PET/CT Recognition of Costal Cartilage Infection After Breast Implant Surgery.

BACKGROUND: Postoperative infection of breast implants can lead to implant removal and other complications. This study aimed to investigate the presence of costal cartilage infection following breast implant surgery and the diagnostic role of PET/CT in identifying this rare complication. PATIENTS AND METHODS: A retrospective study included 16 patients with persistent infections after breast implant removal surgery. Patients underwent PET/CT scans before surgery, and surgical plans were made based on PET/CT findings. Surgical procedures were guided by PET/CT, and specimens were collected for pathological examination and microbiological culture. Follow-up assessments were performed at 1, 3, and 12 months postoperatively. RESULTS: Among the 16 patients, 11 were diagnosed with costal cartilage infection, whereas 5 had subcutaneous soft tissue infections. PET/CT accurately identified costal cartilage infection in all cases and localized the infected costal cartilage in the majority of cases. Microbiological culture results showed various pathogens. All patients were cured with one or staged surgery. CONCLUSION: Costal cartilage infection following breast implant surgery is a significant concern. PET/CT plays a crucial role in the accurate diagnosis and localization of infected costal cartilage, aiding in appropriate surgical management. Patients should be closely monitored for the possibility of costal cartilage infection when experiencing persistent symptoms after breast implant surgery.

Assessing the impact of temperature on acute exacerbation of chronic obstructive pulmonary disease hospitalizations in residents of Panzhihua City: a multi-districts study using a distributed lag non-linear model.

BACKGROUND: Temperature fluctuations can impact the occurrence and progression of respiratory system diseases. However, the current understanding of the impact of temperature on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) remains limited. Therefore, our study aims to investigate the relationship between daily mean temperature (DMT) and the risk of AECOPD hospitalizations within Panzhihua City. METHODS: We systematically collected data on AECOPD hospitalizations at Panzhihua Central Hospital from 2015 to 2020 and meteorological factors across Panzhihua City's districts. A two-stage analysis method was used to establish a distributed lag non-linear model to elucidate the influence of DMT on the frequency of admissions for AECOPD. Subgroup analyses were conducted by gender and age to identify populations potentially susceptible to the impact of DMT. RESULTS: A total of 5299 AECOPD hospitalizations cases were included. The DMT and the risk of AECOPD hospitalization showed a non-linear exposure-response pattern, with low temperatures exacerbating the risk of hospitalizations. The lag effects of low temperature and relatively low temperature peaked at 2th day, with the lag effects disappearing at 16-17 days. Females and elders aged ≥ 65 years were more sensitive to effects of low and relatively low temperature at lag 0-4 days, while male AECOPD patients exhibited longer lasting lag effects. CONCLUSIONS: Low temperatures are associated with an increased risk of AECOPD hospitalizations. Females or elders aged ≥ 65 years with chronic obstructive pulmonary disease should pay more attention to taking protective measures in cold environments. These findings are crucial for the formulation of public health policies, as they will help significantly alleviate the burden of AECOPD and improve respiratory health in the face of climate challenges.

Rhodium(III) Complex Noncanonically Potentiates Antitumor Immune Responses by Inhibiting Wnt/ß-Catenin Signaling.

Metal-based chemoimmunotherapy has recently garnered significant attention for its capacity to stimulate tumor-specific immunity beyond direct cytotoxic effects. Such effects are usually caused by ICD via the activation of DAMP signals. However, metal complexes that can elicit antitumor immune responses other than ICD have not yet been described. Herein, we report that a rhodium complex (Rh-1) triggers potent antitumor immune responses by downregulating Wnt/ß-catenin signaling with subsequent activation of T lymphocyte infiltration to the tumor site. The results of mechanistic experiments suggest that ROS accumulation following Rh-1 treatment is a critical trigger of a decrease in ß-catenin and enhanced secretion of CCL4, a key mediator of T cell infiltration. Through these properties, Rh-1 exerts a synergistic effect in combination with PD-1 inhibitors against tumor growth in vivo. Taken together, our work describes a promising metal-based antitumor agent with a noncanonical mode of action to sensitize tumor tissues to ICB therapy.

