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Background We sought to evaluate the effect of mild hypercapnia on brain tissue oxygen tension (Pbto 2 ) and diffusion limitation (impaired ability of oxygen extraction) in a porcine post asphyxial cardiac arrest model. Methods In 16 Bama pigs, asphyxial cardiac arrest was induced by endotracheal tube clamping and remained untreated for another 4 min. After return of spontaneous circulation (ROSC), animals were randomly assigned to mild hypercapnia (end-tidal carbon dioxide (EtCO 2 ): 45 ~ 50 mmHg) and normocapnia (EtCO 2 : 35 ~ 40 mmHg) groups for 12 h. Intracranial pressure (ICP), Pbto 2 , and brain tissue temperature were invasively measured by multimodality monitors. Blood gas analysis, neuron specific enolase (NSE), and S100β were tested at baseline, ROSC 1 h, 6 h, and 12 h. Generalized mixed model with a compound symmetry covariance matrix was used to compare the time-variables of the two groups. Results Twelve (75%) pigs had ROSC and 11 pigs survived for the study period, with 6 pigs in mild hypercapnia group and 5 in the normocapnia group. The mean EtCO 2 in the mild hypercapnia was significantly higher than normocapnia group (48 vs 38 mmHg, p  <  0.001). Compared with normocapnia, mild hypercapnia group had higher Pbto 2 ( p  <  0.001), slightly higher mean arterial pressure ( p  = 0.012) and ICP ( p  = 0.009). There were no differences in cerebral perfusion pressure ( p  = 0.106), gradient of partial pressure of jugular venous bulb oxygen (Pjvo 2 ) and Pbto 2 ( p  = 0.262), difference of partial pressure of jugular venous CO 2 and arterial CO 2 ( p  = 0.546), cardiac output ( p  = 0.712), NSE ( p  = 0.822), and S100β ( p  = 0.759) between the two groups. Conclusions Short term mild hypercapnia post-resuscitation could improve Pbto 2 . However, no corresponding improvements in the gradient of Pjvo 2 to Pbto 2 and biomarkers of neurological recovery were observed in the porcine asphyxial cardiac arrest model.

Heart failure with preserved ejection fraction (HFpEF) is a common public health problem associated with increased morbidity and long-term mortality. However, effective treatment for HFpEF was not discovered yet. In the present study, we aimed to decipher the effects of Periplocin on DOCA-induced heart failure rats and explore the possible underlying mechanisms. We demonstrated that Periplocin could significantly attenuate cardiac structural remodeling and improve cardiac diastolic function. Of note, Periplocin significantly inhibited the recruitment of inflammatory and immune cells and decreased the expression of serum inflammatory cytokines. Meanwhile, Periplocin had the effect of cardiac glycosides to improve cardiomyocyte contractility and calcium transient amplitude. These findings indicate that Periplocin might be a potential medicine to treat HFpEF in patients. Graphical abstract

Background This study aims to investigate the efficacy and safety of glibenclamide treatment in patients with acute aneurysmal subarachnoid hemorrhage (aSAH). Methods The randomized controlled trial was conducted from October 2021 to May 2023 at two university-affiliated hospitals in Beijing, China. The study included patients with aSAH within 48 h of onset, of whom were divided into the intervention group and the control group according to the random number table method. Patients in the intervention group received glibenclamide tablet 3.75 mg/day for 7 days. The primary end points were the levels of serum neuron-specific enolase (NSE) and soluble protein 100B (S100B) between the two groups. Secondary end points included evaluating changes in the midline shift and the gray matter–white matter ratio, as well as assessing the modified Rankin Scale scores during follow-up. The trial was registered at ClinicalTrials.gov (identifier NCT05137678). Results A total of 111 study participants completed the study. The median age was 55 years, and 52% were women. The mean admission Glasgow Coma Scale was 10, and 58% of the Hunt-Hess grades were no less than grade III. The baseline characteristics of the two groups were similar. On days 3 and 7, there were no statistically significant differences observed in serum NSE and S100B levels between the two groups ( P  > 0.05). The computer tomography (CT) values of gray matter and white matter in the basal ganglia were low on admission, indicating early brain edema. However, there were no significant differences found in midline shift and gray matter–white matter ratio ( P  > 0.05) between the two groups. More than half of the patients had a beneficial outcome (modified Rankin Scale scores 0–2), and there were no statistically significant differences between the two groups. The incidence of hypoglycemia in the two groups were 4% and 9%, respectively ( P  = 0.439). Conclusions Treating patients with early aSAH with oral glibenclamide did not decrease levels of serum NSE and S100B and did not improve the poor 90-day neurological outcome. In the intervention group, there was a visible decreasing trend in cases of delayed cerebral ischemia, but no statistically significant difference was observed. The incidence of hypoglycemia did not differ significantly between the two groups.

