Improved Fog Collection on a Hybrid Surface with Acylated Cellulose Coating.

Fog collection serves as an efficient method to alleviate water scarcity in foggy, water-stressed regions. Recent research has focused on constructing a hybrid surface to enhance fog collection efficiency, with one approach being the prevention of liquid film formation at hydrophilic sites. Inspired by the desert beetle, a coating (10-MCC) made by partially acylating microcrystalline cellulose (MCC) exhibits hydrophilic sites alongside a hydrophobic skeleton enabling rapid droplet capture despite its overall hydrophobicity. The captured droplets quickly coalesce into a large droplet driven by the wetting gradient created by the hydrophobic backbone and hydrophilic sites. To achieve greater fog collection efficiency, a hydrophobic-superhydrophobic hybrid surface is formed by combining a coating of 10-MCC with a superhydrophobic surface. The construction of superhydrophobic surfaces typically involves creating a rough surface with a distinctive structure produced by the anodization technique and modifying it with stearic acid. The superhydrophobic surface exhibits excellent corrosion resistance and mechanical stability. Moreover, the hybrid surface shows high efficiency in fog collection, with a tested maximum efficiency of approximately 1.5092 g/cm2/h, 1.77 times that of the original Al sheets. The results demonstrate a remarkable enhancement in fog collection capacity. Furthermore, this work serves as an inspiration for the low-cost and innovative design of engineered surfaces for efficient fog collection.

IL-27 Alleviates Airway Inflammation and Airway Hyperresponsiveness in Asthmatic Mice by Targeting the CD39/ATP Axis of Dendritic Cells.

Interleukin-27 receptor (IL-27R) is expressed in a variety of immune cells and structural cells, including dendritic cells. The mechanism of IL-27 in asthma has not been fully elucidated. This study aimed to examine whether IL-27 regulated the CD39/ATP axis of dendritic cells in asthma. Our results showed that in ovalbumin (OVA)-induced asthma mouse model, IL-27Rα-/- asthmatic mice showed increased airway resistance, increased infiltration of inflammatory cells in lung tissue, proliferation of goblet cells, enhanced expression of Muc5 AC around airway epithelium, increased total number of cells and eosinophils, increased levels of total IgE, OVA-IgE, IL-4, IL-5, IL-13 and IL-17 A, and increased expression of transcription factors GATA-3 and RORγt in lung tissue. The expression of CD39 mRNA and protein in the lung tissue of IL-27Rα-/- asthmatic mice decreased, and the expression of NLRP3, ASC and Caspase-1 in NLRP3 inflammasome components increased. The concentration of ATP was significantly increased compared with WT asthmatic mice. In vitro experiments showed that the expression of CD39 in lung dendritic cells of IL-27Rα-/- asthmatic mice decreased, while the expression of NLRP3 inflammasome components NLRP3, ASC and Caspase-1 increased. These findings indicate that IL-27 directly and indirectly regulates immunoinflammatory responses in asthma by acting on dendritic cells CD39/ATP Axis.

Response of growth performance and cecum microbial community to cyclic heat stress in broilers.

Heat stress (HS) can affect growth performance through alterations in specific gut microbiota, which greatly threatens poultry production. How HS affects the mechanisms of microbial changes in the poultry cecum and the complex interactions between cecal microbial changes and growth performance have not yet been well evaluated. This study was conducted to examine the changes in growth performance and cecal microbiotal community in cyclic heat stress (CHS)-treated broilers. A total of 200 twenty-eight-day-old female Arbor Acres (AA) broilers were equally allotted into neutral ambient temperature group (TN group, 24 ± 1°C, 24 h/day) and CHS group (33 ± 1°C, 8 h/day) with five replicates of 10 broilers each, respectively. Growth performance, cecum microbial diversity, flora composition, and community structure were analyzed on days 35 and 42. The decreased average daily feed intake (ADFI), average daily gain (ADG), and the increased feed/gain ratio (F:G) were observed in heat-stressed broilers on days 35 and 42. The alpha and beta diversity index had no significant changes at the two experimental periods (P > 0.05). At the genus level, CHS significantly increased the relative abundance of Enterococcus at 42 days (P < 0.05). Based on the analysis of linear effect size feature selection, CHS made an enriched Reyranella and a reduced Romboutsia and Ruminiclostridium at 35 days of age (P < 0.05). CHS made an enriched Weissella and Enterococcus at 42 days of age (P < 0.05). The present study revealed that CHS reduces broiler growth performance and alters the microbial community of the cecum microbiota and the abundance of species. These findings are of critical importance to alleviate the negative effects of CHS on broiler chickens' growth performance by maintaining gut microbial balance.