Inhibition of ANGPTL8 protects against diabetes-associated cognitive dysfunction by reducing synaptic loss via the PirB signaling pathway.

BACKGROUND: Type 2 diabetes mellitus (T2D) is associated with an increased risk of cognitive dysfunction. Angiopoietin-like protein 8 (ANGPTL8) is an important regulator in T2D, but the role of ANGPTL8 in diabetes-associated cognitive dysfunction remains unknown. Here, we explored the role of ANGPTL8 in diabetes-associated cognitive dysfunction through its interaction with paired immunoglobulin-like receptor B (PirB) in the central nervous system. METHODS: The levels of ANGPTL8 in type 2 diabetic patients with cognitive dysfunction and control individuals were measured. Mouse models of diabetes-associated cognitive dysfunction were constructed to investigate the role of ANGPTL8 in cognitive function. The cognitive function of the mice was assessed by the Barnes Maze test and the novel object recognition test, and levels of ANGPTL8, synaptic and axonal markers, and pro-inflammatory cytokines were measured. Primary neurons and microglia were treated with recombinant ANGPTL8 protein (rA8), and subsequent changes were examined. In addition, the changes induced by ANGPTL8 were validated after blocking PirB and its downstream pathways. Finally, mice with central nervous system-specific knockout of Angptl8 and PirB-/- mice were generated, and relevant in vivo experiments were performed. RESULTS: Here, we demonstrated that in the diabetic brain, ANGPTL8 was secreted by neurons into the hippocampus, resulting in neuroinflammation and impairment of synaptic plasticity. Moreover, neuron-specific Angptl8 knockout prevented diabetes-associated cognitive dysfunction and neuroinflammation. Mechanistically, ANGPTL8 acted in parallel to neurons and microglia via its receptor PirB, manifesting as downregulation of synaptic and axonal markers in neurons and upregulation of proinflammatory cytokine expression in microglia. In vivo, PirB-/- mice exhibited resistance to ANGPTL8-induced neuroinflammation and synaptic damage. CONCLUSION: Taken together, our findings reveal the role of ANGPTL8 in the pathogenesis of diabetes-associated cognitive dysfunction and identify the ANGPTL8-PirB signaling pathway as a potential target for the management of this condition.

Omentin-1 attenuates lipopolysaccharide-induced inflammation and osteogenic differentiation in periodontal ligament stem cells and reduces M1 macrophages polarization through repressing endoplasmic reticulum stress.

Periodontitis is featured as the periodontium's pathologic destruction caused by the host's overwhelmed inflammation. Omentin-1 has been reported to be aberrantly downregulated in patients with periodontitis, but the specific regulation of Omentin-1 during the pathogenesis of periodontitis remains unclear. In this study, human periodontal ligament stem cells (hPDLSCs) were stimulated by lipopolysaccharide (LPS) from Porphyromonas gingivalis to establish an in vitro inflammatory periodontitis model. hPDLSCs were treated with recombinant human Omentin-1 (250, 500 and 750ng/mL) for 3h before LPS stimulation. Results revealed that Omentin-1 significantly inhibited LPS-induced inflammation in hPDLSCs through reducing the production of proinflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6) and downregulating the expression of Cox2 and iNOS. Meanwhile, Omentin-1 significantly enhanced alkaline phosphatase (ALP) activity and Alizarin red-stained area, accompanied by increasing expression osteogenic markers BMP2, OCN and Runx2, confirming that Omentin-1 restores osteogenic differentiation in LPS-induced hPDLSCs. In addition, the conditioned medium (CM) from LPS-induced hPDLSCs was harvested to culture macrophages, which resulted in macrophage polarization towards M1, while CM from Omentin-1-treated hPDLSCs reduced M1 macrophages polarization and elevated M2 polarization. Furthermore, Omentin-1 also inhibited LPS-triggered endoplasmic reticulum (ER) stress in hPDLSCs, and additional treatment of the ER stress activator tunicamycin (TM) partially reversed the functions of Omentin-1 on inflammation, osteogenic differentiation and macrophages polarization. In summary, Omentin-1 exerted a protective role against periodontitis through inhibiting inflammation and enhancing osteogenic differentiation of hPDLSCs, providing a novelty treatment option for periodontitis.

