Healthy dietary patterns are associated with exposure to environmental chemicals in a pregnancy cohort.

Healthy dietary patterns, such as the alternate Mediterranean diet and alternate Healthy Eating Index, benefit cardiometabolic health. However, several food components of these dietary patterns are primary sources of environmental chemicals. Here, using data from a racially and ethnically diverse US cohort, we show that healthy dietary pattern scores were positively associated with plasma chemical exposure in pregnancy, particularly for the alternate Mediterranean diet and alternate Healthy Eating Index with polychlorinated biphenyls and per- and poly-fluoroalkyl substances. The associations appeared stronger among Asian and Pacific Islanders. These findings suggest that optimizing the benefits of a healthy diet requires concerted regulatory efforts aimed at lowering environmental chemical exposure.

Additional mechanism for selective absorption of cholesterol and Phytosterols.

Phytosterols are structurally similar to cholesterol but they are much less absorbed (<2%) than cholesterol (>50%) in the intestine. We hypothesize that phytosterols are poor substrates of intestinal acyl-CoA: cholesterol acyltransferase 2 (ACAT2), and thus minimal phytosterol esters are formed and packed into chylomicrons, leading to their low absorption. Two isotope tracing models, including a radioactive hamster microsomal ACAT2 reaction model and a differentiated Caco-2 cell model, were established to examine the specificity of ACAT2 to various sterols, including cholesterol, sitosterol, stigmasterol, and campesterol. Both models consistently demonstrated that only cholesterol but not phytosterols could be efficiently esterified by ACAT2 in a time- and dose-dependent manner. Molecular docking further suggested that unfavorable interactions existed between ACAT2 and phytosterols. In conclusion, phytosterols are poor substrates of ACAT2 and thus minimally absorbed. This work provides a theoretical basis for the use of phytosterol-based supplements in treating dyslipidemia and preventing heart diseases.

Phenotypic subgroup in serologically active clinically quiescent systemic lupus erythematosus: A cluster analysis based on CSTAR cohort.

BACKGROUND: Serologically active clinically quiescent (SACQ) is a state within systemic lupus erythematosus (SLE) characterized by elevated serologic markers without clinical activity. The heterogeneity in SACQ patients poses challenges in disease management. This multicenter prospective study aimed to identify distinct SACQ subgroups and assess their utility in predicting organ damage. METHODS: SACQ was defined as a sustained period of at least 6 months with persistent serologic activity, marked by positive anti-double-stranded DNA (dsDNA) antibodies and/or hypocomplementemia, and without clinical activity. Cluster analysis was employed, utilizing 16 independent components to delineate phenotypes. FINDINGS: Among the 4,107 patients with SLE, 990 (24.1%) achieved SACQ within 2.0 ± 2.3 years on average. Over a total follow-up of 7,105.1 patient years, 340 (34.3%) experienced flares, and 134 (13.5%) developed organ damage. Three distinct SACQ subgroups were identified. Cluster 1 (n = 219, 22.1%) consisted predominantly of elderly males with a history of major organ involvement at SLE diagnosis, showing the highest risk of severe flares (16.4%) and organ damage (27.9%). Cluster 2 (n = 279, 28.2%) was characterized by milder disease and a lower risk of damage accrual (5.7%). Notably, 86 patients (30.8%) in cluster 2 successfully discontinued low-dose glucocorticoids, with 49 of them doing so without experiencing flares. Cluster 3 (n = 492, 49.7%) featured the highest proportion of lupus nephritis and a moderate risk of organ damage (11.8%), with male patients showing significantly higher risk of damage (hazard ratio [HR] = 4.51, 95% confidence interval [CI], 1.82-11.79). CONCLUSION: This study identified three distinct SACQ clusters, each with specific prognostic implications. This classification could enhance personalized management for SACQ patients. FUNDING: This work was funded by the National Key R&D Program (2021YFC2501300), the Beijing Municipal Science & Technology Commission (Z201100005520023), the CAMS Innovation Fund (2021-I2M-1-005), and National High-Level Hospital Clinical Research Funding (2022-PUMCH-D-009).

Metabolic Profiling of Cochlear Organoids Identifies α-Ketoglutarate and NAD+ as Limiting Factors for Hair Cell Reprogramming.

