The Mediating Effect of Depression on the Relationship between Loneliness and Substance Use in Korean Adolescents.

Substance use among adolescents is a major emerging health problem worldwide. Although loneliness and depression are major risk factors for substance use, few studies have examined the relationship between loneliness, depression, and substance use in adolescents. This study aimed to determine the mediating effect of depression on the relationship between loneliness and substance use among Korean adolescents, based on the data from 53,310 adolescents from the 17th Korea Youth Risk Behavior Web-based Survey in 2021. Using a complex sample analysis module, hierarchical logistic regression analysis was employed to confirm the mediating effect of depression on the relationship between loneliness and substance use. The results showed that loneliness and depression have a significant effect on substance use (smoking, drinking alcohol, and drug use). Depression was found to have a partial mediating effect on the relationship between loneliness and substance use. Overall, the results suggested that loneliness and depression in adolescents increase substance use, and loneliness can affect substance use through depression. Therefore, proactive strategies to prevent and reduce loneliness and depression in adolescents can be effective in preventing substance use.

Relationship between a Low-Carbohydrate, High-Fat Diet and Risk of Metabolic Syndrome in Korean Women.

Background: Prevalence of metabolic syndrome with aging is higher in women than in men, and it increases after menopause. Interventions to reduce the risk of metabolic syndrome in women are important. A low-carbohydrate, high-fat diet is effective in weight loss and improvement cardiovascular risk factors including abdominal circumference, blood pressure, and blood lipid profile. We aimed to determine the relationship between a low-carbohydrate, high-fat diet and the risk of metabolic syndrome in Korean women. Methods: This cross-sectional study was conducted using secondary data from the 2014-2018 Korean National Health and Nutrition Examination Survey. Overall, 8,222 women aged >19 yr were included. The effect of a low-carbohydrate, high-fat diet on the risk of metabolic syndrome was analyzed by multiple logistic regression analysis using a complex sampling procedure. Results: The diet significantly reduced the likelihood of metabolic syndrome development (P=0.044). In addition, regardless of the fat type, the diet significantly reduced the likelihood of low high-density lipoprotein cholesterolemia (low-carbohydrate, high-total fat, P=0.013; low-carbohydrate, high-unsaturated fat, P=0.006; low-carbohydrate, high-saturated fat, P=0.006). Conclusion: A low-carbohydrate, high-fat diet is an important intervention that can reduce the risk of metabolic syndrome, and the reduced consumption of carbohydrates can decrease the risk of low high-density lipoprotein cholesterolemia regardless of fat type. Therefore, it is necessary to actively explore the potential of this diet, targeting Asians, including Koreans.

Mediating Effect of Humanism on the Relationship between Task Performance Competence and Holistic Nursing Competence for Clinical Nurses.

This is a cross-sectional descriptive study that investigates the mediating effect of humanism on the relationship between task performance and holistic nursing competence among clinical nurses. The participants were nurses with more than one year of work experience in general hospitals in South Korea, recruited using convenience sampling. A total of 227 data samples were collected. A self-reported questionnaire including the task performance competence scale, holistic nursing competence scale, and humanism scale was used for the survey. Data were analyzed using the t-test, analysis of variance, Pearson's correlation coefficients, and hierarchical multiple regression after checking for normal distribution. The results showed that task performance competence, holistic nursing competence, and humanism differed according to characteristics such as gender, age, educational level, marital status, position, length of career, and job and salary satisfaction. Task performance competence was positively correlated with holistic nursing competence and humanism. A positive correlation was also observed between holistic nursing competence and humanism. A partial mediating effect of humanism in the relationship between task performance competence and holistic nursing competence was confirmed. Thus, to increase nurses' holistic nursing competence, it is necessary to improve task performance competence and formulate a continuous and repetitive education program that includes humanism.

Translationally controlled tumor protein restores impaired memory and altered synaptic protein expression in animal models of dementia.

