Acid-assisted synthesis of core-shell Prussian blue cathode for sodium-ion batteries.

In recent years, core-shell structured Prussian Blue Analogues (PBAs) have been considered as highly promising cathode materials for sodium-ion batteries. Reducing production costs and simplifying the preparation method for core-shell PBAs have also become crucial considerations. This paper presents a novel approach for the first time: by acid-treating the as-synthesized solution from a simple coprecipitation reaction, a high-crystallinity, sodium-rich Mn2+-doped iron hexacyanoferrate (Fe/MnHCF) shell material is self-grown on the surface of manganese hexacyanoferrate (MnHCF). This method significantly improves the electrochemical properties of the MnHCF material. The core-shell structured PBA exhibits excellent cycling performance (with a capacity retention of 95.5 % for 400 cycles at 1 A/g) and high rate performance (134.2mAh/g@10 mA/g, 95.2mAh/g@1 A/g). In this article, we explore the growth mechanism of the high-sodium content, high-crystallinity shell structure and introduce a green chelating agent that is better suited for the crystallization of Mn and Fe-type PBA systems. Our study demonstrates that Mn2+ doping enhances the conductivity of the shell material. Meanwhile, the heterojunction structure of MnHCF@Fe/MnHCF conducive to charge separation and migration. This straightforward synthesis strategy offers a novel approach for fabricating high-performance core-shell structured Prussian Blue Analogue materials.

State transitions of coupled Gi-protein: Insights into internal water channel dynamics within dopamine receptor D3 from in silico submolecular analyses.

Dopamine is a crucial neurotransmitter in the central nervous system (CNS) that facilitates communication among neurons. Activation of dopamine receptors in the CNS regulates key functions such as movement, cognition, and emotion. Disruption of these receptors can result in severe neurological diseases. Although recent research has elucidated the structure of D3R in complex with Gi-protein, revealing the binding and activation mechanisms, the precise conformational changes induced by G-protein activation and GDP/GTP exchange remain unclear. In this study, atomic-level long-term molecular dynamics (MD) simulations were employed to investigate the dynamics of D3R in complex with different states of Gi-protein and ß-arrestin. Our simulations revealed distinct molecular switches within D3R and fluctuations in the distance between Ras and helical domains of G-protein across different G-protein-D3R states. Notably, the D3R-GTP-Gi state exhibited increased activity compared with the D3R-empty-Gi state. Additionally, analyses of potential of mean force (PMF) and free energy landscapes for various systems revealed the formation of a continuous water channel exclusively in the D3R-Gi-GTP state. Furthermore, allosteric communication pathways were proposed for active D3R bound to Gi-protein. This study offers insights into the activation mechanism when Gi-protein interacts with active D3R, potentially aiding in developing selective drugs targeting the dopaminergic system.

Enhanced endoplasmic reticulum stress signaling disrupts porcine sertoli cell function in response to Bisphenol A exposure.

Bisphenol A (BPA), a pervasive substance in our daily lives and livestock excreta, poses significant threats due to its infiltration into foods and water sources. BPA has adverse impacts on male reproductive function, particularly affecting the critical Sertoli (ST) cells that play a pivotal role in the process of spermatogonia differentiating into spermatozoa. In this study, we examined the prevalence of BPA within the pig industry and delved into the impact of BPA exposure on the motility of boar sperm, the function of pig ST cells, as well as the underlying molecular mechanisms involved. This study revealed spatial disparities in the global distribution of BPA and its analogue contamination, utilizing data compiled from 130 comprehensive studies. The average concentration of BPA found in pig feed ranges from 9.7 to 47.9 µg/kg, while in serum, it averages between 55.1 and 75.6 ng/L. The BPA concentration in feed exhibits a negative correlation with sperm viability and the percentage of progressive motile spermatozoa. Exposure to BPA reduced sperm motility in boar and ST cell activity at both 6 and 24 h. The transcriptome analysis revealed that, compared to untreated control cells, endoplasmic reticulum stress (ERS)-related genes were upregulated in ST cells exposed to BPA at 6 and 24 h. This activation of ERS in ST cells was mediated by receptor protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring protein-1α (IRE1α), and activating transcription factor 6 (ATF6). Additionally, BPA exposure triggered oxidative stress and a proinflammatory response mediated by the transcription factor NF-κB, accompanied by an increase in downstream proinflammatory cytokines. BPA exposure also led to apoptosis in ST cells and upregulated the expression levels of pro-apoptosis proteins. However, inhibiting ERS activity with 4-PBA attenuated the BPA-induced inflammatory response and apoptosis in ST cells. Our findings suggest that BPA induced apoptosis and inflammatory response in porcine ST cells through persistent activation of ERS, thereby compromising the normal function of these cells.

