Examining the association between delay discounting, delay aversion and physical activity in Chinese adults with type-2 diabetes mellitus.

BACKGROUND: The role of physical activity in diabetes is critical, influencing this disease's development, man-agement, and overall outcomes. In China, 22.3% of adults do not meet the minimum level of physical activity recommended by the World Health Organization. Therefore, it is imperative to identify the factors that contributing to lack of physical activity must be identified. AIM: To investigate the relationship among delay discounting, delay aversion, glycated hemoglobin (HbA1c), and various levels of physical activity in Chinese adults diagnosed with type 2 diabetes mellitus (T2DM). METHODS: In 2023, 400 adults with T2DM were recruited from the People's Hospital of Linxia Hui Autonomous Prefecture of Gansu Province. A face-to-face questionnaire was used to gather demographic data and details on physical activity, delay discounting, and delay aversion. In addition, HbA1c levels were measured in all 400 participants. The primary independent variables considered were delay discounting and delay aversion. The outcome variables included HbA1c levels and different intensity levels of physical activity, including walking, moderate physical activity, and vigorous physical activity. Multiple linear regression models were utilized to assess the relationship between delay discounting, delay aversion, and HbA1c levels, along with the intensity of different physical activity measured in met-hours per week. RESULTS: After controlling for the sample characteristics, delay discounting was negatively associated with moderate physical activity (ß = -2.386, 95%CI: -4.370 to -0.401). Meanwhile, delay aversion was negatively associated with the level of moderate physical activity (ß = -3.527, 95% CI: -5.578 to -1.476) in the multiple linear regression model, with statistically significant differences. CONCLUSION: Elevated delay discounting and increased delay aversion correlated with reduced levels of moderate physical activity. Result suggests that delay discounting and aversion may influence engagement in moderate physical activity. This study recommends that health administration and government consider delay discounting and delay aversion when formulating behavioral intervention strategies and treatment guidelines involving physical activity for patients with T2DM, which may increase participation in physical activity. This study contributes a novel perspective to the research on physical activity in adults with T2DM by examining the significance of future health considerations and the role of emotional responses to delays.

Spatiotemporal variations, sources, and atmospheric transformation potential of volatile organic compounds in an industrial zone based on high-resolution measurements in three plants.

Industrial emissions are significant sources of volatile organic compounds (VOCs). This study conducted a field campaign at high temporal and spatial resolution to monitor VOCs within three plants in an industrial park in southern China. VOC concentrations showed significant spatial variability in this industrial zone, with median concentrations of 75.22, 40.53, and 29.41 µg/m3 for the total VOCs in the three plants, respectively, with oxygenated VOCs (OVOCs) or aromatics being the major VOCs. Spatial variability within each plant was also significant but VOC-dependent. Seasonal variations in the VOC levels were governed by their industrial emissions, meteorological conditions, and photochemical losses, and they were different for the four groups of VOCs. The temporal and spatial variations in the VOC compositions suggest similar sources of each class of VOCs during different periods of the year in each plant. The diurnal patterns of VOCs (unimodal or bimodal) clearly differed from those at most industrial/urban locations previously, reflecting a dependence on industrial activities. The secondary transformation potential of VOCs also varied temporally and spatially, and aromatics generally made the predominant contributions in this industrial park. The loss rate of OH radicals and ozone formation potential were highly correlated, but the linear relationship substantially changed in summer and autumn due to the intensive emissions of an OVOC species. The lifetime cancer and non-cancer risks via occupational inhalation of the VOCs in the plants were acceptable but merit attention. Taking the secondary transformation potential and health risks into consideration, styrene, xylene, toluene, trichloroethylene, and benzene were proposed to be the priority VOCs regulated in the plants.

Ningxin-Tongyu-Zishen formula alleviates the senescence of granulosa cells on D-galactose-induced premature ovarian insufficiency mice.