Establishment and engineering application of viscoelastic-plastic constitutive laws for creep modeling in interbedded rock masses.

In order to study the creep behavior of the surrounding rock of the interbedded rock mass tunnel considering the time-dependent deformation, this paper proposes a viscoelastic-plastic seven-element model considering the stress threshold, and derives and establishes its creep equation under three-dimensional stress state. At the same time, the UMAT (User-defined Material) subroutine of the model is developed based on the ABAQUS software. The rationality of the seven-element model and the effectiveness of the subprogram are verified by rheological test results. Finally, the UMAT subroutine is applied to the numerical simulation of the creep behavior of soft and hard interbedded rock tunnels with different rock inclinations (α). The results show that the different rock inclination angles have different effects on the horizontal displacement of the ground above the tunnel, settlement deformation, and the convergence of the tunnel section. With the increase of the rock inclination (0 ≤ α ≤ 90°), the horizontal displacement of the surface on both sides is antisymmetric. When α is 0°, 45° and 90°, the horizontal displacement on both sides is equivalent. Surface subsidence decreases and then increases slowly. When α is 0° and 45°, the surface subsidence is the largest (12.4 mm) and the smallest (11.1 mm), respectively. The convergence values of the tunnel section change according to different parts of the tunnel. The convergence values of the arch top and arch bottom decrease continuously, and their maximum convergence values are 23.4 mm and 17.3 mm, respectively. The change trend of the arch waist and arch shoulder convergence values is the opposite. When α is 0°, the convergence value of the arch waist is maximum (3.5 mm). When α is 15°, the convergence value of the arch shoulder is the maximum (2.0 mm).

Betaine ameliorates heat stress-induced apoptosis by affecting oxidative and endoplasmic reticulum stress in mouse Leydig cells.

In order to explore the potential protective role of betaine in heat stress (HS)-elicited apoptosis in mouse Leydig cells (mLCs). Betaine at 16 mm exerted a greater inhibitory effect on HS-induced viability attenuation of cells, which also significantly suppressed the heat shock protein 70 level in HS-treated cells. Furthermore, betaine ameliorated certain negative effects, including increased cell apoptotic ratio, enhancement of apoptosis-related modulator caspase-3 activity, reduced activity levels of such antioxidant enzymes as SOD, CAT, GSH-Px, and MDA upregulation, and inhibited the protein levels of critical endoplasmic reticulum (ER) stress indices like CHOP and GRP78 in mLCs exposed to HS. Besides, treatment of cells with betaine significantly restored diminished testosterone production in response to HS. Correspondingly, betaine effectively rescued the reduced serum testosterone concentration in vivo. In summary, betaine ameliorated HS-induced apoptosis by affecting oxidative and ER stress, thereby providing benefits for the treatment of hyperthermia-related impairment in mLCs.

Antibody-dependent enhancement of porcine reproductive and respiratory syndrome virus infection downregulates the levels of interferon-gamma/lambdas in porcine alveolar macrophages in vitro.