Cochlear hair cells are the sensory cells responsible for transduction of acoustic signals. In mammals, damaged hair cells do not regenerate, resulting in permanent hearing loss. Reprogramming of the surrounding supporting cells to functional hair cells represent a novel strategy to hearing restoration. However, cellular processes governing the efficient and functional hair cell reprogramming are not completely understood. Employing the mouse cochlear organoid system, detailed metabolomic characterizations of the expanding and differentiating organoids are performed. It is found that hair cell differentiation is associated with increased mitochondrial electron transport chain (ETC) activity and reactive oxidative species generation. Transcriptome and metabolome analyses indicate reduced expression of oxidoreductases and tricyclic acid (TCA) cycle metabolites. The metabolic decoupling between ETC and TCA cycle limits the availability of the key metabolic cofactors, α-ketoglutarate (α-KG) and nicotinamide adenine dinucleotide (NAD+). Reduced expression of NAD+ in cochlear supporting cells by PGC1α deficiency further impairs hair cell reprogramming, while supplementation of α-KG and NAD+ promotes hair cell reprogramming both in vitro and in vivo. These findings reveal metabolic rewiring as a central cellular process during hair cell differentiation, and highlight the insufficiency of key metabolites as a metabolic barrier for efficient hair cell reprogramming.

Physiology, Biochemistry, and Transcriptomics Jointly Reveal the Phytotoxicity Mechanism of Acetochlor on Pisum sativum L.

Acetochlor, as a commonly used pre-emergent herbicide, can be toxic to crops and affect production if used improperly. However, the toxic mechanism of acetochlor on plants is not fully understood. The present study used a combination of transcriptomic analysis and physiological measurements to investigate the effects of short-term (15-day) exposure to different concentrations of acetochlor (1, 10, 20 mg/kg) on the morphology, physiology, and transcriptional levels of pea seedlings, aiming to elucidate the toxic response and resistance mechanisms in pea seedlings under herbicide stress. The results showed that the toxicity of acetochlor to pea seedlings was dose-dependent, manifested as dwarfing and stem base browning with increasing concentrations, especially at 10 mg/kg and above. Analysis of the antioxidant system showed that from the 1 mg/kg treatment, malondialdehyde, superoxide dismutase, peroxidase, and glutathione peroxidase in peas increased with increasing concentrations of acetochlor, indicating oxidative damage. Analysis of the glutathione (GSH) metabolism system showed that under 10 mg/kg treatment, the GSH content of pea plants significantly increased, and GSH transferase activity and gene expression were significantly induced, indicating a detoxification response in plants. Transcriptomic analysis showed that after acetochlor treatment, differentially expressed genes in peas were significantly enriched in the phenylpropane metabolic pathway, and the levels of key metabolites (flavonoids and lignin) were increased. In addition, we found that acetochlor-induced dwarfing of pea seedlings may be related to gibberellin signal transduction. Environ Toxicol Chem 2024;00:1-15. © 2024 SETAC.

Constructing Sn-Cu2O Lithiophilicity Nanowires as Stable and High-Performance Lithium Metal Anodes.

Lithium (Li) metal batteries (LMBs) have garnered significant research attention due to their high energy density. However, uncontrolled Li dendrite growth and the continuous accumulation of "dead Li" directly lead to poor electrochemical performance in LMBs, along with serious safety hazards. These issues have severely hindered their commercialization. In this study, a lithiophilic layer of Sn-Cu2O is constructed on the surface of copper foam (CF) grown with Cu nanowire arrays (SCCF) through a combination of electrodeposition and plasma reduction. Sn-Cu2O, with excellent lithiophilicity, reduces the Li nucleation barrier and promotes uniform Li deposition. Simultaneously, the high surface area of the nanowires reduces the local current density, further suppressing the Li dendrite growth. Therefore, at 1 mA cm-2, the half cells and symmetric cells achieve high Coulombic efficiency (CE) and stable operation for over 410 cycles and run smoothly for more than 1350 h. The full cells using an LFP cathode demonstrate a capacity retention rate of 90.6% after 1000 cycles at 5 C, with a CE as high as 99.79%, suggesting excellent prospects for rapid charging and discharging and long-term cyclability. This study provides a strategy for modifying three-dimensional current collectors for Li metal anodes, offering insights into the construction of stable, safe, and fast-charging LMBs.

