Tert-Butylhydroquinone Mitigates T-2-Toxin-Induced Testicular Dysfunction by Targeting Oxidative Stress, Inflammation, and Apoptosis in Rats.

Tert-butylhydroquinone (tBHQ) has emerged as a promising candidate for mitigating the adverse effects of T-2-induced reproductive toxicity. The protective effects of tBHQ on rat sperm quality, testicular injury, apoptosis, and inflammation induced by T-2 toxin exposure were investigated. Histopathological examination of testicular tissues revealed severe damage in the T-2-treated group, characterized by disorganized germ cell arrangement, thinning of the convoluted seminiferous tubule walls, and significant cellular necrosis. However, tBHQ administration, either as a preventive or therapeutic measure, mitigated this structural damage. Image analysis confirmed an increase in the cross-sectional area and height of the convoluted seminiferous tubules in the tBHQ-treated groups compared to the T-2-treated group (p < 0.05), indicating tBHQ's efficacy in alleviating testicular damage. Additionally, tBHQ treatment significantly inhibited T-2-induced apoptosis of testicular tissue cells, as evidenced by the results showing reduced apoptotic cell counts and downregulation of the BAX/BCL2 ratio and caspase-3 expression (p < 0.05). tBHQ significantly increased the concentrations of the antioxidant factors SOD, CAT, TAC, and GSH-PX. Furthermore, tBHQ attenuated the inflammatory response induced by T-2 exposure, as indicated by the decreased mRNA expression of the proinflammatory cytokines Tnf, Il1, and Il10 in testicular tissue (p < 0.05). Additionally, tBHQ treatment alleviated the decline in serum testosterone induced by the T-2 and promoted testosterone synthesis gene expression, including for the genes 17ß-HSD and Cyp11a1, in rat testes (p < 0.05). These findings underscore tBHQ's role as a therapeutic agent combatting T-2-induced reproductive toxicity, highlighting its antioxidative, anti-apoptotic, and anti-inflammatory properties. Further elucidation of tBHQ's mechanisms of action may offer novel strategies for preventing and treating reproductive disorders induced by environmental toxins.

Proteome-wide Mendelian randomization implicates nephronectin as an actionable mediator of the effect of obesity on COVID-19 severity.

Obesity is a major risk factor for Coronavirus disease (COVID-19) severity; however, the mechanisms underlying this relationship are not fully understood. As obesity influences the plasma proteome, we sought to identify circulating proteins mediating the effects of obesity on COVID-19 severity in humans. Here, we screened 4,907 plasma proteins to identify proteins influenced by body mass index using Mendelian randomization. This yielded 1,216 proteins, whose effect on COVID-19 severity was assessed, again using Mendelian randomization. We found that an s.d. increase in nephronectin (NPNT) was associated with increased odds of critically ill COVID-19 (OR = 1.71, P = 1.63 × 10-10). The effect was driven by an NPNT splice isoform. Mediation analyses supported NPNT as a mediator. In single-cell RNA-sequencing, NPNT was expressed in alveolar cells and fibroblasts of the lung in individuals who died of COVID-19. Finally, decreasing body fat mass and increasing fat-free mass were found to lower NPNT levels. These findings provide actionable insights into how obesity influences COVID-19 severity.

GLP-1 RA Improves Diabetic Retinopathy by Protecting the Blood-Retinal Barrier through GLP-1R-ROCK-p-MLC Signaling Pathway.

Background: GLP-1 receptor agonists (GLP-1RA) are common clinical agents that are clinically protective against diabetic complications, such as diabetic retinopathy (DR). Previous studies have shown that the RhoA/ROCK pathway plays an important role in the development of DR. However, the specific mechanism of action between GLP-1RA and DR remains unclear. The aim of this study was thus to investigate the main mechanism involved in the protective effect of GLP-1RA on DR. Methods: Type 2 diabetic mice were fed a high-sugar, high-fat diet. Changes in the retinal structure were observed via HE staining and transmission electron microscopy. The expression of retinal GLP-1R, blood-retinal barrier- (BRB-) related proteins, inflammatory factors, and related pathway proteins were studied via Western blot or immunohistochemistry/immunofluorescence analysis. Results: GLP-1RA treatment reduced the blood glucose and lipid levels as well as the body weight of the diabetic mice while also improving retinal thickness, morphology, and vascular ultrastructure. Moreover, restored GLP-1R expression, increased Occludin and ZO-1 levels, and decreased albumin expression led to reduced retinal leakage and improved the BRB by inhibiting the RhoA/ROCK pathway. Conclusions: We found that the protective effect of GLP-1RA on the retina may be realized through the GLP-1R-ROCK-p-MLC signaling pathway.