Fc gamma receptor-mediated antibody-dependent enhancement (ADE) can promote virus invasion of target cells, sometimes exacerbating the severity of the disease. ADE may be an enormous hurdle to developing efficacious vaccines for certain human and animal viruses. ADE of porcine reproductive and respiratory syndrome virus (PRRSV) infection has been demonstrated in vivo and in vitro. However, the effect of PRRSV-ADE infection on the natural antiviral immunity of the host cells is yet to be well investigated. Specifically, whether the ADE of PRRSV infection affects the levels of type II (interferon-gamma, IFN-γ) and III (interferon-lambdas, IFN-λs) interferons (IFNs) remains unclear. In this study, our results showed that PRRSV significantly induced the secretion of IFN-γ, IFN-λ1, IFN-λ3, and IFN-λ4 in porcine alveolar macrophages (PAMs) in early infection, and weakly inhibited the production of IFN-γ, IFN-λ1, IFN-λ3, and IFN-λ4 in PAMs in late infection. Simultaneously, PRRSV infection significantly increased the transcription of interferon-stimulated gene 15 (ISG15), ISG56, and 2', 5'-oligoadenylate synthetase 2 (OAS2) in PAMs. In addition, our results showed that PRRSV infection in PAMs via the ADE pathway not only significantly decreased the synthesis of IFN-γ, IFN-λ1, IFN-λ3, and IFN-λ4 but also significantly enhanced the generation of transforming growth factor-beta1 (TGF-ß1). Our results also showed that the ADE of PRRSV infection significantly reduced the mRNAs of ISG15, ISG56, and OAS2 in PAMs. In conclusion, our studies indicated that PRRSV-ADE infection suppressed innate antiviral response by downregulating the levels of type II and III IFNs, hence facilitating viral replication in PAMs in vitro. The ADE mechanism demonstrated in the present study furthered our understanding of persistent pathogenesis following PRRSV infection mediated by antibodies.

LOW DOSE OF ESMOLOL ATTENUATES SEPSIS-INDUCED IMMUNOSUPPRESSION VIA MODULATING T-LYMPHOCYTE APOPTOSIS AND DIFFERENTIATION.

ABSTRACT: Background: Immunosuppression caused by immune cell apoptosis and an imbalance of T helper 2 cells (T H 2) and T helper 1 cells (T H 1), is associated with poor outcomes in septic patients. Esmolol was reported to improve survival by modulating immune responses in septic shock. Whether esmolol could alleviate sepsis-induced immunosuppression and the optimal dose are unclear. Methods: Four hours after cecal ligation and puncture (CLP), Wistar rats were randomized into CLP, CLP + E-5 (esmolol: 5 mg·kg -1 ·h -1 ) and CLP + E-18 (esmolol: 18 mg·kg -1 ·h -1 ) groups. Eight rats were underwent sham operation. Eighteen hours after CLP, hemodynamics and organ histological injuries were evaluated, peripheral blood mononuclear cells apoptosis and T-lymphocyte subsets counts were determined by flow cytometry, and the expression of p-Akt, Bcl-2, cleaved Caspase-3, and p-Erk1/2 in splenic CD4 + T-lymphocytes was determined by western blot and immunohistochemistry. ß 1 -Adrenoreceptor expressions were evaluated using real-time polymerase chain reaction and immunohistochemistry. Results: Cecal ligation and puncture induced tachycardia, hypotension, hyperlactatemia, and multiple organ injury. Heart rate was unchanged in the CLP + E-5 group but decreased in the CLP + E-18 group. Hypotension, lactatemia, and multiple organ injuries were improved only in the CLP + E-5 group. T-lymphocyte apoptosis and T H 2/T H 1 ratio was decreased in CLP + E-5 but not in CLP + E-18. p-Akt and Bcl-2 expressions were increased, while cleaved Caspase-3 and p-Erk1/2 expressions were decreased in CLP + E-5. ß 1 -Adrenoreceptor expressions were unchanged in both CLP + E-5 and CLP + E-18 groups. Conclusions: Low dose of esmolol reduced T-lymphocyte apoptosis and restored T H 2/T H 1 ratio in septic shock. Esmolol might modulate Akt/Bcl-2/Caspase-3 pathway to relieve T-lymphocyte apoptosis and inhibit Erk1/2 activity to decrease T H 0 differentiation to T H 2. Esmolol may be a potential immunoregulator of septic shock.

Effect of dietary supplemental vitamin C and betaine on the growth performance, humoral immunity, immune organ index, and antioxidant status of broilers under heat stress.