Cobalt‐based spinel oxide is a promising electrocatalyst for oxygen evolution reaction (OER) because of its low cost, excellent activity and stability. Herein, we designed the CuMnxCo2O4 electrocatalyst with tunable electronic structure via Mn‐doping to enhance OER performance. Results showed that the CuMn0.5Co2O4 catalyst prepared by calcined at 600°C exhibited high crystalline without impurity phase, and possessed the enhanced Co2+/Co3+ ratio and high concentration of oxygen vacancies, which were facilitated to enhance OER performance. Electrochemical test results showed the CuMn0.5Co2O4 catalyst had high OER performance with a low overpotential of 340 mV at the current density of 10 mA ⋅ cm−2 and a smaller Tafel slope of 69.8 mV ⋅ dec−1. TOF and ECSA results illustrated that the more intrinsic catalytic activity on the CuMn0.5Co2O4 catalyst. After 1000 cycles, the catalyst exhibited high stability with the 8 1.7 % of current retention rate. The OER activity enhancement mechanism of was further analyzed, which were mainly ascribed to the conversion of variable Co2+/Co3+ and enhanced oxygen vacancies. Spinel Phase for Oxygen Evolution Reaction: The synthesized CuMn0.5Co2O4 catalyst possessed the enhanced Co2+/Co3+ ratio and oxygen vacancies, enhancing absorption capacity of OH− and electron transport capacity, which improved OER performance of catalyst. The CuMn0.5Co2O4 catalyst exhibited high OER performance with a low overpotential of 340 mV at the current density of 10 mA ⋅ cm−2 and a smaller Tafel slope of 69.8 mV ⋅ dec−1.

PpCAD2 was originally isolated from the ‘Wangkumbae’ pear (Pyrus pyrifolia Nakai), and it encodes for cinnamyl alcohol dehydrogenase (CAD), which is a key enzyme in the lignin biosynthesis pathway. In order to verify the function of PpCAD2, transgenic tomato (Solanum lycopersicum) ‘Micro-Tom’ plants were generated using over-expression constructs via the agrobacterium-mediated transformation method. The results showed that the PpCAD2 over-expression transgenic tomato plant had a strong growth vigor. Furthermore, these PpCAD2 over-expression transgenic tomato plants contained a higher lignin content and CAD enzymatic activity in the stem, leaf and fruit pericarp tissues, and formed a greater number of vessel elements in the stem and leaf vein, compared to wild type tomato plants. This study clearly indicated that overexpressing PpCAD2 increased the lignin deposition of transgenic tomato plants, and thus validated the function of PpCAD2 in lignin biosynthesis.

A disorder in pears that is known as ‘hard-end’ fruit affects the appearance, edible quality, and market value of pear fruit. RNA-Seq was carried out on the calyx end of ‘Whangkeumbae’ pear fruit with and without the hard-end symptom to explore the mechanism underlying the formation of hard-end. The results indicated that the genes in the phenylpropanoid pathway affecting lignification were up-regulated in hard-end fruit. An analysis of differentially expressed genes (DEGs) identified three NAC transcription factors, and RT-qPCR analysis of PpNAC138, PpNAC186, and PpNAC187 confirmed that PpNAC187 gene expression was correlated with the hard-end disorder in pear fruit. A transient increase in PpNAC187 was observed in the calyx end of ‘Whangkeumbae’ fruit when they began to exhibit hard-end symptom. Concomitantly, the higher level of PpCCR and PpCOMT transcripts was observed, which are the key genes in lignin biosynthesis. Notably, lignin content in the stem and leaf tissues of transgenic tobacco overexpressing PpNAC187 was significantly higher than in the control plants that were transformed with an empty vector. Furthermore, transgenic tobacco overexpressing PpNAC187 had a larger number of xylem vessel elements. The results of this study confirmed that PpNAC187 functions in inducing lignification in pear fruit during the development of the hard-end disorder.

