Comparative analysis of the gut bacteria and fungi in migratory demoiselle cranes (Grus virgo) and common cranes (Grus grus) in the Yellow River Wetland, China.

Introduction: Gut microbiota are closely related to the nutrition, immunity, and metabolism of the host and play important roles in maintaining the normal physiological activities of animals. Cranes are important protected avian species in China, and they are sensitive to changes in the ecological environment and are thus good environmental indicators. There have been no reports examining gut fungi or the correlation between bacteria and fungi in wild Demoiselle cranes (Grus virgo) and Common cranes (Grus grus). Related research can provide a foundation for the protection of rare wild animals. Methods: 16S rRNA and ITS high-throughput sequencing techniques were used to analyze the gut bacterial and fungal diversity of Common and Demoiselle cranes migrating to the Yellow River wetland in Inner Mongolia. Results: The results revealed that for gut bacteria α diversity, Chao1 index in Demoiselle cranes was remarkably higher than that in Common cranes (411.07 ± 79.54 vs. 294.92 ± 22.38), while other index had no remarkably differences. There was no remarkable difference in fungal diversity. There were marked differences in the gut microbial composition between the two crane species. At the phylum level, the highest abundance of bacteria in the Common crane and Demoiselle crane samples was Firmicutes, accounting for 87.84% and 74.29%, respectively. The highest abundance of fungi in the guts of the Common and Demoiselle cranes was Ascomycota, accounting for 69.42% and 57.63%, respectively. At the genus level, the most abundant bacterial genus in the Common crane sample was Turicibacter (38.60%), and the most abundant bacterial genus in the Demoiselle crane sample was Catelicoccus (39.18%). The most abundant fungi in the Common crane sample was Penicillium (6.97%), and the most abundant fungi in the Demoiselle crane sample was Saccharomyces (8.59%). Correlation analysis indicated that there was a significant correlation between gut bacteria and fungi. Discussion: This study provided a research basis for the protection of cranes. Indeed, a better understanding of the gut microbiota is very important for the conservation and management of wild birds, as it not only helps us to understand their life history and related mechanisms, but also can hinder the spread of pathogenic microorganisms.

Leonurus japonicus Houtt. Modulates Neuronal Apoptosis in Intracerebral Hemorrhage: Insights from Network Pharmacology and Molecular Docking.

ETHNOPHARMACOLOGICAL RELEVANCE: Leonurus japonicus Houtt. (Labiatae), commonly known as Chinese motherwort, is a herbaceous flowering plant that is native to Asia. It is widely acknowledged in traditional medicine for its diuretic, hypoglycemic, antiepileptic properties and neuroprotection. Currently, Leonurus japonicus (Leo) is included in the Pharmacopoeia of the People's Republic of China. Traditional Chinese Medicine (TCM) recognizes Leo for its myriad pharmacological attributes, but its efficacy against ICH-induced neuronal apoptosis is unclear. AIMS OF THE STUDY: This study aimed to identify the potential targets and regulatory mechanisms of Leo in alleviating neuronal apoptosis after ICH. MATERIALS AND METHODS: The study employed network pharmacology, UPLC-Q-TOF-MS technique,molecular docking, pharmacodynamic studies, western blotting, and immunofluorescence techniques to explore its potential mechanisms. RESULTS: Leo was found to assist hematoma absorption, thus improving the neurological outlook in an ICH mouse model. Importantly, molecular docking highlighted JAK as Leo's potential therapeutic target in ICH scenarios. Further experimental evidence demonstrated that Leo adjusts JAK1 and STAT1 phosphorylation, curbing Bax while augmenting Bcl-2 expression. CONCLUSION: Leo showcases potential in mitigating neuronal apoptosis post-ICH, predominantly via the JAK/STAT mechanism.

STIRUnet: SwinTransformer and inverted residual convolution embedding in unet for Sea-Land segmentation.