Heat stress (HS) has become one of the important factors affecting the development of animal husbandry. The purpose of this experiment was to investigate whether vitamin C (Vc) and betaine (Bet) improve immune organ index and humoral immunity by enhancing the antioxidant status of immune organs, thus protecting broilers from HS-induced injuries. A total of 200 28-day-old Ross 308 broilers were randomly assigned into 5 groups (n = 4 replicates/group, 10 broilers/replicate) which were reared at different ambient temperatures (24 ± 1°C or 33 ± 1°C). The control group fed basal diet, while high-temperature groups were either fed a basal diet (HS group) or a basal diet supplemented with 250-mg Vc/kg diet (HSVc group), 1000-mg Bet/kg diet (HSBet group), and 250-mg Vc plus 1000 mg Bet/kg diet (HSVcBet group), respectively. On day 42, growth performance, humoral immune function, immune organ index, and antioxidant capacity were measured. HS reduced the productive performance of broilers, antibody potency against the Newcastle disease virus (NDV) and sheep red blood cells (SRBC), indices of thymus and bursa, and antioxidant capacity of immune organs. Adding Vc alone or in combination with Bet improved performance, NDV and SRBC antibody potency, thymus and bursa indices, and antioxidant capacity of immune organs in heat-stressed broilers, with the most effective being combination. In summary, HS reduces the antioxidant capacity and immune organ development status of broiler immune organs. Vc and/or Bet can improve the development of immune organs and restore part of the production performance by regulating the antioxidant status of immune organs, among which the combined addition of Vc and Bet has the best effect.

MicroRNA-19a Inhibition Directly and Indirectly Ameliorates Th2 Airway Inflammation in Asthma by Targeting RUNX3.

Disruption of T-cell differentiation is characteristic of airway inflammation in allergic asthma. How miR-19a works in asthma has not been completely elucidated. This study aimed to examine whether microRNA-19a regulates helper T-cell proliferation and to identify the factors involved and the underlying mechanisms. Our results showed that miR-19a levels were upregulated in parallel with a reduction in RUNX3 expression in a house dust mite (HDM)-induced murine model of asthma. A dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay showed that RUNX3 was a direct target of miR-19a. Inhibiting the expression of miR-19a attenuated inflammation and mucus production, induced Th1 cells, suppressed the Th2 inflammatory response, and repressed dendritic cell (DC) maturation by increasing RUNX3 expression in WT asthmatic mice but not RUNX3+/- mice. In vitro experiments revealed that miR-19a inhibition could target RUNX3 to induce Th1 polarization and inhibit Th2 polarization by directly acting on naïve CD4+ T cells or indirectly mediating the maturation and antigen-presenting abilities of DCs. These findings indicate that miR-19a directly and indirectly regulates immunoinflammatory responses in asthma by targeting RUNX3.

IL-13 Regulates Orai1 Expression in Human Bronchial Smooth Muscle Cells and Airway Remodeling in Asthma Mice Model via LncRNA H19.

Background: Increased proliferation and hypertrophy of airway smooth muscle cells (ASMCs) contribute substantially to airway remodeling in asthma. Interleukin (IL)-13 regulates ASMC proliferation by increasing Orai1 expression, the pore-forming subunit of store-operated Ca2+ entry (SOCE). The underlying mechanisms of this effect are not fully understood. Methods: Bioinformatic analysis identified an interaction between microRNA 93-5p (miR-93-5p) and long non-coding RNA (lncRNA) H19, and between miR-93-5p and Orai1. RNA interference was used to investigate H19 knockdown on IL-13-induced proliferation and migration of in vitro cultured human bronchial smooth muscle cells (hBSMCs). Functional relevance of H19 in airway inflammation and airway remodeling was investigated in murine models of acute and chronic asthma. Results: IL-13 concentration-dependently increased the expression of H19 and Orai1 and decreased the expression of miR-93-5p in hBSMCs. H19 knockdown partly reversed the effects of IL-13 on the expression of miR-93-5p and Orai1 and attenuated the proliferation and migration of hBSMCs promoted by IL-13. IL-13-promoted expression of Orai1 was attenuated by miR-93-5p mimic and increased by miR-93-5p inhibitor. IL-13-promoted proliferation of hBSMCs was increased by miR-93-5p inhibitor but not affected by miR-93-5p mimic, whereas IL-13-promoted migration of hBSMCs was increased by miR-93-5p inhibitor and attenuated by miR-93-5p mimic. The inhibiting effect of H19 knockdown on IL-13-induced Orai1 expression and the proliferation and migration of hBSMCs was counteracted by miR-93-5p inhibitor but only marginally or not impacted by miR-93-5p mimic. The expression of H19 and Orai1 was higher in the lungs of asthmatic mice than in control mice. In asthmatic mice, H19 siRNA reduced Orai1 expression, inflammatory cell infiltration, goblet cell hyperplasia, collagen deposition and smooth muscle mass in the lungs. Conclusion: H19 may mediate the effects of IL-13 on Orai1 expression by inhibition of miR-93-5p in hBSMCs. H19 may be a therapeutic target for airway inflammation and airway remodeling.

