The Notch signaling-regulated angiogenesis in rheumatoid arthritis: pathogenic mechanisms and therapeutic potentials.

Angiogenesis plays a key role in the pathological process of inflammation and invasion of the synovium, and primarily drives the progression of rheumatoid arthritis (RA). Recent studies have demonstrated that the Notch signaling may represent a new therapeutic target of RA. Although the Notch signaling has been implicated in the M1 polarization of macrophages and the differentiation of lymphocytes, little is known about its role in angiogenesis in RA. In this review, we discourse the unique roles of stromal cells and adipokines in the angiogenic progression of RA, and investigate how epigenetic regulation of the Notch signaling influences angiogenesis in RA. We also discuss the interaction of the Notch-HIF signaling in RA's angiogenesis and the potential strategies targeting the Notch signaling to improve the treatment outcomes of RA. Taken together, we further suggest new insights into future research regarding the challenges in the therapeutic strategies of RA.

Deciphering the neural mechanisms of miR-134 in major depressive disorder with population-based and person-specific imaging transcriptomic techniques.

MiR-134 has emerged as a potential molecular biomarker for the detection and management of major depressive disorder (MDD). Nevertheless, the specific effects of miR-134 as a regulatory element on brain function and its implications for the clinical presentation of MDD are not yet fully understood. In order to investigate the potential neural mechanisms that contribute to the relationship between miR-134 and MDD, we employed a parallel two-stage cross-scale multi-omics approach. This involved utilizing the anterior cingulate cortex (ACC) functional connectivity as a means to connect microscopic molecular structures with macroscopic brain function in two separate cohorts: the MDD-I dataset (56 MDD patients and 51 healthy controls) and the MDD-II dataset (57 MDD patients and 52 healthy controls). We found a stable ACC functional dysconnectivity pattern of MDD and established the hierarchical cross-scale association from molecular organizations of miR-134 target genes to macroscopic brain functional dysconnectivity and associated behavior, as revealed by population-based analysis. Additionally, our person-specific imaging transcriptomic study revealed that individual exosomal miR-134 expression levels impact on individual clinical symptoms of MDD by modulating ACC-related functional dysconnectivity. Together, our findings provide compelling evidence of the correlation between miR-134 and depression across multi scales within the gene-brain-behavior context.

Hierarchical fluctuation shapes a dynamic flow linked to states of consciousness.

Consciousness arises from the spatiotemporal neural dynamics, however, its relationship with neural flexibility and regional specialization remains elusive. We identified a consciousness-related signature marked by shifting spontaneous fluctuations along a unimodal-transmodal cortical axis. This simple signature is sensitive to altered states of consciousness in single individuals, exhibiting abnormal elevation under psychedelics and in psychosis. The hierarchical dynamic reflects brain state changes in global integration and connectome diversity under task-free conditions. Quasi-periodic pattern detection revealed that hierarchical heterogeneity as spatiotemporally propagating waves linking to arousal. A similar pattern can be observed in macaque electrocorticography. Furthermore, the spatial distribution of principal cortical gradient preferentially recapitulated the genetic transcription levels of the histaminergic system and that of the functional connectome mapping of the tuberomammillary nucleus, which promotes wakefulness. Combining behavioral, neuroimaging, electrophysiological, and transcriptomic evidence, we propose that global consciousness is supported by efficient hierarchical processing constrained along a low-dimensional macroscale gradient.

Removal Efficiency of Sulfapyridine from Contaminated Surface Water by Carboxylated Graphene Oxide Blended PVDF Composite Ultrafiltration Membrane with Activated Carbon.

