Pt Single-Atoms on Structurally-Integrated 3D N-Doped Carbon Tubes Grid for Ampere-Level Current Density Hydrogen Evolution.

To date, the excellent mass-catalytic activities of Pt single-atoms catalysts (Pt-SACs) toward hydrogen evolution reaction (HER) are categorically confirmed; however, their high current density performance remains a challenge for practical applications. Here, a binder-free approach is exemplified to fabricate self-standing superhydrophilic-superaerphobic Pt-SACs cathodes by directly anchoring Pt-SAs via Pt-NxC4-x coordination bonds to the structurally-integrated 3D nitrogen-doped carbon tubes (N-CTs) array grid (denoted as Pt@N-CTs). The 3D Pt@N-CTs cathode with optimal Pt-SACs loading is capable of operating at a high current density of 1000 mA cm-2 with an ultralow overpotential of 157.9 mV with remarkable long-term stability over 11 days at 500 mA cm-2. The 3D super-wettable free-standing Pt@N-CTs possess interconnected vertical and lateral N-CTs with hierarchical-sized open channels, which facilitates the mass transfer. The binder-free immobilization adding to the large surface area and 3D-interconnected open channels endow Pt@N-CTs cathodes with high accessible active sites, electrical conductivity, and structural stability that maximize the utilization efficiency of Pt-SAs to achieve ampere-level current density HER at low overpotentials.

CTRP6 alleviates endometrial fibrosis by regulating Smad3 pathway in intrauterine adhesion†.

Intrauterine adhesion (IUA) is manifestations of endometrial fibrosis and excessive extracellular matrix deposition. C1q/tumor necrosis factor-related protein-6 (CTRP6) is a newly identified adiponectin paralog which has been reported to modulate the fibrosis process of several diseases; however, the endometrial fibrosis function of CTRP6 remains unknown. Our study aimed to assess the role of CTRP6 in endometrial fibrosis and further explore the underlying mechanism. Here, we found that the expression of CTRP6 was downregulated in the endometrial tissues of IUA. In vitro experiments demonstrated the reduced level of CTRP6 in facilitated transforming growth factor-ß1 (TGF-ß1)-induced human endometrial stromal cells (HESCs). In addition, CTRP6 inhibited the expression of α-smooth muscle actin (α-SMA) and collagen I in TGF-ß1-treated HESCs. Mechanistically, CTRP6 activated the AMP-activated protein kinase (AMPK) and protein kinase B (AKT) pathway in HESCs, and AMPK inhibitor (AraA) or PI3K inhibitor (LY294002) pretreatment abolished the protective effect of CTRP6 on TGF-ß1-induced fibrosis. CTRP6 markedly decreased TGF-ß1-induced Smad3 phosphorylation and nuclear translocation, and AMPK or AKT inhibition reversed these effects. Notably, CTRP6-overexpressing treatment alleviated the fibrosis of endometrium in vivo. Therefore, CTRP6 ameliorates endometrial fibrosis, among which AMPK and AKT are essential for the anti-fibrotic effect of CTRP6 via the Smad3 pathway. Taken together, CTRP6 may be a potential therapeutic target for the treatment of intrauterine adhesion.

Aggregation-Induced Emission Phosphorescence Featured Au-Ag Coordination Polymer with a Diphosphine N-Heterocyclic Carbene Ligand for Highly Sensitive Detection of Cr(VI).

Luminescent materials with aggregation-induced emission (AIE) characteristics have been recognized as highly selective and sensitive probes for the detection of toxic metal ions in recent years. In this paper, a Au-Ag cluster-based coordination polymer [Au3Ag3(L)2(CN)6(H2O)2]n [1, L = 1,3-bis((diphenylphosphanyl)methyl)-4,5-dihydro-imidazolylidene] was prepared by in situ generation of the diphosphine N-heterocyclic carbene (PCNHCP)-type ligand L in the presence of the corresponding metal salts. Compound 1 exhibited 530 nm phosphorescence under 380 nm excitation with a QY of 6.30% and a lifetime (τ) of 7.14 µs in the solid state. 1 showed good AIE behavior in the mixture of MeOH/H2O while the best aggregation state (fwater = 90%, QY = 6.79%, τ = 6.70 µs) exhibited selective and sensitive emission quenching toward Cr(VI) ions. Ultralow detection limits of 9.7 ppb (w/w) for Cr2O72- and 17.9 ppb (w/w) for CrO42- were achieved.

