Regular transient limb ischemia improves endothelial function and inhibits endothelial cell apoptosis to prevent atherosclerosis in rabbit.

AIMS: Regular transient limb ischemia (RTLI) can prevent atherosclerosis (AS) progression in hypercholesterolemic rabbits. This study aimed to investigate the minimum effective intensity and possible mechanisms of RTLI for preventing atherosclerosis. METHODS: Eighty rabbits were divided into eight groups: normal (N), high cholesterol (H), three RTLI [three RTLI cycles every other day (R3qod), three RTLI cycles daily (R3qd), and six RTLI cycles daily (R6qd), each cycle of RTLI included 5 min of limb ischemia followed by 5 min limb reperfusion], and three correlated sham RTLI [sham ischemia for 30 min once every other day (S3qod), sham ischemia for 30 min once daily (S3qd), and sham ischemia for 60 min once daily (S6qd)]. Rabbits in group N were kept normally, while the others were fed 1% cholesterol diet for 12 weeks. The RTLI and sham RTLI groups were received RTLI or sham RTLI procedure, respectively. The plaque area in the thoracic aorta was determined by oil red O staining, and quantifying the ratio of plaque area to intimal area (PA/IA). Endothelium-dependent and -independent relaxation were also determined. Endothelial cell were isolated from abdominal aorta of rabbits, and the apoptosis ratio was detected using flow cytometry. RESULTS: The PA/IA and early apoptotic cell ratio was significantly lower as well as the endothelium-dependent relaxation response was higher in group R6qd than those in groups H and S6qd, while those in the R3qod group was not significantly different from those in groups H and S3qod, as well as those in the R3qd group showed no significant difference compared to those in groups H and S3qd. CONCLUSIONS: Six cycles of RTLI daily was the optimal effective intensity to prevent AS progression in rabbits. Endothelial function improvement and apoptosis inhibition might contribute to the anti-AS effects.

High-resolution In-situ Structures of Mammalian Mitochondrial Respiratory Supercomplexes in Reaction within Native Mitochondria.

Mitochondria play a pivotal role in ATP energy production through oxidative phosphorylation, which occurs within the inner membrane via a series of respiratory complexes. Despite extensive in-vitro structural studies, revealing the atomic details of their molecular mechanisms in physiological states remains a major challenge, primarily because of the loss of the native environment during purification. Here, we directly image porcine mitochondria using an in-situ cryo-electron microscopy approach. This enables us to determine the structures of various high-order assemblies of respiratory supercomplexes in their native states, achieving up to 1.8-Å local resolution. We identify four major supercomplex organizations: I1III2IV1, I1III2IV2, I2III2IV2, and I2III4IV2, which can potentially expand into higher-order arrays on the inner membranes. The formation of these diverse supercomplexes is largely contributed by 'protein-lipids-protein' interactions, which in turn dramatically impact the local geometry of the surrounding membranes. Our in-situ structures also capture numerous reactive intermediates within these respiratory supercomplexes, shedding light on the dynamic processes of the ubiquinone/ubiquinol exchange mechanism in complex I and the Q-cycle in complex III. By comparing supercomplex structures from mitochondria treated under distinct conditions, we elucidate how conformational changes and ligand binding states interplay between complexes I and III in response to environmental redox alterations. Our approach, by preserving the native membrane environment, enables structural studies of mitochondrial respiratory supercomplexes in reaction at high resolution across multiple scales, spanning from atomic-level details to the broader subcellular context.

Global prevalence of poor sleep quality in cancer patients: A systematic review and meta-analysis.

