Biomaterials-mediated radiation-induced diseases treatment and radiation protection.

In recent years, the intersection of the academic and medical domains has increasingly spotlighted the utilization of biomaterials in radioactive disease treatment and radiation protection. Biomaterials, distinguished from conventional molecular pharmaceuticals, offer a suite of advantages in addressing radiological conditions. These include their superior biological activity, chemical stability, exceptional histocompatibility, and targeted delivery capabilities. This review comprehensively delineates the therapeutic mechanisms employed by various biomaterials in treating radiological afflictions impacting the skin, lungs, gastrointestinal tract, and hematopoietic systems. Significantly, these nanomaterials function not only as efficient drug delivery vehicles but also as protective agents against radiation, mitigating its detrimental effects on the human body. Notably, the strategic amalgamation of specific biomaterials with particular pharmacological agents can lead to a synergistic therapeutic outcome, opening new avenues in the treatment of radiation- induced diseases. However, despite their broad potential applications, the biosafety and clinical efficacy of these biomaterials still require in-depth research and investigation. Ultimately, this review aims to not only bridge the current knowledge gaps in the application of biomaterials for radiation-induced diseases but also to inspire future innovations and research directions in this rapidly evolving field.

CXCL10 and IL15 co-expressing chimeric antigen receptor T cells enhance anti-tumor effects in gastric cancer by increasing cytotoxic effector cell accumulation and survival.

Chimeric antigen receptor (CAR) T cells have demonstrated outstanding therapeutic success in hematological malignancies. Yet, their efficacy against solid tumors remains constrained due to inadequate infiltration of cytotoxic T and CAR-T cells in the tumor microenvironment (TME), a factor correlated with poor prognosis in patients with solid tumors. To overcome this limitation, we engineered CAR-T cells to secrete CXCL10 and IL15 (10 × 15 CAR-T), which sustain T cell viability and enhance their recruitment, thereby amplifying the long-term cytotoxic capacity of CAR-T cells in vitro. In a xenograft model employing NUGC4-T21 cells, mice receiving 10 × 15 CAR-T cells showed superior tumor reduction and extended survival rates compared to those treated with second-generation CAR-T cells. Histopathological evaluations indicated a pronounced increase in cytotoxic T cell accumulation in the TME post 10 × 15 CAR-T cell treatment. Therefore, the synergistic secretion of CXCL10 and IL15 in these CAR-T cells enhances T cell recruitment and adaptability within tumor tissues, improving tumor control. This approach may offer a promising strategy for advancing CAR-T therapies in the treatment of solid tumors.

Astrocyte atrophy induced by L-PGDS/PGD2/Src signaling dysfunction in the central amygdala mediates postpartum depression.

BACKGROUND: Postpartum depression (PPD) is a serious psychiatric disorder that has significantly adverse impacts on maternal health. Metabolic abnormalities in the brain are associated with numerous neurological disorders, yet the specific metabolic signaling pathways and brain regions involved in PPD remain unelucidated. METHODS: We performed behavioral test in the virgin and postpartum mice. We used mass spectrometry imaging (MSI) and targeted metabolomics analyses to investigate the metabolic alternation in the brain of GABAAR Delta-subunit-deficient (Gabrd-/-) postpartum mice, a specific preclinical animal model of PPD. Next, we performed mechanism studies including qPCR, Western blot, immunofluorescence staining, electron microscopy and primary astrocyte culture. In the specific knockdown and rescue experiments, we injected the adeno-associated virus into the central amygdala (CeA) of female mice. RESULTS: We identified that prostaglandin D2 (PGD2) downregulation in the CeA was the most outstanding alternation in PPD, and then validated that lipocalin-type prostaglandin D synthase (L-PGDS)/PGD2 downregulation plays a causal role in depressive behaviors derived from PPD in both wild-type and Gabrd-/- mice. Furthermore, we verified that L-PGDS/PGD2 signaling dysfunction-induced astrocytes atrophy is mediated by Src phosphorylation both in vitro and in vivo. LIMITATIONS: L-PGDS/PGD2 signaling dysfunction may be only responsible for the depressive behavior rather than maternal behaviors in the PPD, and it remains to be seen whether this mechanism is applicable to all depression types. CONCLUSION: Our study identified abnormalities in the L-PGDS/PGD2 signaling in the CeA, which inhibited Src phosphorylation and induced astrocyte atrophy, ultimately resulting in the development of PPD in mice.

