Search

ObjectiveChemotherapy-induced peripheral neuropathy (CIPN) is a common and severe adverse reaction in taxane-based chemotherapy. This study aimed to analyze the risk factors of peripheral neuropathy in patients with breast cancer receiving paclitaxel chemotherapy to provide a reference for the early prevention of CIPN.MethodsWe included 350 patients with breast cancer who received chemotherapy for the first time at the Tangshan People’s Hospital between August 2022 and June 2023 and were followed for at least 3 months after the end of chemotherapy. The incidence of CIPN in patients with breast cancer was calculated, and risk factors for CIPN were analyzed using logistic regression analysis.ResultsThe incidence rate of CIPN was 79.1%. Multifactor logistic regression analysis indicated that age ≥45 years [odds ratio (OR)=5.119, 95% confidence interval (CI)=1.395–18.780] and ≥60 years (OR=9.366, 95% CI=1.228–71.421), history of hypertension (OR=3.475, 95% CI=1.073–11.250), cumulative dose of chemotherapy drugs >900 mg (OR=4.842, 95% CI=1.961–5.946), vitamin D deficiency (OR=6.214, 95% CI=2.308–16.729), abnormal alanine aminotransferase (OR=3.154, 95% CI=1.010–9.844), anemia before chemotherapy (OR=2.770, 95% CI=1.093–7.019), infusion duration of chemotherapy drugs >30 min (OR=3.673, 95% CI=1.414–9.539), body mass index ≥24 kg/m2 (OR=8.139, 95% CI=1.157–57.240), mild depression (OR=4.546, 95% CI=1.358–15.223), and major depression (OR=4.455, 95% CI=1.237–16.037) increased the risk of CIPN. Having a regular caregiver (OR=0.223, 95% CI=0.087–0.573), high levels of physical activity (OR=0.071, 95% CI=0.008–0.647), and strong social support (OR=0.048, 95% CI=0.003–0.682) were protective factors against CIPN.ConclusionClinical attention should be paid to patients with these risk factors, and active and effective preventive measures should be taken to reduce the occurrence of CIPN and improve the quality of life.

Background: The field's understanding of the association between sluggish cognitive tempo (SCT) and sleep is severely limited by the lack of multi-method and multi-informant research designs that move beyond global ratings, often focused on a limited number of sleep-related domains, such as daytime sleepiness. The current study begins to address these limitations by using actigraphy, daily sleep diary, and self- and parent-report global ratings of sleep in adolescents, a developmental period marked by changes in SCT, sleep, and circadian function. As SCT and sleep are also associated with ADHD symptoms, we tested these associations in a sample of adolescents with and without ADHD. Methods: Adolescents (N = 302; M age = 13.17 years, 44.7% female) with (n = 162) and without ADHD (n = 140) and parents completed global ratings of sleep and daytime sleepiness, and adolescents completed a measure of circadian preference. Adolescents also wore actigraphs for approximately two weeks, during which daily diaries were completed. Results: Above and beyond demographic characteristics (i.e., sex, race, and family income), pubertal development, medication use, and ADHD group status, adolescents' self-reported SCT symptoms were uniquely associated with shorter sleep duration and later sleep onset per both actigraphy and daily diary. SCT symptoms were also uniquely associated with longer sleep onset latency and poorer overall sleep (per daily diary), more sleep/wake problems and daytime sleepiness (per adolescent rating), more difficulties initiating and maintaining sleep (per parent rating), and later eveningness preference (per adolescent rating). Nearly all significant effects remained in sensitivity analyses controlling for adolescent- or parent-reported ADHD symptom dimensions. Conclusions: Findings provide the strongest evidence to date for SCT being uniquely linked to poorer sleep, greater daytime sleepiness, and a later evening circadian preference across subjective and objective measures. Longitudinal studies are needed to evaluate predictive and bidirectional associations.