In this study, sulfapyridine (SPY), an antibiotic that is less commonly treated by membrane filtration techniques but is frequently detected in the aqueous environment and at higher concentrations than other detected antibiotics, was selected for investigation. A composite ultrafiltration membrane for the removal of sulfapyridine (SPY) antibiotics from water was fabricated using polyvinylidene fluoride (PVDF), polyvinylpyrrolidone (PVP), and carboxyl-functionalized graphene oxide (CFGO) as additives. The changes in retention rate and pure water flux of sulfapyridine by the composite ultrafiltration membrane were investigated by changing the ratios of the prepared ultrafiltration membrane materials under the conditions of low-pressure operation to explore the optimal experimental conditions. The results showed that the addition of PVP and CFGO significantly increased the number of membrane pores and their pore size. The addition of CFGO in the membrane significantly improved the hydrophilicity of the membrane. The contact angle decreased from 83.7 to 31.6°. Compared to ordinary PVDF ultrafiltration membranes, the membrane's pure water flux increased nearly three times to 2612.95 L/(m2·h). The removal rate of SPY was 56.26% under the optimal conditions. When the composite ultrafiltration membrane was combined with activated carbon, the removal rate of SPY was 92.67%, which was nine times higher than that of activated carbon alone. At this time, the flux of the composite membrane was 2610.23 L/(m2·h). This study proposes a simple, efficient, and low production cost solution for the removal of sulfapyridine from water.

The human mediodorsal thalamus: Organization, connectivity, and function.

The human mediodorsal thalamic nucleus (MD) is crucial for higher cognitive functions, while the fine anatomical organization of the MD and the function of each subregion remain elusive. In this study, using high-resolution data provided by the Human Connectome Project, an anatomical connectivity-based method was adopted to unveil the topographic organization of the MD. Four fine-grained subregions were identified in each hemisphere, including the medial (MDm), central (MDc), dorsal (MDd), and lateral (MDl), which recapitulated previous cytoarchitectonic boundaries from histological studies. The subsequent connectivity analysis of the subregions also demonstrated distinct anatomical and functional connectivity patterns, especially with the prefrontal cortex. To further evaluate the function of MD subregions, partial least squares analysis was performed to examine the relationship between different prefrontal-subregion connectivity and behavioral measures in 1012 subjects. The results showed subregion-specific involvement in a range of cognitive functions. Specifically, the MDm predominantly subserved emotional-cognition domains, while the MDl was involved in multiple cognitive functions especially cognitive flexibility and inhibition. The MDc and MDd were correlated with fluid intelligence, processing speed, and emotional cognition. In conclusion, our work provides new insights into the anatomical and functional organization of the MD and highlights the various roles of the prefrontal-thalamic circuitry in human cognition.

Neuroticism vulnerability factors of anxiety symptoms in adolescents and early adults: an analysis using the bi-factor model and multi-wave longitudinal model.

BACKGROUND: Neuroticism and stress are important vulnerability factors in the development and outcome of anxiety symptoms. However, as neuroticism is a heterogeneity trait, it is still unclear how different neuroticism factors contribute to anxiety symptoms independently or in conjunction with stress. Thus, different factors of neuroticism were extracted in the present longitudinal study using the bi-factor model. The prediction effect of these different factors on anxiety symptoms and their combined effects with stress in both adolescent and adult samples were examined. METHOD: Participants (592 adolescents and 638 young adults) in Hunan China were included. In the initial assessment in our longitudinal study, participants were asked to complete measurements that assessed neuroticism, stress, and anxiety symptoms. Next, a monthly assessment of stress and anxiety symptoms was completed for the subsequent 6 months. The bi-factor model was used to extract different factors of neuroticism. The hierarchical linear model was used to analyze longitudinal multi-wave data. RESULT: Several model fit indices were used to evaluate the bi-factor model fit for neuroticism (adolescent: Tucker-Lewis index (TLI) = 0.957, comparative fit index (CFI) = 0.973, RMSEA = 0.040, Chi-Square = 80.471; early adults: TLI = 0.957, CFI = 0.973, RMSEA = 0.042, Chi-Square = 88.465). The results of hierarchical linear modeling analyses indicated that the general factor of neuroticism possessed a predictive effect on anxiety symptoms (adolescents: F = 36.77, p < 0.0001, early adults: F = 30.44, p < 0.0001); The negative effect factor only had the prediction effect on anxiety symptoms in early adults (adolescents: F = 0.65, p > 0.05; early adults: F = 4.84, p < 0.05); No prediction of self-reproach factor was found on anxiety symptoms (adolescents: F = 3.79, p > 0.05; early adults: F = 0.02, p > 0.05); the interactive effects of the general factor and stress on anxiety symptoms were only found in early adulthood (adolescents: F = 0.13, p > 0.05; early adults: F = 11.55, p < 0.01). CONCLUSION: Our results suggested that the bi-factor model achieved a satisfactory fit for neuroticism measurement and supported that the anxiety symptoms were induced by the main effects of the general factor in both age samples and the negative factor only in adults. The general factor of neuroticism, but not the negative factor could make an additive effect for anxiety symptoms in face of stress, which meant that the homogeneity of neuroticism played a more significant role in further anxiety symptoms than heterogeneity when coping with stress.