Photocatalytic toluene oxidation with nickel-mediated cascaded active units over Ni/Bi2WO6 monolayers.

Adsorption and activation of C-H bonds by photocatalysts are crucial for the efficient conversion of C-H bonds to produce high-value chemicals. Nevertheless, the delivery of surface-active oxygen species for C-H bond oxygenation inevitably needs to overcome obstacles due to the separated active centers, which suppresses the catalytic efficiency. Herein, Ni dopants are introduced into a monolayer Bi2WO6 to create cascaded active units consisting of unsaturated W atoms and Bi/O frustrated Lewis pairs. Experimental characterizations and density functional theory calculations reveal that these special sites can establish an efficient and controllable C-H bond oxidation process. The activated oxygen species on unsaturated W are readily transferred to the Bi/O sites for C-H bond oxygenation. The catalyst with a Ni mass fraction of 1.8% exhibits excellent toluene conversion rates and high selectivity towards benzaldehyde. This study presents a fascinating strategy for toluene oxidation through the design of efficient cascaded active units.

Itaconate as a key player in cardiovascular immunometabolism.

Cardiovascular diseases (CVDs) are the leading cause of death globally, resulting in a major health burden. Thus, an urgent need exists for exploring effective therapeutic targets to block progression of CVDs and improve patient prognoses. Immune and inflammatory responses are involved in the development of atherosclerosis, ischemic myocardial damage responses and repair, calcification, and stenosis of the aortic valve. These responses can involve both large and small blood vessels throughout the body, leading to increased blood pressure and end-organ damage. While exploring potential avenues for therapeutic intervention in CVDs, researchers have begun to focus on immune metabolism, where metabolic changes that occur in immune cells in response to exogenous or endogenous stimuli can influence immune cell effector responses and local immune signaling. Itaconate, an intermediate metabolite of the tricarboxylic acid (TCA) cycle, is related to pathophysiological processes, including cellular metabolism, oxidative stress, and inflammatory immune responses. The expression of immune response gene 1 (IRG1) is upregulated in activated macrophages, and this gene encodes an enzyme that catalyzes the production of itaconate from the TCA cycle intermediate, cis-aconitate. Itaconate and its derivatives have exerted cardioprotective effects through immune modulation in various disease models, such as ischemic heart disease, valvular heart disease, vascular disease, heart transplantation, and chemotherapy drug-induced cardiotoxicity, implying their therapeutic potential in CVDs. In this review, we delve into the associated signaling pathways through which itaconate exerts immunomodulatory effects, summarize its specific roles in CVDs, and explore emerging immunological therapeutic strategies for managing CVDs.

Bergenin alleviates proliferative arterial diseases by modulating glucose metabolism in vascular smooth muscle cells.

BACKGROUND: Vascular smooth muscle cell (VSMC) proliferation and phenotypic switching are key mechanisms in the development of proliferative arterial diseases. Notably, reprogramming of the glucose metabolism pattern in VSMCs plays an important role in this process. PURPOSE: The aim of this study is to investigate the therapeutic potential and the mechanism underlying the effect of bergenin, an active compound found in Bergenia, in proliferative arterial diseases. METHODS: The effect of bergenin on proliferative arterial disease was evaluated using platelet-derived growth factor (PDGF)-stimulated VSMCs and a mouse model of carotid artery ligation. VSMC proliferation and phenotypic switching were evaluated in vitro using cell counting kit-8, 5-ethynyl-2-deoxyuridine incorporation, scratch, and transwell assays. Carotid artery neointimal hyperplasia was evaluated in vivo using hematoxylin and eosin staining and immunofluorescence. The expression of proliferation and VSMC contractile phenotype markers was evaluated using PCR and western blotting. RESULTS: Bergenin treatment inhibited PDGF-induced VSMC proliferation and phenotypic switching and reduced neointimal hyperplasia in the carotid artery ligation model. Additionally, bergenin partially reversed the PDGF-induced Warburg-like glucose metabolism pattern in VSMCs. RNA-sequencing data revealed that bergenin treatment significantly upregulated Ndufs2, an essential subunit of mitochondrial complex I. Ndufs2 knockdown attenuated the inhibitory effect of bergenin on PDGF-induced VSMC proliferation and phenotypic switching, and suppressed neointimal hyperplasia in vivo. Conversely, Ndufs2 overexpression enhanced the protective effect of bergenin. Moreover, Ndufs2 knockdown abrogated the effects of bergenin on the regulation of glucose metabolism in VSMCs. CONCLUSION: These findings suggest that bergenin is effective in alleviating proliferative arterial diseases. The reversal of the Warburg-like glucose metabolism pattern in VSMCs during proliferation and phenotypic switching may underlie this therapeutic mechanism.