Self-Employment Transitions and Health Outcomes in Later Life: Evidence From China.

Background and Objectives: Self-employment is a vital alternative to waged employment for older workers. Recent research has shown that employment transitions frequently occur when individuals approach retirement. However, evidence of how older people's health changes when they switch between self and waged employment is lacking, particularly outside Western contexts. To address this research gap, we explored the health impact of employment transitions for the older working population in China by hukou (urban or rural household registration status), region, and education. Research Design and Methods: We employed fixed effect models to examine the impact of employment transitions on cognitive, mental, and physical health and life satisfaction drawing on data from four waves (2011, 2013, 2015, and 2018) of the China Health and Retirement Longitudinal Study (N = 4,606). Given China's unique context, we analyzed the results of agricultural and nonagricultural work separately. Results: Individuals transitioning into or remaining in self-employment had lower self-rated health and life satisfaction than those remaining in waged employment. There was no significant difference in cognitive functioning or depressive symptoms. Additionally, those who transitioned from self-employment into waged employment rated their health worse than those who remained in waged employment. The health impacts were more apparent for agricultural than nonagricultural self-employment, particularly for older workers living in urban regions with rural hukou and lower education levels. Discussion and Implications: Most older Chinese transitioning into or staying self-employed are or were pushed into self-employment due to their low human capital and socioeconomic status, which affects their subsequent health. Pension reform and policies supporting older adults to stay in the workforce could help close the economic and health gaps between rural and urban older adults.

Early Weaning Inhibits Intestinal Stem Cell Expansion to Disrupt the Intestinal Integrity of Duroc Piglets via Regulating the Keap1/Nrf2 Signaling.

There are different stress resistance among different breeds of pigs. Changes in intestinal stem cells (ISCs) are still unclear among various breeds of piglets after early weaning. In the current study, Taoyuan Black and Duroc piglets were slaughtered at 21 days of age (early weaning day) and 24 days of age (3 days after early weaning) for 10 piglets in each group. The results showed that the rate of ISC-driven epithelial renewal in local Taoyuan Black pigs hardly changed after weaning for 3 days. However, weaning stress significantly reduced the weight of the duodenum and jejunum in Duroc piglets. Meanwhile, the jejunal villus height, tight junction-related proteins (ZO-1, Occludin, and Claudin1), as well as the trans-epithelial electrical resistance (TEER) values, were down-regulated after weaning for 3 days in Duroc piglets. Moreover, compared with Unweaned Duroc piglets, the numbers of Olfm4+ ISC cells, PCNA+ mitotic cells, SOX9+ secretory progenitor cells, and Villin+ absorptive cells in the jejunum were reduced significantly 3 days after weaning. And ex vivo jejunal crypt-derived organoids exhibited growth disadvantages in weaned Duroc piglets. Notably, the Keap1/Nrf2 signaling activities and the expression of HO-1 were significantly depressed in weaned Duroc piglets compared to Unweaned Duroc piglets. Thus, we can conclude that ISCs of Duroc piglets were more sensitive to weaning stress injury than Taoyuan Black piglets, and Keap1/Nrf2 signaling is involved in this process.

Current applications of tumor local ablation (TLA) combined with immune checkpoint inhibitors in breast cancer treatment.