Cingulum White Matter Integrity as a Mediator Between Harm Avoidance and Hostility.

As a textbook manifestation of an aggressive attitude, hostility can pose a serious threat to both an individual's life and the security of society at large. Past evidence suggests that some anxiety-related traits may be more prone to giving rise to hostility. However, many aspects of hostility, such as, determining the susceptible temperament for hostility, the neural basis of hostility, and the underlying mechanisms through which having a susceptible temperament generates hostility in a healthy brain, remain unclear. In this study, we sought to delve into these questions by assessing temperament and brain white matter integrity using self-report questionnaires and diffusion tensor imaging in a sizable sample of healthy adults (n = 357). First, we investigated the relationship between hostility and the four temperaments of the Cloninger model. Then, we investigated which white matter tracts were significantly correlated with hostility using a whole-brain analysis. Finally, we used a mediation analysis to explore the tripartite relationship between vulnerability temperament, the fractional anisotropy (FA) value of the white matter, and hostility. Our results suggest that a harm avoidance temperament may be susceptible to hostility and that the cingulum may be a key white matter region responsible for hostility. Based on these results, we developed a temperament-brain-attitude pathway showing how harm avoidance temperament could affect the brain and ultimately lead to hostility.

YB-1 transferred by gastric cancer exosomes promotes angiogenesis via enhancing the expression of angiogenic factors in vascular endothelial cells.

BACKGROUND: Angiogenesis is important for the progression of gastric cancer (GC). Y-box binding protein 1 (YB-1) predicts advanced disease and indicates neovasculature formation in GC tissues, while the related mechanisms remain elusive. Exosomes mediate intercellular communications via transferring various molecules including proteins, lipids, mRNAs, and microRNAs, while the cargos of GC exosomes and the related mechanisms in GC angiogenesis were rarely reported except for several microRNAs. METHODS: In this study, human umbilical vein endothelial cells (HUVECs) were, respectively, treated by the exosomes isolated from the YB-1 transfected and the control SGC-7901 cells (SGC-7901-OE-Exo and SGC-7901-NC-Exo), and their apoptosis, proliferation, migration, invasion, and angiogenesis were, sequentially, compared. The levels of angiogenic factors including VEGF, Ang-1, MMP-9 and IL-8 in the exosome-treated HUVECs and the GC-derived exosomes were, separately, detected using PCR and Western blotting as well as RNA sequencing assays. RESULTS: We observed the consistent level of YB-1 in the exosomes and their originated GC cells, and the internalization of exosomes into HUVECs. Comparing with SGC-7901-NC-Exo, SGC-7901-OE-Exo significantly inhibited the apoptosis but promoted the proliferation, migration, invasion, and angiogenesis of HUVECs, within which the increased mRNA and protein levels of VEGF, Ang-1, MMP-9 and IL-8 were demonstrated. Meanwhile, mRNA levels of VEGF, Ang-1, MMP-9 and IL-8 showed no significant difference between SGC-7901-NC-Exo and SGC-7901-OE-Exo, although statistically higher mRNA of YB-1 was detected in the SGC-7901-OE-Exo. CONCLUSIONS: Our findings illustrate YB-1 as the key component of exosome to promote GC angiogenesis by upregulating specific angiogenic factors in the exosome-treated endothelial cells but not in the exosomes themselves.