IntroductionUrban ecological instruction is an important method of sustainable development that couples the needs of the population and the environment, thus facilitating high-quality development. This study aimed to transform existing large-scale considerations of ecological urban construction to provide a more grounded evaluation framework. We constructed an integrated framework that considers economic, environmental, social, cultural, and ecological factors and their contribution to urban ecological construction.MethodsWe used methods of subjective and objective empowerment, exploratory spatial data analysis, and the obstacle degree model to explore spatiotemporal variations in urban ecological construction.ResultsOur results showed that: (1) From 2006 to 2018, urban ecological construction in the Yellow River basin (YRB) exhibited a “polycentric” spatial differentiation pattern and a significant, gradually decreasing “center-periphery” spatial distribution trend. (2) High–high areas (with high agglomeration and high urban ecological construction) in the YRB are mainly distributed in Shandong Province and the adjacent regions, whereas low–low areas are mainly distributed in south–central Ningxia Province and southern Gansu Province. (3) Analysis of urban ecological construction characteristics across different city scales, functional types, spatial carriers, and basin locations shows that the urban ecological construction level is directly proportional to the scale of the city. The level of urban ecological construction is relatively higher in the Shandong Peninsula urban agglomeration, in the priority development area of the North China Plain, and in the downstream and right bank of the YRB. Spatial differences are mainly controlled by the net difference between regions from the upstream and midstream scales, as well as intra-regional differences between the left and right banks. (4) Marked differences can be observed in the obstacles to ecological construction in different types of cities.DiscussionTypical barriers in cities in the YRB include the total water resources per capita, energy consumption per unit of GDP, the proportion of research and development investment in fiscal expenditure, the number of books in public libraries per 10,000 people, and land use efficiency. In the future, urban ecological construction should be based on the development conditions of each individual city, and should be improved according to local conditions to achieve the construction high-quality ecological cities.

Background: Mindfulness training has been shown to promote positive mental health outcomes and related changes in neural networks such as the default mode network, which has a central node in the posterior cingulate cortex (PCC). Previous work from our group reported on the impact of a novel, neurofeedback augmented mindfulness training (NAMT) task on regulation of PCC hemodynamic activity in typically developing adolescents. The present pilot study aimed to expand on this finding by examining the pre-post changes of the NAMT task on resting-state functional connectivity of the PCC. Methods: Thirty-one typically developing adolescents (14.77 ± 1.23 years; 45% female) underwent a resting-state functional magnetic resonance imaging scan both before and after completing the NAMT task. A linear mixed effects model was used to assess for changes in functional connectivity of the PCC across the two resting-state runs. Results: Data did not support the hypothesized decrease in connectivity between the PCC seed and other DMN regions from pre- to post-NAMT task. However, we observed a significant increase in functional connectivity between the PCC and a cluster encompassing the left hippocampus and amygdala following completion of the NAMT task (run 1 Fisher's Z = 0.16; run 2 Fisher's Z = 0.26). Conclusion: Although preliminary, this finding suggests NAMT has the potential to strengthen connectivity between default mode and salience regions. We speculate that such changed connectivity may facilitate enhanced self-referential and emotional processing in adolescents. Clinical trial registration: https://clinicaltrials.gov/, identifier NCT04053582. [ABSTRACT FROM AUTHOR]

High‐frequency oscillatory activity in cognition‐related neural circuits during wakefulness consistently induces the growth of dendritic spines and axonal terminals. Although these structural changes are essential for cognitive functions, it is hypothesized that if these newly expanded structures fail to establish functional connections, they may become superfluous. Sleep is believed to facilitate the reduction of such redundant structures to maintain neural homeostasis. However, the mechanisms underlying this pruning process during sleep remain poorly understood. In this study, that melatonin type 3 receptors (MT3Rs) are selectively expressed in the stellate neurons of the medial entorhinal cortex (MEC) is demonstrated, an area where high melatonin levels are detected during sleep. Activation of MT3Rs during sleep initiates the shrinkage of dendritic spines in stellate neurons by downregulating neural network activity and dephosphorylating synaptic proteins in the MEC. This process is disrupted when MT3R expression is knocked down or when MT3Rs are blocked during sleep. Notably, interference with MT3Rs in the MEC during sleep impairs the acquisition of spatial memory but does not affect object memory acquisition following sleep. These findings reveal novel molecular mechanisms involving melatonin and MT3Rs in the regulation of dendritic spine shrinkage during sleep, which is crucial for the acquisition and consolidation of spatial memory. [ABSTRACT FROM AUTHOR]