Breast cancer is one of the most common cancers in women globally, posing significant challenges to treatment because of the diverse and complex pathological and molecular subtypes. The emergence of immune checkpoint inhibitors (ICIs) has revolutionized the treatment of breast cancer, particularly for triple-negative breast cancer (TNBC), significantly improving patient outcomes. However, the overall tumor response rate remains suboptimal due to drug resistance to ICIs. This resistance is primarily due to the immune-suppressive tumor microenvironment (TME), tumor cells' ability to evade immune surveillance, and other complex immune regulatory mechanisms. To address these challenges, clinical researchers are actively exploring combinatorial therapeutic strategies with ICIs. Tumor local ablation (TLA) technology is anticipated to overcome resistance to ICIs and enhance therapeutic efficacy by ablating tumor tissue, releasing tumor antigens, remodeling the TME, and stimulating local and systemic immune responses. Combination therapy with TLA and ICIs has demonstrated promising results in preclinical breast cancer studies, underscoring the feasibility and importance of addressing drug resistance mechanisms in breast cancer. This provides novel strategies for breast cancer treatment and is expected to drive further advancements in the field.

Comparative single-cell multiome identifies evolutionary changes in neural progenitor cells during primate brain development.

Understanding the cellular and genetic mechanisms driving human-specific features of cortical development remains a challenge. We generated a cell-type resolved atlas of transcriptome and chromatin accessibility in the developing macaque and mouse prefrontal cortex (PFC). Comparing with published human data, our findings demonstrate that although the cortex cellular composition is overall conserved across species, progenitor cells show significant evolutionary divergence in cellular properties. Specifically, human neural progenitors exhibit extensive transcriptional rewiring in growth factor and extracellular matrix (ECM) pathways. Expression of the human-specific progenitor marker ITGA2 in the fetal mouse cortex increases the progenitor proliferation and the proportion of upper-layer neurons. These transcriptional divergences are primarily driven by altered activity in the distal regulatory elements. The chromatin regions with human-gained accessibility are enriched with human-specific sequence changes and polymorphisms linked to intelligence and neuropsychiatric disorders. Our results identify evolutionary changes in neural progenitors and putative gene regulatory mechanisms shaping primate brain evolution.

Pinocembrin alleviates LPS-induced depressive-like behavior in mice via the NLRP3/DCC signaling pathway.

OBJECTIVE: Depression, a prevalent and severe mental disorder, continues to be a significant area of research concerning its pathogenesis and therapeutic approaches. Conventional antidepressants are often limited by delayed therapeutic effects and notable adverse reactions, necessitating the development of innovative and efficacious treatment modalities. Multiple lines of evidence suggest that peripheral and central inflammation play a role in depression, and that anti-inflammatory drugs can ameliorate depressive symptoms in patients with inflammation-related depression. Pinocembrin (PB), a natural bioactive compound, is renowned for its anti-inflammatory and antioxidant properties, while the effect and mechanism of PB are still unclear. Consequently, this study employs PB as an intervention to investigate its effects on depression in mice model, with the objective of establishing a novel therapeutic strategy and foundational data for the treatment of depression. METHODS: (1) The acute inflammation model used lipopolysaccharide (LPS) to induce depression-like behavior in mice by injecting LPS intraperitoneally at a dose of 0.83 mg/kg. The effects of PB (20 mg/kg, i.p.) and the NLRP3 inflammasome inhibitor MCC950 (10 mg/kg, i.p.) on improving depression behavior in mice were evaluated. (2) To explore the specific mechanism of PB in improving depression-like behavior in LPS mice by regulating NLRP3 and Netrin-1/DCC pathway. RESULTS: The results showed that after intraperitoneal injection of LPS, the mice exhibited a significant decrease in body weight, sucrose preference score, and a significant increase in tail suspension immobility time. Treatment with PB and MCC950 increased the sucrose preference score and decreased the tail suspension immobility time. Besides, PB and MCC950 could inhibit the expression of NLRP3 related neuroinflammation, down-regulated the Netrin-1/DCC signaling pathway, and improved hippocampal neuroplasticity in mice. CONCLUSION: In conclusion, PB significantly improved LPS-induced depression-like behavior in mice by reducing the expression of hippocampal NLRP3 inflammasome and down-regulating the Netrin-1/DCC signaling pathway. Additionally, PB was found to regulate α-amino-3-hydroxy-5-methyl-4 isoxazole receptor (AMPAR) and postsynaptic density 95 (PSD95), protecting excitatory synaptic transmission and enhancing synaptic plasticity. This study demonstrates the effectiveness of PB in improving depressive symptoms induced by LPS and provides a new strategy for the clinical treatment of depression.