Fine particulate matter (PM 2.5 ) pollution remains a major threat to public health. As the physical barrier against inhaled air pollutants, airway epithelium is a primary target for PM 2.5  and influenza viruses, two major environmental insults. Recent studies have shown that PM 2.5  and influenza viruses may interact to aggravate airway inflammation, an essential event in the pathogenesis of diverse pulmonary diseases. Airway epithelium plays a critical role in lung health and disorders. Thus far, the mechanisms for the interactive effect of PM 2.5  and the influenza virus on gene transcription of airway epithelial cells have not been fully uncovered. In this present pilot study, the transcriptome sequencing approach was introduced to identify responsive genes following individual and co-exposure to PM 2.5  and influenza A (H3N2) viruses in a human bronchial epithelial cell line (BEAS-2B). Enrichment analysis revealed the function of differentially expressed genes (DEGs). Specifically, the DEGs enriched in the xenobiotic metabolism by the cytochrome P450 pathway were linked to PM 2.5  exposure. In contrast, the DEGs enriched in environmental information processing and human diseases, such as viral protein interaction with cytokines and cytokine receptors and epithelial cell signaling in bacterial infection, were significantly related to H3N2 exposure. Meanwhile, co-exposure to PM 2.5  and H3N2 affected G protein-coupled receptors on the cell surface. Thus, the results from this study provides insights into PM 2.5 - and influenza virus-induced airway inflammation and potential mechanisms.

Summary Hard‐end, superficial scald and cork spot are prevalent physiological disorders in pear fruit, characterized by an increase in lignin deposition, which impairs the fruit quality and reduces farmer income. Although calcium deficiency is known to exacerbate symptoms of these lignin‐related disorders, the underlying mechanisms remain poorly understood. In this study, we aimed to elucidate the regulatory network through which calcium modulates lignin deposition‐induced physiological disorders, using hard‐end disorder as a model. Our results showed that WRKY46, a transcription factor, is upregulated in hard‐end fruit but downregulated by calcium treatment. WRKY46 directly activates the transcription of NAC187, which in turn activates the expression of CCR, promoting lignin accumulation. Furthermore, CML38, a calcium sensor protein, enhances the transactivation capacity of WRKY46 via physical interaction. Calcium disrupts the CML38/WRKY46‐NAC187‐CCR cascade, ultimately suppressing lignin biosynthesis. Additionally, the upregulation of WRKY46, CML38 and NAC187 correlates with reduced Ca2+ levels in the fruit. Collectively, these data suggest that the development of lignin‐related physiological disorders in pear fruit is mediated by the CML38/WRKY46‐NAC187‐CCR regulatory module, which is enhanced by reduced Ca2+ levels. This module plays a dual role in both lignin accumulation and Ca2+ level reduction, shedding new light on the role of calcium in modulating fruit quality.

The Milky Way underwent significant transformations in its early history, characterised by violent mergers and satellite galaxy accretion. However, recent observations reveal notable star formation events over the past 4 Gyr, likely triggered by perturbations from the Sagittarius dwarf galaxy. Here, we present chemical signatures of this accretion event, using the [Fe/H] (metallicity) and [O/Fe] (oxygen abundance) ratios of thin-disc stars. In the normalised age-metallicity plane, we identify a discontinuous V-shape structure at z max (maximum vertical distance from the disc plane)  < 0.4 kpc in the local disc, interrupted by a star formation burst between 4 and 2 Gyr ago. This event is characterised by a significant increase in oxygen abundance, resulting in a distinct [O/Fe] gradient and the formation of young O-rich stars. These stars have larger birth radii, indicating formation in the outer disc followed by radial migration to the Solar neighbourhood. Simulations of late satellite infall suggest that the passage of the Sagittarius dwarf galaxy may have contributed to the observed increase in oxygen abundance in the local disc. Enhanced star formation rates in our galaxy during the past 2–4 Gyr is known from survey data, and this is likely linked to Sagittarius dwarf galaxy’s passage. Here, authors show an increase in oxygen (O) abundance during this period, suggesting satellite accretion contribution to the observed O abundances.

The hard-end is a disorder of pear fruit, however, the mechanisms underlying its development remain unknown. In this study, we found that the hard-end fruit contained a higher transcript abundance level of ethylene-response factor 1b-like ( PpERF1b-like ) and released more ethylene compared to normal pear. In the ethephon treated normal fruit, flesh tissues accumulated more lignin together with elevated expression of PpERF1b-like . Overexpressing PpERF1b-like transiently in fruit and stably in callus increased lignin accumulation and the expression of lignin biosynthesis genes; the opposite results were observed in fruit showing repressed expression of PpERF1b-like . These results confirmed the role of PpERF1b-like in promoting hard-end formation through promoting lignin synthesis. This study provided valuable information for further clarifying the regulation of hard-end formation in pear.