OBJECTIVE: Poor sleep quality is common in patients with cancer, but the prevalence rates varied widely across studies. This systematic review and meta-analysis examined the pooled prevalence of poor sleep quality among patients with cancer. METHODS: Systematic literature searches were independently conducted in the major databases (Web of Science, PubMed, EMBASE and PsycINFO). Studies that reported the prevalence of poor sleep quality in patients with cancer were analyzed using a random effects model. Funnel plots and Egger's tests were used to assess publication bias. Statistical analyses were performed using R software. RESULTS: A total of 59 epidemiological studies involving 16,223 patients were included. The pooled prevalence of poor sleep quality in patients with cancer was 57.4% [95% confidence interval (CI): 53.3% - 61.6%]. Additionally, three comparative studies with 372 patients and 412 healthy controls were included. Compared to healthy controls, patients with cancer had a significantly higher risk for poor sleep quality [odd ratio (OR) = 3.0; 95%CI: 1.2-7.2; P < 0.05]. Subgroup analyses of the studies revealed that studies from Middle East & North Africa region and low income countries, and on gynecological cancer as well as those with a lower cut-off value of sleep quality (all P < 0.01) reported a higher prevalence of poor sleep quality. Meta-regression analyses showed that higher prevalence of poor sleep quality was associated with higher prevalence of comorbid depression (P < 0.05) and anxiety (P < 0.01), but was associated with a lower education level (P < 0.05) and alcohol use ratio (P < 0.05). CONCLUSION: Poor sleep quality is common among patients with cancer. Considering the overall high prevalence rate and negative impact of poor sleep quality, appropriate measures to identify and improve poor sleep quality are needed to enhance the clinical outcomes in this group.

Role of histone variants H2BC1 and H2AZ.2 in H2AK119ub nucleosome organization and Polycomb gene silencing.

Ubiquitination of histone H2A at lysine 119 residue (H2AK119ub) plays critical roles in a wide range of physiological processes, including Polycomb gene silencing 1,2 , replication 3-5 , DNA damage repair 6-10 , X inactivation 11,12 , and heterochromatin organization 13,14 . However, the underlying mechanism and structural basis of H2AK119ub remains largely elusive. In this study, we report that H2AK119ub nucleosomes have a unique composition, containing histone variants H2BC1 and H2AZ.2, and importantly, this composition is required for H2AK119ub and Polycomb gene silencing. Using the UAB domain of RSF1, we purified H2AK119ub nucleosomes to a sufficient amount and purity. Mass spectrometry analyses revealed that H2AK119ub nucleosomes contain the histone variants H2BC1 and H2AZ.2. A cryo-EM study resolved the structure of native H2AK119ub nucleosomes to a 2.6A resolution, confirming H2BC1 in one subgroup of H2AK119ub nucleosomes. Tandem GST-UAB pulldown, Flag-H2AZ.2, and HA-H2BC1 immunoprecipitation revealed that H2AK119ub nucleosomes could be separated into distinct subgroups, suggesting their composition heterogeneity and potential dynamic organization. Knockout or knockdown of H2BC1 or H2AZ.2 reduced cellular H2AK119ub levels, establishing H2BC1 and H2AZ.2 as critical determinants of H2AK119ub. Furthermore, genomic binding profiles of H2BC1 and H2AZ.2 overlapped significantly with H2AK119ub binding, with the most significant overlapping in the gene body and intergenic regions. Finally, assays in developing embryos reveal an interaction of H2AZ.2, H2BC1, and RING1A in vivo . Thus, this study revealed, for the first time, that the H2AK119ub nucleosome has a unique composition, and this composition is required for H2AK119ub and Polycomb gene silencing.

Characterization of a novel sucrose phosphorylase from Paenibacillus elgii and its use in biosynthesis of α-arbutin.

α-Arbutin, a naturally occurring glycosylated derivative of hydroquinone (HQ), effectively inhibits melanin biosynthesis in epidermal cells. It is widely recognized as a fourth-generation whitening agent within the cosmetic industry. Currently, enzymatic catalysis is universally deemed the safest and most efficient method for α-arbutin synthesis. Sucrose phosphorylase (SPase), one of the most frequently employed glycosyltransferases, has been extensively reported for α-arbutin synthesis. In this study, a previously reported SPase known for its effectiveness in synthesizing α-arbutin, was used as a probe sequence to identify a novel SPase from Paenibacillus elgii (PeSP) in the protein database. The sequence similarity between PeSP and the probe was 39.71%, indicating a degree of novelty. Subsequently, the gene encoding PeSP was coexpressed with the molecular chaperone pG-Tf2 in Escherichia coli, significantly improving PeSP's solubility. Following this, PeSP was characterized and employed for α-arbutin biosynthesis. The specific activity of co-expressed PeSP reached 169.72 U/mg, exhibited optimal activity at 35℃ and pH 7.0, with a half-life of 3.6 h under the condition of 35℃. PeSP demonstrated excellent stability at pH 6.5-8.5 and sensitivity to high concentrations of metal ions. The kinetic parameters Km and kcat/Km were determined to be 14.50 mM and 9.79 min- 1·mM- 1, respectively.The reaction conditions for α-arbutin biosynthesis using recombinant PeSP were optimized, resulting in a maximum α-arbutin concentration of 52.60 g/L and a HQ conversion rate of 60.9%. The optimal conditions were achieved at 30℃ and pH 7.0 with 200 U/mL of PeSP, and by combining sucrose and hydroquinone at a molar ratio of 5:1 for a duration of 25 h.