Multiple signal amplification strategy induced by biomarkers of lung cancer: A self-powered biosensing platform adapted for smartphones.

Lung cancer is a major malignant cancer with low survival rates, and early diagnosis is crucial for effective treatment. Herein, a biosensing platform that is self-powered derived from a capacitor-coupled EBFC has been developed for ultra-sensitive real-time identification of microRNA-21 (miRNA-21) with the assistance of a mobile phone. The flexible substrate of the platform is prepared on a carbon paper modified with graphdiyne and gold nanoparticles. The biosensor employs DNAzyme-mediated dual strand displacement amplification, which enhances the signal output intensity of the EBFC and improves selectivity. The coupling of the capacitor with the EBFC significantly amplifies the sensing signal, causing a 10.6-fold surge in current respond and further improving the sensitivity of the sensing platform. The established detection approach demonstrates a linear relationship varied from 0.0001 to 10,000 pM, with a sensitivity down to 32.3 aM as the minimum detectable limit, which has been effectively utilized for detecting miRNA-21 in practical samples. This sensing system provides strong support for the construction of portable detection devices, and the strategy of the platform construction provides an effective method for ultra-sensitive and accurate detection of miRNA, holding great potential in clinical diagnosis, prognosis evaluation, and drug screening for cancer.

The Accumulation of Phenyllactic Acid Impairs Host Glutamine Metabolism and Inhibits African Swine Fever Virus Replication: A Novel Target for the Development of Anti-ASFV Drugs.

African swine fever (ASF) is a highly contagious and hemorrhagic disease caused by infection with the African swine fever virus (ASFV), resulting in a mortality rate of up to 100%. Currently, there are no effective treatments and commercially available vaccines for ASF. Therefore, it is crucial to identify biochemicals derived from host cells that can impede ASFV replication, with the aim of preventing and controlling ASF. The ASFV is an acellular organism that promotes self-replication by hijacking the metabolic machinery and biochemical resources of host cells. ASFV specifically alters the utilization of glucose and glutamine, which are the primary metabolic sources in mammalian cells. This study aimed to investigate the impact of glucose and glutamine metabolic dynamics on the rate of ASFV replication. Our findings demonstrate that ASFV infection favors using glutamine as a metabolic fuel to facilitate self-replication. ASFV replication can be substantially inhibited by blocking glutamine metabolism. The metabolomics analysis of the host cell after late-stage ASFV infection revealed a significant disruption of normal glutamine metabolic pathways due to the abundant expression of PLA (phenyllactic acid). Pretreatment with PLA also inhibited ASFV proliferation and glutamine consumption following infection. The metabolomic analysis also showed that PLA pretreatment greatly slowed down the metabolism of amino acids and nucleotides that depend on glutamine. The depletion of these building blocks directly hindered the replication of ASFV by decreasing the biosynthetic precursors produced during the replication of ASFV's progeny virus. These findings provide valuable insight into the possibility of pursuing the development of antiviral drugs against ASFV that selectively target metabolic pathways.

Change of physiochemical characteristics, nutritional quality, and volatile compounds of Chenopodium quinoa Willd. during germination.

