Emotional task is one of the main methods to study the attention bias and emotional function of affective disorder.Functional near-infrared spectroscopy(fNIRS)studies based on emotional tasks in patients with affective disorders have shown that facial emotion recognition task,the emotional stroop effect,and the emotion induction task combined with fNIRS technology have clinical value in the diagnosis and treatment of affective disorders.The defects of attention function and emotional processing in patients with affective disorders are related to abnormal activation of the left prefrontal cortex,especially the differences in brain activation patterns are related to depressive symptoms in patients with depressive disorders.The future direction of using fNIRS to study emotional tasks is to combine a variety of neuroimaging methods to conduct large-sample longitudinal cohort studies to obtain more objective bases for diagnosis and treatment,and to compare the differences in activation areas of different emotional stimulation materials.

The breakthrough progress of implantable brain-computer interfaces (iBCIs) technology in the field of clinical trials has attracted widespread attention from both academia and industry. The development and advancement of this technology have provided new solutions for the rehabilitation of patients with movement disorders. However, challenges from many aspects make it difficult for iBCIs to further implement and transform technologies. This paper illustrates the key challenges restricting the large-scale development of iBCIs from the perspective of system implementation, then discusses the latest clinical application progress in depth, aiming to provide new ideas for researchers. For the system implementation part, we have elaborated the front-end signal collector, signal processing and decoder, then the effector. The most important part of the front-end module is the neural electrode, which can be divided into two types: piercing and attached. These two types of electrodes are newly classified and described. In the signal processing and decoder section, we have discussed the experimental paradigm together with signal processing and decoder for the first time and believed that the experimental paradigm acts as a learning benchmark for decoders that play a pivotal role in iBCIs systems. In addition, the characteristics and roles of the effectors commonly used in iBCIs systems, including cursors and robotic arms, are analyzed in detail. In the clinical progress section, we have divided the latest clinical progress into two categories: functional rehabilitation and functional replacement from the perspective of the application scenarios of iBCIs. Functional rehabilitation and functional replacement are two different types of application, though the boundary between the two is not absolute. To this end, we have first introduced the corresponding clinical trial progress from the three levels: application field, research team, and clinical timeline, and then conducted an in-depth discussion and analysis of their functional boundaries, in order to provide guidance for future research. Finally, this paper mentions that the key technical challenges in the development of iBCIs technology come from multiple aspects. First of all, from the signal acquisition level, high-throughput and highly bio-compatible neural interface designing is essential to ensure long-term stable signal acquisition. The electrode surface modification method and electrode packaging were discussed. Secondly, in terms of decoding performance, real-time, accurate, and robust algorithms have a decisive impact on improving the reliability of iBCIs systems. The third key technology is from the perspective of practicality, we believe that the signal transmission mode of wireless communication is the trend of the future, but it still needs to overcome challenges such as data transmission rate and battery life. Finally, we believe that issues such as ethics, privacy, and security need to be addressed through legal, policy, and technological innovation. In summary, the development of iBCIs technology requires not only the unremitting efforts of scientific researchers, but also the participation and support of policymakers, medical professionals, technology developers, and all sectors of society. Through interdisciplinary collaboration and innovation, iBCIs technology will achieve wider clinical applications in the future and make important contributions to improving the quality of life of patients.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Background/Aims: Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking. Methods: Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth. Results: Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy. Conclusions UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.

This study aimed to investigate the chemical constituents of supercritical extract from Qi-nan Aquilariae Lignum Resinatum by silica gel column chromatography, thin-layer chromatography, and semi-preparative high-performance liquid chromatography. One new elemane-type and one new eudesmane-type sesquiterpene compounds were isolated from the extract, and their structures were identified by MS, UV, IR, NMR, and ECD spectroscopic techniques, and named aquqinanol C(1) and aquqinanol D(2). Both compounds are novel compounds. The neuroprotective effect of the compounds on CORT-induced PC12 cell damage was determined in vitro. The results showed that compounds 1 and 2 exhibited a certain protective effect against CORT-induced damage in PC12 cells.
Rats ; Animals ; Qi ; Sesquiterpenes/pharmacology* ; Molecular Structure