This study describes the effects of translationally controlled tumor protein (TCTP) on mice with memory impairment caused by scopolamine (SCO) administration. Specifically, memory functions and expression levels of hippocampal synaptic proteins in 7- to 12-month-old SCO-treated wild-type (WT-SCO) mice were compared to those of TCTP-overexpressing (TG) and TCTP knocked-down (KD) mice similarly treated with SCO. Passive-avoidance tasks were performed with WT, TG, and KD mice for four weeks after intraperitoneal injection of SCO or saline followed by an acquisition test. After completing behavioral studies, hippocampi of all mice groups were collected and their synaptic protein contents were subjected to Western blotting or immunohistochemical analyses, and compared with those of 5x familial Alzheimer's disease (5xFAD) mice and postmortem AD patients. Results of passive avoidance tests revealed that SCO-induced memory impairment was repaired in TCTP-TG mice, but not in TCTP-KD mice. Hippocampal expression levels of synaptophysin, synapsin-1, and PSD-95 were increased in TCTP-TG mice treated with SCO (TG-SCO) but decreased in TCTP-KD mice treated with SCO (KD-SCO). Decreased levels of TCTP, synaptophysin, and PSD-95 were also found in hippocampi of 5xFAD mice and AD patients. Expression levels of p-CREB/CREB and brain-derived neurotrophic factor (BDNF) in TCTP-TG and TG-SCO mice were similar to or increased compared to those in WT mice, but decreased in TCTP-KD and KD-SCO mice. BDNF immunoreactivity was restored in CA1 regions of hippocampi of TG-SCO mice, but not in KD-SCO mice. These results suggest that TCTP can restore damaged memory in mice possibly through restored synaptic protein expression.

Enhanced delivery of a low dose of aducanumab via FUS in 5×FAD mice, an AD model.

BACKGROUND: Aducanumab (Adu), which is a human IgG1 monoclonal antibody that targets oligomer and fibril forms of beta-amyloid, has been reported to reduce amyloid pathology and improve impaired cognition after administration of a high dose (10 mg/kg) of the drug in Alzheimer's disease (AD) clinical trials. The purpose of this study was to investigate the effects of a lower dose of Adu (3 mg/kg) with enhanced delivery via focused ultrasound (FUS) in an AD mouse model. METHODS: The FUS with microbubbles opened the blood-brain barrier (BBB) of the hippocampus for the delivery of Adu. The combined therapy of FUS and Adu was performed three times in total and each treatment was performed biweekly. Y-maze test, Brdu labeling, and immunohistochemical experimental methods were employed in this study. In addition, RNA sequencing and ingenuity pathway analysis were employed to investigate gene expression profiles in the hippocampi of experimental animals. RESULTS: The FUS-mediated BBB opening markedly increased the delivery of Adu into the brain by approximately 8.1 times in the brains. The combined treatment induced significantly less cognitive decline and decreased the level of amyloid plaques in the hippocampi of the 5×FAD mice compared with Adu or FUS alone. Combined treatment with FUS and Adu activated phagocytic microglia and increased the number of astrocytes associated with amyloid plaques in the hippocampi of 5×FAD mice. Furthermore, RNA sequencing identified that 4 enriched canonical pathways including phagosome formation, neuroinflammation signaling, CREB signaling and reelin signaling were altered in the hippocami of 5×FAD mice receiving the combined treatment. CONCLUSION: In conclusion, the enhanced delivery of a low dose of Adu (3 mg/kg) via FUS decreases amyloid deposits and attenuates cognitive function deficits. FUS-mediated BBB opening increases adult hippocampal neurogenesis as well as drug delivery. We present an AD treatment strategy through the synergistic effect of the combined therapy of FUS and Adu.

Striatal ZBTB16 Is Associated With Cognitive Deficits in Alzheimer Disease Mice.