Hepatic steatosis, the first step in the development of nonalcoholic fatty liver disease (NAFLD), is frequently observed in the aging population. However, the underlying molecular mechanism remains largely unknown. In this study, we first employed GSEA enrichment analysis to identify short‐chain acyl‐CoA dehydrogenase (SCAD), which participates in the mitochondrial β‐oxidation of fatty acids and may be associated with hepatic steatosis in elderly individuals. Subsequently, we examined SCAD expression and hepatic triglyceride content in various aged humans and mice and found that triglycerides were markedly increased and that SCAD was upregulated in aged livers. Our further evidence in SCAD‐ablated mice suggested that SCAD deletion was able to slow liver aging and ameliorate aging‐associated fatty liver. Examination of the molecular pathways by which the deletion of SCAD attenuates steatosis revealed that the autophagic degradation of lipid droplets, which was not detected in elderly wild‐type mice, was maintained in SCAD‐deficient old mice. This was due to the decrease in the production of acetyl‐coenzyme A (acetyl‐CoA), which is abundant in the livers of old wild‐type mice. In conclusion, our findings demonstrate that the suppression of SCAD may prevent age‐associated hepatic steatosis by promoting lipophagy and that SCAD could be a promising therapeutic target for liver aging and associated steatosis. [ABSTRACT FROM AUTHOR]

Learning leads to rapid microstructural changes in gray (GM) and white (WM) matter. Do these changes continue to accumulate if task training continues, and can they be reverted by sleep? We addressed these questions by combining structural and diffusion weighted MRI and high-density EEG in 16 subjects studied during the physiological sleep/wake cycle, after 12 h and 24 h of intense practice in two different tasks, and after post-training sleep. Compared to baseline wake, 12 h of training led to a decline in cortical mean diffusivity. The decrease became even more significant after 24 h of task practice combined with sleep deprivation. Prolonged practice also resulted in decreased ventricular volume and increased GM and WM subcortical volumes. All changes reverted after recovery sleep. Moreover, these structural alterations predicted cognitive performance at the individual level, suggesting that sleep's ability to counteract performance deficits is linked to its effects on the brain microstructure. The cellular mechanisms that account for the structural effects of sleep are unknown, but they may be linked to its role in promoting the production of cerebrospinal fluid and the decrease in synapse size and strength, as well as to its recently discovered ability to enhance the extracellular space and the clearance of brain metabolites.

Liraglutide, an analog of human glucagon‐like peptide‐1 (GLP‐1), has been found to improve hepatic steatosis in clinical practice. However, the underlying mechanism remains to be fully defined. Increasing evidence suggests that retinoic acid receptor‐related orphan receptor α (RORα) is involved in hepatic lipid accumulation. In the current study, we investigated whether the ameliorating impact of liraglutide on lipid‐induced hepatic steatosis is dependent on RORα activity and examined the underlying mechanisms. Cre‐loxP‐mediated, liver‐specific Rorα knockout (Rora LKO) mice, and littermate controls with a Roraloxp/loxp genotype were established. The effects of liraglutide on lipid accumulation were evaluated in mice challenged with a high‐fat diet (HFD) for 12 weeks. Moreover, mouse AML12 hepatocytes expressing small interfering RNA (siRNA) of Rora were exposed to palmitic acid to explore the pharmacological mechanism of liraglutide. The results showed that liraglutide treatment significantly alleviated HFD‐induced liver steatosis, marked by reduced liver weight and triglyceride accumulation, improved glucose tolerance and serum levels of lipid profiles and aminotransferase. Consistently, liraglutide also ameliorated lipid deposits in a steatotic hepatocyte model in vitro. In addition, liraglutide treatment reversed the HFD‐induced downregulation of Rora expression and autophagic activity in mouse liver tissues. However, the beneficial effect of liraglutide on hepatic steatosis was not observed in Rora LKO mice. Mechanistically, the ablation of Rorα in hepatocytes diminished liraglutide‐induced autophagosome formation and the fusion of autophagosomes and lysosomes, resulting in weakened autophagic flux activation. Thus, our findings suggest that RORα is essential for the beneficial impact of liraglutide on lipid deposition in hepatocytes and regulates autophagic activity in the underlying mechanism. [ABSTRACT FROM AUTHOR]