The impacts of varying germination periods (0-72 h) on morphological properties, proximate composition, amino acid profile, GABA levels, antioxidant attributes, polyphenol content (both free and bound), and volatile compounds of quinoa were evaluated. Germination significantly increased the content of fiber, amino acids, GABA, polyphenols, and in-vitro antioxidant activities in quinoa. The optimal nutritional quality and antioxidant capacity of quinoa were observed during the 36-72 h germination period. We examined the dynamics of 47 phenolic compounds in quinoa during germination and noted a substantial rise in free phenolic acids and bound flavonoids post-germination. A total of 53 and 84 volatile compounds were respectively identified in ungerminated quinoa and germinated quinoa. It was found that the germination period of 24-48 h contributed to reducing the presence of undesirable flavors. TEM analysis revealed significant structural damage to the ultrastructure and relaxation of the cell wall in germinated quinoa grains.

CTRP3 alleviates mitochondrial dysfunction and oxidative stress injury in pathological cardiac hypertrophy by activating UPRmt via the SIRT1/ATF5 axis.

Pathological cardiac hypertrophy is an independent risk factor for heart failure. Disruption of mitochondrial protein homeostasis plays a key role in pathological cardiac hypertrophy; however, the mechanism of maintaining mitochondrial homeostasis in pathological cardiac hypertrophy remains unclear. In this study, we investigated the regulatory mechanisms of mitochondrial protein homeostasis in pathological cardiac hypertrophy. Wildtype (WT) mice, knockout mice, and mice transfected with lentivirus overexpressing mouse C1q-tumor necrosis factor-related protein-3 (CTRP3) underwent transverse aortic constriction or sham surgery. After 4 weeks, cardiac function, mitochondrial function, and oxidative stress injury were examined. For mechanistic studies, neonatal rat cardiomyocytes were treated with small interfering RNA or overexpression plasmids for the relevant genes. CTRP3 overexpression attenuated transverse aortic constriction (TAC) induced pathological cardiac hypertrophy, mitochondrial dysfunction, and oxidative stress injury compared to that in WT mice. TAC or Ang II resulted in compensatory activation of UPRmt, but this was not sufficient to counteract pathologic cardiac hypertrophy. CTRP3 overexpression further induced activation of UPRmt during pathologic cardiac hypertrophy and thereby alleviated pathologic cardiac hypertrophy, whereas CTRP3 knockout or knockdown inhibited UPRmt. ATF5 was a key regulatory molecule of UPRmt, as ATF5 knockout prevented the cardioprotective effect of CTRP3 in TAC mice. In vitro, SIRT1 was identified as a possible downstream CTRP3 effector molecule, and SIRT1 knockout blocked the cardioprotective effects of CTRP3. Our results also suggest that ATF5 may be regulated by SIRT1. Our study demonstrates that CTRP3 activates UPRmt via the SIRT1/ATF5 axis under pathological myocardial hypertrophy, thus attenuating mitochondrial dysfunction and oxidative stress injury.

Rattan Pepper Polysaccharide Regulates DSS-Induced Intestinal Inflammation and Depressive Behavior through Microbiota-Gut-Brain Axis.

Inflammatory bowel disease (IBD) is a chronic and recurrent disease. Increasing evidence suggests a higher incidence of depression in IBD patients compared with the general population, but the underlying mechanism remains uncertain. Rattan pepper polysaccharide (RPP) is an important active ingredient of rattan pepper, yet its effects and mechanisms on intestinal inflammation and depression-like behavior remain largely unknown. This study aims to investigate the ameliorating effect of RPP on dextran sulfate sodium salt (DSS)-induced intestinal inflammation and depression-like behavior as well as to reveal its mechanism. Our results indicate that RPP effectively ameliorated intestinal microbiota imbalance and metabolic disorders of short-chain fatty acids (SCFAs) and bile acids in mice with DSS-induced inflammation, contributing to the recovery of intestinal Th17/Treg homeostasis. Importantly, RPP effectively alleviated brain inflammation caused by intestinal inflammatory factors entering the brain through the blood-brain barrier. This effect may be attributed to the inhibition of the TLR4/NF-κB signaling pathway, which alleviates neuroinflammation, and the activation of the CREB/BDNF signaling pathway, which improves synaptic dysfunction. Therefore, our findings suggest that RPP may play a role in alleviating DSS-induced gut inflammation and depression-like behavior through the microbiota-gut-brain axis.