Malic enzymes in cancer: Regulatory mechanisms, functions, and therapeutic implications.

Malic enzymes (MEs) are metabolic enzymes that catalyze the oxidation of malate to pyruvate and NAD(P)H. While researchers have well established the physiological metabolic roles of MEs in organisms, recent research has revealed a link between MEs and carcinogenesis. This review collates evidence of the molecular mechanisms by which MEs promote cancer occurrence, including transcriptional regulation, post-transcriptional regulation, post-translational protein modifications, and protein-protein interactions. Additionally, we highlight the roles of MEs in reprogramming energy metabolism, suppressing senescence, and modulating the tumor immune microenvironment. We also discuss the involvement of these enzymes in mediating tumor resistance and how the development of novel small-molecule inhibitors targeting MEs might be a good therapeutic approach. Insights through this review are expected to provide a comprehensive understanding of the intricate relationship between MEs and cancer, while facilitating future research on the potential therapeutic applications of targeting MEs in cancer management.

Brain region-specific action of ketamine as a rapid antidepressant.

Ketamine has been found to have rapid and potent antidepressant activity. However, despite the ubiquitous brain expression of its molecular target, the N-methyl-d-aspartate receptor (NMDAR), it was not clear whether there is a selective, primary site for ketamine's antidepressant action. We found that ketamine injection in depressive-like mice specifically blocks NMDARs in lateral habenular (LHb) neurons, but not in hippocampal pyramidal neurons. This regional specificity depended on the use-dependent nature of ketamine as a channel blocker, local neural activity, and the extrasynaptic reservoir pool size of NMDARs. Activating hippocampal or inactivating LHb neurons swapped their ketamine sensitivity. Conditional knockout of NMDARs in the LHb occluded ketamine's antidepressant effects and blocked the systemic ketamine-induced elevation of serotonin and brain-derived neurotrophic factor in the hippocampus. This distinction of the primary versus secondary brain target(s) of ketamine should help with the design of more precise and efficient antidepressant treatments.

Associations between Long-Term Dietary Coenzyme Q10 Intake and New-Onset Hypertension in Adults: Insights from a Nationwide Prospective Cohort Study.

Coenzyme Q10 (CoQ10) supplementation appears to be associated with a lower blood pressure. Nevertheless, it remains unclear whether food-sourced CoQ10 will affect new-onset hypertension in general adults. This study investigated the relationship between dietary CoQ10 intake and new-onset hypertension among the general population. Participants without hypertension at baseline from the China Health and Nutrition Survey (CHNS) prospective cohort study were included (n = 11,428). Dietary CoQ10 intake was collected by validated dietary recalls and the food weighing method. Linear and non-linear relationships between dietary CoQ10 intake and new-onset hypertension were analyzed using multivariable Cox proportional hazards models and restricted cubic splines. During follow-up (median: 6 years), 4006 new-onset hypertension cases were documented. Compared with non-consumers, the hazard ratio (HR) and 95% confidence interval (CI) from quintile 2 to 4 total dietary CoQ10 were 0.83 (0.76, 0.91), 0.86 (0.78, 0.94) and 1.01 (0.92, 1.11); total plant-derived CoQ10 were 0.80 (0.73, 0.88), 1.00 (0.91, 1.09) and 1.10 (1.00, 1.20); and animal-derived CoQ10 were 0.65 (0.59, 0.71), 0.58 (0.53, 0.64) and 0.68 (0.62, 0.75). The lowest risk was found at moderate intake, with a non-linear relationship (P nonlinearity < 0.05). Furthermore, the overall inverse association was stronger among individuals without alcohol consumption or eating a low-fat diet. Moderate long-term dietary CoQ10 intake might be protective against new-onset hypertension. However, it follows a non-linear relationship and excessive intake may increase the risk of new-onset hypertension in the Chinese population.

