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Abstract We revisit the masses of heavy quarkonium double-gluon hybrid mesons with exotic quantum numbers J PC = 1−+ and 2+− in the framework of the QCD sum rules. Considering the double-gluon hybrid meson operators in the octet-octet color structure, we have constructed two independent interpolating currents with J PC = 1−+ and five independent currents with J PC = 2+−. For the interpolating currents with antisymmetric glueball operator, there exist non-local divergences in one kind of additional Feynman diagrams of the tri-gluon condensate, which will give important contributions to the sum rule stabilities and mass predictions. We use the diagrammatic renormalization to cancel out such divergences. At the leading order of α s , the two-point correlation functions and spectral densities can be expressed in the analytic form of the generalized hypergeometric functions and Meijer’s G-functions. After performing the numerical analysis, we predict the masses of the 1−+ and 2+− charmonium double-gluon hybrid mesons to be around 6.1 − 7.2 GeV and 6.3 − 6.4 GeV, respectively. For the bottomonium systems, their masses are predicted to be 13.7 − 14.3 GeV and 12.6 − 13.3 GeV for the 1−+ and 2+− channels, respectively. Besides, it is possible to hunt for these charmonium hybrids in the radiative decays of bottomonium mesons in BelleII experiment. Further investigations on these hybrid states in various theoretical and phenomenological methods are also anticipated in the future.

Background: Schizophrenia (SCZ) is a prevalent and serious mental disorder, and the exact pathophysiology of this condition is not fully understood. In previous studies, it has been proven that ferroprotein levels are high in SCZ. It has also been shown that this inflammatory response may modify fibromodulin. Accumulating evidence indicates a strong link between metabolism and ferroptosis. Therefore, the present study aims to identify ferroptosis‐linked hub genes to further investigate the role that ferroptosis plays in the development of SCZ. Material and methods: From the GEO database, four microarray data sets on SCZ (GSE53987, GSE38481, GSE18312, and GSE38484) and ferroptosis‐linked genes were extracted. Using the prefrontal cortex expression matrix of SCZ patients and healthy individuals as the control group from GSE53987, weighted gene co‐expression network analysis (WGCNA) was performed to discover SCZ‐linked module genes. From the feed, genes associated with ferroptosis were retrieved. The intersection of the module and ferroptosis-linked genes was done to obtain the hub genes. Then, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and Gene Set Enrichment Analysis (GSEA) were conducted. The SCZ diagnostic model was established using logistic regression, and the GSE38481, GSE18312, and GSE38484 data sets were used to validate the model. Finally, hub genes linked to immune infiltration were examined. Results: A total of 13 SCZ module genes and 7 hub genes linked to ferroptosis were obtained: DECR1, GJA1, EFN2L2, PSAT1, SLC7A11, SOX2, and YAP1. The GO/KEGG/GSEA study indicated that these hub genes were predominantly enriched in mitochondria and lipid metabolism, oxidative stress, immunological inflammation, ferroptosis, Hippo signaling pathway, AMP‐activated protein kinase pathway, and other associated biological processes. The diagnostic model created using these hub genes was further confirmed using the data sets of three blood samples from patients with SCZ. The immune infiltration data showed that immune cell dysfunction enhanced ferroptosis and triggered SCZ. Conclusion: In this study, seven critical genes that are strongly associated with ferroptosis in patients with SCZ were discovered, a valid clinical diagnostic model was built, and a novel therapeutic target for the treatment of SCZ was identified by the investigation of immune infiltration.