The foreign bully, the guest and the low-income knowledge worker: performing multiple versions of whiteness in China.

With the rise of China's economy, more and more white Westerners are moving to China for better job or business opportunities. In addition to the so-called transnational elites, there are an increasing number of middle-stratum white migrants whose lived experiences in China are marked by notable tensions between privileges and precariousness. Based on research in Beijing and Xi'an, this paper examines how white migrants from different backgrounds make strategic choices in coping with the decline of white skin privilege in China and feelings of insecurity in a highly competitive Chinese labour market. It identifies China as a new frontier zone where the meanings of whiteness are contested and reconstructed in interracial encounters between white migrants and various groups of Chinese. I argue that although these white migrants have little control over the multiple and contradictory ways that they are racialised in Chinese society, they still demonstrate a certain degree of agency in manipulating the Chinese gazes for their benefits through the strategic performance of different versions of whiteness.

Between privileges and precariousness: Remaking whiteness in China's teaching English as a second language industry.

 This research examines the multiple and contradictory racialization of white identities in China's booming ESL (English as a second language) industry. China represents a new geography of whiteness studies beyond Euro-America due to the transformation of corporeal whiteness into a minority identity as a result of international migration. This research makes distinctions between white privilege as a form of structural domination in Western societies and white-skin privilege as a form of embodied racial capital in China, which can be easily transformed into white-skin vulnerability. It interprets the tension between white-skin privilege and precariousness as a concurrent and mutually constitutive process that foregrounds the open-ended nature of white racial formation in China. By focusing on the intersections between global white supremacist ideologies and local Chinese constructions of self/Other relations, this project explores new forms of racialization beyond the Black/white, superiority/inferiority binaries in the Western context.

Esta investigación examina la racialización múltiple y contradictoria de identidades blancas en la industria en auge del ESL (inglés como segundo idioma) en China. China representa una geografía nueva de estudios de blancura más allá de Euro­América debido a la transformación de la blancura corpórea en la identidad de una minoría como resultado de una migración internacional. Esta investigación hace distinciones entre el privilegio blanco como una forma de dominación estructural en sociedades occidentales y el privilegio de piel blanca como una forma de capital racial corporeizado en China, el cual puede ser fácilmente transformado en vulnerabilidad de la piel blanca. Interpreta la tensión entre el privilegio de piel blanca y la precariedad como un proceso concurrente y mutuamente constitutivo que destaca la naturaleza abierta de la formación racial blanca en China. Al enfocarse en las intersecciones entre las ideologías supremacistas blancas globales y las construcciones chinas locales de las relaciones sí­mismo/otro, este proyecto explora nuevas formas de racialización más allá de los binarios negro/blanco, superioridad/inferioridad en el contexto occidental. [privilegio de piel blanca, precariedad, neoliberalismo racial, profesores de inglés extranjeros, China].

Impact of Apocrine Gland Residue on Bromhidrosis Clinical Efficacy: A Self-controlled Case Series Study.

