Explore the vast range of titles available.

Background Close relationships have been observed among impulsivity, depression, hopelessness, and suicidal ideation in depressed patients. However, the precise mechanism that connects these psychological symptoms remains unclear. This study aims to explore the mediation effect of depression and hopelessness on the relationship between impulsivity and suicidal ideation in depressed patients. Methods A total of 258 depressed patients were evaluated using the Hamilton Depression Scale, the Beck Hopelessness Scale, the Scale for Suicide Ideation, and the Barratt Impulsiveness Scale. A path analysis was afterwards performed to determine the specified relationships in the proposed model. Results The relationship between impulsivity and suicidal ideation was found to be serially mediated by depression and hopelessness. The mediating effect of depression and hopelessness accounted for 26.59% of the total effect. Specifically, in the pathway from impulsivity to hopelessness, the mediating effect of depression accounted for 40.26%. Moreover, the relationship between impulsivity and suicidal ideation was mediated by hopelessness, with the mediating effect accounting for 12.41%. It is important to note that these relationships were observed to be independent of age and marital status. Furthermore, the proposed model demonstrated a good fit with the data. Conclusions This study identified a serial mediation pathway between impulsivity and suicidal ideation, mediated by depression and hopelessness. Our findings indicate that impulsivity indirectly influences suicidal ideation through its association with depression, which subsequently contributes to feelings of hopelessness. These results emphasize the importance of addressing symptoms of depression and hopelessness in the prevention and intervention efforts targeting individuals with depression. Additionally, monitoring and addressing impulsivity levels may also be crucial in reducing the risk of suicidal ideation among this population. These findings provide valuable insights for future preventive programs and interventions aimed at mitigating suicidal ideation in individuals with depression.

Against the backdrop of artificial intelligence (AI) empowering the medical industry, achieving symmetric coordination between patients and medical intelligent systems has emerged as a key factor in enhancing the efficacy of medical human–computer collaborative diagnosis. This study systematically identified the factors influencing the effectiveness of human–machine collaborative diagnosis in healthcare by combining literature analysis with expert interviews, based on the Socio-technical Systems Theory. It constructed a symmetric evaluation framework consisting of 19 indicators across four dimensions: user, technology, task, and environment. An integrated DEMATEL method incorporating symmetric logic was employed to quantitatively analyze the interdependent relationships among factors and identify 18 key factors. Subsequently, ISM was applied to analyze the dependency relationships between these key factors, thereby constructing a clear multi-level hierarchical structure model. Through hierarchical construction of a multi-level hierarchical structure model, four core paths driving diagnostic effectiveness were revealed. The research shows that optimizing user behavior mechanisms and technology adaptability and strengthening dynamic coordination strategies between tasks and the environment can effectively achieve the two-way symmetric mapping of the medical human–machine system from fuzzy decision-making to precise output. This has not only improved the efficacy of medical human–computer collaborative diagnosis, but also provided a theoretical basis and practical guidance for optimizing the practical application of medical human–computer collaborative diagnosis.

Optical vector analysis (OVA) capable of achieving magnitude and phase responses is essential for the fabrication and application of emerging optical devices. Conventional OVA often has to make compromises among resolution, dynamic range, and bandwidth. Here we show an original method to meet the measurement requirements for ultra-wide bandwidth, ultra-high resolution, and ultra-large dynamic range simultaneously, based on an asymmetric optical probe signal generator (ASG) and receiver (ASR). The ASG and ASR remove the measurement errors introduced by the modulation nonlinearity and enable an ultra-large dynamic range. Thanks to the wavelength-independence of the ASG and ASR, the measurement range can increase by 2  N times by applying an N -tone optical frequency comb without complicated operation. In an experiment, OVA with a resolution of 334 Hz (2.67 attometer in the 1550-nm band), a dynamic range of > 90 dB and a measurement range of 1.075 THz is demonstrated. Typical methods for optical vector analysis have tradeoffs among resolution, dynamic range, and bandwidth. The authors use an asymmetric optical probe signal generator and receiver to perform attometer resolution measurement over a THz of bandwidth while maintaining high dynamic range, aiming to characterize emerging optical devices.