Nanocomposites based on nanoceria regulate the immune microenvironment for the treatment of polycystic ovary syndrome.

The immune system is closely associated with the pathogenesis of polycystic ovary syndrome (PCOS). Macrophages are one of the important immune cell types in the ovarian proinflammatory microenvironment, and ameliorate the inflammatory status mainly through M2 phenotype polarization during PCOS. Current therapeutic approaches lack efficacy and immunomodulatory capacity, and a new therapeutic method is needed to prevent inflammation and alleviate PCOS. Here, octahedral nanoceria nanoparticles with powerful antioxidative ability were bonded to the anti-inflammatory drug resveratrol (CeO2@RSV), which demonstrates a crucial strategy that involves anti-inflammatory and antioxidative efficacy, thereby facilitating the proliferation of granulosa cells during PCOS. Notably, our nanoparticles were demonstrated to possess potent therapeutic efficacy via anti-inflammatory activities and effectively alleviated endocrine dysfunction, inflammation and ovarian injury in a dehydroepiandrosterone (DHEA)-induced PCOS mouse model. Collectively, this study revealed the tremendous potential of the newly developed nanoparticles in ameliorating the proinflammatory microenvironment and promoting the function of granulosa cells, representing the first attempt to treat PCOS by using CeO2@RSV nanoparticles and providing new insights in combating clinical PCOS.

Effect of obstructive sleep apnea on semen quality.

BACKGROUND: Obstructive sleep apnea (OSA) has several notable complications such as hypertension and diabetes. Studies have also shown that OSA is associated with erectile dysfunction and reduced androgen levels. However, the effect of OSA on semen quality remains poorly studied. METHODS: Men attending a tertiary reproductive center for semen analysis were tested with a portable sleep breathing monitor. Patients were divided into four groups based on their apnea hypopnea index: none, mild, moderate, and severe obstructive sleep apnea. Differences between groups were assessed using χ2, and associations were tested with multiple regression analysis. RESULTS: We included a total of 175 male subjects with a mean age of 32.2 ± 3.6 years. There were significant differences between groups in progressive sperm motility (%) (43 ± 16, 42 ± 17, 36 ± 18, 29 ± 18, respectively; p = 0.002), total motility (%) (59 ± 19, 59 ± 20, 49 ± 21, 42 ± 20, respectively; p = 0.010), and vitality (%) (80 ± 10, 81 ± 11, 79 ± 8, 72 ± 19, respectively; p = 0.039). Asthenospermia (progressive motility < 35%) was significantly more common in subjects with OSA (χ2 = 5.195, p = 0.023). In multiple regression models, after adjusting for age and body mass index, apnea hypopnea index remained negatively and significantly associated with progressive motility, total motility, and vitality. CONCLUSIONS: OSA is an independent risk factor for sperm motility and vitality, and further investigation is now needed to determine if continuous positive pressure ventilation or other therapies can improve semen quality in these patients.

A Novel Photoluminescent Ag/Cu Cluster Exhibits a Chromic Photoluminescence Response towards Volatile Organic Vapors.

A new Ag/Cu bimetallic cluster [Ag10Cu6(bdppthi)2(C≡CPh)12(EtOH)2](ClO4)4 (1, bdppthi = N,N'-bis(diphenylphosphanylmethyl)-tetrahydroimidazole) exhibited strong phosphorescent (PL) emission at 644 nm upon excitation at 400 nm. Removal of the coordinated EtOH molecules in 1 resulted in derivative 1a, which exhibited significant red-shifted emission at 678 nm. The structure and PL of 1 was restored on exposure to EtOH vapor. Cluster 1a also exhibited a vapor-chromic PL response towards other common organic solvent vapors including acetone, MeOH and MeCN. A PMMA film of 1a was developed as a reusable visible sensor for MeCN.

C1QTNF6 participates in the pathogenesis of PCOS by affecting the inflammatory response of granulosa cells‡.

Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease. It has been reported that chronic low-grade inflammation might participate in its pathogenesis. C1q and TNF related 6 (C1QTNF6) is a newly identified adiponectin paralog associated with inflammation. The aim of the present study was to investigate the role of C1QTNF6 in the development of chronic inflammation in PCOS and the underlying molecular mechanism. After analyzing the expression of C1QTNF6 in the serum and granulosa cells (GCs) of PCOS patients and healthy controls, we verified the roles of C1QTNF6 in inflammation through dehydroepiandrosterone-induced PCOS mouse models and cell models of lipopolysaccharide (LPS)-induced inflammation. The results demonstrated that C1QTNF6 expression in the serum and GCs of patients with PCOS was significantly elevated compared with those of the controls, and similar results were observed in the serum and ovary of PCOS mouse models. In PCOS mice and C1QTNF6-overexpressing PCOS mice, serum levels of pro-inflammatory factors including C-reactive protein (CRP), interleukin 6 (IL6), and tumor necrosis factor-α (TNFα) were increased, while the opposite effects were observed when C1QTNF6 was down-regulated in PCOS mice. Furthermore, C1QTNF6 overexpression up-regulated the levels of TNFα, IL6, and CRP and activated the AKT/NF-κB pathway in LPS-treated KGN cells, whereas C1QTNF6 knockdown and BAY-117082 (an NF-κB inhibitor) treatment resulted in the opposite effects. Taken together, our results indicate that C1QTNF6 is involved in the pathogenesis of PCOS by affecting the inflammatory response via the AKT/NF-κB signaling pathway.

Phenylethyl isothiocyanate induces oxidative damage of porcine kidney cells mediated by reactive oxygen species.

The aim of this study is to confirm the toxic effect of phenylethyl isothiocyanate (PEITC) on porcine kidney cells (PK-15) and explore the effect of oxidative damage mediated by reactive oxygen species (ROS) induced by PEITC in PK-15 cells. Porcine kidney cell line (PK-15) was treated with PEITC (2, 5, and 10 µM) for 24 hours, and the oxidative damage mediated by PEITC through ROS was investigated. The survival rate of PK-15 cells decreased in a dose-dependent manner after the treatment of PEITC in a dose-dependent manner. A high concentration of PEITC (10 µM) can change cell morphology, increase the content of malondialdehyde, ROS, and lactate dehydrogenase, and decrease the activity of SOD, CAT, GSH-PX, and GSH. PEITC has a toxic effect on PK-15 cells by inducing oxidative stress in PK-15 cells through the generation of ROS.

Differential effects of Chinese high-fat dietary habits on lipid metabolism: mechanisms and health implications.

BACKGROUND: The traditional Chinese diet blends lard with vegetable oil, keeping the fatty acid balance intake ratio of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids at nearly 1:1:1. However, the effects of a mixture of lard and vegetable oil on lipid metabolism have never been researched. In the present study, by simulating Chinese high-fat dietary habits, we explored the effects of a mixture of lard and vegetable oil on lipid metabolism. METHODS: We randomly assigned 50 male C57BL/6 J mice to 5 groups (10 in each group) and fed them lard, sunflower oil (SFO), soybean oil (SBO), lard blended with sunflower oil (L-SFO), or lard blended with soybean oil (L-SBO) for 12 weeks. RESULTS: We found that the final body weights of mice in the lard group were significantly higher than those of mice in the SFO and SBO groups. Body fat rate and volume of fat cell of the lard group were significantly higher than those of the SFO, SBO, and L-SBO groups. Liver triglyceride level of the lard group increased significantly compared to the other groups. Although body fat rate and liver triglyceride level in the SBO and SFO groups decreased compared to those in the other groups, the high-density lipoprotein cholesterol/low-density lipoprotein cholesterol ratio were also significantly decreased in the SBO and SFO groups. CONCLUSIONS: We found that a lard diet induced accumulation of body fat, liver and serum lipids, which can increase the risk of obesity, non-alcoholic fatty acid liver disease, and atherosclerosis. The vegetable oil diet resulted in cholesterol metabolism disorders even though it did not lead to obesity. The mixed oil diet induced body fat accumulation, but did not cause lipid accumulation in the liver and serum. Thus, differential oil/fat diets have an impact on differential aspects in mouse lipid metabolism.