Sodium selenite attenuates zearalenone-induced apoptosis through inhibition of endoplasmic reticulum stress in goat trophoblast cells.

Zearalenone (ZEL)-induced apoptosis in different cells is mediated by various molecular mechanisms, including endoplasmic reticulum (ER) stress. Selenium, an inorganic micronutrient, has several cytoprotective properties, but its potential protective action against ZEL-induced apoptosis in trophoblast cells and the precise mechanisms remain unclear. In this study, we investigated the effects of sodium selenite, a predominant chemical form of selenium, on cell viability, apoptosis, and progesterone (P4) production in ZEL-treated goat trophoblast cell line and explored the underlying molecular mechanisms. ZEL treatment repressed cell viability and promoted apoptosis, which was accompanied by an enhancement of the activity of caspase 3, a key executioner of apoptosis. ZEL treatment was involved in the upregulation of malonaldehyde (MDA) levels and was implicated in the reduction of the protein expression of selenoprotein S (SELS), thereby triggering protein expression of ER stress biomarkers (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP)). However, sodium selenite attenuates these adverse effects, including increases in apoptotic rate, caspase 3 activity, MDA, GRP78, and CHOP expression and decreases in SELS expression in cells treated with ZEL or Thapsigargin (Tg, an ER stress agonist). Simultaneously, 4-phenylbutyric acid (4-PBA, an ER stress antagonist) treatment significantly alleviated the ZEL-induced deleterious effects on cells in response to ZEL, similarly to sodium selenite. In addition, sodium selenite supplementation effectively rescued the ZEL-induced decrease in P4 production in ZEL-treated cells. In summary, these findings suggest that ZEL triggers apoptosis in goat trophoblast cells by downregulating SELS expression and activating the ER stress signaling pathway and that sodium selenite protects against these detrimental effects. This study provides novel insights into the benefits of using selenium against ZEL-induced apoptosis and cellular damage.

Zinc Protects against Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in TM3 Leydig Cells.

Heat stress (HS)-induced apoptosis in Leydig cells is mediated by various molecular mechanisms, including endoplasmic reticulum (ER) stress. Zinc, an inorganic mineral element, exhibits several cytoprotective properties, but its potential protective action against Leydig cell apoptosis and the related molecular mechanisms has not been fully elucidated. In this study, we evaluated the effects of zinc sulfate, a predominant chemical form of zinc, exerted on cell viability, apoptosis, and testosterone production in HS-treated TM3 Leydig cells and investigated the underlying signaling pathways. HS treatment inhibited cell viability and induced apoptosis, which was accompanied by the induction of the activity of caspase 3, an executioner of apoptosis, involved in the expression of pro-apoptotic protein B cell lymphoma 2-associated X protein (Bax), and in the reduction of the expression of anti-apoptotic protein B cell lymphoma 2 (Bcl-2), thereby activating ER stress marker protein expression (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP)). However, zinc sulfate led to the attenuation of deleterious effects, including increases in apoptosis, caspase-3 activity, Bax, GRP78, and CHOP expression, and decreases in cell viability and Bcl-2 protein expression in cells treated with HS or thapsigargin (an ER stress activator). Furthermore, 4-phenylbutyric acid (an ER stress inhibitor) treatment markedly alleviated the HS-induced adverse effects in cells exposed to HS, which was similar to zinc sulfate. Additionally, zinc sulfate supplementation in the culture medium effectively restored the HS-induced decrease in testosterone levels in HS-treated cells. In summary, these findings indicate that HS triggers apoptosis in TM3 Leydig cells via the ER stress pathway and that zinc confers protection against these detrimental effects. This study provides new insights into the benefits of using zinc against HS-induced apoptosis and cell injury.

