroptosis. Folic acid reduced NLRP3 inflammasome-mediated pyroptosis by down-regulating the Hippo signaling pathway, thereby effectively reducing T2DM-induced damage in H9C2 cells and animals.</p

    Molecular Simulation and Experimental Study of CO<sub>2</sub> Absorption in Ionic Liquid Reverse Micelle

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    The structure and dynamics for CO<sub>2</sub> absorption in ionic liquid reverse micelle (ILRM) were studied using molecular simulations. The ILRM consisted of 1-butyl-3-methylimidazolium tetrafluoroborate ([bmim]­[BF<sub>4</sub>]) ionic liquid (IL) as the micelle core, the benzylhexadecyldimethylammonium ([BHD]<sup>+</sup>) chloride ([Cl]<sup>−</sup>) was the cationic surfactant, and benzene was used as the continuous solvent phase in this study. The diffusivity values of this ILRM system were also experimentally determined. Simulations indicate that there is ion exchange between the IL anion ([BF<sub>4</sub>]<sup>−</sup>) and the surfactant anion ([Cl]<sup>−</sup>). It was also found that the [bmim]­[BF<sub>4</sub>] IL exhibits small local density at the interface region between the IL core and the [BHD]<sup>+</sup> surfactant cation layer, which leads to a smaller density for the [bmim]­[BF<sub>4</sub>] IL inside the reverse micelle (RM) compared with the neat IL. These simulation findings are consistent with experimental results. Both our simulations and experimental results show that [bmim]­[BF<sub>4</sub>] inside the RM diffuses 5–26 times faster than the neat IL, which is partly due to the fast <i>particle</i> diffusion for the ILRM nanodroplet (IL and surfactant) as a whole in benzene solvent compared with neat [bmim]­[BF<sub>4</sub>] diffusion. Additionally, it was found that [bmim]­[BF<sub>4</sub>] IL solved in benzene diffuses 2 orders of magnitude faster than the neat IL. Lastly, simulations show that CO<sub>2</sub> molecules are absorbed in four different regions of the ILRM system, that is, (I) in the IL inner core, (II) in the [BHD]<sup>+</sup> surfactant cation layer, (III) at the interface between the [BHD]<sup>+</sup> surfactant cation layer and benzene solvent, and (IV) in the benzene solvent. The CO<sub>2</sub> solubility was found to decrease in the order II > III ∼ IV > I, while the CO<sub>2</sub> diffusivity and permeability decrease in the following order: IV > III > II > I

    Table_1_Role of gut microbiota and inflammatory factors in acute respiratory distress syndrome: a Mendelian randomization analysis.XLSX

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    BackgroundAcute respiratory distress syndrome (ARDS) is a serious lung ailment marked by significant inflammation and damage in the alveoli and capillaries of the lungs. Recent research suggests a strong correlation between the onset and advancement of ARDS and an imbalance in the gut microbiota (GM).MethodsIn this investigation, Mendelian randomization (MR) analysis was utilized, drawing on data from publicly accessible genome-wide association studies. The primary focus was on examining the interplay between GM, inflammatory factors (IFs) and ARDS. Instrumental variables were established through genetic modifications of GM and IFs. Various statistical analysis methods including the inverse-variance weighted model, MR-Egger method and Wald ratio test were applied for comprehensive data analysis.ResultsEight bacterial taxa within the GM demonstrated a potential causal link with development of ARDS. Notably, the phylum Actinobacteria and the genus Intestinibacter exhibited a negative association with the risk of ARDS. However, Erysipelotrichales (id. 2,148), Victivallis (id. 2,256), Ruminococcaceae UCG014 (id. 11,371), Eubacterium ruminantium group (id. 11,340), Erysipelotrichaceae (id. 2,149) and Erysipelotrichia (id. 2,147) demonstrated a positive association with ARDS risk. Additionally, the study identified a potential causal relationship between the inflammatory factors interleukin-16 and C-C motif chemokine 3 with the occurrence of ARDS.ConclusionThis study strongly suggests that the interaction between gut microbiota (GM) and inflammatory factors (IFs) significantly contributes to the pathogenesis of acute respiratory distress syndrome (ARDS). This underscores their crucial involvement in both the initiation and advancement of this severe lung disorder.</p

    Wrist coordinate system.

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    <p>Horizontal plane(red), sagittal plane(green) and coronal plane(blue).</p

    Projection views.

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    <p>(a) Axillary view. Original radial boundary (dotted line) was translated toward the ulnar side (yellow arrow). Red dot shows the axis point. (b) Axis projection view. Figure shows the risk zone (RZ), including the RD, UD, RV, and UV quadrants. The safe zone (SZ) is denoted by the green area. Blue lines mark the boundaries. (c) Screw cross-section view. Circles represent the cross-section of the screw, and purple areas represent the trajectory of the screw. We could not accurately identify the screw’s position when it was perpendicular on AP radiographs.</p

    The Scaphoid Safe Zone: A Radiographic Simulation Study to Prevent Cortical Perforation Arising from Different Views

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    <div><p>Purpose</p><p>The purpose of this study was to simulate and calculate the probability of iatrogenic perforation of the scaphoid cortical bone when internal fixation appeared to be safe on radiographs. The results will assist surgeons in determining proper screw placement.</p><p>Methods</p><p>Thirty scaphoids were reconstructed using computed tomography data and image-processing software. Different central axes were determined by the software to simulate the surgical views. The safe zone (SZ) and risk zone (RZ) were identified on the axial projection radiographs by comparing the scaphoid bone stenosis measured by the fluoroscopic radiographs with a three-dimensional reconstruction of the scaphoid stenosis. Each original axial projection radiograph was zoomed and compiled to match a calculated average image. The RZ, SZ, and probability of perforations in various quadrants were calculated.</p><p>Results</p><p>Using a volar view (approach), the mean risks of cortical perforation were 25% with screws and 36% with k-wires. Using a dorsal view (approach), the mean risks of cortical perforation were 18% with screws and 30% with k-wires. A high risk of perforation was detected at the ulnar–dorsal zone.</p><p>Conclusion</p><p>Surgeons should be wary of screws that appear to lie close to the scaphoid cortex on both anteroposterior (AP) and lateral radiographs, particularly in the ulnar–dorsal and radial–dorsal quadrants, because such screws are likely to perforate the cortex. The position of the internal fixator should be assessed using a diagram outlining the various SZs. Therapeutic, Level III.</p></div
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