Ningxin-Tongyu-Zishen formula (NTZF) is a clinical experience formula for the treatment of premature ovarian insufficiency (POI) in traditional Chinese medicine (TCM), and the potential mechanism is unknown. For in vivo experiments, POI mouse models (C57BL/6 mice), were constructed by subcutaneous injection of D-galactose (D-gal, 200 mg/kg). After treatment of NTZF (10.14, 20.27, 40.54 g/kg;) or estradiol valerate (0.15 mg/kg), ovarian function, oxidative stress (OS) and protein expression of Sirt1/p53 were evaluated. For in vitro experiments, H2O2 (200 µM) was used to treat KGN to construct ovarian granulosa cells (OGCs) cell senescence model. Pretreatment with NTZF (1.06 mg/mL) or p53 inhibitor (Pifithrin-α, 1 µM) was performed before induction of senescence, and further evaluated the cell senescence, OS, mRNA and protein expression of Sirt1/p53. In vivo, NTZF improved ovarian function, alleviated OS and Sirt1/p53 signaling abnormalities in POI mice. In vitro experiments showed that NTZF reduced the level of OS and alleviated the senescence of H2O2-induced KGN. In addition, NTZF activated the protein expression of Sirt1, inhibited the mRNA transcription and protein expression of p53 and p21. Alleviating OGCs senescence and protecting ovarian function through Sirt1/p53 is one of the potential mechanisms of NTZF in the treatment of POI.

Prediction of the benign and malignant nature of masses in COPD background based on Habitat-based enhanced CT radiomics modeling: A preliminary study.

BACKGROUND: It is difficult to differentiate between chronic obstructive pulmonary disease (COPD)-peripheral bronchogenic carcinoma (COPD-PBC) and inflammatory masses. OBJECTIVE: This study aims to predict COPD-PBC based on clinical data and preoperative Habitat-based enhanced CT radiomics (HECT radiomics) modeling. METHODS: A retrospective analysis was conducted on clinical imaging data of 232 cases of postoperative pathological confirmed PBC or inflammatory masses. The PBC group consisted of 82 cases, while the non-PBC group consisted of 150 cases. A training set and a testing set were established using a 7:3 ratio and a time cutoff point. In the training set, multiple models were established using clinical data and radiomics texture changes within different enhanced areas of the CT mass (HECT radiomics). The AUC values of each model were compared using Delong's test, and the clinical net benefit of the models was tested using decision curve analysis (DCA). The models were then externally validated in the testing set, and a nomogram of predicting COPD-PBC was created. RESULTS: Univariate analysis confirmed that female gender, tumor morphology, CEA, Cyfra21-1, CT enhancement pattern, and Habitat-Radscore B/C were predictive factors for COPD-PBC (P< 0.05). The combination model based on these factors had significantly higher predictive performance [AUC: 0.894, 95% CI (0.836-0.936)] than the clinical data model [AUC: 0.758, 95% CI (0.685-0.822)] and radiomics model [AUC: 0.828, 95% CI (0.761-0.882)]. DCA also confirmed the higher clinical net benefit of the combination model, which was validated in the testing set. The nomogram developed based on the combination model helped predict COPD-PBC. CONCLUSION: The combination model based on clinical data and Habitat-based enhanced CT radiomics can help differentiate COPD-PBC, providing a new non-invasive and efficient method for its diagnosis, treatment, and clinical decision-making.

Analysis and experimental validation of necroptosis-related molecular classification, immune signature and feature genes in Alzheimer's disease.

Necroptosis, a programmed cell death pathway, has been demonstrated to be activated in Alzheimer's disease (AD). However, the precise role of necroptosis and its correlation with immune cell infiltration in AD remains unclear. In this study, we conducted non-negative matrix factorization clustering analysis to identify three subtypes of AD based on necroptosis-relevant genes. Notably, these subtypes exhibited varying necroptosis scores, clinical characteristics and immune infiltration signatures. Cluster B, characterized by high necroptosis scores, showed higher immune cell infiltration and was associated with a more severe pathology, potentially representing a high-risk subgroup. To identify potential biomarkers for AD within cluster B, we employed two machine learning algorithms: the least absolute shrinkage and selection operator regression and Random Forest. Subsequently, we identified eight feature genes (CARTPT, KLHL35, NRN1, NT5DC3, PCYOX1L, RHOQ, SLC6A12, and SLC38A2) that were utilized to develop a diagnosis model with remarkable predictive capacity for AD. Moreover, we conducted validation using bulk RNA-seq, single-nucleus RNA-seq, and in vivo experiments to confirm the expression of these feature genes. In summary, our study identified a novel necroptosis-related subtype of AD and eight diagnostic biomarkers, explored the roles of necroptosis in AD progression and shed new light for the clinical diagnosis and treatment of this disease.