Single-Benzene-Based Solvatochromic Chromophores: Color-Tunable and Bright Fluorescence in the Solid and Solution States.

The search for structurally simple chromophores with superior fluorescence brightness and a wide range of solvent compatibility is highly desirable. Herein, a new type of single-benzene-based solvatochromic chromophore with a symmetric bifunctional structure, in which azetidine and ethoxycarbonyl moieties serve as the electron-donating and -withdrawing groups, respectively, is reported. This chromophore exhibits an extraordinary wide range of solvent compatibility and preserves excellent fluorescence quantum yields from nonpolar n-hexane to polar methanol and even in water. Unusually, the symmetric structure of the chromophore shows a distinct color change from bright green to red with increasing solvent polarity and possesses large Stokes shifts (λ=132-207 nm) in the tested solvents. Moreover, this single-benzene-based chromophore displays good photochemical stability in both solution and solid states, and even exhibits reversible mechanochromic luminescence.

General autophagy-dependent and -independent lipophagic processes collaborate to regulate the overall level of lipophagy in yeast.

ABBREVIATION: AP: autophagosome; ATG: autophagy related; CMA: chaperone-mediated autophagy; ESCRT: endosomal sorting complex required for transport; FA: fatty acid; LD: lipid droplet; Ld microdomains: liquid-disordered microdomains; NL: neutral lipid.

MiR-142-3p Regulates ILC1s by Targeting HMGB1 via the NF-κB Pathway in a Mouse Model of Early Pregnancy Loss.

OBJECTIVE: Innate lymphoid cells (ILCs) are a class of newly discovered immunocytes. Group 1 ILCs (ILC1s) are identified in the decidua of humans and mice. High mobility group box 1 (HMGB1) is predicted to be one of the target genes of miR-142-3p, which is closely related to pregnancy-related diseases. Furthermore, miR-142-3p and HMGB1 are involved in regulating the NF-κB signaling pathway. This study aimed to examine the regulatory effect of miR-142-3p on ILC1s and the underlying mechanism involving HMGB1 and the NF-κB signaling pathway. METHODS: Mouse models of normal pregnancy and abortion were constructed, and the alterations of ILC1s, miR-142-3p, ILC1 transcription factor (T-bet), and pro-inflammatory cytokines of ILC1s (TNF-α, IFN-γ and IL-2) were detected in mice from different groups. The targeting regulation of HMGB1 by miR-142-3p in ILC1s, and the expression of HMGB1 in normal pregnant mice and abortive mice were investigated. In addition, the regulatory effects of miR-142-3p and HMGB1 on ILC1s were detected in vitro by CCK-8, Annexin-V/PI, ELISA, and RT-PCR, respectively. Furthermore, changes of the NF-κB signaling pathway in ILC1s were examined in the different groups. For the in vivo studies, miR-142-3p-Agomir was injected in the uterus of abortive mice to evaluate the abortion rate and alterations of ILC1s at the maternal-fetal interface, and further detect the expression of HMGB1, pro-inflammatory cytokines, and the NF-κB signaling pathway. RESULTS: The number of ILC1s was significantly increased, the level of HMGB1 was significantly upregulated, and that of miR-142-3p was considerably downregulated in the abortive mice as compared with the normal pregnant mice (all P<0.05). In addition, miR-142-3p was found to drastically inhibit the activation of the NF-κB signaling pathway (P<0.05). The number of ILC1s and the levels of pro-inflammatory cytokines were significantly downregulated and the activation of the NF-κB signaling pathway was inhibited in the miR-142-3p Agomir group (all P<0.05). CONCLUSION: miR-142-3p can regulate ILC1s by targeting HMGB1 via the NF-κB signaling pathway, and attenuate the inflammation at the maternal-fetal interface in abortive mice.

Effect of obstructive sleep apnea on in vitro fertilization outcomes in women with polycystic ovary syndrome.