Association between immunity and viral shedding duration in non-severe SARS-CoV-2 Omicron variant-infected patients.

Background: Coronavirus disease 2019 (COVID-19) is a respiratory-related disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). More than 200 countries worldwide are affected by this disease. The Omicron variant of SARS-CoV-2 is the major epidemic variant worldwide and is characterized by higher infectivity. However, the immunity and risk factors for prolonged viral elimination in patients with non-severe SARS-CoV-2 Omicron variant infections are unclear. Therefore, this study aimed to examine the relationship between immunity and duration of viral elimination in non-severe SARS-CoV-2 Omicron variant-infected patients in Shanghai. Methods: In total, 108 non-severe SARS-CoV-2 Omicron variant-infected patients from Shanghai New International Expo Center Fangcang Shelter Hospital were recruited in this study. They were further allocated to the early elimination (EE) and prolonged elimination (PE) groups according to SARS-CoV-2 nucleic acid positivity duration. Results: Compared to patients with EE, those with PE had increased serum concentrations of interleukin (IL)-5, IL-6, and IL-8; higher neutrophil count and neutrophil-to-lymphocyte ratio (NLR); lower lymphocyte, eosinophil, and red blood cell counts; and lower concentrations of hemoglobin and albumin (ALB). In lymphocyte subpopulation analysis, lower numbers of CD3+ T cells, CD4+ T cells, CD8+ T cells, and NK cells and a higher CD4/CD8 ratio were observed in patients with PE. In addition, correlation analysis results revealed that cycle threshold values of SARS-CoV-2 Omicron variant ORF1ab and N were negatively correlated with IL-6 and IL-8 levels and positively correlated with eosinophil count in patients with COVID-19. Finally, multivariate regression analysis showed that ALB, CD4/CD8 ratio, NLR, and eosinophil count were predictors of the SARS-CoV-2 Omicron variant elimination. Conclusion: In this study, we identified that the ALB, CD4/CD8 ratio, NLR, and eosinophil count were risk factors for prolonged viral elimination in non-severe SARS-CoV-2 Omicron variant-infected patients. These factors might be efficient indicators in the diagnosis, evaluation, and prognosis monitoring of the disease.

Boron Attenuates Heat Stress-Induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress in Mouse Granulosa Cells.

Heat stress-induced apoptosis in granulosa cells is mediated by multiple apoptotic signaling pathways, including endoplasmic reticulum (ER) stress. Boron is a naturally occurring trace element with several cytoprotective properties. Nonetheless, the molecular mechanisms involved in the protective functions of boron in granulosa cells undergoing apoptosis caused by heat stress (HS) remain unclear. In this study, we investigated the role of boric acid, a predominant chemical form of boron, in HS-induced apoptotic damage in mouse granulosa cells (mGCs) and explored the underlying mechanisms. We found that HS treatment suppressed cell viability; increased the apoptotic rate of cells; potentiated the activity of caspase-3, a key player in the caspase-mediated apoptotic signaling pathway; and activated ER stress markers, including glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) in mGCs. However, boric acid treatment effectively alleviated the effects of both HS-induced and thapsigargin (an ER stress agonist)-induced apoptosis, such as the enhanced activity of caspase-3 and increase in GRP78 and CHOP expression. Moreover, treatment with 4-phenylbutyrate (4-PBA), an ER stress antagonist, significantly attenuated these HS-induced adverse effects in mGCs. In addition, boric acid supplementation in the culture medium significantly restored the decreased estradiol levels in heat-treated mGCs. The administration of boric acid to female mice previously exposed to hyperthermal conditions effectively restored the levels of serum estradiol in vivo. Collectively, these findings suggest that HS induces apoptosis in mGCs via ER stress pathways and that boron has a protective effect against these adverse effects. This study provides novel insights into the benefits of using boron against heat-induced apoptosis.