Ntsr1 contributes to pulmonary hypertension by enhancing endoplasmic reticulum stress via JAK2-STAT3-Thbs1 signaling.

Pulmonary hypertension (PH) is a severe clinical syndrome with pulmonary vascular remodeling and poor long-term prognosis. Neurotensin receptor 1 (Ntsr1), serve as one of the G protein-coupled receptors (GPCRs), implicates in various biological processes, but the potential effects of Ntsr1 in PH development are unclear. The Sugen/Hypoxia (SuHx) or monocrotaline (MCT) induced rat PH model was used in our study and the PH rats showed aggravated pulmonary artery remodeling and increased right ventricular systolic pressure (RVSP). Our results revealed that Ntsr1 induced endoplasmic reticulum (ER) stress response via ATF6 activation contributed to the development of PH. Moreover, RNA-sequencing (RNA-seq) and phosphoproteomics were performed and the Ntsr1-JAK2-STAT3-thrombospondin 1 (Thbs1)-ATF6 signaling was distinguished as the key pathway. In vitro, pulmonary artery smooth muscle cells (PASMCs) under hypoxia condition showed enhanced proliferation and migration properties, which could be inhibited by Ntsr1 knockdown, JAK2 inhibitor (Fedratinib) treatment, STAT3 inhibitior (Stattic) treatment, Thbs1 knockdown or ATF6 knockdown. In addition, adeno-associated virus 1 (AAV1) were used to knockdown the expression of Ntsr1, Thbs1 or ATF6 in rats and reversed the phenotype of PH. In summary, our results reveal that Ntsr1-JAK2-STAT3-Thbs1 pathway can induce enhanced ER stress via ATF6 activation and increased PASMC proliferation and migration capacities, which can be mechanism of the pulmonary artery remodeling and PH. Targeting Ntsr1 might be a novel therapeutic strategy to ameliorate PH.

Zbtb16 increases susceptibility of atrial fibrillation in type 2 diabetic mice via Txnip-Trx2 signaling.

Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia, and recent epidemiological studies suggested type 2 diabetes mellitus (T2DM) is an independent risk factor for the development of AF. Zinc finger and BTB (broad-complex, tram-track and bric-a-brac) domain containing 16 (Zbtb16) serve as transcriptional factors to regulate many biological processes. However, the potential effects of Zbtb16 in AF under T2DM condition remain unclear. Here, we reported that db/db mice displayed higher AF vulnerability and Zbtb16 was identified as the most significantly enriched gene by RNA sequencing (RNA-seq) analysis in atrium. In addition, thioredoxin interacting protein (Txnip) was distinguished as the key downstream gene of Zbtb16 by Cleavage Under Targets and Tagmentation (CUT&Tag) assay. Mechanistically, increased Txnip combined with thioredoxin 2 (Trx2) in mitochondrion induced excess reactive oxygen species (ROS) release, calcium/calmodulin-dependent protein kinase II (CaMKII) overactivation, and spontaneous Ca2+ waves (SCWs) occurrence, which could be inhibited through atrial-specific knockdown (KD) of Zbtb16 or Txnip by adeno-associated virus 9 (AAV9) or Mito-TEMPO treatment. High glucose (HG)-treated HL-1 cells were used to mimic the setting of diabetic in vitro. Zbtb16-Txnip-Trx2 signaling-induced excess ROS release and CaMKII activation were also verified in HL-1 cells under HG condition. Furthermore, atrial-specific Zbtb16 or Txnip-KD reduced incidence and duration of AF in db/db mice. Altogether, we demonstrated that interrupting Zbtb16-Txnip-Trx2 signaling in atrium could decrease AF susceptibility via reducing ROS release and CaMKII activation in the setting of T2DM.