Association between adherence to life's simple 7 metrics and risk of obstructive sleep apnea among adults in the United States.

BACKGROUND: We aimed to explore the impact of adherence to Life's Simple 7 (LS7) metrics on risk of obstructive sleep apnea (OSA), and the impact of inflammation on the association, in adults in the United States. METHODS: Data from 13,825 community-dwelling adults aged ≥ 20 years recruited in the National Health and Nutrition Examination Surveys (NHANES) 2005-2008, 2015-2018 was analyzed. The LS7 score was calculated based on the AHA definition of LS7 metrics. The diagnosis of OSA was based on self-reported symptoms of sleep disturbance using a standard questionnaire. The Multivariable Apnea Prediction (MAP) Index score was also calculated to assess the risk of OSA. Log-binominal regression and negative binomial regression were performed to estimate the associations between LS7 and OSA and MAP index, with odds ratios (ORs) and prevalence ratios (PRs) and their 95% confidence intervals (CIs) calculated. Mediation analysis was performed to estimate the mediating effects of inflammatory indicators on the associations. RESULTS: A total of 4473 participants (32.4%) had OSA, and the mean MAP index was 0.39. In fully adjusted log-binominal regression models, with total score < 6 as the reference, the ORs (95% CIs) for risk of OSA were 0.90 (0.73, 1.10), 0.76 (0.65, 0.89), 0.78 (0.64, 0.95), and 0.45 (0.38, 0.54) for total score = 6, total score = 7, total score = 8, and total score > 8, respectively (P for trend < 0.001). When LS7 score was analyzed as a continuous variable, each 1-point increase in LS7 score was associated with a 15% decrease in OSA risk (P < 0.001). In negative binominal regression models, the adjusted PRs (95% CIs) for the MAP index were 0.93 (0.90, 0.97), 0.87 (0.84, 0.91), 0.80 (0.77, 0.84), and 0.55 (0.53, 0.57) for total score = 6, total score = 7, total score = 8, and total score > 8, respectively (P for trend < 0.001). For each 1-point increase in LS7 score, the risk of OSA decreased by 13% (P < 0.001). Consistent results were observed in subgroup analysis. Mediation analysis indicated that inflammatory factors, including blood cell count, neutrophil count, and C-reactive protein, positively mediated the association of LS7 with OSA, with a mediation proportion of 0.022 (P = 0.04), 0.02 (P = 0.04), and 0.02 (P = 0.02), respectively. CONCLUSIONS: In a nationally representative sample of US adults, adherence to LS7 metrics was independently associated with reduced OSA risk. Inflammation plays a mediating role in the association between LS7 and OSA.

Establishing a risk prediction model for residual pulmonary vascular obstruction after regular anticoagulant therapy for non-high-risk pulmonary embolism.