PURPOSE: In Alzheimer disease (AD), brain regions such as the cortex and the hippocampus show abundant amyloid load which correlates with cognitive function decline. Prior to the significant development of AD pathophysiology, patients report the manifestation of neuropsychiatric symptoms, indicating a functional interplay between basal ganglia structures and hippocampal regions. Zinc finger and BTB domain-containing protein 16 (ZBTB16) is a transcription factor that controls the expression of downstream genes and the involvement of ZBTB16 in the striatum undergoing pathological aging in AD and the resulting behavioral phenotypes has not yet been explored. METHODS: To study molecular alterations in AD pathogenesis, we analyzed the brain from amyloid precursor protein (APP)/ presenilin 1 (PS1) transgenic mice. The molecular changes in the striatal region of the brain were analyzed via the immunoblotting, and the quantitative RNA sequencing. The cognitive impairments of APP/PS1 mice were assessed via 3 behavioral tests: 3-chamber test, Y-maze test, and noble object recognition test. And multielectrode array experiments for the analysis of the neuronal activity of the striatum in APP/PS1 mice was performed. RESULTS: We found that the alteration in ZBTB16 levels that occurred in the early ages of the pathologically aging striatum coalesces with the disruption of transcriptional dysregulation while causing social memory deficits, anxiety-like behavior. The early ZBTB16 knockdown treatment in the striatum of APP/PS1 mice rescued cognition that continued into later age. CONCLUSION: This study demonstrates that perturbation of transcriptional regulation of ZBTB16 during pathological aging may influence cognitive impairments and reveals a potent approach to targeting the transcriptional regulation of the striatum for the treatment of AD.

Reliability and Validity of the Korean Version of the High-Performance Work System Scale (HPWS-K).

The application of the concept of high-performance work system (HPWS) to nurses can improve the quality of nursing care by enhancing nurse supply and patient safety culture. This study aimed to test the validity and reliability of the Korean version of the HPWS Scale (HPWS-K) and verify its adequacy for measuring HPWS within the context of nurses working in Korean hospitals. Data analyses were performed by using data from 214 nurses engaged in patient care in Korean general hospitals with over 300 beds, with SPSS version 22.0 and AMOS version 26.0 software. The data collected were translated into Korean and the adapted Korean version was back-translated into English by bilingual nursing professionals. The content validity of the HPWS-K was tested by administering it to 10 participants, and the collected data underwent reliability and validity testing. In the exploratory factor analysis, the total variance explained was 49.97%, and the instrument's reliability (Cronbach's α) was 0.87. A one-factor confirmatory factor analysis showed an acceptable model fit. The results confirmed the feasibility of using the HPWS-K with Korean nurses, and its application in this context is expected to contribute to creating a safe and effective healthcare environment in Korea.

Combined Effects of Smartphone Overdependence and Stress on Depression and Suicide-Related Behaviors among High School Students.

This study aimed to identify smartphone overdependency and stress' combined effects on depression and suicide-related behaviors, such as suicidal ideation, plans, and attempts, among Korean high school students. Cross-sectional secondary data analysis was conducted using data from the 2020 Korea Youth Risk Behavior Web-based Survey. This study included 25,987 high school students. Data were analyzed using descriptive analysis, Rao-Scott chi-square test, and logistic regression based on a complex sample design. Regardless of smartphone overdependence, some stress and high stress were associated with higher depression than no stress and no smartphone overdependence. Furthermore, regardless of smartphone overdependence, some stress and high stress were associated with greater depression and suicidal ideation than no stress and no smartphone overdependence. However, only high stress was associated with suicide plans and attempts. Additionally, stress with smartphone overdependence increased the risk of depression and suicide-related behaviors, whereas the absence of stress did not significantly affect depression and suicide-related behaviors. Therefore, to prevent depression and suicide-related behaviors among high school students, continuous monitoring of and interventions to reduce stress levels should be prioritized. Moreover, as stress combined with smartphone overdependence increases the likelihood of depression and suicide-related behaviors, educational programs to prevent smartphone overdependence should be developed.

Photoluminescence Path Bifurcations by Spin Flip in Two-Dimensional CrPS4.