Repair and regeneration of small intestine: A review of current engineering approaches.

The small intestine (SI) is difficult to regenerate or reconstruct due to its complex structure and functions. Recent developments in stem cell research, advanced engineering technologies, and regenerative medicine strategies bring new hope of solving clinical problems of the SI. This review will first summarize the structure, function, development, cell types, and matrix components of the SI. Then, the major cell sources for SI regeneration are introduced, and state-of-the-art biofabrication technologies for generating engineered SI tissues or models are overviewed. Furthermore, in vitro models and in vivo transplantation, based on intestinal organoids and tissue engineering, are highlighted. Finally, current challenges and future perspectives are discussed to help direct future applications for SI repair and regeneration.

SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis.

BACKGROUND: Plenty of long non-coding RNAs (lncRNAs) play vital roles in the progression of atherosclerosis. Small nucleolar RNA host gene 6 (SNHG6) is a well known lncRNA that is aberrantly high expressed in atherosclerosis patients. However, its function and basic mechanism in atherosclerosis events have not been well clarified. METHODS: The expression patterns of SNHG6, miR-135a-5p, ROCK1 and ROCK2 in clinical samples and cells were detected by RT-qPCR assays. Cell Counting Kit-8 (CCK-8), flow cytometry assays, ELISA and reactive oxygen species (ROS) and malondialdehyde (MDA) detection, were performed to assess cell viability, apoptosis, inflammation and oxidative stress, respectively. Western blot analysis was carried out to examine the protein levels of Bax, Bcl-2, and SNHG6. Luciferase reporter and RIP assays were used to confirm the true interaction between SNHG6 and miR-135a-5p, or miR-135a-5p and ROCK. RESULTS: The levels of SNHG6, ROCK1 and ROCK2 were notably increased and miR-135a-5p was decreased in atherosclerosis patients and oxidized low-density lipoprotein (ox-LDL)-treated HUVECs. Knockdown of SNHG6 alleviated ox-LDL-induced injury of HUVECs, while this effect was partly reversed by miR-135a-5p inhibitor. Moreover, overexpression of ROCKs aggravated miR-135a-5p-alleviated atherosclerosis cell injury. SNHG6 contributed to ROCK expression through sequestering miR-135a-5p as a molecular sponge. CONCLUSION: SNHG6 functions as a promoter in atherosclerosis events by targeting miR-135a-5p/ROCK axis in ox-LDL-stimulated HUVECs. This finding will help to develop a novel therapeutic strategy for atherosclerosis.

Coupled Temporal Fluctuation and Global Signal Synchronization of Spontaneous Brain Activity in Hypnosis for Respiration Control: An fMRI Study.

Hypnosis is a psychological technology proved to be effective in respiratory motion control, which is essential to reduce radiation dose during radiotherapy. This study explored the neural mechanisms and cognitive neuroscience of hypnosis for respiration control by functional magnetic resonance imaging with a within-subject design of 15 healthy volunteers in rest state (RS) and hypnosis state (HS). Temporal fluctuation and signal synchronization of brain activity were employed to investigate the altered physiological performance in hypnosis. The altered correlations between temporal fluctuation and signal synchronization were examined within large scale of intrinsic networks which were identified by seed-wise functional connectivity. As a result, hypnosis was observed with increased activity in the right calcarine, bilateral fusiform gyrus and left middle temporal gyrus, and with decreased activity in the left cerebellum posterior lobe (inferior semilunar lobule part). Compared to RS, enhanced positive correlations were observed between temporal fluctuation and signal synchronization in HS. Most importantly, coupled correlation was observed between temporal fluctuation and global signal synchronization within the identified intrinsic networks (R = 0.3843, p > 0.05 in RS; R = 0.6212, p < 0.005 in HS). The findings provide implications for the neural basis of hypnosis for respiratory motion control and suggest the involvement of emotional processing and regulation of perceptual consciousness in hypnosis.