BackgroundMitochondrial dysfunction is an important factor in the pathogenesis of schizophrenia. However, the relationship between mitophagy and schizophrenia remains to be elucidated.MethodsSingle-cell RNA sequencing datasets of peripheral blood and brain organoids from SCZ patients and healthy controls were retrieved. Mitophagy-related genes that were differentially expressed between the two groups were screened. The diagnostic model based on key mitophagy genes was constructed using two machine learning methods, and the relationship between mitophagy and immune cells was analyzed. Single-cell RNA sequencing data of brain organoids was used to calculate the mitophagy score (Mitoscore).ResultsWe found 7 key mitophagy genes to construct a diagnostic model. The mitophagy genes were related to the infiltration of neutrophils, activated dendritic cells, resting NK cells, regulatory T cells, resting memory T cells, and CD8 T cells. In addition, we identified 12 cell clusters based on the Mitoscore, and the most abundant neurons were further divided into three subgroups. Results at the single-cell level showed that Mitohigh_Neuron established a novel interaction with endothelial cells via SPP1 signaling pathway, suggesting their distinct roles in SCZ pathogenesis.ConclusionWe identified a mitophagy signature for schizophrenia that provides new insights into disease pathogenesis and new possibilities for its diagnosis and treatment.

Abstract Background Melancholic depression (MD) is one of the most prevalent and severe subtypes of major depressive disorder (MDD). Previous studies have revealed inconsistent results regarding alterations in grey matter volume (GMV) of the hippocampus and amygdala of MD patients, possibly due to overlooking the complexity of their internal structure. The hippocampus and amygdala consist of multiple and functionally distinct subregions, and these subregions may play different roles in MD. This study aims to investigate the volumetric alterations of each subregion of the hippocampus and amygdala in patients with MD and non-melancholic depression (NMD). Methods A total of 146 drug-naïve, first-episode MDD patients (72 with MD and 74 with NMD) and 81 gender-, age-, and education-matched healthy controls (HCs) were included in the study. All participants underwent magnetic resonance imaging (MRI) scans. The subregional segmentation of hippocampus and amygdala was performed using the FreeSurfer 6.0 software. The multivariate analysis of covariance (MANCOVA) was used to detect GMV differences of the hippocampal and amygdala subregions between three groups. Partial correlation analysis was conducted to explore the relationship between hippocampus or amygdala subfields and clinical characteristics in the MD group. Age, gender, years of education and intracranial volume (ICV) were included as covariates in both MANCOVA and partial correlation analyses. Results Patients with MD exhibited a significantly lower GMV of the right hippocampal tail compared to HCs, which was uncorrelated with clinical characteristics of MD. No significant differences were observed among the three groups in overall and subregional GMV of amygdala. Conclusions Our findings suggest that specific hippocampal subregions in MD patients are more susceptible to volumetric alterations than the entire hippocampus. The reduced right hippocampal tail may underlie the unique neuropathology of MD. Future longitudinal studies are required to better investigate the associations between reduced right hippocampal tail and the onset and progression of MD.

Abstract We have studied the strong decay properties of the recently observed $$T^a_{c{\bar{s}0}}(2900)^{++/0}$$ T c s ¯ 0 a ( 2900 ) + + / 0 by considering it as a $$cu{\bar{d}}{\bar{s}}/cd{\bar{u}}{\bar{s}}$$ c u d ¯ s ¯ / c d u ¯ s ¯ fully open-flavor tetraquark state with $$I(J^P)=1(0^+)$$ I ( J P ) = 1 ( 0 + ) . In the framework of QCD sum rules, we have calculated the three-point correlation functions of the two-body strong decay processes $$T^a_{c\bar{s}0}(2900)^{++}\rightarrow D_s^+\pi ^+$$ T c s ¯ 0 a ( 2900 ) + + → D s + π + , $$D^+K^+, D_s^{*+}\rho ^+$$ D + K + , D s ∗ + ρ + and $$D_{s1}^+\pi ^+$$ D s 1 + π + . The full width of $$T^a_{c{\bar{s}0}}(2900)^{++/0}$$ T c s ¯ 0 a ( 2900 ) + + / 0 is obtained as $$161.7\pm 94.8$$ 161.7 ± 94.8 MeV, which is consistent with the experimental observation. We predict the relative branching ratios as $$\Gamma (T\rightarrow D_s\pi ): \Gamma (T\rightarrow DK):\Gamma (T\rightarrow D_s^{*} \rho ):\Gamma (T\rightarrow D_{s1}\pi )\approx 1.00:1.10:0.04:0.43$$ Γ ( T → D s π ) : Γ ( T → D K ) : Γ ( T → D s ∗ ρ ) : Γ ( T → D s 1 π ) ≈ 1.00 : 1.10 : 0.04 : 0.43 , implying that the main decay modes of $$T^a_{c{\bar{s}0}}(2900)^{++/0}$$ T c s ¯ 0 a ( 2900 ) + + / 0 state are $$D_s\pi $$ D s π and DK channels in our calculations. However, the P-wave decay mode $$D_{s1}\pi $$ D s 1 π is also comparable and important by including the uncertainties. To further identify the nature of $$T^a_{c\bar{s}0}(2900)^{++/0}$$ T c s ¯ 0 a ( 2900 ) + + / 0 , we suggest confirming them in the DK and $$D_{s}\pi $$ D s π final states, and measuring the above ratios in future experiments.