Ultrathin layered crystals of coordinated chromium(III) are promising not only as two-dimensional (2D) magnets but also as 2D near-infrared (NIR) emitters due to long-range spin correlation and efficient transition between high- and low-spin excited states of Cr3+ ions. In this study, we report on the dual-band NIR photoluminescence (PL) of CrPS4 and show that its excitonic emission bifurcates into fluorescence and phosphorescence depending on thickness, temperature, and defect density. In addition to the spectral branching, the biexponential decay of PL transients, also affected by the three factors, could be well described within a three-level kinetic model for Cr(III). In essence, the PL bifurcations are governed by activated reverse intersystem crossing from the low- to high-spin states, and the transition barrier becomes lower for thinner 2D samples because of surface-localized defects. Our findings can be generalized to 2D solids of coordinated metals and will be valuable in realizing groundbreaking magneto-optic functions and devices.

Transcriptomic analysis in the striatum reveals the involvement of Nurr1 in the social behavior of prenatally valproic acid-exposed male mice.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder that exhibits neurobehavioral deficits characterized by abnormalities in social interactions, deficits in communication as well as restricted interests, and repetitive behaviors. The basal ganglia is one of the brain regions implicated as dysfunctional in ASD. In particular, the defects in corticostriatal function have been reported to be involved in the pathogenesis of ASD. Surface deformation of the striatum in the brains of patients with ASD and their correlation with behavioral symptoms was reported in magnetic resonance imaging (MRI) studies. We demonstrated that prenatal valproic acid (VPA) exposure induced synaptic and molecular changes and decreased neuronal activity in the striatum. Using RNA sequencing (RNA-Seq), we analyzed transcriptome alterations in striatal tissues from 10-week-old prenatally VPA-exposed BALB/c male mice. Among the upregulated genes, Nurr1 was significantly upregulated in striatal tissues from prenatally VPA-exposed mice. Viral knockdown of Nurr1 by shRNA significantly rescued the reduction in dendritic spine density and the number of mature dendritic spines in the striatum and markedly improved social deficits in prenatally VPA-exposed mice. In addition, treatment with amodiaquine, which is a known ligand for Nurr1, mimicked the social deficits and synaptic abnormalities in saline-exposed mice as observed in prenatally VPA-exposed mice. Furthermore, PatDp+/- mice, a commonly used ASD genetic mouse model, also showed increased levels of Nurr1 in the striatum. Taken together, these results suggest that the increase in Nurr1 expression in the striatum is a mechanism related to the changes in synaptic deficits and behavioral phenotypes of the VPA-induced ASD mouse model.

Incidence and risk factors of progressive nasal inner nuclear layer thickening after surgical peeling of epiretinal membrane.

To assess incidence and risk factors of postoperative progressive nasal inner nuclear layer (INL) thickening after epiretinal membrane (ERM) surgery. Progressive nasal INL thickening was defined as 1.5-fold increase in thickness of nasal INL after ERM surgery compared to preoperative examination. Kaplan-Meier survival analysis was done to compare the cumulative risk ratio between groups stratified by presence of progressive nasal INL thickening. Logistic regression was performed to identify possible risk factors. Progressive nasal INL thickening occurred in 13.0% of ERM removal patients. Patients without progressive nasal INL thickening showed better visual acuity recovery compared to patients with nasal INL thickening (p = 0.029). Presence of cystoid space in inner retinal layer before surgery (odds ratio [OR] = 0.143, 95% confidence interval [CI] 0.028-0.736; p = 0.020), older age (OR = 0.896, 95% CI 0.817-0.982, p = 0.020), and thicker preoperative central macular thickness (OR = 0.994, 95% CI 0.988-1.000, p = 0.039) were correlated inversely with thickening of nasal INL. Correlation between nasal INL thickness and postoperative visual outcome was significant. Absence of cystoid space before ERM surgery, younger age, and thinner central macular thickness were risk factors for progressive postoperative nasal INL thickening. Progressive nasal INL thickening may serve as a new biomarker for worsened visual symptom after ERM surgery.