Mitophagy-related genes could facilitate the development of septic shock during immune infiltration.

Septic shock often occurs following critically low blood pressure in patients with sepsis, and is accompanied by a high death rate. Although mitophagy is associated with infection and immune responses, its role in septic shock remains unknown. This study screened effective mitophagy-related genes (MRGs) for medical practice and depicted immune infiltration situations in patients with septic shock. Gene expression profiles of GSE131761 from the Gene Expression Omnibus database were compiled for differential analysis, weighted gene co-expression network analysis, and immune infiltration analysis, while other GSE series were used as validation datasets. A series of validation methods were used to verify the robustness of hub genes, while a nomogram and prognosis model were established for medical practice. Six genes were screened via combinations of differentially expressed genes, weighted gene co-expression network analysis, and MRGs. From this, 3 hub genes (MAP1LC3B, ULK1, and CDC37) were chosen for subsequent analysis based on different validation methods. Gene set enrichment analysis showed that leukocyte trans-endothelial migration and the p53 signaling pathway were abnormally activated during septic shock. Immune infiltration analysis indicated that the imbalance of neutrophils and CD4 naive T cells was significantly correlated with septic shock progression. A nomogram was generated based on MAP1LC3B, ULK1, and CDC37, as well as age. The stability of our model was confirmed using a calibration plot. Importantly, patients with septic shock with the 3 highly expressed hub genes displayed worse prognosis than did patients without septic shock. MAP1LC3B, ULK1, and CDC37 are considered hub MRGs in the development of septic shock and could represent promising diagnostic and prognostic biomarkers in blood tissue. The validated hub genes and immune infiltration pattern expand our knowledge on MRG functional mechanisms, which provides guidance and direction for the development of septic shock diagnostic and therapeutic markers.

A cutting-edge strategy for spinal cord injury treatment: resident cellular transdifferentiation.

Spinal cord injury causes varying degrees of motor and sensory function loss. However, there are no effective treatments for spinal cord repair following an injury. Moreover, significant preclinical advances in bioengineering and regenerative medicine have not yet been translated into effective clinical therapies. The spinal cord's poor regenerative capacity makes repairing damaged and lost neurons a critical treatment step. Reprogramming-based neuronal transdifferentiation has recently shown great potential in repair and plasticity, as it can convert mature somatic cells into functional neurons for spinal cord injury repair in vitro and in vivo, effectively halting the progression of spinal cord injury and promoting functional improvement. However, the mechanisms of the neuronal transdifferentiation and the induced neuronal subtypes are not yet well understood. This review analyzes the mechanisms of resident cellular transdifferentiation based on a review of the relevant recent literature, describes different molecular approaches to obtain different neuronal subtypes, discusses the current challenges and improvement methods, and provides new ideas for exploring therapeutic approaches for spinal cord injury.

A pair of diastereoisomeric C-glucofuranosyl flavones from the flowers of Gypsophila oldhamiana.

Two new C-glucofuranosyl flavones apigenin 6-C-ß-glucofuranoside (1) and apigenin 6-C-α-glucofuranoside (2) together with four known compounds (3-6) were isolated from the flowers of Gypsophila oldhamiana. Their structures were elucidated on the basis of extensive spectroscopic analyses. These compounds were evaluated for the cytotoxic activities against four human cancer cell lines and did not exhibit any significant bioactivities (IC50 values > 10 µM).

Baseline High-Sensitivity C-Reactive Protein as a Predictor of Adverse Clinical Events in Patients with Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: A Meta-Analysis.