Unraveling the causes of sarcopenia: Roles of neuromuscular junction impairment and mitochondrial dysfunction.

Sarcopenia is a systemic skeletal muscle disease characterized by a decline in skeletal muscle mass and function. Originally defined as an age-associated condition, sarcopenia presently also encompasses muscular atrophy due to various pathological factors, such as intensive care unit-acquired weakness, inactivity, and malnutrition. The exact pathogenesis of sarcopenia is still unknown; herein, we review the pathological roles of the neuromuscular junction and mitochondria in this condition. Sarcopenia is caused by complex and interdependent pathophysiological mechanisms, including aging, neuromuscular junction impairment, mitochondrial dysfunction, insulin resistance, lipotoxicity, endocrine factors, oxidative stress, and inflammation. Among these, neuromuscular junction instability and mitochondrial dysfunction are particularly significant. Dysfunction in neuromuscular junction can lead to muscle weakness or paralysis. Mitochondria, which are plentiful in neurons and muscle fibers, play an important role in neuromuscular junction transmission. Therefore, impairments in both mitochondria and neuromuscular junction may be one of the key pathophysiological mechanisms leading to sarcopenia. Moreover, this article explores the structural and functional alterations in the neuromuscular junction and mitochondria in sarcopenia, suggesting that a deeper understanding of these changes could provide valuable insights for the prevention or treatment of sarcopenia.

Discovery of astragaloside IV against high glucose-induced apoptosis in retinal ganglion cells: Bioinformatics and in vitro studies.

OBJECTIVE: To examine the therapeutic mechanism of astragaloside IV (AS-IV) in the management of retinal ganglion cell (RGC) injury induced by high glucose (HG), a comprehensive approach involving the integration of network pharmacology and conducting in vitro and in vivo experiments was utilized. METHODS: A rat model of diabetic retinopathy (DR) injury was created by administering streptozotocin through intraperitoneal injection. Additionally, a model of RGC injury induced by HG was established using a glucose concentration of 0.3 mmol/mL. Optical coherence tomography (OCT) images were captured 8 weeks after the injection of AS-IV. AS-IV and FBS were added to the culture medium and incubated for 48 h. The viability of cells was assessed using a CCK-8 assay, while the content of reactive oxygen species (ROS) was measured using DCFH-DA. Apoptosis was evaluated using Annexin V-PI. To identify the targets of AS-IV, hyperglycemia, and RGC, publicly available databases were utilized. The Metascape platform was employed for conducting GO and KEGG enrichment analyses. The STRING database in conjunction with Cytoscape 3.7.2 was used to determine common targets of protein-protein interactions (PPIs) and to identify the top 10 core target proteins in the RGC based on the MCC algorithm. qRT-PCR was used to measure the mRNA expression levels of the top10 core target proteins in RGCs. RESULTS: OCT detection indicated that the thickness of the outer nucleus, and inner and outer accessory layers of the retina increased in the AS-IV treated retina compared to that in the DM group but decreased compared to that in the CON group. Coculturing RGC cells with AS-IV after HG induction resulted in a significant increase in cell viability and a decrease in ROS and apoptosis, suggesting that AS-IV can reduce damage to RGC cells caused by high glucose levels by inhibiting oxidative stress. There were 14 potential targets of AS-IV in the treatment of RGC damage induced by high glucose levels. The top 10 core target proteins identified by the MCC algorithm were HIF1α, AKT1, CTNNB1, SMAD2, IL6, SMAD3, IL1ß, PPARG, TGFß1, and NOTCH3. qRT-PCR analysis showed that AS-IV could upregulate the mRNA expression levels of SMAD3, TGF-ß1, and NOTCH3, and downregulate the mRNA expression levels of HIF1α, AKT1, CTNNB1, SMAD2, SMAD3, and IL-1ß in high glucose-induced RGC cells. CONCLUSION: The findings of this study validate the efficacy of astragaloside IV in the treatment of DR and shed light on the molecular network involved. Specifically, HIF1α, AKT1, CTNNB1, SMAD2, SMAD3, and IL-1ß were identified as the crucial candidate molecules responsible for the protective effects of astragaloside IV on RGCs.