Significance of Altered Fatty Acid Transporter Expressions in Uterine Cervical Cancer and Its Precursor Lesions.

BACKGROUND: High-risk human papilloma virus (HR HPV) infection is a major factor leading to the development of uterine cervical cancer. Data suggest that alterations in lipid metabolism are related to the pathogenesis of cervical cancer. Specifically, the uptake of exogenous fatty acids and their intracellular storage in lipid droplets enables cancer cells to survive and adapt to the changing tumor environment. MATERIALS AND METHODS: We compared the immunohistochemical expression of fatty acid transport protein 4 (FATP4), and cluster of differentiation 36/fatty acid translocase (CD36/FAT) in normal cervical epithelium, low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), and squamous cell carcinoma (SCC) tissues of the uterine cervix. We also investigated the clinicopathological implications of these fatty acid transporters in SCC. RESULTS: Compared with that in normal cervical tissues, the expression of FATP4 was lower in LSIL (p=0.002), HSIL (p=0.006), and SCC (p=0.001). In contrast, CD36 expression was higher in SCC tissues than in normal cervical tissues (p<0.001). In normal cervical tissues, HR HPV-infected lesions exhibited a decrease in FATP4 (p<0.001) and an increase of CD36 (p=0.134), compared to those that were not infected with HR HPV. High CD36 expression was associated with a shorter recurrence-free survival (p<0.001). However, high FATP4 levels showed no significant correlation with the clinicopathological parameters of SCC. CONCLUSION: Altered expression levels of FATP4 and CD36 are unique features that might be related to HR HPV infection and promote tumorigenesis and progression of cervical cancer.

Dysfunction of striatal MeCP2 is associated with cognitive decline in a mouse model of Alzheimer's disease.

Rationale: Cerebral Methyl-CpG binding Protein 2 (MeCP2) is involved in several psychiatric disorders that are concomitant with cognitive dysfunction. However, the regulatory function of striatal MeCP2 and its association with Alzheimer's disease (AD) has been largely neglected due to the absence of amyloid plaque accumulation in the striatal region until the later stages of AD progression. Considerable evidence indicates that neuropsychiatric symptoms related to cognitive decline are involved with striatal dysfunction. To this respect, we investigated the epigenetic function of striatal MeCP2 paralleling the pathogenesis of AD. Methods: We investigated the brain from amyloid precursor protein (APP)/presenilin1 (PS1) transgenic mice and postmortem brain samples from normal subjects and AD patients. The molecular changes in the brain, particularly in the striatal regions, were analyzed with thioflavin S staining, immunohistochemistry, immunoblotting, and MeCP2 chromatin immunoprecipitation sequencing (ChIP-seq). The cognitive function of APP/PS1 mice was assessed via three behavioral tests: 3-chamber test (3CT), Y-maze test (YMT), and passive avoidance test (PA). A multi-electrode array (MEA) was performed to analyze the neuronal activity of the striatum in APP/PS1 mice. Results: Striatal MeCP2 expression was increased in the younger (6 months) and older (10 months) ages of APP/PS1 mice, and the genome-wide occupancy of MeCP2 in the younger APP/PS1 showed dysregulated binding patterns in the striatum. Additionally, we confirmed that APP/PS1 mice showed behavioral deficits in multiple cognitive behaviors. Notably, defective cognitive phenotypes and abnormal neuronal activity in old APP/PS1 mice were rescued through the knock-down of striatal MeCP2. Conclusion: We found that the MeCP2-mediated dysregulation of the epigenome in the striatum is linked to the defects in cognitive behavior and neuronal activity in the AD animal model, and that this alteration is initiated even in the very early stages of AD pathogenesis. Together, our data indicates that MeCP2 may be a potential target for the diagnosis and treatment of AD at asymptomatic and symptomatic stages.

Hole doping effect of MoS2 via electron capture of He+ ion irradiation.