Targeting Transient Receptor Potential Melastatin-2 (TRPM2) Enhances Therapeutic Efficacy of Third Generation EGFR Inhibitors against EGFR Mutant Lung Cancer.

There is an urgent need to fully understand the biology of third generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs), particularly osimertinib, and to develop mechanism-driven strategies to manage their acquired resistance. Transient receptor potential melastatin-2 (TRPM2) functions as an important regulator of Ca2+ influx, but its role in mediating therapeutic efficacies of EGFR-TKIs and acquired resistance to EGFR-TKIs has been rarely studied. This study has demonstrated a previously undiscovered role of suppression of TRPM2 and subsequent inhibition of Ca2+ influx and induction of ROS and DNA damage in mediating apoptosis induction and the therapeutic efficacy of osimertinib against EGFR mutant NSCLC. The rebound elevation represents a key mechanism accounting for the emergence of acquired resistance to osimertinib and other third generation EGFR-TKIs. Accordingly, targeting TRPM2 is a potentially promising strategy for overcoming and preventing acquired resistance to osimertinib, warranting further study in this direction including the development of cancer therapy-optimized TRPM2 inhibitors.

Bile Acid Injection Regulated Blood Glucose in T2DM Rats Via the TGR5/GLP-1 Rather than FXR/FGF15 Pathway.

Background and Aims: Type 2 Diabetes mellitus (T2DM) has reached an epidemic status worldwide. Targeting bile acid signaling has therapeutic potential for treating T2DM. However, the effect of bile acid on T2DM and related mechanisms remains unclear. Here, we explored the role of bile acid in T2DM and elucidated the mechanisms involved. Methods: We established an STZ-induced rat model of T2DM and divided it into an bile acid-treated group and saline control group according to the random number table method. We incubated the bile acid-treated group with human bile acid via middle small intestine intubation and the saline control group was incubated with the same amount of normal saline. We compared the fasting body mass, fasting blood glucose (FBG), 2-hour postprandial blood glucose (2h-PG), fasting plasma insulin (FINS), fasting plasma triglyceride (TG), cholesterol, and total bile acid levels between the two groups one week before surgery and one to four weeks after surgery. Mechanically, Western blot, IHC, and ELISA assays were employed to detect the effect of bile acid on the TGR5/GLP-1 and FXR/FGF15 pathways. Results: Bile acid injection could increase the FINS level and decrease the 2h-PBG level of T2DM rats. In addition, bile acid injection did not affect FBG, fasting body mass, TG, CH, and total bile acid. At the same time, bile acid injection could activate the TGR5/GLP-1 pathway but could not influence the FXR/FGF15 pathway. Conclusion: Bile acids treatment promotes glucose homeostasis in the STZ-induced T2MD rat model via the following mechanism by activating the TGR5/GLP-1 signaling pathway rather than FXR/FGF15 pathway to improve glucose tolerance and thus achieve glucose homeostasis. The bile acid/TGR5/GLP-1 signaling pathway may be a crucial mechanism of controlling the blood glucose of T2DM rats, and TGR5/GLP-1 pathway may constitute novel targets for treating T2DM.

Raman-guided exploration of placental microplastic exposure: Unraveling the polymeric tapestry and assessing developmental implications.

The prevalence of microplastics in human tissues and their potential reproductive toxicity have been increasingly documented, yet their appearance in the placenta and the impact of microplastic exposure on human fertility and pregnancy remains uncertain. Utilizing an inVia™ confocal Raman microspectroscopy by Renishaw equipped with a detection threshold as low as 0.25 µm, our study examined the microplastics in the placentas of 50 women post-delivery and investigated their correlations with gestational age, and neonatal length and weight. We found that 40 microplastic particles were identified across 31 of 50 placentas, averaging 2.35 ± 1.25 µm in size and ranging from 1.03 to 6.84 µm. Seven distinct polymer types were detected, with PTFE, PS, and ABS being the most prevalent. Notably, no significant difference across the normal, PTFE, and PS groups for all demographic variables examined was identified, nor as pathological alterations of placental tissues. In conclusion, our findings demonstrate the presence of seven microplastic polymers in human placentas, with PTFE, PS, and ABS being the most prevalent. However, maternal and neonatal parameters were not affected, and further studies are necessary to elucidate the effects of microplastics on developmental outcomes and fetal health.

Isolation of Mouse Pancreatic Endothelial Cells.