Circ_0068481 Affects the Human Pulmonary Artery Smooth Muscle Cells' Progression by miR-361-3p/KLF5 Axis.

BACKGROUND: Uncontrolled proliferation of pulmonary artery smooth muscle cells (PASMCs) contributes to the pathogenesis of pulmonary arterial hypertension (PAH). In this work, we defined the precise part of circ_0068481 in PASMC proliferation and migration induced by hypoxia. We hypothesized that circ_0068481 enhanced hypoxia-induced PASMC proliferation, invasion, and migration through the microRNA (miR)-361-3p/Krüppel-like factor 5 (KLF5) pathway. METHODS: Human PASMCs (hPASMCs) were exposed to hypoxic (3% O2) conditions. Circ_0068481, miR-361-3p, and KLF5 levels were gauged by qRT-PCR and western blot. Cell viability, proliferation, invasion, and migration were detected by XTT, EdU incorporation, transwell, and wound-healing assays, respectively. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays were performed to confirm the direct relationship between miR-361-3p and circ_0068481 or KLF5. RESULTS: Circ_0068481 expression was increased in the serum of PAH patients and hypoxia-induced hPASMCs. Downregulation of circ_0068481 attenuated hypoxia-induced promotion in hPASMC proliferation, invasion, and migration. Circ_0068481 directly targeted miR-361-3p, and miR-361-3p downregulation reversed the inhibitory effects of circ_0068481 silencing on hypoxia-induced hPASMC proliferation, invasion, and migration. KLF5 was a direct miR-361-3p target, and miR-361-3p upregulation mitigated hypoxia-induced hPASMC proliferation, invasion, and migration by inhibiting KLF5 expression. Moreover, circ_0068481-induced KLF5 expression by binding to miR-361-3p in hypoxic hPASMCs. CONCLUSIONS: Circ_0068481 knockdown ameliorated hypoxia-induced hPASMC proliferation, invasion, and migration at least in part through the miR-361-3p/KLF5 axis.

Work conflict: Another trigger to smartphone addiction of individuals with high rumination?

With the widespread use of smartphones, many people spend much time on smartphones for shopping, learning, socializing, and so on, which can affect an individual's mental health and work performance. Especially, individual perceived conflict at work may increase their social anxiety and thus raise the risk of their smartphone addiction. This study collected data from 577 corporate employees in China through convenience sampling to explain the influence mechanism of work conflict on smartphone addiction and to verify the moderating role of rumination. Statistical results show that relationship conflicts, task conflicts, and process conflicts positively affect smartphone addiction by enhancing social anxiety. Moreover, rumination positively moderates the relationship between work conflict and smartphone addiction. People with high rumination are more likely to escape reality due to conflict at work, which further enhances their smartphone addiction behaviors. Our study suggests that a relatively harmonious working atmosphere should be established within organizations, especially for employees with rumination. Work conflict is a predisposing factor for social anxiety and smartphone addiction in individuals with high rumination.

Dipeptidyl peptidase 4 inhibition sensitizes radiotherapy by promoting T cell infiltration.

Radiotherapy could regulate systemic antitumor immunity, while the immune state in the tumor microenvironment (TME) also affects the efficacy of radiotherapy. We have found that higher CD8+ T cell infiltration is associated with longer overall survival of lung adenocarcinoma and melanoma patients receiving radiotherapy. 8-Gray radiation increased the transcriptional levels of chemokines in tumor cells in vitro. However, it was not sufficient to induce significant lymphocyte infiltration in vivo. Dipeptidyl peptidase 4 (DPP4) has been reported to inactivate chemokines via post-translational truncation. Single-cell sequencing revealed that dendritic cells (DCs) had a higher DPP4 expression among other cells in the TME and upregulated DPP4 expression after radiation. Combining a DPP4 inhibitor with radiotherapy could promote chemokines expression and T cell infiltration in the TME, enhancing the antitumor effect of radiotherapy. Moreover, this therapy further enhanced the therapeutic efficacy of anti-PD-1. In this study, we demonstrated the underlying mechanism of why radiotherapy failed to induce sufficient T cell infiltration and proposed an effective strategy to promote T cell infiltration and sensitize radiotherapy. These findings demonstrate the translational value of DPP4 inhibition as a complementary approach to enhance the efficacy of radiotherapy and the combination of radiotherapy with immunotherapy.