Beyond the general purpose of noble gas ion sputtering, which is to achieve functional defect engineering of two-dimensional (2D) materials, we herein report another positive effect of low-energy (100 eV) He+ ion irradiation: converting n-type MoS2 to p-type by electron capture through the migration of the topmost S atoms. The electron capture ability via He+ ion irradiation is valid for supported bilayer MoS2; however, it is limited at supported monolayer MoS2 because the charges on the underlying substrates transfer into the monolayer under the current condition for He+ ion irradiation. Our technique provides a stable and universal method for converting n-type 2D transition metal dichalcogenides (TMDs) into p-type semiconductors in a controlled fashion using low-energy He+ ion irradiation.

Combined Effects of Unhealthy Lifestyle Behaviors on Metabolic Syndrome among Postmenopausal Women.

This study aimed to identify the combined effects of unhealthy lifestyle behaviors, including diet, sedentary behavior, and physical activity on metabolic syndrome (MS) and components of MS among postmenopausal women. Secondary data analysis was conducted using the Korean National Health and Nutrition Examination Survey (2014-2018) with a cross-sectional study design. Logistic regression analysis was conducted with data from 6114 Korean postmenopausal women. While no significant effects of unhealthy lifestyle behaviors, either individually or as a combination, were found for MS, prolonged sedentary behavior without poor dietary behavior and insufficient physical activity was associated with increased likelihood of abdominal obesity (adjusted odds ratio [AOR]: 1.59, 95% confidence interval [CI]: 1.10-2.29) and impaired fasting glucose (AOR: 1.54, 95% CI: 1.13-2.10). The combination of poor dietary behavior and prolonged sedentary behaviors was also associated with increased likelihood of abdominal obesity (AOR: 1.48, 95% CI: 1.10-2.00) and impaired fasting glucose (AOR: 1.49, 95% CI: 1.14-1.96). In addition, prolonged sedentary behavior and insufficient physical activity together were associated with increased likelihood of abdominal obesity (AOR: 2.81, 95% CI: 1.90-4.20) and impaired fasting glucose (AOR: 1.59, 95% CI: 1.13-2.24). Finally, combining poor dietary behavior, prolonged sedentary behavior, and insufficient physical activity was also associated with increased likelihood of abdominal obesity (AOR: 2.05, 95% CI: 1.50-2.80) and impaired fasting glucose (AOR: 1.71, 95% CI: 1.32-2.23). Strategies for replacing sedentary behavior of postmenopausal women with activities are warranted for prevention of abdominal obesity and impaired fasting glucose.

Subanesthetic ketamine rapidly alters medial prefrontal miRNAs involved in ubiquitin-mediated proteolysis.

Ketamine is a dissociative anesthetic and a non-competitive NMDAR antagonist. At subanesthetic dose, ketamine can relieve pain and work as a fast-acting antidepressant, but the underlying molecular mechanism remains elusive. This study aimed to investigate the mode of action underlying the effects of acute subanesthetic ketamine treatment by bioinformatics analyses of miRNAs in the medial prefrontal cortex of male C57BL/6J mice. Gene Ontology and KEGG pathway analyses of the genes putatively targeted by ketamine-responsive prefrontal miRNAs revealed that acute subanesthetic ketamine modifies ubiquitin-mediated proteolysis. Validation analysis suggested that miR-148a-3p and miR-128-3p are the main players responsible for the subanesthetic ketamine-mediated alteration of ubiquitin-mediated proteolysis through varied regulation of ubiquitin ligases E2 and E3. Collectively, our data imply that the prefrontal miRNA-dependent modulation of ubiquitin-mediated proteolysis is at least partially involved in the mode of action by acute subanesthetic ketamine treatment.

Impact of Job Engagement on the Quality of Nursing Services: The Effect of Person-Centered Nursing in South Korean Nurses.