Comprehensive profiling of serum glycosphingolipids to discover the diagnostic biomarkers of lung cancer and uncover the variation of glycosphingolipid networks in different lung cancer subtypes.

Glycosphingolipids are glycolipid complexes formed by an oligosaccharide chain covalently linked to a ceramide backbone and play important roles in the occurrence and metastasis of lung cancer. In this study, an UHPLC-HRMS method was developed for the comprehensive profiling of glycosphingolipids, with an in-house library constructed for data interpretation. Serum glycosphingolipids were profiled in 31 healthy controls (HCs) and 92 lung cancer patients with different pathologic subtypes. Over 1700 glycosphingolipids were detected in human serum based on the novel method. A total of 567 differential glycosphingolipids (adjusted P < 0.05, and fold change > 2) were found between lung cancer patients and HCs. Glycosphingolipids can be used as potential biomarkers for lung cancer diagnosis, with sensitivity much higher than that of traditional serum tumor markers. The levels of most glycosphingolipids in squamous cell carcinoma (Squa) were significantly lower than those in small cell lung cancer (SCLC) and adenocarcinoma (Aden). The highest Cer1P abundance in SCLC patients among the three different subtypes of lung cancer was thought to be related to the high malignancy and metastasis of SCLC. An artificial neural network (ANN) model was constructed for the discrimination of the three different subtypes of lung cancer, with accuracy higher than 93%. Beyond providing biomarkers and statistical models for the diagnosis of lung cancer and discrimination of lung cancer subtypes, this study uncovered the variation of glycosphingolipid networks in different subtypes of lung cancer and thereby provided a novel insight to study the pathogenesis of lung cancer and explore therapeutic targets.

Flexomagnetoelectric Effect in Sr_{2}IrO_{4} Thin Films.

Symmetry engineering is explicitly effective to manipulate and even create phases and orderings in strongly correlated materials. Flexural stress is universally practical to break the space-inversion or time-reversal symmetry. Here, by introducing strain gradient in a centrosymmetric antiferromagnet Sr_{2}IrO_{4}, the space-inversion symmetry is broken accompanying a nonequivalent O p-Ir d orbital hybridization along the z axis. Thus, an emergent polar phase and out-of-plane magnetic moment have been simultaneously observed in these asymmetric Sr_{2}IrO_{4} thin films, which both are absent in its ground state. Furthermore, upon the application of a magnetic field, such polarization can be controlled by modifying the occupied d orbitals through spin-orbit interaction, giving rise to a flexomagnetoelectric effect. This Letter provides a general strategy to artificially design multiple symmetries and ferroic orderings in strongly correlated systems.

The promotion of cell proliferation and invasion in cutaneous squamous cell carcinomas after ARNT downregulation is associated with CXCL3.

The aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor associated with adaptive responses to cellular stress. Its role in cutaneous squamous cell carcinoma (cSCC) remains poorly understood. The aim of this study was to investigate the role of ARNT in cSCC. Immunohistochemistry revealed downregulation of ARNT in cSCC, precancerous lesions (actinic keratosis), and cells. Knockdown of ARNT in A431 and SCL-1 cells significantly enhanced cell growth and metastasis. Microarray analysis and Ingenuity Pathway Analysis confirmed that loss of ARNT in A431 cells was highly correlated with cell growth and movement and upregulated CXCL3 expression. Cellular and xenograft experiments further confirmed that ARNT regulates cSCC proliferation and invasiveness in a CXCL3-dependent manner. ARNT may regulate CXCL3 expression through ROS-STAT3 pathway. In conclusion, this study demonstrates that ARNT plays a critical role in the development of cSCC and significantly affects the proliferation and metastatic ability of cSCC cells. It has the potential to serve as an ideal treatment target for cSCC.

Apigenin inhibits lipid metabolism of hepatocellular carcinoma cells by targeting the histone demethylase KDM1A.