Abstract Background Diabetes was commonly seen in chronic total occlusion (CTO) patients but data regarding the impact of successful percutaneous coronary intervention (PCI) on clinical outcome of CTO patients with diabetes was controversial. And importantly, no studies have compared quality of life (QOL) after CTO-PCI in patients with and without diabetes. Methods Consecutive patients undergoing elective CTO-PCI were prospectively enrolled from Apr. 2018 to May 2021. Patients were subdivided into 2 groups: Diabetes and No Diabetes. Detailed baseline characteristics, assessment of symptoms and QOL, angiographic and procedural details, in-hospital complications, and 1 month and 1 year follow-up data were collected. These data were analyzed accordingly for risk predictors of clinical outcome in patients who have diabetes and received successful CTO-PCI. Results A total of 1076 patients underwent CTO-PCI attempts. Diabetes was present in 374 (34.76%) patients, who had more hypertension, previous PCI and stroke. Regarding the coronary lesions, diabetic patients suffered more LCX lesion, multivessel disease, number of lesions per patient, blunt stump, calcification and higher J-CTO score (p 0.05). Number of lesions per patient was an independent risk factor of MACE and all-cause mortality (p 0.05). Conclusions Successful CTO-PCI could represent an effective strategy improving clinical outcome, symptoms and QOL in CTO patients with diabetes.

As the essential amino acids, branched-chain amino acid (BCAA) from diets is indispensable for health. BCAA supplementation is often recommended for patients with consumptive diseases or healthy people who exercise regularly. Latest studies and ours reported that elevated BCAA level was positively correlated with metabolic syndrome, diabetes, thrombosis and heart failure. However, the adverse effect of BCAA in atherosclerosis (AS) and its underlying mechanism remain unknown. Here, we found elevated plasma BCAA level was an independent risk factor for CHD patients by a human cohort study. By employing the HCD-fed ApoE−/− mice of AS model, ingestion of BCAA significantly increased plaque volume, instability and inflammation in AS. Elevated BCAA due to high dietary BCAA intake or BCAA catabolic defects promoted AS progression. Furthermore, BCAA catabolic defects were found in the monocytes of patients with CHD and abdominal macrophages in AS mice. Improvement of BCAA catabolism in macrophages alleviated AS burden in mice. The protein screening assay revealed HMGB1 as a potential molecular target of BCAA in activating proinflammatory macrophages. Excessive BCAA induced the formation and secretion of disulfide HMGB1 as well as subsequent inflammatory cascade of macrophages in a mitochondrial-nuclear H2O2 dependent manner. Scavenging nuclear H2O2 by overexpression of nucleus-targeting catalase (nCAT) effectively inhibited BCAA-induced inflammation in macrophages. All of the results above illustrate that elevated BCAA promotes AS progression by inducing redox-regulated HMGB1 translocation and further proinflammatory macrophage activation. Our findings provide novel insights into the role of animo acids as the daily dietary nutrients in AS development, and also suggest that restricting excessive dietary BCAA consuming and promoting BCAA catabolism may serve as promising strategies to alleviate and prevent AS and its subsequent CHD.