Objective:To explore the effect of long noncoding RNA(lncRNA)THAP7-AS1 on the glycolysis of gastric cancer(GC)cells by regulating methyltransferase-like 3(METTL3)mediated N6-methyladenosine(m6A)modification. Methods:Gene Expression Profiling Interactive Analysis(GEPIA)database was used to analyze the expression levels of THAP7-AS1 and METTL3 in GC tissues and their relationship with the overall survival of GC patients.Real-time fluorescence quantitative PCR and Western blotting were used to analyze the expression of THAP7-AS1,METTL3 mRNA,glucose transporter 1(GLUT1)mRNA,and METTL3 protein in GC tissues and paracancerous tissues samples collected from 80 GC patients in Department of Oncology,The Third Affiliated Hospital of Zunyi Medical University(the First People's Hospital of Zunyi),and the relationship between THAP7-AS1 levels and the clinicopathological characteristics of GC patients was analyzed.Real-time fluorescence quantitative PCR and Western blotting were used to verify the expression of THAP7-AS1,METTL3 mRNA,GLUT1 mRNA,and METTL3 protein in GES-1,BGC-823 and SGC-7901 cells.Lentiviral infection was used to knock-down THAP7-AS1 or overexpress METTL3 BGC-823 and SGC-7901 cells,and real-time fluorescence quantitative PCR and Western blotting were used to examine effect of different treatment on the expression of THAP7-AS1,METTL3 mRNA,GLUT1 mRNA,and METTL3 protein;colorimetry assay was used to detect the m6A modification level in the total RNA;methylated RNA immunoprecipitation(MeRIP)-quantitative PCR(qPCR)was used to detect the GLUT1 m6A modification level;glycolysis stress test kits were used to detect the extracellular acidification rate(ECAR),glucose uptake and lactate production of treated GC cells;Western blotting was used to examine the expression levels of METTL3,GLUT1,M2 type pyruvate kinase(PKM2)and lactic dehydrogenase(LDHA)proteins in treated GC cells;EdU staining,wound healing assay and Transwell invasion assay were used to evaluate the proliferation,migration and invasion of treated GC cells.Finally,a mouse model of subcutaneously transplanted GC tumor was established using nude mice,and the effect of knocking-down THAP7-AS1 was assessed by measuring the tumor volume and weight,as well as the expression levels of METTL3 and GLUT1 proteins in transplanted GC tumor tissues. Results:Analysis of the GEPIA database showed that the expression levels of THAP7-AS1 and METTL3 was higher in GC tissue than those in normal gastric tissues,and the expression levels of THAP7-AS1 and METTL3 are negatively correlated with overall survival of GC patients(P＜0.05).Compared with the paracancerous tissues(or normal gastric epithelial cells),the expression levels of THAP7-AS1,METTL3 mRNA,GLUT1 mRNA and METTL3 protein was significantly increased in GC tissues(or GC cells),and the higher the expression of THAP7-AS1,the higher the TNM stage,the lower the degree of tumor differentiation,and the easier the occurrence of microvascular infiltration and lymph node metastasis(P＜0.05).Knocking-down of THAP7-AS1 down-regulated the expression levels of METTL3 mRNA,GLUT1 mRNA and METTL3 protein,the m6A modification levels in total RNA and GLUT1,the ECAR levels,the glucose uptake,the lactate production,EdU positive rate,scratch healing rate,the number of invaded cells,and the expression levels of glycolysis-related proteins(METTL3,GLUT1,PKM2 and LDHA)in GC cells(P＜0.05).Overexpression of METTL3 could partially reverse these effects of THAP7-AS1 knock-down(P＜0.05).In vivo experiments showed that THAP7-AS1 knock-down can obviously inhibit the growth of transplanted GC tumors(P＜0.05). Conclusion:lncRNA THAP7-AS1 can promote the glycolysis which further promotes the proliferation,migration and invasion of GC cells by regulating METTL3 mediated m6A modification.

An innovative sandwich-structural Fe-based metal-organic framework magnetic material(Fe3O4@SW-MIL-101-NH2)was fabricated using a facile solvothermal method.The characteristic properties of the material were investigated by field emission scanning electron microscopy,transmission electron mi-croscopy(TEM),energy-dispersive X-ray spectroscopy,Fourier transform infrared spectroscopy,X-ray powder diffraction,vibrating sample magnetometry,and Brunauer-Emmett-Teller measurements.Fe3O4@SW-MIL-101-NH2 is associated with advantages,such as robust magnetic properties,high specific surface area,and satisfactory storage stability,as well as good selective recognition ability for chlorogenic acid(CA)and its metabolites via chelation,hydrogen bonding,and π-interaction.The results of the static adsorption experiment indicated that Fe3O4@SW-MIL-101-NH2 possessed a high adsorption capacity toward CA and its isomers,cryptochlorogenic acid(CCA)and neochlorogenic acid(NCA),and the adsorption behaviors were fitted using the Langmuir adsorption isotherm model.Then,a strategy using magnetic solid-phase extraction(MSPE)and ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry(UPLC-Q-TOF MS/MS)was developed and suc-cessfully employed for the selective pre-concentration and rapid identification of CA metabolites in rat plasma,urine,and feces samples.This work presents a prospective strategy for the synthesis of magnetic adsorbents and the high-efficiency pretreatment of CA metabolites.