BACKGROUND: The development of cancer is accompanied by metabolic reprogramming, and the liver serves as a central hub for lipid transportation. Apigenin, a plant-derived flavonoid, demonstrates potent anticancer properties across various cancer types and exhibits promising potential as a therapeutic agent for cancer treatment. However, there are limited studies focusing on the downstream targets of apigenin. Moreover, there are few reports on the impact of apigenin in lipid metabolism within liver cancer cells. PURPOSE: The objective is to elucidate the metabolic mechanism underlying the inhibitory effect of apigenin on liver cancer progression, search for downstream targets and provide reliable data support for the clinical trials of apigenin. METHODS: Anticancer effects of apigenin were detected at cellular and molecular levels in vitro, and downstream targets of apigenin, especially metabolic pathway genes, were analyzed by transcriptome. Next, the downstream target of apigenin was verified and the biological function of the downstream target was examined. Finally, the downstream target of apigenin was further verified by restoring target gene expression. RESULTS: Cellular molecular experiments showed that Apigenin inhibited the proliferation, migration, invasion and lipid metabolism of hepatocellular carcinoma (HCC) cells. Transcriptome analysis showed apigenin widely regulates histone demethylase, particularly histone H3K4 lysine demethylase 1A (KDM1A). Apigenin treatment inhibited the expression of KDM1A protein and mRNA levels in liver cancer cells, molecular docking predicted the interaction between apigenin and KDM1A. Furthermore, downregulation KDM1A inhibited the proliferation and lipid metabolism of HCC cells, in the same way, overexpressing KDM1A promoted proliferation of HCC cells. Finally, restoring KDM1A expression partially attenuated the effects of apigenin on lipid metabolism in HCC cells. CONCLUSION: In conclusion, our study provides compelling evidence that apigenin inhibits liver cancer progression and elucidates its mechanism of action in regulating lipid metabolism. Specifically, we find that apigenin suppresses the progression of HCC cells by downregulating genes involved in lipid metabolism. Additionally, our results indicate that KDM1A acts as a downstream target of apigenin in the inhibition of lipid metabolism in HCC. These findings offer experimental support for the potential use of apigenin as a therapeutic agent for liver cancer, highlighting its relevance in future clinical applications.

Chronic diesel exhaust exposure induced pulmonary vascular remodeling a potential trajectory for traffic related pulmonary hypertension.

BACKGROUND: As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. However, its impact on pulmonary vessels is still unclear. METHODS: To explore the effects of DE exposure on pulmonary vascular remodeling, our study analyzed the number and volume of small pulmonary vessels in the diesel engine testers (the DET group) from Luoyang Diesel Engine Factory and the controls (the non-DET group) from the local water company, using spirometry and carbon content in airway macrophage (CCAM) in sputum. And then we constructed a rat model of chronic DE exposure, in which 12 rats were divided into the DE group (6 rats with 16-week DE exposure) and the control group (6 rats with 16-week clean air exposure). During right heart catheterization, right ventricular systolic pressure (RVSP) was assessed by manometry. Macrophage migration inhibitory factor (MIF) in lung tissues and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA, respectively. Histopathological analysis for cardiovascular remodeling was also performed. RESULTS: In DET cohort, the number and volume of small pulmonary vessels in CT were positively correlated with CCAM in sputum (P<0.05). Rat model revealed that chronic DE-exposed rats had elevated RVSP, along with increased wall thickness of pulmonary small vessels and right the ventricle. What's more, the MIF levels in BALF and lung tissues were higher in DE-exposed rats than the controls. CONCLUSION: Apart from airway remodeling, DE also induces pulmonary vascular remodeling, which will lead to cardiopulmonary dysfunction.

Contagion of depression: a double-edged sword.

Depression is a significant mental health issue with extensive economic implications, and recent studies suggest it may be transmitted between individuals. However, the mechanisms of this contagion remain unclear, and the social buffering effect has been understudied. This research employs three rodent models, including stress crossover, cohabitation-induced, and non-contact induced depression contagion models, to explore these mechanisms. Here, we report that that naive mice cohabiting with depressed mice showed increased corticosterone levels and depressive behaviors, unlike those with stressed mice, who did not exhibit these changes and even mitigated desperation in stressed mice. Non-contact cohabitation did not produce significant behavioral differences, but exposure to bedding from depressed mice reduced sucrose preference in naive mice. This study introduces reliable models of depression contagion, suggesting it operates independently of stress transmission. The interplay between depression contagion and social buffering may vary in different contexts. These findings provide new insights into the mechanisms of depression contagion and potential strategies for preventing depressive disorders.