Extraction of coastline from optical remote sensing images is of paramount importance for coastal zone management, erosion monitoring, and intelligent ocean construction. However, nearshore marine environment complexity presents a challenge when capturing small-scale and detailed information regarding coastlines. Furthermore, the presence of numerous tidal flats, suspended sediments, and coastal biological communities exacerbates the reduction in segmentation accuracy, which is particularly noticeable in medium-high-resolution remote sensing image segmentation tasks. Most previous related studies, based primarily on convolutional neural networks (CNNs) or traditional feature extraction methods, faced challenges in detailed pixel-level refinement and lacked comprehensive understanding of the studied images. Therefore, we proposed a new U-shaped deep learning model (STIRUnet) that combines the excellent global modeling ability of SwinTransformer with an improved CNN using an inverted residual module. The proposed method has the capability of global supervised feature learning and layer-by-layer feature extraction, and we conducted sea-land segmentation experiments using GF-HNCD and BSD remote sensing image datasets to validate the performance of the proposed model. The results indicate the following: 1) suspended sediments and coastal biological communities are major contributors to coastline blurring, and 2) the recovery of minute features (e.g., narrow watercourses and microscale artificial structures) effectively enhances edge details and leads to more realistic segmentation outcomes. The findings of this study are highly important in relation of accurate extraction of sea-land information in complex marine environments, and they offer novel insights regarding mixed-pixel identification.

Construction of a novel S-type γ-Bi2O3/CeO2 heterojunction for highly efficient photocatalytic degradation of antibiotics.

Cubic nanoparticles of CeO2 were partly covered on the tetrahedron surface of γ-Bi2O3 through a hydrothermal reaction and then a calcination process to construct a novel S-type γ-Bi2O3/CeO2 heterojunction. The optimized sample removed 96% of lomefloxacin and 81% of tetracycline. During the cycling test, the photocatalytic efficiency of lomefloxacin and tetracycline was maintained above 87% and 80%, respectively, for five consecutive cycles. According to XRD and Raman spectra characterization, the sample after cycling held a stable crystal structure. Holes, OH-˙, O2˙, and electrons participated in the degradation of lomefloxacin, while tetracycline was removed via the effect of the former three active substances. Based on theoretical calculation and experimental tests, the excellent photocatalytic activity of γ-Bi2O3/CeO2 came from the fast transfer of charge carriers along the S-type path. Moreover, the CB electrons of γ-Bi2O3 and VB holes of CeO2 were preserved to generate free radicals for antibiotic degradation. The colony numbers of Escherichia coli were 1.50 × 10-6 CFU mL-1 and 1.39 × 10-6 CFU mL-1 in solutions after the degradation of the two pollutants, which represents the non-toxicity of the final products. The γ-Bi2O3/CeO2 sample has a potential application for antibiotic removal from modern sewage.

Unveiling the Synergy of Architecture and Anion Vacancy on Bi2Te3-x@NPCNFs for Fast and Stable Potassium Ion Storage.

Large volume strain and slow kinetics are the main obstacles to the application of high-specific-capacity alloy-type metal tellurides in potassium-ion storage systems. Herein, Bi2Te3-x nanocrystals with abundant Te-vacancies embedded in nitrogen-doped porous carbon nanofibers (Bi2Te3-x@NPCNFs) are proposed to address these challenges. In particular, a hierarchical porous fiber structure can be achieved by the polyvinylpyrrolidone-etching method and is conducive to increasing the Te-vacancy concentration. The unique porous structure together with defect engineering modulates the potassium storage mechanism of Bi2Te3, suppresses structural distortion, and accelerates K+ diffusion capacity. The meticulously designed Bi2Te3-x@NPCNFs electrode exhibits ultrastable cycling stability (over 3500 stable cycles at 1.0 A g-1 with a capacity degradation of only 0.01% per cycle) and outstanding rate capability (109.5 mAh g-1 at 2.0 A g-1). Furthermore, the systematic ex situ characterization confirms that the Bi2Te3-x@NPCNFs electrode undergoes an "intercalation-conversion-step alloying" mechanism for potassium storage. Kinetic analysis and density functional theory calculations reveal the excellent pseudocapacitive performance, attractive K+ adsorption, and fast K+ diffusion ability of the Bi2Te3-x@NPCNFs electrode, which is essential for fast potassium-ion storage. Impressively, the assembled Bi2Te3-x@NPCNFs//activated-carbon potassium-ion hybrid capacitors achieve considerable energy/power density (energy density up to 112 Wh kg-1 at a power density of 1000 W kg-1) and excellent cycling stability (1600 cycles at 10.0 A g-1), indicating their potential practical applications.