Background: The incidence of pulmonary embolism (PE) has been on the rise annually. Despite receiving regular sequential anticoagulation therapy, some patients with non-high-risk acute PE (APE) continue to experience residual pulmonary vascular obstruction (RPVO). This study sought to identify the risk factors for RPVO following 3 months of sequential anticoagulation therapy for non-high-risk PE. Machine learning techniques were utilized to construct a clinical prediction model for predicting the occurrence of RPVO. Methods: A total of 254 acute non-high-risk PE patients were included in this study, all of whom were admitted to the Third People's Hospital of Yunnan Province between 2020 and 2023. After 3 months of regular anticoagulant treatment, computed tomography pulmonary angiography (CTPA) were reviewed to identify the presence of RPVO. Patients were then categorized into either the thrombolysis group or the thrombosis residue group. Throughout the study period, 49 patients were excluded due to missing data, irregular treatment, or loss to follow-up. Clinical symptoms, physical signs, and laboratory results of 205 PE patients were recorded. Correlation and collinearity analyses were conducted on relevant risk factors, and significance tests were performed. Heat maps illustrating the relationships between influencing factors were generated. Predictors were selected using least absolute shrinkage and selection operator (LASSO) regression, followed by multivariate logistic regression analysis to create a predictive model. Internal validation of the model was also carried out. Results: By searching the literature to understand all the clinical indicators that may affect the efficacy of anticoagulation therapy. A total of 205 patients with non-high-risk acute pulmonary thromboembolism were evaluated for various risk factors. Five independent factors were identified by multivariable analysis-age, chronic obstructive pulmonary disease (COPD), acratia, pulmonary systolic blood pressure (PASP), and major arterial embolism-and their P value, odds ratio (OR) and confidence interval (CI) were as follows: (P=0.012, OR =1.123; 95% CI: 1.026-1.23), (P=0.002, OR =13.30; 95% CI: 2.673-66.188), (P=0.001, OR =14.009; 95% CI: 2.782-70.547), (P=0.003, OR =1.061; 95% CI: 1.020-1.103) and (P<0.001, OR =18.128; 95% CI: 3.853-85.293), which may indicate a poor prognosis after standard anticoagulant therapy. A nomogram was constructed using these variables and internally validated. The receiver operating characteristic (ROC) curves of the model demonstrated strong predictive accuracy, with an area under the curve (AUC) of 0.94 (95% CI: 0.89-0.96) for the training set and 0.93 (95% CI: 0.88-0.95) for the validation set. Calibration curves were utilized to assess the practicality of the nomogram. Conclusions: A novel predictive model was developed based on a single-center retrospective study to identify patients with RPVO following anticoagulant therapy for acute non-high-risk PE. This model may aid in the early detection of patients, prompt adjustment of treatment, and ultimately lead to a decrease in adverse outcomes.

Non-antibiotic pharmaceutical phenylbutazone binding to MexR reduces the antibiotic susceptibility of Pseudomonas aeruginosa.

Antimicrobial resistance has been an increasingly serious threat to global public health. The contribution of non-antibiotic pharmaceuticals to the development of antibiotic resistance has been overlooked. Our study found that the anti-inflammatory drug phenylbutazone could protect P. aeruginosa against antibiotic mediated killing by binding to the efflux pump regulator MexR. In this study, antibiotic activity against P. aeruginosa alone or in combination with phenylbutazone was evaluated in vitro and in vivo. Resazurin accumulation assay, transcriptomic sequencing, and PISA assay were conducted to explore the underlying mechanism for the reduced antibiotic susceptibility caused by phenylbutazone. Then EMSA, ITC, molecular dynamic simulations, and amino acid substitutions were used to investigate the interactions between phenylbutazone and MexR. We found that phenylbutazone could reduce the susceptibility of P. aeruginosa to multiple antibiotics, including parts of ß-lactams, fluoroquinolones, tetracyclines, and macrolides. Phenylbutazone could directly bind to MexR, then promote MexR dissociating from the mexA-mexR intergenic region and de-repress the expression of MexAB-OprM efflux pump. The overexpressed MexAB-OprM pump resulted in the reduced antibiotic susceptibility. And the His41 and Arg21 residues of MexR were involved in the phenylbutazone-MexR interaction. We hope this study would imply the potential risk of antibiotic resistance caused by non-antibiotic pharmaceuticals.

Association between percutaneous absorption of benzophenone-3 and N, N-diethyl-m-toluamide among the general adult population.