Preliminary study on the effect of lumbar axial rotation on bone mineral density measured by DXA and QCT.

Currently, the relationship between axial rotation of the vertebrae and bone mineral density (BMD) measured by dual-energy X-ray absorptiometry (DXA) and quantitative computed tomography (QCT) remains controversial. The aim of this study is to quantitatively assess the effect of vertebral rotation on volumetric bone mineral density (v-BMD) and areal bone mineral density (a-BMD), further to propose the corrected strategies. To achieve this, a phantom, which was rotated from 0° to 25° in 5° increments, was utilized. Bone mineral content (BMC), a-BMD, v-BMD, and projected area (p-AREA) were measured. The Kruskal-Wallis non-parametric test or one-way ANOVA was used to examine the differences in variables between the different groups. The Pearson and Spearman correlation was used to test the relationships between quantitative parameters and rotated angles. Linear regression analysis was used to evaluate the relationship between angles and quantitative parameters. The findings indicate that, as the angle increased, a-BMD and v-BMD decreased (P < 0.001) , and the p-AREA increased (P < 0.001), but the BMC stays constant. The rotated angle was negative correlated (r = - 0.925, P < 0.001) with a-BMD and v-BMD (r = - 0.880, P < 0.001), positive (r = 0.930, P = < 0.001) correlated with p-AREA. The linear regression analysis showed that a-BMD = 0.808-0.01 × Angle and v-BMD = 151.808-1.588 × Angle. This study showed that, axial rotation might lead to a lower measured for a-BMD and v-BMD, it should be modified. This gives clinicians some insights into how to deal with osteoporosis in scoliosis patients. It's essential for clinicians to incorporate these findings into their diagnostic processes to prevent potential misdiagnosis and over-treatment of osteoporosis.

Grifola frondosa polysaccharide's therapeutic potential in oxazolone-induced ulcerative colitis.

Grifola frondosa polysaccharide (GFP) is a consumable fungus recognized for its potential health advantages. The present study aimed to investigate the development and potential etiologies of ulcerative colitis (UC) utilizing oxazolone (OXZ) as an inducer in mice, along with assessing the therapeutic effects of GFP at varying doses in UC mice, with sulfasalazine (SASP) serving as the positive control. The obtained results indicated that OXZ intervention in mice induced numerous physical manifestations of UC, including increased disease activity index (DAI), decreased goblet cell division, enhanced fibrosis, reduced expression of Claudin1 and Zona encludens protein1 (ZO-1), decreased proliferative activity of colonic mucosal epithelial cells, disturbed oxidation balance, and alterations in intestinal flora. Nonetheless, GFP intervention significantly ameliorated or even resolved these abnormal indicators to a considerable extent. Consequently, this study suggests that GFP might serve as a prebiotic to regulate intestinal flora, mitigate enterotoxin production, restore oxidative balance, thereby reducing the generation of inflammatory mediators, restoring the intestinal barrier, and ultimately improving OXZ-induced UC in mice. GFP demonstrates promising potential as a candidate drug for colitis treatment and as a dietary supplement for alleviating intestinal inflammatory issues.

Improved contingent screening strategy increased trisomy 21 detection rate in the second trimester.

PURPOSE: This study aimed to establish suitable threshold values for biochemical indicators in low-risk pregnant women who underwent second trimester screening and design strategies for consecutive prenatal testing to increase trisomy 21 detection. METHODS: This study examined singleton pregnant women who underwent double, triple, or quadruple screening in the second trimester over six years. To obtain adequate detection efficiency for low-risk pregnancies, threshold values for serum biochemical indicators were established, and a cost-effectiveness assessment of the improved contingent screening strategy was conducted. RESULTS: Participants were included in serum double- (n = 88,550), triple- (n = 29,991), and quadruple-screening (n = 15,004) groups. Threshold values were defined as having a free beta subunit of human chorionic gonadotropin (free ß-hCG) multiple of the median (MoM) ≥ 2.50, alpha-fetoprotein (AFP) MoM ≤ 0.50, or unconjugated estriol (uE3) MoM ≤ 0.70 for low risk. Low-risk pregnancies, comprising 1.35% (988/73,183), 4.45% (1,171/26,286), and 11.91% (1,559/13,085) of the double-, triple-, and quadruple-screening groups, respectively, underwent further non-invasive prenatal screening. In the double-, triple-, and quadruple-screening groups, we detected 11.76% (2/17), 40.00% (2/5), and 66.67% (2/3) of trisomy 21 cases with false negative results, respectively, with the overall detection rates of 85.00% (85/100), 90.63% (29/32), and 95.24% (20/21), respectively, and decreased ratio of overall costs of 5.26%, 16.63%, and 24.36%, respectively. CONCLUSION: Utilizing threshold values of AFP, free ß-hCG, and uE3 to trigger further non-invasive prenatal screening may increase trisomy 21 detection in pregnancies deemed low risk in the second trimester while reducing the overall costs of screening strategies.