Background Data regarding the impact of successful chronic total occlusion treated with percutaneous coronary intervention (CTO‐PCI) on symptoms and quality of life (QOL) in elderly patients (≥75 years) are unknown. This prospective study aimed to assess whether successful CTO‐PCI could improve the symptoms and QOL in elderly patients (≥75 years). Methods and Results Consecutive patients who underwent elective CTO‐PCI were prospectively enrolled and subdivided into 3 groups based on age: age

BackgroundA low estimated glomerular filtration rate (eGFR eGFR ≥ 60 mL/min/1.73 m2 (n = 482), 60 > eGFR ≥ 30 mL/min/1.73 m2 (n = 161), and eGFR 0.05).ConclusionSuccessful PCI effectively improved symptoms and QOL of CTO patients with low eGFR.

Abstract Background Contrast-induced nephropathy (CIN) is one of major and serious complications in patients undergoing percutaneous coronary intervention (PCI). It is unknown whether increased urinary adiponectin (UAPN), a sensitive marker for early renal function impairment, is associated with an increased risk of CIN. Therefore, we prospectively investigate the association of UAPN with CIN. Methods We prospectively enrolled 208 patients who were undergoing elective PCI. The baseline UAPN was assessed prior to PCI. The ROC analysis was used to evaluate the predictive value of UAPN for CIN. Multivariate logistic regression analysis was performed to analyze the independent risk factors for CIN. Results Of 208 patients, CIN occurred in 19 patients (9.13%), and 6 of them (2.88%) required dialysis. Patients with CIN had a higher UAPN level than those without CIN (17.15 ± 12.36 vs. 10.29 ± 3.04 ng/ml, P 124 μmol/L (OR, 4.210; 95% CI, 1.297–13.669; P

Abstract Background Biochemical marker has revolutionized the approach to the diagnosis of heart failure. However, it remains difficult to assess stability of the patient. As such, novel means of stratifying disease severity are needed. C1q/TNF-Related Protein 3 (CTRP3) and C1q/TNF-Related Protein 9 (CTRP9) are novel adipokines that contribute to energy homeostasis with additional anti-inflammatory and anti-ischemic properties. The aim of our study is to evaluate concentrations of CTRP3 and CTRP9 in patients with HFrEF (heart failure with reduced ejection fraction) and whether associated with mortality. Methods Clinical data and plasma were obtained from 176 healthy controls and 168 patients with HFrEF. CTRP3 and CTRP9 levels were evaluated by enzyme-linked immunosorbent assay. Results Both CTRP3 and CTRP9 concentrations were significantly decreased in the HFrEF group compared to the control group (p

Nϵ-carboxymethyl-lysine (CML), an advanced glycation end product, is involved in vascular calcification (VC) in diabetic atherosclerosis. This study aimed to investigate the effects of CML on VC in diabetic atherosclerosis induced by vascular smooth muscle cell (VSMC)–derived foam cells. Human studies, animal studies and cell studies were performed. The human study results from 100 patients revealed a poor blood glucose and lipid status and more severe coronary lesions and stenosis in patients with coronary artery disease and diabetes mellitus. Intraperitoneal injection of streptozotocin combined with a high-fat diet was used to build a diabetic atherosclerosis model in ApoE−/− mice. The animal study results indicated that CML accelerated VC progression in diabetic atherosclerosis by accelerating the accumulation of VSMC-derived foam cells in ApoE−/− mice. The cell study results illustrated that CML induced VSMC-derived foam cells apoptosis and aggravated foam cells calcification. Consistent with this finding, calcium content and the expression levels of alkaline phosphatase, bone morphogenetic protein 2 and runt-related transcription factor 2 were significantly elevated in A7r5 cells treated with oxidation-low-density lipoprotein and CML. Thus, we concluded that CML promoted VSMC-derived foam cells calcification to aggravate VC in diabetic atherosclerosis, providing evidence for the contribution of foam cells to diabetic VC.