Mitochondria-lysosome-extracellular vesicles axis and nanotheranostics in neurodegenerative diseases.

The intricate functional interactions between mitochondria and lysosomes play a pivotal role in maintaining cellular homeostasis and proper cellular functions. This dynamic interplay involves the exchange of molecules and signaling, impacting cellular metabolism, mitophagy, organellar dynamics, and cellular responses to stress. Dysregulation of these processes has been implicated in various neurodegenerative diseases. Additionally, mitochondrial-lysosomal crosstalk regulates the exosome release in neurons and glial cells. Under stress conditions, neurons and glial cells exhibit mitochondrial dysfunction and a fragmented network, which further leads to lysosomal dysfunction, thereby inhibiting autophagic flux and enhancing exosome release. This comprehensive review synthesizes current knowledge on mitochondrial regulation of cell death, organelle dynamics, and vesicle trafficking, emphasizing their significant contributions to neurodegenerative diseases. Furthermore, we explore the emerging field of nanomedicine in the management of neurodegenerative diseases. The review provides readers with an insightful overview of nano strategies that are currently advancing the mitochondrial-lysosome-extracellular vesicle axis as a therapeutic approach for mitigating neurodegenerative diseases.

Circadian regulation of microglia function: Potential targets for treatment of Parkinson's Disease.

Circadian rhythms are involved in the regulation of many aspects of the body, including cell function, physical activity and disease. Circadian disturbance often predates the typical symptoms of neurodegenerative diseases and is not only a non-motor symptom, but also one of the causes of their occurrence and progression. Glial cells possess circadian clocks that regulate their function to maintain brain development and homeostasis. Emerging evidence suggests that the microglial circadian clock is involved in the regulation of many physiological processes, such as cytokine release, phagocytosis, and nutritional and metabolic support, and that disruption of the microglia clock may affect multiple aspects of Parkinson's disease, especially neuroinflammation and α-synuclein processes. Herein, we review recent advances in the circadian control of microglia function in health and disease, and discuss novel pharmacological interventions for microglial clocks in neurodegenerative disorders.

Ginsenosides retard atherogenesis via remodelling host-microbiome metabolic homeostasis.

BACKGROUND AND PURPOSE: Panax ginseng is widely applied in the adjuvant treatment of cardiometabolic diseases in clinical practice without clear mechanisms. This study aims to clearly define the efficacy and underlying mechanism of P. ginseng and its active components in protecting against atherosclerosis. EXPERIMENTAL APPROACH: The anti-atherogenic efficacy of total ginseng saponin extract (TGS) and its components was evaluated on Ldlr-/- mice. Gut microbial structure was analysed by 16S rRNA sequencing and PCR. Bile acid profiles were revealed using targeted metabolomics with LC-MS/MS analysis. The contribution of gut microbiota to atherosclerosis was assessed by co-housing experiments. KEY RESULTS: Ginsenoside Rb1, representing protopanaxadiol (PPD)-type saponins, increased intestinal Lactobacillus abundance, resulting in enhanced bile salt hydrolase (BSH) activity to promote intestinal conjugated bile acid hydrolysis and excretion, followed by suppression of enterohepatic farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) signal, and thereby increased cholesterol 7α-hydroxylase (CYP7A1) transcriptional expression and facilitated metabolic elimination of cholesterol. Synergistically, protopanaxatriol (PPT)-type saponins, represented by ginsenoside Rg1, protected against atherogenesis-triggered gut leak and metabolic endotoxaemia. Ginsenoside Rg1 directly induced mucin production to nutritionally maintain Akkermansia muciniphila, which reciprocally inhibited gut permeation. Rb1/Rg1 combination, rather than a single compound, can largely mimic the holistic efficacy of TGS in protecting Ldlr-/- mice from atherogenesis. CONCLUSION AND IMPLICATIONS: Our study provides strong evidence supporting TGS and ginsenoside Rb1/Rg1 combinations as effective therapies against atherogenesis, via targeting different signal nodes by different components and may provide some elucidation of the holistic mode of herbal medicines.