The preventive effect of liraglutide on the lipotoxic liver injury via increasing autophagy.

INTRODUCTION AND OBJECTIVES: The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing. Previous studies indicated that Liraglutide, glucagon-like peptide-1 analogue, could regulate glucose homeostasis as a valuable treatment for Type 2 Diabetes. However, the precise effect of Liraglutide on NAFLD model in rats and the mechanism remains unknown. In this study, we investigated the molecular mechanism by which Liraglutide ameliorates hepatic steatosis in a high-fat diet (HFD)-induced rat model of NAFLD in vivo and in vitro. MATERIALS AND METHODS: NALFD rat models and hepatocyte steatosis in HepG2 cells were induced by HFD and palmitate fatty acid treatment, respectively. AMPK inhibitor, Compound C was added in HepG2 cells. Autophagy-related proteins LC3, Beclin1 and Atg7, and AMPK pathway-associated proteins were evaluated by Western blot and RT-PCR. RESULTS: Liraglutide enhanced autophagy as showed by the increased expression of the autophagy markers LC3, Beclin1 and Atg7 in HFD rats and HepG2 cells treated with palmitate fatty acid. In vitro, The AMPK inhibitor exhibited an inhibitory effect on Liraglutide-induced autophagy enhancement with the deceased expression of LC3, Beclin1 and Atg7. Additionally, Liraglutide treatment elevated AMPK levels and TSC1, decreased p-mTOR expression. CONCLUSIONS: Liraglutide could upregulate autophagy to decrease lipid over-accumulation via the AMPK/mTOR pathway.

Vps15 is critical to mediate autophagy in AngII treated HUVECs probably by PDK1/PKC signaling pathway.

AIMS: Vps15 is an important regulator on the activity of class III PI3K in autophagy induction. AngII plays a positive role of autophagy in the early protection of endothelial cells. In this study, the expression of Vps15 was knocked down using the specific shRNA to investigate the effects of Vps15 on cell autophagy, senescence and apoptosis in HUVECs stimulated by AngII. The associated cell signaling pathway was also explored. MATERIALS AND METHODS: MDC staining was applied to show autophagic bodies. Cell senescence was detected using ß-galactosidase staining. Cell apoptosis was examined by flow cytometry using Annexin V-FITC/PI staining. And western blot was used to evaluate the ratio of LC3-II/I and the activation of associated cell signaling pathway. KEY FINDINGS: Cell autophagy induced by AngII was inhibited in HUVECs transfected with Vps15-shRNA, while cell senescence and apoptosis were enhanced. Rescue experiment revealed that cell autophagy was activated after Vps15 reexpression, while cell senescence and apoptosis were inhibited. Moreover, the phosphorylations of PDK1 and PKC substrates were increased after AngII treatment, which were decreased by Vps15 knockdown. Pretreatment of cells with the inhibitor for PDK1 or PKC attenuated cell autophagy after AngII stimulation, yet promoted cell senescence and apoptosis. The phosphorylations of both PDK1 and PKC were inhibited in cells pretreated with PDK1 inhibitor. Only the activation of PKC was inhibited when the inhibitor for pan-PKC was used. SIGNIFICANCE: These results suggested that Vps15 was critical to the protective autophagy in HUVECs induced by AngII, and PDK1/PKC signaling pathway was probably involved.

MoS2 decorated CdS hybrid heterojunction for enhanced photoelectrocatalytic performance under visible light irradiation.