STUDY OBJECTIVES: Polycystic ovary syndrome (PCOS) confers a high risk of obstructive sleep apnea (OSA). Here we investigated the effect of OSA on first in vitro fertilization (IVF) cycle metrics and outcomes in patients with PCOS. METHODS: This was a prospective cohort study of patients with PCOS undergoing their first IVF at a single tertiary center between October 1, 2021, and September 30, 2022. Patients were screened for OSA before IVF and grouped accordingly. Clinical and IVF cycle data were compared between groups. RESULTS: OSA was found in 37.2% of 156 patients with PCOS, with longer infertility duration (4.3 ± 2.5 vs. 3.4 ± 2.0 years) and lower levels of anti-Müllerian and luteinizing hormones than patients without OSA (6.44 ± 2.96 vs 8.69 ± 4.03 µg/L and 6.30 ± 5.02 vs 8.46 ± 6.09 U/L). Antral follicle count was lower in patients with OSA (28.9 ± 12.4 vs 33.2 ± 12.9). During ovarian stimulation, patients with OSA required significantly higher doses of gonadotropin (2080.8 ± 1008.7 vs 1682.8 ± 619.9 U) and had lower peak estradiol level (4473.5 ± 2693.0 vs 5455.7 ± 2955.1 pmol/L) and fewer retrieved oocytes, high-quality, and available embryos (17.8 ± 7.2 vs 21.9 ± 10.5, 4.5 ± 4.4 vs 6.2 ± 4.6, 5.2 ± 4.3 vs 7.4 ± 5.0). Eleven patients were excluded for having no embryos or missing transfer. Therefore, we analyzed the outcome of the first embryo transfer in 145 patients. The biochemical and clinical pregnancy rates were lower in patients with OSA than patients without OSA (51.9% vs 66.7% and 42.3% vs 60.2%). OSA was independently associated with clinical pregnancy rate after controlling for several confounders (P = .043). CONCLUSIONS: OSA impairs female fertility in patients with polycystic ovary syndrome, suggesting an adverse effect on in vitro fertilization cycle stimulation characteristics and clinical outcomes. CITATION: Zhang Q, Wang Z, Ding J, et al. Effect of obstructive sleep apnea on in vitro fertilization outcomes in women with polycystic ovary syndrome. J Clin Sleep Med. 2024;20(1):31-38.

Astaxanthin Alleviates Hepatic Lipid Metabolic Dysregulation Induced by Microcystin-LR.

Microcystin-LR (MC-LR), frequently generated by cyanobacteria, has been demonstrated to raise the likelihood of liver disease. Few previous studies have explored the potential antagonist against MC-LR. Astaxanthin (ASX) has been shown to possess various beneficial effects in regulating lipid metabolism in the liver. However, whether ASX could alleviate MC-LR-induced hepatic lipid metabolic dysregulation is as yet unclear. In this work, the important roles and mechanisms of ASX in countering MC-LR-induced liver damage and lipid metabolic dysregulation were explored for the first time. The findings revealed that ASX not only prevented weight loss but also enhanced liver health after MC-LR exposure. Moreover, ASX effectively decreased triglyceride, total cholesterol, aspartate transaminase, and alanine aminotransferase contents in mice that were elevated by MC-LR. Histological observation showed that ASX significantly alleviated lipid accumulation and inflammation induced by MC-LR. Mechanically, ASX could significantly diminish the expression of genes responsible for lipid generation (Srebp-1c, Fasn, Cd36, Scd1, Dgat1, and Pparg), which probably reduced lipid accumulation induced by MC-LR. Analogously, MC-LR increased intracellular lipid deposition in THLE-3 cells, while ASX decreased these symptoms by down-regulating the expression of key genes in the lipid synthesis pathway. Our results implied that ASX played a crucial part in lipid synthesis and effectively alleviated MC-LR-induced lipid metabolism dysregulation. ASX might be developed as a novel protectant against hepatic impairment and lipid metabolic dysregulation associated with MC-LR. This study offers new insights for further management of MC-LR-related metabolic diseases.

Prevalence of cancer-related cognitive impairment among patients with nasopharyngeal carcinoma: a cross-sectional study.