Inflammation in patients with coronary artery disease (CAD) has been linked to adverse clinical outcomes. A useful biomarker for measuring inflammation levels, high-sensitivity C-reactive protein (hs-CRP) in the blood can be used to detect the presence of low-grade inflammation. This study sought to assess the predictive value of baseline hs-CRP levels for adverse clinical events in CAD patients undergoing percutaneous coronary intervention (PCI). To investigate this topic, a meta-analysis was performed. We conducted a systematic search of PubMed, Embase, and the Cochrane Library for original articles reporting the correlation between hs-CRP levels and adverse clinical events in CAD patients undergoing PCI. We followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines and conducted a meta-analysis by extracting relevant data. Our pooled calculations yielded hazard ratios or odds ratios with 95% confidence intervals. A total of 28 studies comprising 60544 patients were included in this analysis. High baseline hs-CRP levels predicted increased risk for major adverse cardiac events (P = 0.037), major adverse cardiac and cerebrovascular events (P = 0.020), all-cause mortality (P = 0.001), cardiovascular mortality (P < 0.001), death and/or myocardial infarction (P = 0.017) in patients, as well as restenosis (P < 0.001). However, there was no association between elevated baseline hs-CRP levels and thrombosis. In conclusion, in CAD patients undergoing PCI, baseline hs-CRP levels are reliable predictors of major adverse cardiac events, major adverse cardiac and cerebrovascular events, all-cause mortality, cardiovascular mortality, death and/or myocardial infarction, and restenosis. Therefore, hs-CRP can effectively assist in prognosis determination for CAD patients undergoing PCI.

A heterozygous pathogenic variant in the ATP6V1A gene triggering epilepsy in a large Chinese pedigree.

Epilepsy is one of the most common disorders in children, with an incidence rate of approximately 5%. Although an increasing number of genes have been demonstrated to be pathogenic factors in epilepsy, evidence for a potential pathogenic role of ATP6V1A remains limited. Herein, the clinical and genetic data of a 5-year-old boy who experienced seizures at 9 months of age are collected. Genetic variants are screened using whole-exome sequencing (WES), and the effects of the candidate variants are further validated at both the RNA and protein levels. WES reveals a heterozygous variant [NM_001690.4: c .1132 C>T, p.Leu378Phe] of the ATP6V1A gene. This variant is not reported in the public database, but is predicted to be deleterious by multiple software packages, and classified as a variant of unknown significance following the American College of Medical Genetics and Genomics guidelines. Quantitative PCR and western blotting further confirm its down-regulatory role in both the RNA and protein expression of ATP6V1A. This case report confirms the pathogenicity of ATP6V1A in epilepsy with solid experimental evidence, thereby expanding the phenotype spectrum of ATP6V1A variants. More importantly, we show that seizures triggered by ATP6V1A variants could be controlled by Levetiracetam, crucially rescuing the development of the patient.

Structural Engineering-Enabled Joule Heating Effect Cooperated with Capillary Effect Toward Fast Spreading of Droplets for High-Flux Separation of Viscous Emulsion.

Viscous emulsions with poor fluidity and high adhesion are extremely difficult to separate. Herein, high-flux separation of viscous emulsions is realized by developing structural engineered collagen fibers (CFs)-based composite membrane that featured 3D conductive hierarchical fiber structure with the spaced carbon nanofibers (CNFs) and activated carbon (AC) serving as conductive network and competitive adsorption-based demulsifying sites, respectively. The as-designed membrane structure boosts fast spreading of emulsion droplets on membrane surface aided by the synergistic effect of joule heat in situ generated by the spaced CNFs and the capillary effect derived from CFs, which guarantees the full contact of viscous emulsions with the spaced AC for achieving ultra-efficient demulsifying. The permeation of resultant oily filtrate is accelerated by the capillary effect of hierarchically fibrous structured CFs to exhibit fast transport kinetics, therefore accomplishing high-flux separation. The structural engineered membrane achieves high-performance separation toward different viscous emulsions (55.4-123.7 mPa·s) with separation efficiency >99.9% and flux high up to 259 L m-2 h-1 . The investigations provide a novel structural engineering strategy for realizing high-performance separation of viscous emulsions.

Global prevalence of poor sleep quality in military personnel and veterans: A systematic review and meta-analysis of epidemiological studies.