Apocrine sweat gland excision is a successful surgical treatment for bromhidrosis used in clinical practice due to its efficacy and unobtrusive postoperative scar. However, a small quantity of apocrine sweat gland residue is an unavoidable intraoperative concern to minimize losses of the dermal vascular network induced by extensive excision of the apocrine sweat glands. However, the relationship between the degree of remaining glands and clinical efficacy is yet unknown. This study looked at the histopathology of preexcision and postexcision specimens from bromhidrosis patients to see a connection between residual apocrine sweat glands and clinical efficacy following apocrine sweat gland excision. Methods: Twenty-one patients with bromhidrosis were recruited from April 2018 to December 2020. In this study, a description self-controlled case series was applied, with the patient preoperative sample as the control. The entire axillary skin was excised before and immediately after apocrine sweat gland excision, and skin tissue hemotoxylin-and-eosin staining was conducted to assess and compare the remnant apocrine sweat glands. Furthermore, preoperative and 6-month postoperative NRS-11 odor scores were analyzed, as well as patient satisfaction after surgery. Results: All patients had variable degrees of apocrine sweat gland excision residue, but they all passed clinical cure criteria and presented a high patient satisfaction rate. Conclusions: Apocrine sweat gland excision with a small quantity of apocrine sweat gland remnant can nevertheless result in a favorable clinical outcome and high patient satisfaction of bromhidrosis.

Caspase-3-dependent peritubular capillary dysfunction is pivotal for the transition from acute to chronic kidney disease after acute ischemia-reperfusion injury.

Ischemia-reperfusion injury (IRI) is a major risk factor for chronic renal failure. Caspase-3, an effector responsible for apoptosis execution, is activated within the peritubular capillary (PTC) in the early stage of IRI-induced acute kidney injury (AKI). Recently, we showed that caspase-3-dependent microvascular rarefaction plays a key role in fibrosis development after mild renal IRI. Here, we further characterized the role of caspase-3 in microvascular dysfunction and progressive renal failure in both mild and severe AKI, by performing unilateral renal artery clamping for 30/60 min with contralateral nephrectomy in wild-type (C57BL/6) or caspase-3-/- mice. In both forms of AKI, caspase-3-/- mice showed better long-term outcomes despite worse initial tubular injury. After 3 wk, they showed reduced PTC injury, decreased PTC collagen deposition and α-smooth muscle actin expression, and lower tubular injury scores compared with wild-type animals. Caspase-3-/- mice with severe IRI also showed better preservation of long-term renal function. Intravital imaging and microcomputed tomography revealed preserved PTC permeability and better terminal capillary density in caspase-3-/- mice. Collectively, these results demonstrate the pivotal importance of caspase-3 in regulating long-term renal function after IRI and establish the predominant role of PTC dysfunction as a major contributor to progressive renal dysfunction.NEW & NOTEWORTHY Our findings demonstrate the pivotal importance of caspase-3 in regulating renal microvascular dysfunction, fibrogenesis, and long-term renal impairment after acute kidney injury induced by ischemia-reperfusion injury. Furthermore, this study establishes the predominant role of peritubular capillary integrity as a major contributor to progressive renal dysfunction after ischemia-reperfusion injury.

Application of evidence-based nursing in patients with acute myocardial infarction complicated with heart failure.

OBJECTIVE: To explore the application of evidence-based nursing (EBN) in patients with acute myocardial infarction (AMI) complicated with heart failure. METHODS: A total of 76 patients with acute myocardial infarction complicated with heart failure after Percutaneous Transluminal Coronary Intervention (PCI) were admitted to the Department of Cardiology of our hospital from April 2018 to October 2019 and randomly divided into the control group and the experimental group, with 38 patients in each group. The control group received routine nursing and the experimental group received EBN nursing. Self-rating Anxiety Scale (SAS), Self-rating Depression Scale (SDS) scores, quality of life, long-term treatment efficacy, and nursing satisfaction in the two groups before and after nursing were compared and analyzed. RESULTS: In terms of SAS and SDS, the experimental group after nursing had remarkably lower scores than the control group (t=6.468, 4.025, all P < 0.001). The quality-of-life scores of patients in both groups after nursing were better, and the increase in the experimental group was more evident (all P < 0.05). Left Ventricular Ejection Fraction (LVEF) in the experimental group was significantly higher compared with the control group (t=2.480, P < 0.05), while Left Ventricular Diastolic Diameter (LVDd) and Brain Natriuretic Peptide (BNP) were significantly lower (t=3.824, 12.241, all P < 0.001). Considering the total nursing satisfaction, the experimental group demonstrated a higher satisfaction rate (P < 0.05). CONCLUSION: EBN is beneficial for patients with AMI complicated with heart failure, and it is worth being popularized in clinical nursing.