Association between perioperative glucose profiles assessed by the continuous glucose monitoring (CGM) system and prognosis in patients with ST-segment elevation myocardial infarction (STEMI): protocol for a cohort study.

INTRODUCTION: ST-segment elevation myocardial infarction (STEMI) presents a serious cardiovascular condition requiring prompt intervention. Dysglycaemia has been identified as a significant risk factor impacting STEMI prognosis. However, limited research has focused on comprehensively examining the association between glucose dynamics during the perioperative period and patient outcomes. This study aims to address this gap by leveraging continuous glucose monitoring (CGM) technology to gain real-time insights into glucose fluctuations and their potential impact on STEMI prognosis. METHODS AND ANALYSIS: This is a multicentre, prospective, 3-year follow-up cohort study. Between May 2023 and May 2024, 550 eligible STEM patients who underwent percutaneous coronary intervention are expected to be recruited. Using the CGM system, continuous glucose levels will be collected throughout the perioperative phase. Key clinical parameters, including cardiac biomarkers, angiographic findings and major adverse cardiovascular events, will be assessed in relation to glucose profile. ETHICS AND DISSEMINATION: The study was approved by the Medical Research Ethics Committee of The First Affiliated Hospital of University of Science and Technology of China and will be conducted in accordance with the moral, ethical and scientific principles of the Declaration of Helsinki. Written informed consent will be obtained from all participants before any study-related procedures are implemented. Study results will be disseminated through conferences and peer-reviewed scientific journals. TRIAL REGISTRATION NUMBER: ChiCTR2300069662.

The mechanism of selenium regulating the permeability of vascular endothelial cells through selenoprotein O.

Vascular diseases, a leading cause of death in human, are strongly associated with pathological damage to blood vessels. The selenoprotein (Sel) have been reported to play important roles in vascular disease. However, the role of SelO in vascular disease has not been conclusively investigated. The present experiment was to investigate the regulatory mechanism of the effect of SelO on the permeability of vascular endothelial. The H.E staining, FITC-Dextran staining, Dil-AC-LDL staining and FITC-WGA staining showed that vascular structure was damaged, and intercellular junctions were disrupted with selenium (Se)-deficient. Immunohistochemistry, qPCR and Western blot revealed decreased expression of the adhesion plaque proteins vinculin, talin and paxillin, decreased expression of the vascular connectivity effector molecules connexin, claudin-1 and E-cadherin and increased expression of JAM-A and N-cadherin, as well as decreased expression of the ZO-1 signaling pathways ZO-1, Rock, rhoGEF, cingulin and MLC-2. In a screening of 24 Sel present in mice, SelO showed the most pronounced changes in vascular tissues, and a possible association between SelO and vascular intercellular junction effectors was determined using IBM SPSS Statistics 25. Silencing of SelO, vascular endothelial intercellular junction adverse effects present. The regulatory relationship between SelO and vascular endothelial intercellular junctions was determined. The results showed that Se deficiency lead to increased vascular endothelial permeability and vascular tissue damage by decreasing SelO expression, suggesting a possible role for SelO in regulating vascular endothelial permeability.

Injured sensory neurons-derived galectin-3 contributes to neuropathic pain via programming microglia in the spinal dorsal horn.