Characterization of heat stress affecting the growth performance, blood biochemical profile, and redox status in male and female broilers at market age.

This study investigated the effects of acute heat stress (HS), sex, and their interaction on growth performance, serum biochemical and redox status in the later stage broilers. Two hundred 38-day-old Ross 308 chicks were allocated in a factorial arrangement of 2 × 2 (temperatures and sexes) with 5 replicates of 10 bird each. Thermoneutral and heat-stressed broilers were raised at 24 ± 1 °C or 32 ± 1 °C from day 38 to 39, respectively. HS decreased the average daily feed intake (ADFI) and average daily gain (ADG) whereas it increased feed conversion ratio (FCR), rectal temperature (RT), and respiratory rate (RR) in broilers exposed to high temperature for 24 h and 48 h. Moreover, RT, RR, serum glucose, and HDL-C levels increased while triglyceride (TG), total superoxide dismutase (T-SOD), and glutathione peroxidase (GPx) decreased in broilers exposed to high temperature for 12 h. Male broilers had higher final body weight (FBW), ADFI, ADG, total protein carbonyl group, and lower FCR and T-SOD than females in HS condition for 24 h and 48 h. Lower RT, serum albumin, HDL-C, activities of T-SOD and GPx were observed when compared with those of males in HS condition for 12 h. There were significant temperature × sex interactive effects on ADFI, ADG, and TG in broilers exposed to high temperature for 24 h and 48 h. The present study suggests that the acute HS negatively affects growth performance which is accompanied by the disorder of serum nutritional metabolism and imbalance of redox status in later stage broilers. Some parameters presented sexual differences that suggested it may be more effective to alleviate the negative effects of HS when broiler producers take into account the gender of broiler.

Increased miR-223-3p in Leukocytes Positively Correlated with IL-17A in Plasma of Asthmatic Patients.

Asthma is a common airway inflammation with an intricate underlying mechanism. The role played by circulating miRNAs in asthma remains unclear. In the present study, we aimed to investigate the role of miR-223-3p in leukocytes of asthma and identify the relationship between miR-223-3p and inflammatory cytokines in asthma. Using real-time polymerase chain reaction (RT-PCR), we detected miR-223-3p expression in peripheral blood leukocytes from 23 asthmatic patients and 20 healthy controls. The levels of IFN-γ (Th1 cytokine), IL-4 (Th2 cytokine), IL-17A (Th17 cytokine) in plasma were examined using enzyme-linked immunosorbent assay (ELISA). Analysis of variance (ANOVA) and Spearman's test was used for statistical analysis. The expression of miR-223-3p in peripheral blood leukocytes was upregulated in the asthmatic patients compared with that in the healthy controls. Increased miR-223-3p expression was associated with forced expiratory volume in 1-second percent predicted (FEV1% predicted). A positive correlation was noted between miR-223-3p and IL-17A. The findings of this study showed that miR-223-3p plays a vital role in the pathogenesis of asthma and can serve as a novel biomarker for asthma.

The role of isolation rooms, facemasks and intensified hand hygiene in the prevention of nosocomial COVID-19 transmission in a pulmonary clinical setting.

From December 25, 2019 to January 31, 2020, 33 cases of the coronavirus disease 2019 (COVID-19) were identified in the Department of Respiratory and Critical Care Medicine of Zhongnan Hospital of Wuhan University, China, yet none of the affiliated HCWs was infected. Here we analyzed the infection control measures used in three different departments in the Zhongnan Hospital of Wuhan University and correlated the measures with the corresponding infection data of HCWs affiliated with these departments. We found that three infection control measures, namely the isolation of the presumed positive patients, the use of facemasks and intensified hand hygiene play important roles in preventing nosocomial transmission of COVID-19.