Identification of metabolism-related subtypes and feature genes in Alzheimer's disease.

BACKGROUND: Owing to the heterogeneity of Alzheimer's disease (AD), its pathogenic mechanisms are yet to be fully elucidated. Evidence suggests an important role of metabolism in the pathophysiology of AD. Herein, we identified the metabolism-related AD subtypes and feature genes. METHODS: The AD datasets were obtained from the Gene Expression Omnibus database and the metabolism-relevant genes were downloaded from a previously published compilation. Consensus clustering was performed to identify the AD subclasses. The clinical characteristics, correlations with metabolic signatures, and immune infiltration of the AD subclasses were evaluated. Feature genes were screened using weighted correlation network analysis (WGCNA) and processed via Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Furthermore, three machine-learning algorithms were used to narrow down the selection of the feature genes. Finally, we identified the diagnostic value and expression of the feature genes using the AD dataset and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis. RESULTS: Three AD subclasses were identified, namely Metabolism Correlated (MC) A (MCA), MCB, and MCC subclasses. MCA contained signatures associated with high AD progression and may represent a high-risk subclass compared with the other two subclasses. MCA exhibited a high expression of genes related to glycolysis, fructose, and galactose metabolism, whereas genes associated with the citrate cycle and pyruvate metabolism were downregulated and associated with high immune infiltration. Conversely, MCB was associated with citrate cycle genes and exhibited elevated expression of immune checkpoint genes. Using WGCNA, 101 metabolic genes were identified to exhibit the strongest association with poor AD progression. Finally, the application of machine-learning algorithms enabled us to successfully identify eight feature genes, which were employed to develop a nomogram model that could bring distinct clinical benefits for patients with AD. As indicated by the AD datasets and qRT-PCR analysis, these genes were intimately associated with AD progression. CONCLUSION: Metabolic dysfunction is associated with AD. Hypothetical molecular subclasses of AD based on metabolic genes may provide new insights for developing individualized therapy for AD. The feature genes highly correlated with AD progression included GFAP, CYB5R3, DARS, KIAA0513, EZR, KCNC1, COLEC12, and TST.

Protein-coated cobalt oxide-hydroxide nanospheres deliver photosensitizer IR780 iodide for near-infrared light-triggered photodynamic/photothermal/chemodynamic therapy against colon cancer.

Phototherapy has garnered worldwide attention for its minimal invasiveness, controllability, and spatial selectivity in treating cancer. One promising approach involves the use of near-infrared dye IR780, which demonstrates both photodynamic therapy (PDT) and photothermal therapy (PTT) effects under 808 nm laser irradiation. However, this hydrophobic dye's toxicity and limited tumor targeting ability severely hamper its suitability for cancer applications. Herein, a biocompatible nanoplatform CoOOH-IR780@BSA (CoIRB) is developed to efficiently deliver IR780 and provide multi-mode treatments for colon tumors. Due to the nanocarrier coating, CoIRB nanoparticles demonstrated reliable dispersion and stability, and their biotoxicity was substantially reduced for safer blood circulation, which overcame the biological barrier of IR780. The nanoplatform has also shown considerable results in phototherapy in vivo and in vitro experiments, with successful inhibition of MC38 tumor growth through intravenous administration. Additionally, the introduction of cobalt ions could induce Fenton-like reactions to activate the production of toxic hydroxyl radicals (˙OH), exerting an assisted chemodynamic therapy (CDT) effect. Notably, these nanodrugs also exhibited potential as scavengers of reductive glutathione (GSH) and hydrogen sulfide (H2S), leading to amplifying oxidative damage of reactive oxygen species (ROS). Overall, the versatile therapeutic platform, CoIRB, has opened up considerable prospects as a biotherapeutic option for combining PDT/PTT/CDT against colon cancer.