The pancreas is a vital organ for maintaining metabolic balance within the body, in part due to its production of metabolic hormones such as insulin and glucagon, as well as digestive enzymes. The pancreas is also a highly vascularized organ, a feature facilitated by the intricate network of pancreatic capillaries. This extensive capillary network is made up of highly fenestrated endothelial cells (ECs) important for pancreas development and function. Accordingly, the dysfunction of ECs can contribute to that of the pancreas in diseases like diabetes and cancer. Thus, researching the function of pancreatic ECs (pECs) is important not only for understanding pancreas biology but also for developing its pathologies. Mouse models are valuable tools to study metabolic and cardiovascular diseases. However, there has not been an established protocol with sufficient details described for the isolation of mouse pECs due to the relatively small population of ECs and the abundant digestive enzymes potentially released from the acinar tissue that can lead to cell damage and, thus, low yield. To address these challenges, we devised a protocol to enrich and recover mouse pECs, combining gentle physical and chemical dissociation and antibody-mediated selection. The protocol presented here provides a robust method to extract intact and viable ECs from the whole mouse pancreas. This protocol is suitable for multiple downstream assays and may be applied to various mouse models.

Institutional Support for the Career Advancement of Women Faculty in Science and Academic Medicine: Successes, Challenges, and Future Directions.

Institutional support is crucial for the successful career advancement of all faculty but in particular those who are women. Evolving from the past, in which gender disparities were prevalent in many institutions, recent decades have witnessed significant progress in supporting the career advancement of women faculty in science and academic medicine. However, continued advancement is necessary as previously unrecognized needs and new opportunities for improvement emerge. To identify the needs, opportunities, and potential challenges encountered by women faculty, the Women's Leadership Committee of the Arteriosclerosis, Thrombosis, and Vascular Biology Council developed an initiative termed GROWTH (Generating Resources and Opportunities for Women in Technology and Health). The committee designed a survey questionnaire and interviewed 19 leaders with roles and responsibilities in faculty development from a total of 12 institutions across various regions of the United States. The results were compiled, analyzed, and discussed. Based on our interviews and analyses, we present the current status of these representative institutions in supporting faculty development, highlighting efforts specific to women faculty. Through the experiences, insights, and vision of these leaders, we identified success stories, challenges, and future priorities. Our article provides a primer and a snapshot of institutional efforts to support the advancement of women faculty. Importantly, this article can serve as a reference and resource for academic entities seeking ideas to gauge their commitment level to women faculty and to implement new initiatives. Additionally, this article can provide guidance and strategies for women faculty as they seek support and resources from their current or prospective institutions when pursuing new career opportunities.

Protective Effect of Long Noncoding RNA OXCT1-AS1 on Doxorubicin-Induced Apoptosis of Human Myocardial Cells by the Competitive Endogenous RNA Pattern. / Efeito Protetor do RNA Não Codificante Longo OXCT1-AS1 na Apoptose de Células Miocárdicas Humanas Induzida pela Doxorrubicina pelo Padrão Competitivo de RNA Endógeno.

BACKGROUND: The anthracycline chemotherapeutic antibiotic doxorubicin (DOX) can induce cumulative cardiotoxicity and lead to cardiac dysfunction. Long non-coding RNAs (lncRNAs) can function as important regulators in DOX-induced myocardial injury. OBJECTIVE: This study aims to investigate the functional role and molecular mechanism of lncRNA OXCT1 antisense RNA 1 (OXCT1-AS1) in DOX-induced myocardial cell injury in vitro. METHODS: Human cardiomyocytes (AC16) were stimulated with DOX to induce a myocardial cell injury model. OXCT1-AS1, miR-874-3p, and BDH1 expression in AC16 cells were determined by RT-qPCR. AC16 cell viability was measured by XTT assay. Flow cytometry was employed to assess the apoptosis of AC16 cells. Western blotting was used to evaluate protein levels of apoptosis-related markers. Dual-luciferase reporter assay was conducted to verify the binding ability between miR-874-3p and OXCT1-AS1 and between miR-874-3p and BDH1. The value of p<0.05 indicated statistical significance. RESULTS: OXCT1-AS1 expression was decreased in DOX-treated AC16 cells. Overexpression of OXCT1-AS1 reversed the reduction of cell viability and promotion of cell apoptosis caused by DOX. OXCT1-AS1 is competitively bound to miR-874-3p to upregulate BDH1. BDH1 overexpression restored AC16 cell viability and suppressed cell apoptosis under DOX stimulation. Knocking down BDH1 reversed OXCT1-AS1-mediated attenuation of AC16 cell apoptosis under DOX treatment. CONCLUSION: LncRNA OXCT1-AS1 protects human myocardial cells AC16 from DOX-induced apoptosis via the miR-874-3p/BDH1 axis.