Background The purpose of this research was to explore the underlying mechanisms of cognitive impairments in patients with coronary heart disease (CHD) who exhibit depressive symptoms. This was accomplished by recording Event-related potentials (ERPs) during the emotional Stroop task, with a specific focus on the temporal dynamics of attentional bias towards various emotional words. Methods We selected 17 CHD patients with depressive symptoms and 23 CHD patients without depression using a convenience sampling method from the Affiliated Hospital of Weifang Medical University. Each participant completed an emotional Stroop color-word task, and ERPs were recorded during the task to examine cognitive processing. Results CHD patients with depressive symptoms exhibited generally smaller amplitudes of N1, N2, P3 and longer latency of P3 compared to CHD patients without depression. Specifically, the N1 amplitude of negative words was smaller and the P3 amplitude of negative words was larger in the CHD with depressive group compared to the CHD group. Furthermore, within the group of CHD patients with depressive symptoms, negative words elicited a smaller N1 amplitude and larger P3 amplitude compared to positive and neutral words. Conclusions CHD patients with depressive symptoms demonstrate decreased attentional resources, leading to cognitive impairments. Notably, significant attentional bias occurs during both early and later stages of cognitive processing. This bias is primarily characterized by an enhanced automatic processing of negative information at the early stage and difficulty disengaging from such information at the later stage. These findings contribute to the existing literature on the cognitive neural mechanisms underlying depression in CHD patients.

Major depression disorder is a severe mental illness often linked with metabolic disorders. Adiponectin is an adipocyte-secreted circulatory hormone with antidiabetic and glucose/lipid modulation capacities. Studies have demonstrated the pathophysiological roles of adiponectin involved in various neurological disorders, including depression. However, the underlying mechanisms are poorly understood. Here we showed that adiponectin deprivation enhanced antidepressive-like behaviors in the LPS-induced model of depression. APN KO mice displayed increased cytokines (both pro and anti-inflammatory), accompanied by an impaired expression of adiponectin receptors (mRNA/protein level) and decreasing IBA-1 level in the cortex and primary microglia of LPS treated APN KO mice. Further, LPS-treatment significantly reduced p-NFκB expression in the microglia of APN KO mice. However, the Bay11-7082 treatment recovered p-NFκB expression in the cortex of APN KO mice in the presence of LPS. Interestingly, the antidepressant potentials of APN KO mice were abolished by TrkB antagonist K252a, IKK inhibitor Bay11-7082, and AdipoRon suggesting crosstalk between TrkB/BDNF signaling and NFκB in depression. Furthermore, the effects of Bay11-7082 were abolished by a TrkB/BDNF activator (7,8-DHF), indicating a critical role of TrkB/BDNF signaling. Taken together, these findings showed that dysregulated neuroinflammatory status and BDNF signaling might underlie the antidepressive-like behaviors of APN KO mice. NFκB elicited BDNF changes may be accountable for the pathogenesis of LPS induced depression, where APN might present an alternative therapeutic target for depressive disorders.

Background Selective serotonin reuptaker inhibitors, including fluoxetine, are widely studied and prescribed antidepressants, while their exact molecular and cellular mechanism are yet to be defined. We investigated the involvement of HDAC1 and eEF2 in the antidepressant mechanisms of fluoxetine using a lipopolysaccharide (LPS)-induced depression-like behavior model. Methods For in vivo analysis, mice were treated with LPS (2 mg/kg BW), fluoxetine (20 mg/kg BW), HDAC1 activator (Exifone: 54 mg/kg BW) and NH125 (1 mg/kg BW). Depressive-like behaviors were confirmed via behavior tests including OFT, FST, SPT, and TST. Cytokines were measured by ELISA while Iba-1 and GFAP expression were determined by immunofluorescence. Further, the desired gene expression was measured by immunoblotting. For in vitro analysis, BV2 cell lines were cultured; treated with LPS, exifone, and fluoxetine; collected; and analyzed. Results Mice treated with LPS displayed depression-like behaviors, pronounced neuroinflammation, increased HDAC1 expression, and reduced eEF2 activity, as accompanied by altered synaptogenic factors including BDNF, SNAP25, and PSD95. Fluoxetine treatment exhibited antidepressant effects and ameliorated the molecular changes induced by LPS. Exifone, a selective HDAC1 activator, reversed the antidepressant and anti-inflammatory effects of fluoxetine both in vivo and in vitro, supporting a causing role of HDAC1 in neuroinflammation allied depression. Further molecular mechanisms underlying HDAC1 were explored with NH125, an eEF2K inhibitor, whose treatment reduced immobility time, altered pro-inflammatory cytokines, and NLRP3 expression. Moreover, NH125 treatment enhanced eEF2 and GSK3β activities, BDNF, SNAP25, and PSD95 expression, but had no effects on HDAC1. Conclusions Our results showed that the antidepressant effects of fluoxetine may involve HDAC1-eEF2 related neuroinflammation and synaptogenesis.