Emerging studies have demonstrated spinal microglia play a critical role in central sensitization and contribute to chronic pain. Although several mediators that contribute to microglia activation have been identified, the mechanism of microglia activation and its functionally diversified mechanisms in pathological pain are still unclear. Here we report that injured sensory neurons-derived Galectin-3 (Gal3) activates and reprograms microglia in the spinal dorsal horn (SDH) and contributes to neuropathic pain. Firstly, Gal3 is predominantly expressed in the isolectin B4 (IB4)-positive non-peptidergic sensory neurons and significantly up-regulated in dorsal root ganglion (DRG) neurons and primary afferent terminals in SDH in the partial sciatic nerve ligation (pSNL)-induced neuropathic pain model. Gal3 knockout (Gal3 KO) mice showed a significant decrease in mechanical allodynia and Gal3 inhibitor TD-139 produced a significant anti-allodynia effect in the pSNL model. Furthermore, pSNL-induced microgliosis was compromised in Gal3 KO mice. Additionally, intrathecal injection of Gal3 produces remarkable mechanical allodynia by direct activation of microglia, which have enhanced inflammatory responses with TNF-α and IL-1ß up-regulation. Thirdly, using single-nuclear RNA sequencing (snRNA-seq), we identified that Gal3 targets microglia and induces reprogramming of microglia, which may contribute to neuropathic pain establishment. Finally, Gal3 enhances excitatory synaptic transmission in excitatory neurons in the SDH via microglia activation. Our findings reveal that injured sensory neurons-derived Gal3 programs microglia in the SDH and contribute to neuropathic pain.

Association between sarcopenia and osteoarthritis among the US adults: a cross-sectional study.

The association between sarcopenia and OA still presents many uncertainties. We aimed to assess whether sarcopenia is associated with occurrence of OA in US adults. We conducted a cross-sectional study consisting of 11,456 participants from National Health and Nutrition Examination Survey 1999-2006. Sarcopenia was defined by a low muscle mass. The skeletal muscle index (SMI) was calculated as the appendicular skeletal muscle mass divided by body mass indexes (BMI) or body weight. OA status was assessed by using self-reported questionnaire. We evaluated the association between sarcopenia and OA using multivariate regression models. In addition, subgroup and interaction analysis were performed. Sarcopenia was associated with OA when it was defined by the BMI-adjusted SMI (OR = 1.23 [95% CI, 1.01, 1.51]; P = 0.038) and defined by the weight-adjusted SMI (OR = 1.30 [95% CI, 1.10, 1.55]; P = 0.003). Subgroup and interaction analysis found that the strongest positive association mainly exists in smoker (OR = 1.54 [95% CI, 1.21, 1.95], Pint = 0.006), and this association is not significant in other groups. In conclusion, we found that sarcopenia was associated with occurrence of OA. Subgroup analysis revealed that the association between sarcopenia and OA was more pronounced in smoker. Further well-designed prospective cohort studies are needed to assess our results.

GO-PEG Represses the Progression of Liver Inflammation via Regulating the M1/M2 Polarization of Kupffer Cells.

As a highly promising nanomaterial, exploring the impact of the liver, a vital organ, stands out as a crucial focus in the examination of its biological effects. Kupffer cells (KCs) are one of the first immune cells to contact with exotic-substances in liver. Therefore, this study investigates the immunomodulatory effects and mechanisms of polyethylene glycol-modified graphene oxide (GO-PEG) on KCs. Initial RNA-seq and KEGG pathway analyses reveal the inhibition of the TOLL-like receptor, TNF-α and NOD-like receptor pathways in continually stimulated KCs exposed to GO-PEG. Subsequent biological experiments validate that a 48-hour exposure to GO-PEG alleviates LPS-induced KCs immune activation, characterized by a shift in polarization from M1 to M2. The underlying mechanism involves the absorption of double-stranded RNA/single-stranded RNA, inhibiting the activation of TLR3 and TLR7 in KCs. Employing a Kupffer/AML12 cell co-culture model and animal studies, it is observed that GO-PEG indirectly inhibit oxidative stress, mitochondrial dysfunction, and apoptosis in AML12 cells, partially mitigating systemic inflammation and preserving liver tissue/function. This effect is attributed to the paracrine interaction between KCs and hepatocytes. These findings suggest a meaningful and effective strategy for treating liver inflammation, particularly when combined with anti-inflammatory drugs.