FUNDAMENTO: O antibiótico quimioterápico antraciclina doxorrubicina (DOX) pode induzir cardiotoxicidade cumulativa e levar à disfunção cardíaca. RNAs não codificantes longos (lncRNAs) podem funcionar como importantes reguladores na lesão miocárdica induzida por DOX. OBJETIVO: Este estudo tem como objetivo investigar o papel funcional e o mecanismo molecular do RNA antisense lncRNA OXCT1 1 (OXCT1-AS1) na lesão celular miocárdica induzida por DOX in vitro. MÉTODOS: Cardiomiócitos humanos (AC16) foram estimulados com DOX para induzir um modelo de lesão celular miocárdica. A expressão de OXCT1-AS1, miR-874-3p e BDH1 em células AC16 foi determinada por RT-qPCR. A viabilidade das células AC16 foi medida pelo ensaio XTT. A citometria de fluxo foi empregada para avaliar a apoptose de células AC16. Western blotting foi utilizado para avaliar os níveis proteicos de marcadores relacionados à apoptose. O ensaio repórter de luciferase dupla foi conduzido para verificar a capacidade de ligação entre miR-874-3p e OXCT1-AS1 e entre miR-874-3p e BDH1. O valor de p<0,05 indicou significância estatística. RESULTADOS: A expressão de OXCT1-AS1 foi diminuída em células AC16 tratadas com DOX. A superexpressão de OXCT1-AS1 reverteu a redução da viabilidade celular e a promoção da apoptose celular causada pela DOX. OXCT1-AS1 está ligado competitivamente ao miR-874-3p para regular positivamente o BDH1. A superexpressão de BDH1 restaurou a viabilidade das células AC16 e suprimiu a apoptose celular sob estimulação com DOX. A derrubada do BDH1 reverteu a atenuação da apoptose de células AC16 mediada por OXCT1-AS1 sob tratamento com DOX. CONCLUSÃO: LncRNA OXCT1-AS1 protege células miocárdicas humanas AC16 da apoptose induzida por DOX através do eixo miR-874-3p/BDH1.

Quantum Computation of Conical Intersections on a Programmable Superconducting Quantum Processor.

Conical intersections (CIs) are pivotal in many photochemical processes. Traditional quantum chemistry methods, such as the state-average multiconfigurational methods, face computational hurdles in solving the electronic Schrödinger equation within the active space on classical computers. While quantum computing offers a potential solution, its feasibility in studying CIs, particularly on real quantum hardware, remains largely unexplored. Here, we present the first successful realization of a hybrid quantum-classical state-average complete active space self-consistent field method based on the variational quantum eigensolver (VQE-SA-CASSCF) on a superconducting quantum processor. This approach is applied to investigate CIs in two prototypical systems─ethylene (C2H4) and triatomic hydrogen (H3). We illustrate that VQE-SA-CASSCF, coupled with ongoing hardware and algorithmic enhancements, can lead to a correct description of CIs on existing quantum devices. These results lay the groundwork for exploring the potential of quantum computing to study CIs in more complex systems in the future.

Anterior cervical discectomy and fusion with zero-profile anchored spacer versus plate and cage for three-level contiguous cervical degenerative disease: A systematic review and meta-analysis.