Geminiviruses constitute the largest group of known plant viruses and cause devastating diseases and economic losses in many crops worldwide. Due to limited naturally occurring resistance genes, understanding plant antiviral defense against geminiviruses is critical for finding host factors of geminiviruses and development of strategies for geminivirus control. Here we identified NbWRKY1 as a positive regulator of plant defense against geminivirus infection. Using tomato yellow leaf curl China virus/tomato yellow leaf curl China betasatellite (TYLCCNV/TYLCCNB) as a representative geminivirus, we found that NbWRKY1 was upregulated in response to TYLCCNV/TYLCCNB infection. Overexpression of NbWRKY1 attenuated TYLCCNV/TYLCCNB infection, whereas knockdown of NbWRKY1 enhanced plant susceptibility to TYLCCNV/TYLCCNB. We further revealed that NbWRKY1 bound to the promoter of the NbWHIRLY1 (NbWhy1) transcription factor and inhibited the transcription of NbWhy1. Consistently, NbWhy1 negatively regulates plant response against TYLCCNV/TYLCCNB. Overexpression of NbWhy1 significantly accelerated TYLCCNV/TYLCCNB infection. Conversely, knockdown of NbWhy1 led to impaired geminivirus infection. Furthermore, we demonstrated that NbWhy1 interfered with the antiviral RNAi defense and disrupted the interaction between calmodulin 3 and calmodulin-binding transcription activator-3. Moreover, the NbWRKY1-NbWhy1 also confers plant antiviral response toward tomato yellow leaf curl virus infection. Taken together, our findings suggest that NbWRKY1 positively regulates plant defense to geminivirus infection by repressing NbWhy1. We propose that the NbWRKY1-NbWhy1 cascade could be further employed to control geminiviruses.

Total synthesis of the proposed noursamycin A has been accomplished, which disproves the original structural assignments. The synthetic strategy described herein has also been employed in the first total synthesis of nicrophorusamide A, a cyclopeptide that is structurally related to noursamycin A.

Low modulus materials that can shape-morph into different three-dimensional (3D) configurations in response to external stimuli have wide-ranging applications in flexible/stretchable electronics, surgical instruments, soft machines and soft robotics. This paper reports a shape-programmable system that exploits liquid metal microfluidic networks embedded in an elastomer matrix, with electromagnetic forms of actuation, to achieve a unique set of properties. Specifically, this materials structure is capable of fast, continuous morphing into a diverse set of continuous, complex 3D surfaces starting from a two-dimensional (2D) planar configuration, with fully reversible operation. Computational, multi-physics modeling methods and advanced 3D imaging techniques enable rapid, real-time transformations between target shapes. The liquid-solid phase transition of the liquid metal allows for shape fixation and reprogramming on demand. An unusual vibration insensitive, dynamic 3D display screen serves as an application example of this type of morphable surface. Low modulus materials that can change shape in response to external stimuli are promising for a wide range of applications. The authors here introduce a shape-reprogrammable construct, based on liquid metal microfluidic networks and electromagnetic actuation, that supports a unique collection of capabilities.

Intake of nutrients and water from diet to maintain life, a typical physiological function of gut, is highly dependent on the extensive immune network, whose imbalance is easy to induce inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC). Clinical strategies to completely cure IBD are poor, so it is urgent to develop novel drugs or targets. Adiponectin (APN), an adipokine from adipocytes, regulates energy metabolism and immune response. High levels APN are inversely associated with CD severity UC colonic fibrosis. However, the mechanism by which APN interferes with IBD remains unclear. This review aims to analyze correlation and molecular mechanism between APN and IBD. APN and AdipoR2 proteins are highly expressed in colon which is a primary organ of IBD, and the target intersection of APN and IBD is huge. APN may interfere with lipid metabolism in IBD individuals through AdipoR1/2, but regulates neural and peripheral immune by AdipoR1 but not AdipoR2 and mediates nutritional and energy homeostasis through AdipoR2 rather than AdipoR1. Besides, APN mediates CRP and IL-6 through AdipoR1/2, AMPK and TNF-α through AdipoR1 and PI3K-Akt, PPARA and PPARG through AdipoR2 to affect IBD progression, which depends on direct interaction between APPL1 and AdipoR1/2. Unexpectedly, AMPK and TNF-α may also interact directly with AdipoR1. APN regulates CD through AdipoR1/2-metabolism process and UC through AdipoR1-inflammation axis or AdipoR2-fibrosis process. APN analogues or AdipoRon which is a dual agonist of AdipoR1/2 potentially reduces colonic fibrosis in UC and fistulae in CD, promotes mucosal healing, repairs intestinal microbiota homeostasis and increases autophagy to alleviate IBD symptoms by weakening TNF-α, IL-6, NLRP3, TGFB1 activities and aggrandizing P-AKT, PPARA, PPARG, INS, IRS1/2, IGF-1, TIMP1, NOD2, SIRT1 levels. Graphic Abstract