BACKGROUND: Multiple studies have confirmed the mutual enhancement of percutaneous permeation of benzophenone-3 (BP-3) and N,N-diethyl-m-toluamide (DEET), which are effective ingredients in sunscreen products and insect repellents, respectively. However, the association between percutaneous absorption of BP-3 and DEET in a large general adult population remains to be elucidated. METHODS: This cross-sectional study included US adults who had available data on urinary BP-3 and two DEET metabolites, 3-(diethylcarbamoyl) benzoic acid (DCBA) and 3-(ethylcarbamoyl) benzoic acid (ECBA), from the National Health and Nutrition Examination Survey (NHANES) conducted in 2015-2016. We conducted three weighted multivariable linear regression models to investigate the potential correlation between percutaneous absorption of BP-3 and DEET, along with trend tests, smooth curve fitting, and subgroup analysis to assess the robustness of the findings. RESULTS: Weighted multivariable linear logistic regression revealed a positive correlation between log10 BP-3 and log10 DCBA (ß = 0.1678, 95 % CI: 0.0970 to 0.2386) as well as log10 ECBA (ß = 0.1416, 95 % CI: 0.0707 to 0.2125), after adjusting for all covariates. After converting log10 BP-3 from a continuous variable to a categorical variable (quartiles), the trend tests showed that the results were stable (all P for trend < 0.05). Smoothed curve fitting demonstrated a linear positive correlation between log10 BP-3 and both log10 DCBA and log10 ECBA. In subgroup analyses, the positive correlation between BP-3 and DEET metabolites was more pronounced in participants who were male, middle-aged, non-Hispanic white, had a moderate PIR level and reported always or most of the time using sunscreen. CONCLUSIONS: Our findings revealed a statistically significant linear and positive correlation between the percutaneous absorption of BP-3 and DEET in the general adult population.

The role of gastrodin in the management of CNS-related diseases: Underlying mechanisms to therapeutic perspectives.

Central nervous system (CNS)-related diseases have a high mortality rate, are a serious threat to physical and mental health, and have always been an important area of research. Gastrodin, the main active metabolite of Gastrodia elata Blume, used in Chinese medicine and food, has a wide range of pharmacological effects, mostly related to CNS disorders. This review aims to systematically summarize and discuss the effects and underlying mechanisms of gastrodin in the treatment of CNS diseases, and to assess its potential for further development as a lead drug in both biomedicine and traditional Chinese medicine. Studies on the pharmacological effects of gastrodin on the CNS indicate that it may exert anti-neurodegenerative, cerebrovascular protective, and ameliorative effects on diabetic encephalopathy, perioperative neurocognitive dysfunction, epilepsy, Tourette's syndrome, depression and anxiety, and sleep disorders through various mechanisms. To date, 110 gastrodin products have been approved for clinical use, but further multicenter clinical case-control studies are relatively scarce. Preclinical studies have confirmed that gastrodin can be used to treat CNS-related disorders. However, important concerns need to be addressed in the context of likely non-specific, assay interfering effects when gastrodin is studied using in vitro and in silico approaches, calling for a systematic assessment of the evidence to date. High-quality clinical trials should have priority to evaluate the therapeutic safety and clinical efficacy of gastrodin. Further experimental research using appropriate in vivo models is also needed, focusing on neurodegenerative diseases, cerebral ischemic and hypoxic diseases, brain damage caused by methamphetamine or heavy metals, and epilepsy.

School Bullying Victimization and Depression Symptoms in Adolescents: The Mediating Role of Internet Addiction and Moderating Role of Living Areas.