OBJECTIVE: To examine the prevalence of cancer-related cognitive impairment (CRCI) and its contributing factors in patients with nasopharyngeal carcinoma (NPC) and explore the relationship between various assessment methods. METHODS: A cross-sectional study was conducted with 367 patients with NPC between March 2022 and April 2024 at Chongqing University Cancer Hospital. The data gathered from the demographic questionnaire, Montreal Cognitive Assessment (MoCA), Functional Assessment of Cancer Therapy-Cognitive Function (FACT-Cog), Self-Rating Anxiety Scale (SAS), and Self-Rating Depression Scale (SDS) were analyzed using logistic regression. RESULTS: Out of 367 participants, males accounted for 271 (73.84%). There were 217 (59.13%) individuals aged between 35-55 years. Cognitive impairment incidence was 58.04% using MoCA and 47.98% using FACT-Cog. Years of education, work condition, age and time since diagnosis (≥ 11 months) were all significantly associated with cognitive impairment using MoCA, the strongest being time since diagnosis (≥ 11 months) (OR = 2.672, 95% CI = 1.191-5.997, P = 0.017). Gender, marital status (married), place of residence (township), place of residence (city), alcohol history, SAS and SDS were all significantly associated with FACT-Cog, the strongest being marital status (married) (OR = 4.100, 95% CI = 1.130-14.87, P = 0.032). CONCLUSION: Patients diagnosed with NPC exhibit susceptibility to CRCI. There was a weak correlation between some aspects of the subjective tests and the objective test scores. Advanced age and disease diagnosis longer than 10 months are associated with a heightened risk of objective cognitive impairment. Furthermore, residing in rural areas, female, married, alcohol history, SAS and SDS increases the likelihood of subjective cognitive impairment. These findings highlight the need to select appropriate assessment scales for different needs and take targeted interventions to address CRCI in patients with NPC.

Dysregulated lncSNHG12 suppresses the invasion and migration of trophoblasts by regulating Dio2/Snail axis to involve in recurrent spontaneous abortion.

Recurrent spontaneous abortion (RSA) is a complex pathological process involving diverse factors, in which the dysregulated functions of trophoblasts cannot be ignored. Long noncoding RNA (lncRNA) has been reported to play a significant role in regulating the functions of trophoblasts in RSA. However, the impact and potential mechanism of lncRNA small nucleolar RNA host gene 12 (lncSNHG12) remain unclear. The role of lncSNHG12 in RSA was investigated through in vivo experiments and clinical samples. Co-IP and RNA pull down were conducted to explore the molecular mechanisms in trophoblasts. Our results showed that lncSNHG12 promoted the migration and invasion of trophoblasts by interacting with Iodothyronine deiodinase 2 (Dio2), which regulating the EMT process of trophoblasts by interacting with Snail. Moreover, in vivo experiments confirmed that lncSNHG12 could improve the fetal absorption rate of the abortion mice. The clinical samples revealed that lncSNHG12, Dio2 and Snail were down-regulated in the villous tissues of RSA patients, and positive correlations were confirmed between lncSNHG12 and Dio2, as well as Dio2 and Snail. In summary, the lncSNHG12/Dio2/Snail axis might be involved in the development of RSA by regulating the invasion and migration of trophoblasts. Abbreviations: RSA, recurrent spontaneous abortion; EVTs, extravillous trophoblasts; EMT, epithelial-to-mesenchymal transition; lncRNA, long non-coding RNA; Dio2, iodothyronine deiodinase 2; SNHGs, small nuclear RNA host genes; snoRNAs, small nuclear cell RNAs; LPS, lipopolysaccharide; De, derived decidua; Jz, junctional zone; Lz, labyrinth zones; RIP, RNA Binding Protein Immunoprecipitation; Co-IP, Co-Immunoprecipitation; RPISeq, RNA-Protein Interaction Prediction.

Cyanidin-3-O-Glucoside Alleviates Alcoholic Liver Injury via Modulating Gut Microbiota and Metabolites in Mice.