An innovative metabolic index for insulin resistance correlates with early neurological deterioration following intravenous thrombolysis in minor acute ischemic stroke patients.

Background and purpose: The composite score for insulin resistance (IR), known as the Metabolic Score of Insulin Resistance (METS-IR), serves as an assessment tool for IR and has been previously linked to symptomatic intracranial hemorrhage and poor functional outcomes in patients with acute ischemic stroke (AIS). Despite these associations, the impact of METS-IR on early neurological deterioration (END) in patients with minor AIS who underwent intravenous administration of recombinant tissue-type plasminogen activator (IV-rtPA) remains inadequately established. This investigation explored the link between METS-IR and END in patients with minor AIS receiving IV-rtPA treatment. Methods: In this study, a cohort comprising 425 consecutive patients with National Institutes of Health Stroke Scale Score (NIHSS)≤5 who underwent IV-rtPA treatment was included. The METS-IR was computed using the formula ln METS-IR=ln (2 × FBG + TG) × BMI/ln (HDL). END was defined as a NIHSS ≥2 within 24 h post IV-rtPA administration, while poor functional outcome was defined as a modified Rankin Scale (mRS) of 2-6. Multivariate logistical regression was performed to investigate the association between METS-IR and both poor functional outcomes and END. Results: Among the 425 enrolled patients, 64 (15.1 %) patients experienced END, while 80 (18.8 %) had poor functional outcomes three months post-discharge. Upon adjusting for confounding factors, a higher METS-IR emerged as an independent predictor for both END and poor functional outcomes. Similarly, noteworthy findings were observed when METS-IR was defined as a categorical group. The restricted cubic spline (RCS) analysis indicated a linear relationship between METS-IR and END (P = 0.593 for non-linearity, P = 0.034 for overall). The incorporation of METS-IR into the conventional model resulted in a significant enhancement of predictive accuracy for both END and poor functional outcomes. Conclusion: METS-IR emerges as an independent predictor for END and poor functional outcome at three months post-discharge in patients with minor AIS subjected to IV-rtPA. Considering its simplicity and clinical accessibility as an indicator of IR, METS-IR may hold guiding significance in clinical practice.

Nanoconfined tandem three-phase photocatalysis for highly selective CO2 reduction to ethanol.

The conversion of CO2 and H2O into ethanol with high selectivity via photocatalysis is greatly desired for effective CO2 resource utilization. However, the sluggish and challenging C-C coupling hinders this goal, with the behavior of *CO holding the key. Here, a nanoconfined and tandem three-phase reaction system is established to simultaneously enhance the *CO concentration and interaction time, achieving an outstanding ethanol selectively of 94.15%. This system utilizes a tandem catalyst comprising an Ag core and a hydrophobic Cu2O shell. The hydrophobic Cu2O shell acts as a CO2 reservoir, effectively overcoming the CO2 mass-transfer limitation, while the Ag core facilitates the conversion of CO2 to CO. Subsequently, CO undergoes continuous reduction within the nanoconfined mesoporous channels of Cu2O. The synergy of enhanced mass transfer, nanoconfinement, and tandem reaction leads to elevated *CO concentrations and prolonged interaction time within the Cu2O shell, significantly reducing the energy barrier for *CO-*CO coupling compared to the formation of *CHO from *CO, as determined by density functional theory calculations. Consequently, C-C coupling preferentially occurs over *CHO formation, producing excellent ethanol selectivity. These findings provide valuable insights into the efficient production of C2+ compounds.