School bullying and depression are both serious social and public health problems among adolescents. Prior studies indicated a correlation between bullying and depression. However, the potential moderators remain largely unexplored. This study aimed to identify the mediating effect of Internet addiction and the moderating effect of living in urban or rural areas in the relationship between school bullying victimization and depression symptoms among Chinese adolescents. This cross-sectional study of adolescents was conducted using two-stage random cluster sampling of students in urban and rural public high schools in China. A moderated mediation model was constructed to uncover the underlying mechanism of school bullying victimization and depression symptoms. A total of 2,376 adolescents (52.65% females, mean age ± SD a 14.69 ± 1.76 years) were included in the study. The prevalence of clinical depression symptoms with a cut-off value of 16 on the Center for Epidemiological Studies Depression Scale (CES-D) was 21.76% (95% CI: 20.15, 23.46), and with a cut-off value of 20 on the CES-D was 13.85% (95% CI: 12.51, 15.30) for overall. Our findings indicated a significant positive association between school bullying victimization and depression symptoms (p < 0.01) and a significant mediating effect of Internet addiction in the association between school bullying victimization and depression symptoms (indirect effect = 1.143, 95% CI: 0.677, 1.609; percentage of mediation: 16.7%, 95% CI: 10.3, 23.1). This indirect relationship was partially moderated by the living in urban or rural areas in the mediation process. Specifically, the effect of school bullying victimization on Internet addiction was greater among urban adolescents (simple slope: 0.774, 95% CI: 0.524, 1.024, p < 0.01) than among rural adolescents (simple slope: 0.337, 95% CI: 0.132, 0.543, p < 0.01), but moderating effect of urban-rural areas was not significant on the relationship between Internet addiction and depression symptoms. These findings highlight the mediating role of Internet addiction and the moderating role of living areas in school bullying victimization and adolescents' depression symptoms, which provide evidence for social work, mental health services, and policy interventions for adolescents in China.

Elastic Nanofibrous Dressings with Mesenchymal Stem Cell-Recruiting and Protecting Characteristics for Promoting Diabetic Wound Healing.

Diabetic wounds that do not heal for a long time challenge global healthcare. Mesenchymal stem cell (MSC) therapy has positive significance in promoting diabetic wound healing. However, traditional MSC therapy involves exogenous MSCs, which brings many limitations and unsatisfactory treatment. Moreover, the maintenance of MSC viability and function is difficult because of the high level of reactive oxygen species (ROS) in diabetic wounds. Therefore, we developed a nanofibrous dressing to recruit and protect endogenous MSCs while avoiding the inherent disadvantages of exogenous MSCs. Ceria nanoparticles capable of ROS scavenging are integrated into the nanofibrous dressings, together with Apt19S, a DNA aptamer with affinity and selectivity for MSCs. In addition, the homogenization and freeze-drying technology give the nanofibrous dressings good elasticity, which protects the wound from external pressure. Further experiments in diabetic mice show that the dressing has excellent endogenous MSC recruitment and anti-inflammatory properties, thereby synergistically promoting diabetic wound healing. This study is expected to explore an efficient method of stem cell therapy, providing a new way to construct high-performance wound dressings.

The influence of task-irrelevant color perception on flanker task performance: Insights from behavioral and ERP data.

Perception of color as a task-relevant stimulus can affect cognition and behavior in the flanker task; however, it remains unclear whether it has the same impact when it is a task-irrelevant stimulus dimension. To this end, we applied four-letter flanker tasks with or without colored (red/blue) to 23 healthy young adults, while recording the event-related potentials (ERPs) and behavioral performance. The flanker task included four kinds of color types: non-color letter (NC), all color letter (AC), flanker color letter (FC), and target color letter (TC), each flanker task included congruent and incongruent conditions. The behavioral data demonstrated the classic conflict effect across all color types of flanker tasks in both reaction times (RTs) and accuracy, the significant interaction and main effect of color type factors were only observed in accuracy. The ERP results showed significant interaction between conflict factor (congruent, incongruent) and color type (NC, AC, FC, and TC), and the color type factor enhanced the fronto-central P2 (180-200 ms), descended the fronto-centro-parietal N2b (260-320 ms), and increased the fronto-central P3b (360-520 ms). The fronto-central P2 and the fronto-central P3b were larger for TC than NC, AC, and FC in the congruent condition, while the fronto-central P3b was smaller for NC than AC, FC, and TC in the incongruent condition. Furthermore, the fronto-centro-parietal N2b was decreased successively in NC, AC, FC, and TC in both congruent and incongruent conditions. Overall, our findings suggested that the task-irrelevant stimuli dimension of color can capture some attentional resources and is affected by the location of color (target/flanker) and the type of task trial (congruent/incongruent) in the flanker task.

The complete chloroplast genome of Blechnopsis orientalis (Linnaeus) C. Presl 1753 (Blechnaceae).