Pervious photocatalysis application of nanostructured suspensions reveals high recombination rates of photogenerated electron-hole pairs, low recycling efficiency and secondary pollution problems. Herein, MoS2@CdS nanocomposites thin films on FTO (fluorine-doped tin oxide) substrates are fabricated using facile electrodeposition by decorating a layer of highly-active MoS2 cocatalyst on CdS film to optimize the interface modification. The hybrid film exhibits enhanced photoelectrocatalytic activity compared to pristine CdS film. The synthesized CdS exhibits a bandgap of 2.42 eV with the conduct band at ca. -0.25 V vs. RHE, while MoS2 reveals a bandgap of 1.73 eV with the valance band at ca. 1.59 V vs. RHE. The appropriate band alignment between the hybrid films favours the electrons transfer thus the charge recombination are suppressed. The MoS2@CdS film yields a highest photocurrent of 15.2 mA/cm2 at 0 V vs. Ag/AgCl under visible light illumination (λ ≧ 420 nm), exhibiting a 5.2 times enhancement as compared to that of CdS film (2.9 mA/cm2). The structural integration of MoS2 with CdS will be a promising strategy to develop a high-efficient and low-cost non-noble metal cocatalyst for solar energy conversion.

Investigation on the Neural Mechanism of Hypnosis-Based Respiratory Control Using Functional MRI.

Respiratory control is essential for treatment effect of radiotherapy due to the high dose, especially for thoracic-abdomen tumor, such as lung and liver tumors. As a noninvasive and comfortable way of respiratory control, hypnosis has been proven effective as a psychological technology in clinical therapy. In this study, the neural control mechanism of hypnosis for respiration was investigated by using functional magnetic resonance imaging (fMRI). Altered spontaneous brain activity as well as neural correlation of respiratory motion was detected for eight healthy subjects in normal state (NS) and hypnosis state (HS) guided by a hypnotist. Reduced respiratory amplitude was observed in HS (mean ± SD: 14.23 ± 3.40 mm in NS, 12.79 ± 2.49 mm in HS, p=0.0350), with mean amplitude deduction of 9.2%. Interstate difference of neural activity showed activations in the visual cortex and cerebellum, while deactivations in the prefrontal cortex and precuneus/posterior cingulate cortex (PCu/PCC) in HS. Within these regions, negative correlations of neural activity and respiratory motion were observed in visual cortex in HS. Moreover, in HS, voxel-wise neural correlations of respiratory amplitude demonstrated positive correlations in cerebellum anterior lobe and insula, while negative correlations were shown in the prefrontal cortex and sensorimotor area. These findings reveal the involvement of cognitive, executive control, and sensorimotor processing in the control mechanisms of hypnosis for respiration, and shed new light on hypnosis performance in interaction of psychology, physiology, and cognitive neuroscience.

Mechanically robust cryogels with injectability and bioprinting supportability for adipose tissue engineering.

Bioengineered adipose tissues have gained increased interest as a promising alternative to autologous tissue flaps and synthetic adipose fillers for soft tissue augmentation and defect reconstruction in clinic. Although many scaffolding materials and biofabrication methods have been investigated for adipose tissue engineering in the last decades, there are still challenges to recapitulate the appropriate adipose tissue microenvironment, maintain volume stability, and induce vascularization to achieve long-term function and integration. In the present research, we fabricated cryogels consisting of methacrylated gelatin, methacrylated hyaluronic acid, and 4arm poly(ethylene glycol) acrylate (PEG-4A) by using cryopolymerization. The cryogels were repeatedly injectable and stretchable, and the addition of PEG-4A improved the robustness and mechanical properties. The cryogels supported human adipose progenitor cell (HWA) and adipose derived mesenchymal stromal cell adhesion, proliferation, and adipogenic differentiation and maturation, regardless of the addition of PEG-4A. The HWA laden cryogels facilitated the co-culture of human umbilical vein endothelial cells (HUVEC) and capillary-like network formation, which in return also promoted adipogenesis. We further combined cryogels with 3D bioprinting to generate handleable adipose constructs with clinically relevant size. 3D bioprinting enabled the deposition of multiple bioinks onto the cryogels. The bioprinted flap-like constructs had an integrated structure without delamination and supported vascularization. STATEMENT OF SIGNIFICANCE: Adipose tissue engineering is promising for reconstruction of soft tissue defects, and also challenging for restoring and maintaining soft tissue volume and shape, and achieving vascularization and integration. In this study, we fabricated cryogels with mechanical robustness, injectability, and stretchability by using cryopolymerization. The cryogels promoted cell adhesion, proliferation, and adipogenic differentiation and maturation of human adipose progenitor cells and adipose derived mesenchymal stromal cells. Moreover, the cryogels also supported 3D bioprinting on top, forming vascularized adipose constructs. This study demonstrates the potential of the implementation of cryogels for generating volume-stable adipose tissue constructs and provides a strategy to fabricate vascularized flap-like constructs for complex soft tissue regeneration.