Alcoholic liver disease (ALD) is primarily caused by long-term excessive alcohol consumption. Cyanidin-3-O-glucoside (C3G) is a widely occurring natural anthocyanin with multiple biological activities. This study aims to investigate the effects of C3G isolated from black rice on ALD and explore the potential mechanism. C57BL/6J mice (male) were fed with standard diet (CON) and Lieber-DeCarli liquid-fed (Eth) or supplemented with a 100 mg/kg/d C3G Diet (Eth-C3G), respectively. Our results showed that C3G could effectively ameliorate the pathological structure and liver function, and also inhibited the accumulation of liver lipids. C3G supplementation could partially alleviate the injury of intestinal barrier in the alcohol-induced mice. C3G supplementation could increase the abundance of Norank_f_Muribaculaceae, meanwhile, the abundances of Bacteroides, Blautia, Collinsella, Escherichia-Shigella, Enterococcus, Prevotella, [Ruminococcus]_gnavus_group, Methylobacterium-Methylorubrum, Romboutsia, Streptococcus, Bilophila, were decreased. Spearman's correlation analysis showed that 12 distinct genera were correlated with blood lipid levels. Non-targeted metabolic analyses of cecal contents showed that C3G supplementation could affect the composition of intestinal metabolites, particularly bile acids. In conclusion, C3G can attenuate alcohol-induced liver injury by modulating the gut microbiota and metabolites, suggesting its potential as a functional food ingredient against alcoholic liver disease.

Manipulating Coupled Field Enhancement in Slot-under-Groove Nanoarrays for Universal Surface-Enhanced Raman Scattering.

Surface-enhanced Raman scattering (SERS) is an ultrasensitive spectroscopic technique that can identify materials and chemicals based on their inelastic light-scattering properties. In general, SERS relies on sub-10 nm nanogaps to amplify the Raman signals and achieve ultralow-concentration identification of analytes. However, large-sized analytes, such as proteins and viruses, usually cannot enter these tiny nanogaps, limiting the practical applications of SERS. Herein, we demonstrate a universal SERS platform for the reliable and sensitive identification of a wide range of analytes. The key to this success is the prepared "slot-under-groove" nanoarchitecture arrays, which could realize a strongly coupled field enhancement with a large spatial mode distribution via the hybridization of gap-surface plasmons in the upper V-groove and localized surface plasmon resonance in the lower slot. Therefore, our slot-under-groove platform can simultaneously deliver high sensitivity for small-sized analytes and the identification of large-sized analytes with a large Raman gain.

CTRP6 regulates M1 macrophage polarization via the PPAR-γ/NF-κB pathway and reprogramming glycolysis in recurrent spontaneous abortion.

Aberrant polarization and functions of decidual macrophages are closely related to recurrent spontaneous abortion (RSA). C1q/tumor necrosis factor-related protein 6 (CTRP6) is a member of the adiponectin paralog family, and plays indispensable roles in inflammation, glucose uptake and tumor metastasis. However, the regulatory effect of CTRP6 on macrophage polarization and glycolysis in RSA and the underlying mechanisms have not been fully elucidated. In the present study, we first found that CTRP6 expression was positively correlated with the M1 macrophage marker (CD86) in decidual tissues by dual immunofluorescence analysis. In vitro experiments indicated that CTRP6 could facilitate M1 macrophage activation through the PPAR-γ/NF-κB pathway and manipulate the glycolysis of macrophages. Notably, in addition to silencing CTRP6, treatment with a PPAR-γ agonist (GW1929) inhibited M1 macrophage polarization and rescued embryo absorption in vivo. Taken together, these results identify previously unrevealed functions of CTRP6 in macrophage transformation during RSA.

LncRNA AOC4P recruits TRAF6 to regulate EZH2 ubiquitination and participates in trophoblast glycolysis and M2 macrophage polarization which is associated with recurrent spontaneous abortion.

During embryo implantation, trophoblast cells rely on large amounts of energy produced by glycolysis for their rapid growth and invasion. The disorder of trophoblast metabolism may lead to recurrent spontaneous abortion (RSA). Lactate, which is produced by the glycolysis of trophoblast cells during early pregnancy, can promote the polarization of M2 macrophages and maintain an anti-inflammatory environment at the maternal-fetal interface. Our study found that amine oxidase copper-containing 4 pseudogene (AOC4P) was abnormally increased in villi from RSA patients. It inhibited the glycolysis of trophoblast cells and thus hindered the polarization of M2 macrophages. Further studies showed that AOC4P combines with tumor necrosis factor receptor-associated factor 6 (TRAF6) to upregulate TRAF6 expression. TRAF6 acted as an E3 ubiquitin ligase to promote ubiquitination and degradation of zeste homolog 2 (EZH2). These results provided new insights into the important role played by AOC4P at the maternal-fetal interface.