Oxidative Stress and Endoplasmic Reticulum Stress Are Involved in the Protective Effect of Alpha Lipoic Acid Against Heat Damage in Chicken Testes.

Heat stress (HS) causes testicular injury, resulting in decreased fertility. Alpha-lipoic acid (ALA) is a well-known antioxidant. The aim of this study was to investigate the protective effects of ALA on HS-induced testicular damage in chickens. Histological changes; biomarkers of oxidative stress, including glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA); markers of endoplasmic reticulum (ER) stress, including glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP); apoptosis-related modulators, including Bax, Bcl-2, and caspase 3, in testicular tissue and serum testosterone levels were evaluated in chickens under heat stress. Heat stress induces spermatogenic cell abnormalities in chicken testes. Compared to the HS group, the histomorphological abnormalities in testicular tissue were visibly ameliorated, with significant increases in the enzyme activities of GPx, SOD, and CAT, increased serum testosterone concentration, and decreased MDA levels in the ALA + HS group. Consistent with these results, compared with the HS group, the protein levels of GRP78, CHOP, caspase 3, and Bax were significantly decreased, whereas Bcl-2, StAR, and 3ß-HSD protein levels were increased in the ALA + HS group. Collectively, these findings suggest that ALA significantly ameliorates the heat-induced histomorphological abnormalities in the testes and decreased testosterone production by potentiating the activities of anti-oxidative enzymes (GPx, SOD, and CAT), inhibiting ER stress-related apoptotic pathways (Bax, Bcl-2, and caspase 3), and increasing steroidogenic gene (StAR and 3ß-HSD) expression in chickens.

Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells.

Heat stress induces apoptosis in various cells. Selenium, an essential micronutrient, has beneficial effects in maintaining the cellular physiological functions. However, its potential protective action against chronic heat stress (CHS)-induced apoptosis in granulosa cells and the related molecular mechanisms are not fully elucidated. In this study, we investigated the roles of selenium in CHS-induced apoptosis in mouse granulosa cells and explored its underlying mechanism. The heat treatment for 6-48 h induced apoptosis, potentiated caspase 3 activity, increased the expression levels of apoptosis-related gene BAX and ER stress markers, glucose-regulated protein 78 (GRP78), and CCAAT/enhancer binding protein homologous protein (CHOP) in mouse granulosa cells. The treatment with ER stress inhibitor 4-PBA significantly attenuated the adverse effects caused by CHS. Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP. Additionally, treatment of the cells with 5 ng/mL selenium significantly ameliorated the levels of estradiol, which were decreased in response to heat exposure. Consistently, administering selenium supplement alleviated the hyperthermia-caused reduction in the serum estradiol levels in vivo. Together, our findings indicate that selenium has protective effects on CHS-induced apoptosis via inhibition of the ER stress pathway. The current study provides new insights in understanding the role of selenium during the process of heat-induced cell apoptosis.

Modular Synthesis of Nona-Decasaccharide Motif from Psidium guajava Polysaccharides: Orthogonal One-Pot Glycosylation Strategy.

The synthesis of long, branched, and complex carbohydrate sequences remains a challenging task in chemical synthesis. Reported here is an efficient and modular one-pot synthesis of a nona-decasaccharide and shorter sequences from Psidium guajava polysaccharides, which have the potent α-glucosidase inhibitory activity. The synthetic strategy features: 1) several one-pot glycosylation reactions on the basis of N-phenyltrifluoroacetimidate (PTFAI) and Yu glycosylation to streamline the chemical synthesis of oligosaccharides, 2) the successful and efficient assembly sequences (first O3', second O5', final O2') toward the challenging 2,3,5-branched Araf motif, 3) the stereoselective 1,2-cis-glucosylation by reagent control, and 4) the convergent [6+6+7] one-pot coupling reaction for the final assembly of the target nona-decasaccharide. This orthogonal one-pot glycosylation strategy can streamline the chemical synthesis of long, branched, and complicated carbohydrate chains.