Polyethylene microplastics induced inflammation via the miR-21/IRAK4/NF-κB axis resulting to endoplasmic reticulum stress and apoptosis in muscle of carp.

As a widespread environmental pollutant, microplastics pose a great threat to the tissues and organs of aquatic animals. The carp's muscles are necessary for movement and survival. However, the mechanism of injury of polyethylene microplastics (PE-MPs) to carp muscle remains unclear. Therefore, in this study, PE-MPs with the diameter of 8 µm and the concentration of 1000 ng/L were used to feed carp for 21 days, and polyethylene microplastic treatment groups was established. The results showed that PE-MPs could cause structural abnormalities and disarrangement of muscle fibers, and aggravate oxidative stress in muscles. Exposure to PE-MPs reduced microRNA (miR-21) in muscle tissue, negatively regulated Interleukin-1 Receptor Associated Kinase 4 (IRAK4), activated Nuclear Factor Kappa-B (NF-κB) pathway, induced inflammation, and led to endoplasmic reticulum stress and apoptosis. The present study provides different targets for the prevention of muscle injury induced by polyethylene microplastics.

Nano-Bio Interactions: Biofilm-Targeted Antibacterial Nanomaterials.

Biofilm is a spatially organized community formed by the accumulation of both microorganisms and their secretions, leading to persistent and chronic infections because of high resistance toward conventional antibiotics. In view of the tunable physicochemical properties and the related unique biological behavior (e.g., size-, shape-, and surface charge-dependent penetration, protein corona endowed targeting, catalytic- and electronic-related oxidative stress, optical- and magnetic-associated hyperthermia, etc.), nanomaterials-based therapeutics are widely used for the treatment of biofilm-associated infections. In this review, the biological characteristics of biofilm are introduced. And the nanomaterials-based antibacterial strategies are further discussed via biofilm targeting, including preventing biofilm formation, enhancing biofilm penetration, disrupting the mature biofilm, and acting as drug delivery systems. In which, the interactions between biofilm and nanomaterials include mechanical disruption, electron transfer, enzymatic degradation, oxidative stress, and hyperthermia. Additionally, the current advances of nanomaterials for antibacterial nanomaterials by biofilm targeting are summarized. This review aims to present a complete vision of antibacterial nanomaterials-biofilm (nano-bio) interactions, paving the way for the future development and clinical translation of effective antibacterial nanomedicines.

Effect of Baduanjin exercise on executive function in older adults with cognitive frailty: A randomized controlled trial.

OBJECTIVE: To investigate the effectiveness of Baduanjin exercise on executive function in community-dwelling older adults with cognitive frailty. DESIGN: Randomized controlled trial. SETTING: Community residential centers. SUBJECTS: 120 eligible older adults. INTERVENTIONS: Baduanjin training group received supervised Baduanjin training, 60 min sessions three times per week for 24 weeks. The control group did not receive any exercise intervention. MAIN MEASURES: Primary outcome was executive function, assessed using Clock Drawing Test. Secondary outcomes included the subcomponents of executive function (working memory, inhibitory control and cognitive flexibility), attention and cognitive frailty (global cognitive function, physical frailty) assessed using Verbal Fluency Test, Trail Making Test-A/B, Stroop Test, Montreal Cognitive Assessment and Edmonton Frailty Scale, respectively, at baseline and 24 weeks after intervention. RESULTS: After the 24-week intervention, the scores of Clock Drawing Test and Verbal Fluency Test, the Trail Making Test-B time and the Card correct numbers of Stroop Test in Baduanjin training group showed significant improvement compared with control group (all P < 0.05) with small to moderate effect sizes and the significant interaction effect of group by time in the Clock Drawing Test and Trail Making Test-B test (P = 0.003 and P = 0.043); cognitive frailty variables, including Montreal Cognitive Assessment and Edmonton Frail Scale scores, also showed significant improvement (P = 0.002 and P = 0.004) with a moderate effect sizes and a significant interaction effect (P < 0.001, P = 0.013). No adverse events were reported. CONCLUSION: Regular Baduanjin training may be an effective and safe intervention to improve cognitive frailty and executive function in community-dwelling older adults with cognitive frailty. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR2100050857. Data of registration: 8/5/2020, https://www.chictr.org.cn/showproj.html?proj = 133037.