Progress and application of adipose-derived stem cells in the treatment of diabetes and its complications.

Diabetes mellitus (DM) is a serious chronic metabolic disease that can lead to many serious complications, such as cardiovascular disease, retinopathy, neuropathy, and kidney disease. Once diagnosed with diabetes, patients need to take oral hypoglycemic drugs or use insulin to control blood sugar and slow down the progression of the disease. This has a significant impact on the daily life of patients, requiring constant monitoring of the side effects of medication. It also imposes a heavy financial burden on individuals, their families, and even society as a whole. Adipose-derived stem cells (ADSCs) have recently become an emerging therapeutic modality for DM and its complications. ADSCs can improve insulin sensitivity and enhance insulin secretion through various pathways, thereby alleviating diabetes and its complications. Additionally, ADSCs can promote tissue regeneration, inhibit inflammatory reactions, and reduce tissue damage and cell apoptosis. The potential mechanisms of ADSC therapy for DM and its complications are numerous, and its extensive regenerative and differentiation ability, as well as its role in regulating the immune system and metabolic function, make it a powerful tool in the treatment of DM. Although this technology is still in the early stages, many studies have already proven its safety and effectiveness, providing new treatment options for patients with DM or its complications. Although based on current research, ADSCs have achieved some results in animal experiments and clinical trials for the treatment of DM, further clinical trials are still needed before they can be applied in a clinical setting.

Electrochromic Smart Window Based on Transition-Metal Phthalocyanine Derivatives.

Phthalocyanines have been widely investigated as electrochromic materials because of their large conjugated structure. However, they have shown limited applicability due to their complex electrochromism mechanism and low solubility in common organic solvents. Replacement of central metal ions in phthalocyanines affects their stability and is responsible for various electrochromic phenomena, such as color change. Herein, the relationship between the electron d-orbital arrangement in the outermost layer of transition metals and the electrochromic stability of phthalocyanine derivatives has been investigated. An enhanced solubility of phthalocyanines in organic solvents was obtained through the introduction of quaternary tert-butyl substitution. Electrochromic devices fabricated with transition-metal phthalocyanine derivatives showed high response speeds and good stability. The fast color-switching feature between blue/green and blue/purple makes it a promising candidate for smart windows and adaptive camouflage applications.

Formulation and application of the "hospital-to-home + online-to-offline" treatment scheme in caring for and supporting vulnerable patients with chronic heart failure.

BACKGROUND: Chronic heart failure (CHF) is the terminal stage of cardiovascular disease. OBJECTIVE: In this study, the "hospital-to-home + online-to-offline" (H2H + O2O) care scheme was implemented for patients with CHF during vulnerable periods, and its effect was evaluated. METHODS: Patients with CHF in the cardiovascular department of a Class III/Grade A hospital in Jiangxi Province from January to December 2020 were selected using a convenience sampling method and randomly divided into a control and intervention group (n= 100 each). The patients in the control group received routine in-hospital treatment and out-of-hospital follow-up, while in the intervention group, a multi-disciplinary cooperation team with CHF specialist nurses evaluated and stratified the patients before discharge and formulated individualized prescriptions and care plans. Based on the "Health & Happiness" chronic disease follow-up application designed for this study, the specialist nurses provided patients with one-to-one guidance. After three months, the cardiac function, heart failure knowledge, self-care behavior, and re-hospitalization rate of the patients were compared between the two groups. Cardiac function was evaluated by the serum B-type natriuretic peptide (BNP), the left ventricular ejection fraction (LVEF), and a six-minute walking test (6MWT). Heart failure knowledge and self-care behavior was assessed using specific questionaries. RESULTS: The level of cardiac function in the intervention group was significantly higher than that in the control group, and the difference was statistically significant (P< 0.001). The mastery of heart failure knowledge and self-care behavior in the intervention group were significantly higher than those in the control group, and the differences were statistically significant (P< 0.05). The re-hospitalization rate due to CHF in the intervention group was 21.0%, which was lower than that in the control group (35.0%), and the difference was statistically significant (P< 0.05). CONCLUSION: The H2H + O2O care scheme can be used for the transition of vulnerable patients with CHF from the hospital to family care to improve the patients' level of cardiac function, elevate their knowledge level and self-care abilities, and improve their overall health outcomes.