Regional homogeneity and functional connectivity patterns in major depressive disorder, cognitive vulnerability to depression and healthy subjects.

BACKGROUND: Cognitive vulnerability to depression (CVD) is a high risk for depressive disorder. Recent studies focus on individuals with CVD to determine the neural basis of major depressive disorder (MDD) neuropathology. However, whether CVD showed specific or similar brain functional activity and connectivity patterns, compared to MDD, remain largely unknown. METHODS: Here, using resting-state functional magnetic resonance imaging in subjects with CVD, healthy controls (HC) and MDD, regional homogeneity (ReHo) and resting-state functional connectivity (R-FC) analyses were conducted to assess local synchronization and changes in functional connectivity patterns. RESULTS: Significant ReHo differences were found in right posterior lobe of cerebellum (PLC), left lingual gyrus (LG) and precuneus. Compared to HC, CVD subjects showed increased ReHo in the PLC, which was similar to the difference found between MDD and HC. Compared to MDD patients, CVD subjects showed decreased ReHo in PLC, LG, and precuneus. R-FC analyses found increased functional connections between LG and left inferior parietal lobule, posterior cingulate cortex, and dorsolateral prefrontal cortex in CVD compared to both HC and MDD. Moreover, Regional mean ReHo values were positively correlated with Center for Epidemiologic Studies Depression Scale scores. CONCLUSION: These analyses revealed that PLC and functional connections between LG and left inferior parietal lobule, posterior cingulate cortex, and dorsolateral prefrontal cortex may be a potential marker for CVD.

Levels of neuroticism differentially predict individual scores in the depression and anxiety dimensions of the tripartite model: A multiwave longitudinal study.

The associations between neuroticism and depression and anxiety symptoms remain unclear possibly due to the lack of specificity and covariation among common symptoms. The current study hypothesized that neuroticism acts as a vulnerability factor for general distress (GD) and specific depression and anxiety symptoms. We investigated this hypothesis using the "tripartite model" (a well-known dimensional model of anxiety and depression). A sample of 644 college students was recruited from Hunan, China. In the initial stage of this investigation, the students completed self-assessment forms to measure their levels of neuroticism and frequency of daily hassles. The students also reported on their levels of GD and specific depression and anxiety symptoms. The same self-assessment procedure was undertaken once a month for the next 6 months. The results of the hierarchical linear model suggest a significant interaction between neuroticism and the level of stress caused by exposure to increased levels of daily hassles, which can be used as a predictor of future levels of GD and specific anxiety symptoms. However, the same interaction was not a significant predictor of specific depression symptoms. The current findings suggest that neuroticism may be a risk factor for specific anxiety but not for specific depression symptoms in face of stress caused by daily hassles.

Protection of endothelial cells against Ang II-induced impairment: Involvement of both PPARα and PPARγ via PI3K/Akt pathway.

The aim of our study is to explore the involvement of PPARα and PPARγ in Ang II-induced endothelial injury. We found that Ang II significantly elevated the oxidative stress in HUVECs, causing apoptosis and cellular impairment in a time-dependent pattern. Activation of either PPARα by docosahexaenoic acid (DHA) or PPARγ by rosiglitazone protected the endothelial cells. Interestingly, a more significant effect was observed when DHA and rosiglitazone were administrated together. Moreover, we found that this protection was mediated through the PI3K/Akt pathway. Our study may help to understand the mechanism of endothelial dysfunction, contributing to the treatment of hypertension and other endothelial-related diseases.