A comparison of behavioral paradigms assessing spatial memory in tree shrews.

Impairments in spatial navigation in humans can be preclinical signs of Alzheimer's disease. Therefore, cognitive tests that monitor deficits in spatial memory play a crucial role in evaluating animal models with early stage Alzheimer's disease. While Chinese tree shrews (Tupaia belangeri) possess many features suitable for Alzheimer's disease modeling, behavioral tests for assessing spatial cognition in this species are lacking. Here, we established reward-based paradigms using the radial-arm maze and cheeseboard maze for tree shrews, and tested spatial memory in a group of 12 adult males in both tasks, along with a control water maze test, before and after bilateral lesions to the hippocampus, the brain region essential for spatial navigation. Tree shrews memorized target positions during training, and task performance improved gradually until reaching a plateau in all 3 mazes. However, spatial learning was compromised post-lesion in the 2 newly developed tasks, whereas memory retrieval was impaired in the water maze task. These results indicate that the cheeseboard task effectively detects impairments in spatial memory and holds potential for monitoring progressive cognitive decline in aged or genetically modified tree shrews that develop Alzheimer's disease-like symptoms. This study may facilitate the utilization of tree shrew models in Alzheimer's disease research.

Value of applying interactive micro-courses on occupational protection in operating room for nursing trainees.

This study aimed to investigate the application value of an interactive micro class on occupational protection in the operating room for nursing interns. Using a cluster sampling approach, 200 junior college nursing interns were selected as participants at our hospital, who were practicing from June 2020 to April 2021. They were randomly assigned to either the observation group or the control group, with 100 participants in each. Data on teaching-related evaluation indicators, including clarity of teaching objectives, learning atmosphere, rational use of learning resources, effectiveness of teaching process regulation, and degree of students' participation in activities, were collected for both groups. Additionally, the scores of occupational protection assessment in the operating room, which encompassed physical, chemical, biological, environmental, and physiological and psychological factors, were also recorded. The comparative analysis of teaching-related evaluation indicators between the 2 groups revealed statistically significant differences. Specifically, significant differences were found between the 2 groups in the clarity of teaching objectives (P = .007), learning atmosphere (P < .001), rational use of learning resources (P < .001), effectiveness of teaching process regulation (P = .01), and degree of students' participation in activities (P < .001). Furthermore, the scores of all items in the observation group were higher than those in the control group. Additionally, the comparison results of the scores of the occupational protection assessment in the operating room between the 2 groups showed that while there was no statistically significant difference between the 2 groups before the intervention (P > .05). However, after the intervention, statistically significant differences were found between the 2 groups in physical (P < .001), chemical (P = .001), biological (P < .001), environmental (P < .001), and physiological and psychological factors (P < .001). Additionally, the scores of all items in the observation group were higher than those in the control group. The implementation of the interactive micro class enhanced the quality of teaching related to occupational protection in the operating room for interning nurses, thus verifying its benefits in clinical teaching practices.

Hyaluronic Acid-Based Nanocarriers for Anticancer Drug Delivery.

Hyaluronic acid (HA), a main component of the extracellular matrix, is widely utilized to deliver anticancer drugs due to its biocompatibility, biodegradability, non-toxicity, non-immunogenicity and numerous modification sites, such as carboxyl and hydroxyl groups. Moreover, HA serves as a natural ligand for tumor-targeted drug delivery systems, as it contains the endocytic HA receptor, CD44, which is overexpressed in many cancer cells. Therefore, HA-based nanocarriers have been developed to improve drug delivery efficiency and distinguish between healthy and cancerous tissues, resulting in reduced residual toxicity and off-target accumulation. This article comprehensively reviews the fabrication of anticancer drug nanocarriers based on HA in the context of prodrugs, organic carrier materials (micelles, liposomes, nanoparticles, microbubbles and hydrogels) and inorganic composite nanocarriers (gold nanoparticles, quantum dots, carbon nanotubes and silicon dioxide). Additionally, the progress achieved in the design and optimization of these nanocarriers and their effects on cancer therapy are discussed. Finally, the review provides a summary of the perspectives, the lessons learned so far and the outlook towards further developments in this field.