The Characteristics of Macrophage Heterogeneity in Atherosclerotic Aortas.

Macrophage is the main effector cell during atherosclerosis. We applied single-cell RNA sequencing (scRNA) data to investigate the role of macrophage subsets in atherosclerosis. Monocyte and macrophage clusters were divided into 6 subclusters. Each subcluster's markers were calculated and validated by immunofluorescence. Elevated macrophage subclusters in the WD group were subject to enrichment pathway analysis and exhibited different phenotypes. Pseudotime analysis shows the subclusters originate from monocytes. We cultured bone marrow-derived macrophages with CSF-1 and ox-LDL to simulate an atherosclerotic-like environment and detected the transformation of subclusters. Macrophage-Vegfa and Macrophage-C1qb increased in the WD group. Macrophage-Vegfa acquires the characteristics of phagocytosis and immune response, while Macrophage-C1qb is not involved in lipid metabolism. The two subclusters are both enriched in cell movement and migration pathways. Experimental verification proved Monocyte-Ly6C evolved into Macrophage-Vegfa and Macrophage-C1qb during atherosclerosis progression.

Multi-Scale Engineered 2D Carbon Polyhedron Array with Enhanced Electrocatalytic Performance.

Electrocatalyst engineering from the atomic to macroscopic level of electrocatalysts is one of the most powerful routes to boost the performance of electrochemical devices. However, multi-scale structure engineering mainly focuses on the range of atomic-to-particle scale such as hierarchical porosity engineering, while catalyst engineering at the macroscopic level, such as the arrangement configuration of nanoparticles, is often overlooked. Here, a 2D carbon polyhedron array with a multi-scale engineered structure via facile chemical etching, ice-templating induced self-assembly, and high-temperature pyrolysis processes is reported. Controlled phytic acid etching of the carbon precursor introduces homogeneous atomic phosphorous and nitrogen doping, as well as a well-defined mesoporous structure. Subsequent ice-templated self-assembly triggers the formation of a 2D particle array superstructure. The atomic-level doping gives rise to high intrinsic activity, while the well-engineered porous structure and particle arrangement addresses the mass transport limitations at the microscopic particle level and macroscopic electrode level. As a result, the as-prepared electrocatalyst delivers outstanding performance toward oxygen reduction reaction in both acidic and alkaline media, which is better than recently reported state-of-the-art metal-free electrocatalysts. Molecular dynamics simulation together with extensive characterizations indicate that the performance enhancement originates from multi-scale structural synergy.

Low-dose exercise protects the heart against established myocardial infarction via IGF-1-upregulated CTRP9 in male mice.

Regular exercise is recommended as an important component of therapy for cardiovascular diseases in clinical practice. However, there are still major challenges in prescribing an optimized exercise regimen to individual patients with established cardiac disease. Here, we tested the effects of different exercise doses on cardiac function in mice with established myocardial infarction (MI). Exercise was introduced to mice with MI after 4 weeks of surgery. Low-dose exercise (15 min/day for 8 weeks) improved mortality and cardiac function by increasing 44.39% of ejection fractions while inhibiting fibrosis by decreasing 37.74% of distant region. Unlike higher doses of exercise, low-dose exercise consecutively upregulated cardiac expression of C1q complement/tumor necrosis factor-associated protein 9 (CTRP9) during exercise (>1.5-fold). Cardiac-specific knockdown of CTRP9 abolished the protective effects of low-dose exercise against established MI, while cardiac-specific overexpression of CTRP9 protected the heart against established MI. Mechanistically, low-dose exercise upregulated the transcription factor nuclear receptor subfamily 2 group F member 2 by increasing circulating insulin-like growth factor 1 (IGF-1), therefore, upregulating cardiac CTRP9 expression. These results suggest that low-dose exercise protects the heart against established MI via IGF-1-upregulated CTRP9 and may contribute to the development of optimized exercise prescriptions for patients with MI.