OBJECTIVE: To compare the safety, clinical outcomes and radiological results of anterior cervical discectomy and fusion (ACDF) with zero-profile anchored spacer (ZPAS) versus plate and cage (PC) for three-level contiguous cervical degenerative disease (CDD). METHODS: The study was registered at PROSPERO (CRD42024512706). The Web of Science core collection, PubMed and Embase were searched up to February 12, 2024. Review Manager 5.3 was used. The relative risk (RR) and 95% confidence interval (CI) was evaluated for dichotomous data. Continuous data were assessed using the mean difference (MD) and 95% CI. RESULTS: Nine studies comparing ACDF with ZPAS versus PC for three-level contiguous CDD were included. The intraoperative blood loss and operation time in ZPAS were significantly less than those in PC. The subsidence rate, loss of cervical alignment, fusion segmental height and intervertebral disc height were significantly greater in ZPAS than in PC. The cervical alignment and dysphagia rate within 6 months were significantly lower in ZPAS than in PC. The ASD of ZPAS was significantly lower than that of PC according to the sensitivity analysis when one study was excluded. No significant differences were identified in the other aspects. CONCLUSION: Both ACDF with ZPAS and PC were safe and effective procedures. PC was associated with increased surgical trauma. The ZPAS could better decrease the incidence of ASD and dysphagia. ZPAS was also accompanied by high subsidence rate and poor cervical alignment.

Adult-neurogenesis allows for representational stability and flexibility in early olfactory system.

In the early olfactory system, adult-neurogenesis, a process of neuronal replacement results in the continuous reorganization of synaptic connections and network architecture throughout the animal's life. This poses a critical challenge: How does the olfactory system maintain stable representations of odors and therefore allow for stable sensory perceptions amidst this ongoing circuit instability? Utilizing a detailed spiking network model of early olfactory circuits, we uncovered dual roles for adult-neurogenesis: one that both supports representational stability to faithfully encode odor information and also one that facilitates plasticity to allow for learning and adaptation. In the main olfactory bulb, adult-neurogenesis affects neural codes in individual mitral and tufted cells but preserves odor representations at the neuronal population level. By contrast, in the olfactory piriform cortex, both individual cell responses and overall population dynamics undergo progressive changes due to adult-neurogenesis. This leads to representational drift, a gradual alteration in sensory perception. Both processes are dynamic and depend on experience such that repeated exposure to specific odors reduces the drift due to adult-neurogenesis; thus, when the odor environment is stable over the course of adult-neurogenesis, it is neurogenesis that actually allows the representations to remain stable in piriform cortex; when those olfactory environments change, adult-neurogenesis allows the cortical representations to track environmental change. Whereas perceptual stability and plasticity due to learning are often thought of as two distinct, often contradictory processing in neuronal coding, we find that adult-neurogenesis serves as a shared mechanism for both. In this regard, the quixotic presence of adult-neurogenesis in the mammalian olfactory bulb that has been the focus of considerable debate in chemosensory neuroscience may be the mechanistic underpinning behind an array of complex computations.

Biodegradation of polystyrene (PS) and polypropylene (PP) by deep-sea psychrophilic bacteria of Pseudoalteromonas in accompany with simultaneous release of microplastics and nanoplastics.

Plastics dumped in the environment are fragmented into microplastics by various factors (UV, weathering, mechanical abrasion, animal chewing, etc.). However, little is known about plastic fragmentation and degradation mediated by deep-sea microflora. To obtain deep-sea bacteria that can degrade plastics, we enriched in situ for 1 year in the Western Pacific using PS as a carbon source. Subsequently, two deep-sea prevalent bacteria of the genus Pseudoalteromonas (Pseudoalteromonas lipolytica and Pseudoalteromonas tetraodonis) were isolated after 6 months enrichment in the laboratory under low temperature (15 °C). Both showed the ability to degrade polystyrene (PS) and polypropylene (PP), and biodegradation accelerated the generation of micro- and nanoplastics. Plastic biodegradation was evidenced by the formation of carboxyl and carboxylic acid groups, heat resistance decrease and plastic weight loss. After 80 days incubation at 15 °C, the microplastic concentration of PS and PP could be up to 1.94 × 107/L and 5.83 × 107/L, respectively, and the proportion of nanoplastics (< 1 µm) could be up to 65.8 % and 73.6 %. The film weight loss were 5.4 % and 4.5 % of the PS films, and 2.3 % and 1.8 % of the PP films by P. lipolytica and P. tetraodonis, respectively; thus after discounting the weight loss of microplastics, the only 3.9 % and 2.8 % of the PS films, and 1.3 % and 0.7 % of the PP films, respectively, were truly degraded by the two bacteria respectively after 80 days of incubation. This study highlights the role of Pseudoalteromonas in fragmentation and degradation of plastics in cold dark pelagic deep sea.

Advancements in defensive medicine research: Based on current literature.