Adipose-derived stem cells (ADSCs) have the ability to migrate to injury sites and facilitate tissue repair by promoting angiogenesis. However, the therapeutic effect of ADSCs from patients with diabetes is impaired due to oxidative stress. Given that diabetes is a group of metabolic disorders and mitochondria are a major source of reactive oxygen species (ROS), it is possible that mitochondrial ROS plays an important role in the induction of diabetic ADSC (dADSC) dysfunction. ADSCs isolated from diabetic mice were treated with mitoTEMPO, a mitochondrial ROS scavenger, or TEMPO, a universal ROS scavenger, for three passages. The results showed that pretreatment with mitoTEMPO increased the proliferation, multidifferentiation potential, and the migration and proangiogenic capacities of dADSCs to levels similar to those of ADSCs from control mice, whereas pretreatment with TEMPO showed only minor effects. Mechanistically, mitoTEMPO pretreatment enhanced the mitochondrial antioxidant capacity of dADSCs, and knockdown of superoxide dismutase reduced the restored mitochondrial antioxidant capacity and attenuated the proangiogenic effects induced by mitoTEMPO pretreatment. In addition, mitoTEMPO pretreatment improved the survival of dADSCs in diabetic mice with critical limb ischemia, showing protective effects similar to those of control ADSCs. Pretreatment of dADSCs with mitoTEMPO decreased limb injury and improved angiogenesis in diabetic mice with critical limb ischemia. These findings suggested that short-term pretreatment of dADSCs with a mitochondrial ROS scavenger restored their normal functions, which may be an effective strategy for improving the therapeutic effects of ADSC-based therapies in patients with diabetes.

Recent studies show branched-chain amino acid (BCAA) catabolic pathway is defective in obese animals and humans, contributing to the pathogenesis of insulin resistance and diabetes. However, in the context of obesity, various processes including the dysfunctional lipid metabolism can affect insulin sensitivity and glycemic regulation. It remains unclear how BCAA catabolic defect may exert direct impacts on glucose metabolism without the disturbance of obesity. The current study characterized the glucose metabolism in lean mice in which the genetic deletion of PP2Cm leads to moderate BCAA catabolic defect. Interestingly, compared to the wildtype control, lean PP2Cm deficient mice showed enhanced insulin sensitivity and glucose tolerance, lower body weight, and the preference for carbohydrate over lipids utilization. Metabolomics profiling of plasma and tissues revealed significantly different metabolic patterns in the PP2Cm deficient mice, featured by the marked alterations in glucose metabolic processes, including gluconeogenesis/glycolysis, glycogen metabolism, and tricarboxylic acid cycle. The metabolic changes of glucose were predominantly observed in liver but not skeletal muscle or white adipose tissue. The elevated branched-chain keto acids (BCKAs) resulted from the BCAA catabolic defect may play a critical role in regulating the expression of key regulators of glucose metabolic processes and the activity of respiratory Complex II/succinate dehydrogenase in TCA cycle. Together, these results show BCAA catabolic defect significantly alters glucose metabolism in lean mice with some impacts different or even opposite from those in obese mice, highlighting the critical role of BCAA catabolism in glycemic regulation and the complex interplay between macronutrients in lean and obese animals.

The Western meat-rich diet is both high in protein and fat. Although the hazardous effect of a high fat diet (HFD) upon liver structure and function is well recognized, whether the co-presence of high protein intake contributes to, or protects against, HF-induced hepatic injury remains unclear. Increased intake of branched chain amino acids (BCAA, essential amino acids compromising 20% of total protein intake) reduces body weight. However, elevated circulating BCAA is associated with non-alcoholic fatty liver disease and injury. The mechanisms responsible for this quandary remain unknown; the role of BCAA in HF-induced liver injury is unclear. Utilizing HFD or HFD + BCAA models, we demonstrated BCAA supplementation attenuated HFD-induced weight gain, decreased fat mass, activated mammalian target of rapamycin (mTOR), inhibited hepatic lipogenic enzymes, and reduced hepatic triglyceride content. However, BCAA caused significant hepatic damage in HFD mice, evidenced by exacerbated hepatic oxidative stress, increased hepatic apoptosis, and elevated circulation hepatic enzymes. Compared to solely HFD-fed animals, plasma levels of free fatty acids (FFA) in the HFD + BCAA group are significantly further increased, due largely to AMPKα2-mediated adipocyte lipolysis. Lipolysis inhibition normalized plasma FFA levels, and improved insulin sensitivity. Surprisingly, blocking lipolysis failed to abolish BCAA-induced liver injury. Mechanistically, hepatic mTOR activation by BCAA inhibited lipid-induced hepatic autophagy, increased hepatic apoptosis, blocked hepatic FFA/triglyceride conversion, and increased hepatocyte susceptibility to FFA-mediated lipotoxicity. These data demonstrated that BCAA reduces HFD-induced body weight, at the expense of abnormal lipolysis and hyperlipidemia, causing hepatic lipotoxicity. Furthermore, BCAA directly exacerbate hepatic lipotoxicity by reducing lipogenesis and inhibiting autophagy in the hepatocyte.