Caspase-3 Is a Pivotal Regulator of Microvascular Rarefaction and Renal Fibrosis after Ischemia-Reperfusion Injury.

Background Ischemia-reperfusion injury (IRI) is a major risk factor for chronic renal failure. Here, we characterize the different modes of programmed cell death in the tubular and microvascular compartments during the various stages of IRI-induced AKI, and their relative importance to renal fibrogenesis.Methods We performed unilateral renal artery clamping for 30 minutes and contralateral nephrectomy in wild-type mice (C57BL/6) or caspase-3-/- mice.Results Compared with their wild-type counterparts, caspase-3-/- mice in the early stage of AKI had high urine cystatin C levels, tubular injury scores, and serum creatinine levels. Electron microscopy revealed evidence of tubular epithelial cell necrosis in caspase-3-/- mice, and immunohistochemistry showed upregulation of the necroptosis marker receptor-interacting serine/threonine-protein kinase 3 (RIPK3) in renal cortical sections. Western blot analysis further demonstrated enhanced levels of phosphorylated RIPK3 in the kidneys of caspase-3-/- mice. In contrast, caspase-3-/- mice had less microvascular congestion and activation in the early and extension phases of AKI. In the long term (3 weeks after IRI), caspase-3-/- mice had reduced microvascular rarefaction and renal fibrosis, as well as decreased expression of α-smooth muscle actin and reduced collagen deposition within peritubular capillaries. Moreover, caspase-3-/- mice exhibited signs of reduced tubular ischemia, including lower tubular expression of hypoxia-inducible factor-1α and improved tubular injury scores.Conclusions These results establish the pivotal importance of caspase-3 in regulating microvascular endothelial cell apoptosis and renal fibrosis after IRI. These findings also demonstrate the predominant role of microvascular over tubular injury as a driver of progressive renal damage and fibrosis after IRI.

[Determination of trigonelline in coffee powder and instant coffee by ultrasonic extraction and high performance liquid chromatography].

A method of high performance liquid chromatography was established for the analysis of trigonelline in coffee powder and instant coffee. The separation was performed on a BondPak NH2 column (250 mm x 4.6 mm, 5 microm). The mobile phase was methanol-water (82: 18, v/v) at a flow rate of 0.8 mL/min. The detection wavelength was set at 260 nm. The method had good linearity in the range of 1 - 40 mg/L (the correlation coefficient was 0.9998). The repeatability of the method was performed at one day, different days, and by two analysts. The accuracy of the method was evaluated by recovery study. The recoveries were more than 90% with the relative standard deviations less than 3%. The contents of trigonelline in samples were assessed with ultrasonic extraction and hot water extraction, separately, and the regression coefficient between trigonelline contents obtained under the two extraction methods was 0.9964. The method is simple, rapid, highly sensitive, and suitable for the analysis of trigonelline and quality control of coffee samples.

Hydrogen peroxide-induced proline and metabolic pathway of its accumulation in maize seedlings.

Exogenous H(2)O(2) treatment led to a significant accumulation of proline in coleoptiles and radicles of maize seedlings. It also induced an almost immediate and rapid increase of activity of the key enzymes Delta(1)-pyrroline-5-carboxylate synthetase and glutamate dehydrogenase of the glutamate pathway of proline biosynthesis and an up-regulation of Delta(1)-pyrroline-5-carboxylate synthetase gene expression. Activities of the key enzymes arginase and ornithine aminotransferase of the ornithine pathway of proline biosynthesis increased only after 12h of H(2)O(2) treatment. Furthermore, the H(2)O(2) treatment caused an early decrease of the activity of proline dehydrogenase, a key enzyme of proline degradation. These results indicate that H(2)O(2) might be involved in signal transduction events, leading to proline accumulation in maize seedlings, and that the H(2)O(2)-induced proline accumulation is a combined result of the sequential activation of the glutamate and ornithine pathways of proline biosynthesis and the simultaneous inhibition of proline degradation by H(2)O(2).