To investigate and comprehend the evolving research hotspots, cutting-edge trends, and frontiers associated with defensive medicine. The original data was collected from the Web of Science core collection and then subjected to a preliminary retrieval process. Following screening, a total of 654 relevant documents met the criteria and underwent subsequent statistical analysis. Software CiteSpace was employed for conducting a customized visual analysis on the number of articles, keywords, research institutions, and authors associated with defensive medicine. The defensive medicine research network was primarily established in Western countries, particularly the United States, and its findings and conceptual framework have significantly influenced defensive medicine research in other regions. Currently, quantitative methods dominated most studies while qualitative surveys remained limited. Defensive medicine research mainly focused on high-risk medical specialties such as surgery and obstetrics. Research on defensive medicine pertained to the core characteristics of its conceptual framework. An in-depth investigation into the factors that give rise to defensive medicine is required, along with the generation of more generalizable research findings to provide valuable insights for improving and intervening in defensive medicine.

[Meteorological Influences on Annual Variation and Trend of Autumn Surface Ozone in the Pearl River Delta].

Based on the ozone （O3） monitoring data of the Pearl River Delta （PRD） from 2015 to 2022 and the reanalysis of meteorological data, the impact of meteorological conditions on the annual variation and trends of the maximum daily 8-hour average O3 concentration （MDA8-O3） were quantified using multiple linear regression （MLR） and LMG methods. The results indicated that the MLR model constructed using meteorological parameters from individual months in autumn better simulated the variation in MDA8-O3 compared to that in the model built using meteorological parameters from the entire autumn season. The combined influence of total cloud cover, relative humidity, 2 m maximum temperature, and 850 hPa zonal wind led to a reduction of 34.1 µg·m-3 in MAD8-O3 in 2020 compared to that in 2019, with contributions of 31.3%, 45.2%, 15.8%, and 6.7%, respectively. The observed trends of MDA8-O3 in the PRD for September, October, November, and the autumn season during 2015-2022 were 7.3, 5.2, 4.8, and 5.8 µg·ï¼ˆm3·a）-1, respectively. Among these, the trends driven by meteorological factors were 3.6, 2.4, 2.4, and 3.1 µg·ï¼ˆm3·a）-1. Overall, meteorological conditions contributed 53.4% to the variations in autumn MDA8-O3 in the PRD from 2015 to 2022.

A comprehensive physics-based model for the brachial Artery's full flow mediated dilation (FMD) response observed during the FMD test.

In this study, a physics-based model is developed to describe the entire flow mediated dilation (FMD) response. A parameter quantifying the arterial wall's tendency to recover arises from the model, thereby providing a more elaborate description of the artery's physical state, in concert with other parameters characterizing mechanotransduction and structural aspects of the arterial wall. The arterial diameter's behavior throughout the full response is successfully reproduced by the model. Experimental FMD response data were obtained from healthy volunteers. The model's parameters are then adjusted to yield the closest match to the observed experimental response, hence delivering the parameter values pertaining to each subject. This study establishes a foundation based on which future potential clinical applications can be introduced, where endothelial function and general cardiovascular health are inexpensively and noninvasively quantified.

LncRNA HOXA-AS3 promotes cell proliferation and invasion via targeting miR-218-5p/FOXP1 axis in osteosarcoma.

Osteosarcoma is an aggressive form of bone cancer and affects the health in children and adolescents. Although conventional treatment improves the osteosarcoma survival, some patients have metastasis and drug resistance, leading to a worse prognosis. Therefore, it is necessary to explore the molecular mechanism of osteosarcoma occurrence and progression, which could discover the novel treatment for osteosarcoma. Long noncoding RNAs (lncRNAs) have been reported to regulate osteosarcoma occurrence and malignant progression. LncRNA HOXA-AS3 facilitates the tumorigenesis and progression in a variety of human cancers. However, the underlying mechanism of lncRNA HOXA-AS3-induced oncogenesis is poorly determined in osteosarcoma. To address this point, we utilized several cellular biological strategies and molecular approaches to explore the biological functions and mechanisms of lncRNA HOXA-AS3 in osteosarcoma cells. We found that lncRNA HOXA-AS3 facilitates cell proliferation and invasion via targeting miR-218-5p/FOXP1 axis in osteosarcoma. In conclusion, lncRNA HOXA-AS3 could be a promising target for osteosarcoma treatment.