Blechnopsis orientalis (Linnaeus) C. Presl (1753) is a fern used both as food and medicine. It is found primarily in southern China and Southeast Asia, thriving in warm, humid shrublands or sparse forest. The total length of the chloroplast genome is 155,211 bp, including a large single-copy region (LSC, 81,877 bp), a small single-copy region (SSC, 21,500 bp), and two inverted repeat regions (IRs, 25,917 bp). The GC content is 41.3%. A total of 131 genes were annotated, including 88 protein-coding genes, eight rRNA genes, and 35 tRNA genes. The phylogenetic analysis using the maximum-likelihood method showed that B. orientalis and Oceaniopteris gibba were closely related. This study provides genomic resources for phylogenetic genetics and resource exploitation of B. orientalis.

Sarcopenic obesity and osteoporosis: Research progress and hot spots.

Sarcopenic obesity (SO) and osteoporosis (OP) are associated with aging and obesity. The pathogenesis of SO is complex, including glucolipid and skeletal muscle metabolic disorders caused by inflammation, insulin resistance, and other factors. Growing evidence links muscle damage to bone loss. Muscle-lipid metabolism disorders of SO disrupt the balance between bone formation and bone resorption, increasing the risk of OP. Conversely, bones also play a role in fat and muscle metabolism. In the context of aging and obesity, the comprehensive review focuses on the effects of mechanical stimulation, mesenchymal stem cells (MSCs), chronic inflammation, myokines, and adipokines on musculoskeletal, at the same time, the impact of osteokines on muscle-lipid metabolism were also analyzed. So far, exercise combined with diet therapy is the most effective strategy for increasing musculoskeletal mass. A holistic treatment of musculoskeletal diseases is still in the preliminary exploration stage. Therefore, this article aims to improve the understanding of musculoskeletal -fat interactions in SO and OP, explores targets that can provide holistic treatment for SO combined with OP, and discusses current limitations and challenges. We hope to provide relevant ideas for developing specific therapies and improving disease prognosis in the future.

YAP1 status defines two intrinsic subtypes of LCNEC with distinct molecular features and therapeutic vulnerabilities.

PURPOSE: Large cell neuroendocrine carcinoma (LCNEC) is a high-grade neuroendocrine malignancy that, like small cell lung cancer (SCLC), is associated with an absence of druggable oncogenic drivers and dismal prognosis. In contrast to SCLC, however, there is little evidence to guide optimal treatment strategies which are often adapted from SCLC and non-small cell lung cancer (NSCLC) approaches. EXPERIMENTAL DESIGN: To better define the biology of LCNEC, we analyzed cell line and patient genomic data and performed immunohistochemistry and single-cell (sc)RNAseq of core needle biopsies from LCNEC patients and preclinical models. RESULTS: Here, we demonstrate that the presence or absence of YAP1 distinguishes two subsets of LCNEC. The YAP1-high subset is mesenchymal and inflamed and characterized, alongside TP53 mutations, by co-occurring alterations in CDKN2A/B and SMARCA4. Therapeutically, the YAP1-high subset demonstrates vulnerability to MEK and AXL targeting strategies, including a novel preclinical AXL CAR-T cell. Meanwhile, the YAP1-low subset is epithelial and immune-cold and more commonly features TP53 and RB1 co-mutations, similar to those observed in pure SCLC. Notably, the YAP1-low subset is also characterized by expression of SCLC subtype-defining transcription factors - especially ASCL1 and NEUROD1 - and, as expected given its transcriptional similarities to SCLC, exhibits putative vulnerabilities reminiscent of SCLC, including Delta-like ligand 3 (DLL3) and CD56 targeting, as with novel preclinical DLL3 and CD56 CAR T-cells, and DNA damage repair (DDR) inhibition. CONCLUSION: YAP1 defines distinct subsets of LCNEC with unique biology. These findings highlight the potential for YAP1 to guide personalized treatment strategies for LCNEC.