Upper tract urothelial carcinoma accompanied by hyperthermia: A case report.

Upper tract urothelial carcinoma (UTUC) is a relatively rare malignant neoplasm of the urinary system. Due to its highly aggressiveness, the tumor has already undergone invasive growth when most UTUC patients are diagnosed. In addition, the most common cause of fever in cancer patients is infection, and cancer patients with neoplastic fever are relatively rare. We reported a 58-year-old man with invasive high-grade UTUC accompanied by hyperthermia.

'Boomerang' moves and young adults' mental well-being in the United Kingdom.

BACKGROUND: In the UK and many other contemporary Western populations, attaining and maintaining residential independence is an important marker of a young person's successful transition to adulthood. However, employment precarity, partnership breakdown, and difficulties in affording housing may mean that some young adults are unable to maintain residential independence and 'boomerang' back to co-reside with their parents. Although a growing body of literature has explored how such counter-transitions affect parents' mental well-being, little is known about effects on the mental health of the young returnees and whether any such effects vary by gender or socio-economic characteristics. DATA AND METHODS: We use data from 11 waves (2009-2020) of the UK Household Longitudinal Study (UKHLS) and focus on young adults aged 21-35 (N = 9714). We estimate fixed-effects models to analyse the effect of returning to the parental home on changes in young adults' mental well-being measured using scores on the General Health Questionnaire (GHQ) and the Mental Component Summary (MCS) score of the Short Form Health Survey (SF-12). RESULTS: Over the period of observation, 15% of young adults made one or more moves back to the parental home. The fixed-effects analysis showed that returning to the parental home was associated with a reduction (improvement) in GHQ score, although effects were small and did not vary by gender, employment status, partnership status, or presence of a co-resident biological child. No associations were found with changes in MCS score. CONCLUSION: Although cross-sectional results from the UK have shown that the mental health of young adults living with parents is worse than that of young adults living independently, we found no evidence that returning to the parental home was associated with a deterioration in young adults' mental health. On the contrary, returns home were associated with a slight reduction in depressive symptoms suggesting that the benefits of parental support may outweigh possible negative impacts of inability to maintain residential independence. Further research in other settings is needed to assess the extent to which these findings reflect the UK context.

Upregulation of Hsp27 via further inhibition of histone H2A ubiquitination confers protection against myocardial ischemia/reperfusion injury by promoting glycolysis and enhancing mitochondrial function.

Research suggests that ischemic glycolysis improves myocardial tolerance to anoxia and low-flow ischemia. The rate of glycolysis during ischemia reflects the severity of the injury caused by ischemia and subsequent functional recovery following reperfusion. Histone H2AK119 ubiquitination (H2Aub) is a common modification that is primarily associated with gene silencing. Recent studies have demonstrated that H2Aub contributes to the development of cardiovascular diseases. However, the underlying mechanism remains unclear. This study identified Hsp27 (heat shock protein 27) as a H2Aub binding protein and explored its involvement in mediating glycolysis and mitochondrial function. Functional studies revealed that inhibition of PRC1 (polycomb repressive complex 1) decreased H2Aub occupancy and promoted Hsp27 expression through inhibiting ubiquitination. Additionally, it increased glycolysis by activating the NF-κB/PFKFB3 signaling pathway during myocardial ischemia. Furthermore, Hsp27 reduced mitochondrial ROS production by chaperoning COQ9, and suppressed ferroptosis during reperfusion. A delivery system was developed based on PCL-PEG-MAL (PPM)-PCM-SH (CWLSEAGPVVTVRALRGTGSW) to deliver PRT4165 (PRT), a potent inhibitor of PRC1, to damaged myocardium, resulting in decreased H2Aub. These findings revealed a novel epigenetic mechanism connecting glycolysis and ferroptosis in protecting the myocardium against ischemia/reperfusion injury.