Copper/carbon core/shell nanoparticles (CCCSNs) recently have been introduced as an industrial material. In this paper, composites based on high density polyethylene (HDPE), bamboo fiber, CCCSNs, and coupling agent (MAPE) were prepared by melt compounding. The influence of CCCSN content on the resulting composites’ mechanical, biological resistance, and thermal properties was investigated. It was found that CCCSNs within the carbon black matrix were processed well with bamboo fiber-plastic blends through mixing and injection molding. The materials enhanced composite strength and modulus-related properties. Composites with CCCSNs and natural fibers reduced heat capacity and thermal diffusivity. Composites with CCCSN materials also enhanced termite and mold performance. Thus, the material can be used as additive for plastics and other polymers to modify strength properties, biological resistance (e.g., mold and stain), and thermal conductivity properties.

According to the low temperature and high effective bonding problem of microdevices made of degradable polymer PLGA, chemical, plasma, and UV irradiation method are used to study the experimental surface treatment of PLGA films and microdevices bonding process. The results show that all three methods can reduce the surface contact angle of PLGA films, the contact angle increases with time at room temperature, and the PLGA films contact angle is almost unchanged under refrigeration. The PLGA film bonding temperature is significantly reduced after UV irradiation, and the bonding interfaces also generate diffusion cross linking layer are dense and uniform.

HLA-A, -B and -DRB1 allele frequencies and their haplotype frequencies in 21,918 Chinese residents living in Liaoning Province, who were registered as volunteer donors of China Marrow Donor Registry, were investigated. They are composed of 93.37% Han Chinese, 5.1% Manchus, 0.57% Mongols, 0.46% Hui persons, 0.29% Koreans and 0.14% Xibe ethnic group. In total eighteen different HLA-A alleles, forty-eight different HLA-B alleles and fourteen different HLA-DRB1 alleles have been identified. Their frequencies are in agreement with the Hardy-Weinberg equilibrium. For Han Chinese in Liaoning, 1,534 different HLA-A-B-DRB1 haplotypes were identified, with a frequency of higher than 0.01%. A*30-B*13-DRB1*07, A*02-B*46-DRB1*09 and A*02-B*13-DRB1*12 are the most frequent haplotypes among Liaoning Han. While Liaoning Han, Liaoning Manchu, Liaoning Mongol, Liaoning Hui and Liaoning Korean share the northern Han characteristic haplotypes, all minority ethnic groups with the exception of Liaoning Manchu have developed their own unique HLA profiles. This dataset characterizes the HLA allele and haplotype frequencies in the Liaoning area and suggests that it is different from those in other parts of China and ethnic groups, which implicates transplant donor searching strategies and studies on population genetics.

Genome-wide association studies have found that rs17612742 increases the risk of large artery atherosclerotic stroke. The rs17612742 was located in the intron region of Endothelin receptor type A (NRA), which was cellular and gender-heterogeneous. Functional genomics studies of rs17612742 were carried out through some public databases, and it was found that rs17612742 was located in the chromatin open region and promoted the expression of NRA. Compared with the control group, EDNRA expression increased in middle cerebral artery occlusion exposed rodents. However, age heterogeneity of EDNRA expression under physiological and pathological conditions was not observed. In addition, we also discussed how to conduct further empirical studies to provide evidence that rs17612742 confers the risk of large artery atherosclerotic stroke by increasing the expression of NRA. [ABSTRACT FROM AUTHOR]