Crop-Weed Introgression Plays Critical Roles in Genetic Differentiation and Diversity of Weedy Rice: A Case Study of Human-Influenced Weed Evolution.

As an important driving force, introgression plays an essential role in shaping the evolution of plant species. However, knowledge concerning how introgression affects plant evolution in agroecosystems with strong human influences is still limited. To generate such knowledge, we used InDel (insertion/deletion) molecular fingerprints to determine the level of introgression from japonica rice cultivars into the indica type of weedy rice. We also analyzed the impact of crop-to-weed introgression on the genetic differentiation and diversity of weedy rice, using InDel (insertion/deletion) and SSR (simple sequence repeat) molecular fingerprints. Results based on the STRUCTURE analysis indicated an evident admixture of some weedy rice samples with indica and japonica components, suggesting different levels of introgression from japonica rice cultivars to the indica type of weedy rice. The principal coordinate analyses indicated indica-japonica genetic differentiation among weedy rice samples, which was positively correlated with the introgression of japonica-specific alleles from the rice cultivars. In addition, increased crop-to-weed introgression formed a parabola pattern of dynamic genetic diversity in weedy rice. Our findings based on this case study provide evidence that human activities, such as the frequent change in crop varieties, can strongly influence weed evolution by altering genetic differentiation and genetic diversity through crop-weed introgression in agroecosystems.

Abundance and characteristics of microplastics in the Wanquan River estuary, Hainan Island.

As the nexus where rivers and oceans meet, estuaries are vulnerable to microplastic (MP) pollution derived from rivers. However, few studies have focused on the pollution status of MPs in small estuarine areas. Here, the abundance and characteristics of MPs in surface water and sediment samples from a small estuary, the Wanquan River estuary, were studied. The average abundance of MPs was 6573 ± 2659 n/m3 in surface water and 1065 ± 696 n/kg dw in sediment samples from the Wanquan River estuary. Most of the MPs in water samples and sediments were red (92.9 % and 88.1 %) fragments (87.4 % and 95.5 %) with sizes <1.0 mm (90.8 % and 92.4 %) made up of antifouling paint particles (APPs) (83.5 % and 89.8 %), respectively. A significant positive correlation (p < 0.01) was found between the concentration of Cu2+ and the abundance of APPs in sediment samples from the Wanquan River estuary. The APPs in the sediments can act as a continuous source of toxic chemicals (e.g., Cu2+) to marine environments. The results of this study expand our knowledge about MP pollution in small estuaries, and the ecological risk of APPs in the Wanquan River estuary to aquatic organisms should not be ignored.

An integrative investigation of developmental toxicities induced by triphenyltin in a larval coral reef fish, Amphiprion ocellaris.

Triphenyltin (TPT) is widely distributed on coastlines, which makes coral reef fish a potential target of TPT pollution. However, the negative effects of TPT on coral reef fish remain poorly understood. Therefore, in the present study, the larval coral reef fish Amphiprion ocellaris was used to investigate the developmental toxicities of TPT at environmentally relevant concentrations (0, 1, 10 and 100 ng/L). After TPT exposure for 14 d, the cumulative mortality increased, and growth was suppressed. In addition, TPT exposure inhibited the development of melanophores and xanthophores and delayed white strip formation, which might be responsible for the disruption of the genes (erbb3b, mitfa, kit, xdh, tyr, oca2, itk and trim33) related to pigmentation. TPT exposure also attenuated ossification of head skeletal elements and the vertebral column and inhibited the expression of genes (bmp2, bmp4 and sp7) related to skeletal development. The observed developmental toxicities on growth, pigmentation and skeleton development might be associated with the disruption of thyroid hormones and the genes related to thyroid hormone regulation (tshß, thrα, thrß, tg, tpo, dio2, and ttr). In addition, TPT exposure interfered with locomotor and shoaling behavior, and the related genes dbh, avp and avpr1aa. Taken together, our results suggest that TPT pollution might threaten the development of one of the most iconic coral reef fish, which might produce disastrous consequences on the health of coral reef ecosystems.