Improved phyllosphere microbiome composition of tea plant with the application of small peptides in combination with rhamnolipid.

BACKGROUND: Small peptides play a crucial role in plant growth and adaptation to the environment. Exogenous small peptides are often applied together with surfactants as foliar fertilizers, but the impact of small peptides and surfactants on the tea phyllosphere microbiome remains unknown. RESULTS: In this study, we investigated the effects of small peptides and different surfactants on the tea phyllosphere microbiome using 16S and ITS sequencing. Our results showed that the use of small peptides reduced the bacterial diversity of the tea phyllosphere microbiome and increased the fungal diversity, while the use of surfactants influenced the diversity of bacteria and fungi. Furthermore, the addition of rhamnolipid to small peptides significantly improved the tea phyllosphere microbiome community structure, making beneficial microorganisms such as Pseudomonas, Chryseobacterium, Meyerozyma, and Vishniacozyma dominant populations. CONCLUSION: Our study suggests that the combined use of small peptides and surfactants can significantly modify the tea phyllosphere microbiome community structure, particularly for beneficial microorganisms closely related to tea plant health. Thus, this preliminary study offers initial insights that could guide the application of small peptides and surfactants in agricultural production, particularly with respect to their potential for modulating the phyllosphere microbiome community in tea plant management.

Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies.

Epicardial adipose tissue (EAT) is located between the myocardium and visceral pericardium. The unique anatomy and physiology of the EAT determines its great potential in locally influencing adjacent tissues such as the myocardium and coronary arteries. Classified by research methodologies, this study reviews the latest research progress on the role of EAT in cardiovascular diseases (CVDs), particularly in patients with metabolic disorders. Studies based on imaging techniques demonstrated that increased EAT amount in patients with metabolic disorders is associated with higher risk of CVDs and increased mortality. Then, in-depth profiling studies indicate that remodeled EAT may serve as a local mediator of the deleterious effects of cardiometabolic conditions and plays a crucial role in CVDs. Further, in vitro coculture studies provided preliminary evidence that the paracrine effect of remodeled EAT on adjacent cardiomyocytes can promote the occurrence and progression of CVDs. Considering the important role of EAT in CVDs, targeting EAT might be a potential strategy to reduce cardiovascular risks. Several interventions have been proved effective in reducing EAT amount. Our review provides valuable insights of the relationship between EAT, metabolic disorders, and CVDs, as well as an overview of the methodological constructs of EAT-related studies.

Forkhead box O6 (FoxO6) promotes cardiac pathological remodeling and dysfunction by activating Kif15-TGF-ß1 under aggravated afterload.

Pathological cardiac hypertrophy exhibits complex and abnormal gene expression patterns and progresses to heart failure. Forkhead box protein O6 (FoxO6) is a key transcription factor involved in many biological processes. This study aimed to explore the role of FoxO6 in cardiac hypertrophy. Three groups of mice were established: wild-type, FoxO6 knockout, and FoxO6-overexpressing. The mice received daily administration of angiotensin-II (Ang-II) or saline for 4 weeks, after which they were examined for cardiac hypertrophy, fibrosis, and function. Elevated cardiac expression of FoxO6 was observed in Ang-II-treated mice. FoxO6 deficiency attenuated contractile dysfunction and cardiac remodeling, including cardiomyocyte hypertrophy and fibroblast proliferation and differentiation. Conversely, FoxO6 overexpression aggravated the cardiomyopathy and heart dysfunction. Further studies identified kinesin family member 15 (Kif15) as downstream molecule of FoxO6. Kif15 inhibition attenuated the aggravating effect of FoxO6 overexpression. In vitro, FoxO6 overexpression increased Kif15 expression in cardiomyocytes and elevated the concentration of transforming growth factor-ß1 (TGF-ß1) in the medium where fibroblasts were grown, exhibiting increased proliferation and differentiation, while FoxO6 knockdown attenuated this effect. Cardiac-derived FoxO6 promoted pathological cardiac remodeling induced by aggravated afterload largely by activating the Kif15/TGF-ß1 axis. This result further complements the mechanisms of communication among different cells in the heart, providing novel therapeutic targets for heart failure.