Nurses' job engagement could help improve the quality of nursing services, and person-centered nursing is expected to play an important role in this relationship. However, little is known about the role of person-centered nursing in the association between job engagement and quality of nursing services. This study examines the moderating and mediating effects of person-centered nursing on the relationship between the job engagement and the quality of nursing services in Korean nurses. In October 2020, 200 hospital nurses were surveyed at three university hospitals. The moderating and mediating effects of person-centered nursing were determined using hierarchical regression analysis. There was a significant positive correlation between job engagement, person-centered nursing, and quality of nursing services. Person-centered nursing was found to have a mediating and moderating role in the relationship between job engagement and quality of nursing service. In conclusion, in the impact of job engagement on the quality of nursing service, it plays a buffering role, and the job engagement of nurses improves the quality of nursing services through improvement of person-centered nursing. Therefore, this study recommends the development and implementation of an educational program to foster person-centered nursing in order to improve the quality of nursing services.

Upregulation of Fatty Acid Transporters is Associated With Tumor Progression in Non-Muscle-Invasive Bladder Cancer.

As patients with non-muscle-invasive bladder cancer (NMIBC) show a high degree of heterogeneity in tumor recurrence or progression, many clinicians demand a detailed risk stratification. Although modified fatty acid metabolism in cancer cells is reported to reflect malignant phenotypes such as metastasis, the impact of fatty acid transporters on NMIBC has never been investigated. This study examined the clinicopathologic implications of fatty acid transporters such as fatty acid transport protein 4 (FATP4), cluster of differentiation 36/fatty acid translocase (CD36/FAT), and long chain acyl CoA synthetase 1 (ACSL1) in 286 NMIBC cases. This study revealed that FATP4, CD36, and ACSL1 were overexpressed in 123 (43.0%), 43 (15.0%), and 35 (12.2%) NMIBC cases, respectively. High FATP4 in tumor cells was associated with high grade (p = 0.004) and high stage (p = 0.039). High CD36 was related to high grade (p < 0.001), high stage (p = 0.002), and non-papillary growth type (p = 0.004). High ACSL1 showed an association with high grade (p < 0.001), high stage (p = 0.01), non-papillary growth type (p = 0.002), and metastasis (p = 0.033). High FATP4 was an independent factor predicting short overall survival (OS) (hazard ratio = 3.32; 95% confidence interval, 1.07-10.31; p = 0.038). In conclusion, upregulation of FATP4, CD36, and ACSL1 might promote the NMIBC progression and could be exploited in clinical risk stratification and targeted therapy.

Disruption of the astrocyte-neuron interaction is responsible for the impairments in learning and memory in 5XFAD mice: an Alzheimer's disease animal model.

The morphological dynamics of astrocytes are altered in the hippocampus during memory induction. Astrocyte-neuron interactions on synapses are called tripartite synapses. These control the synaptic function in the central nervous system. Astrocytes are activated in a reactive state by STAT3 phosphorylation in 5XFAD mice, an Alzheimer's disease (AD) animal model. However, changes in astrocyte-neuron interactions in reactive or resting-state astrocytes during memory induction remain to be defined. Here, we investigated the time-dependent changes in astrocyte morphology and the number of astrocyte-neuron interactions in the hippocampus over the course of long-term memory formation in 5XFAD mice. Hippocampal-dependent long-term memory was induced using a contextual fear conditioning test in 5XFAD mice. The number of astrocytic processes increased in both wild-type and 5XFAD mice during memory formation. To assess astrocyte-neuron interactions in the hippocampal dentate gyrus, we counted the colocalization of glial fibrillary acidic protein and postsynaptic density protein 95 via immunofluorescence. Both groups revealed an increase in astrocyte-neuron interactions after memory induction. At 24 h after memory formation, the number of tripartite synapses returned to baseline levels in both groups. However, the total number of astrocyte-neuron interactions was significantly decreased in 5XFAD mice. Administration of Stattic, a STAT3 phosphorylation inhibitor, rescued the number of astrocyte-neuron interactions in 5XFAD mice. In conclusion, we suggest that a decreased number of astrocyte-neuron interactions may underlie memory impairment in the early stages of AD.