Poor sleep quality is prevalent among members of the military but rates of poor sleep quality vary between studies. This study examined the global prevalence of poor sleep quality in military personnel and veterans as well as possible moderators of prevalence differences between studies. PubMed, EMBASE, Web of Science, and PsycINFO were systematically searched from their inception dates to September 1, 2022. Studies were included if they were conducted on military personnel and/or veterans and prevalence estimates of poor sleep quality could be generated from assessments with standardized tools. A random-effects model was used to calculate the pooled prevalence and its 95% confidence intervals (CIs). Fifty-nine studies (N = 28,100) were included for analysis with sample sizes ranging from 14 to 8481. Two studies were rated as "high quality" (3.39%), while 57 were rated as "moderate quality" (96.61%). The overall pooled prevalence of poor sleep quality in military personnel and veterans was 69.00% (95% CI: 62.33-75.30%); pooled rates were 57.79% (95% CI: 49.88-65.50%) and 82.88% (95% CI: 74.08-90.21%) for active duty personnel and veterans, respectively. Subgroup analyses indicated study region, study design, sampling method, Pittsburg Sleep Quality Index cut-off values, and service type moderated prevalence of poor sleep quality. Meta-regression analyses indicated sample size, mean age, depression and posttraumatic stress disorder (PTSD) were associated with prevalence differences between studies. Poor sleep quality was more common in both active duty military personnel and veterans who were older and those who reported PTSD or depression. Regular monitoring of sleep quality and sleep hygiene should be promoted in this population. More relevant studies in middle- and low-income countries should also be conducted.

Hikikomori: A perspective from bibliometric analysis.

AIMS: Hikikomori is a common phenomenon reported in Japan and many other countries. However, the broad trends of the research publications on hikikomori are unclear. Therefore, this study examined the patterns of research on hikikomori using bibliometric analysis. METHODS: Relevant publications were searched in Web of Science. Bibliometric analyses were performed with CiteSpace, R and VOSviewer. RESULTS: In total, 297 publications on hikikomori met the eligibility criteria. The International Journal of Social Psychiatry (IF = 10.461) published the most papers (K = 17, or 5.7%) on hikikomori. Takahiro A. Kato from Kyushu University (41; 13.8%; H-index = 18) was the most influential author, while Takahiro A. Kato (total link strength [TLS]: 235), Alan R. Teo (TLS: 157), and Masaru Tateno (TLS: 153) separately had the strongest research collaboration with other researchers. Of all countries that published on hikikomori, Japan had the highest number of publications (K = 91). The keywords "United States" and "psychiatric diagnosis" received the most attention between 2013 and 2015, whereas "health" and "autism spectrum disorder" received the most attention in 2021 and 2022. CONCLUSIONS: Peer-reviewed research publications on hikikomori are growing rapidly and the research trends in this field are also changing.

Detailed analysis of the association between urate deposition and bone erosion in gout: a dual-energy computed tomography study.

Objective: This study aimed to analyze the effect of urate deposition (UD) on bone erosion and examine the association between the volume of monosodium urate (MSU) crystals and an improved bone erosion score method, as measured in the metatarsophalangeal (MTP) joints of patients with gout. Materials and methods: Fifty-six patients diagnosed with gout using the 2015 European League Against Rheumatism and American College of Rheumatology criteria were enrolled. MSU crystals volume at each MTP joint was measured using dual-energy computed tomography (DECT) images. The degree of bone erosion was evaluated with the modified Sharp/van der Heijde (SvdH) erosion scoring system based on CT images. Differences in clinical features between patients with (UD group) and without (non-UD group) UD were assessed, and the correlation between erosion scores and urate crystal volume was analyzed. Results: The UD and non-UD groups comprised 30 and 26 patients, respectively. Among the 560 MTP joints assessed, 80 showed MSU crystal deposition, and 108 showed bone erosion. Bone erosion occurred in both groups but was significantly less severe in the non-UD group (p <0.001). Both groups had equivalent levels of serum uric acid (p=0.200). Symptom duration was significantly longer in the UD group (p=0.009). The UD group also had a higher rate of kidney stones (p=0.023). The volume of MSU crystals was strongly and positively associated with the degree of bone erosion (r=0.714, p <0.001). Conclusion: This study found that patients with UD show significant increased bone erosion than those without UD. The volume of MSU crystals is associated with the improved SvdH erosion score based on CT images, regardless of serum uric acid level, demonstrating the potential of combining DECT and serum uric acid measurements in helping optimize the management of patients with gout.

Systematic reviews and meta-analyses on major depressive disorder: a bibliometric perspective.

Background: There is a vast amount of evidence-based medicine research on the major depressive disorder (MDD) available in the literature, however, no studies on the overall performance, productivity and impact of such research have been published to date. This study explored and mapped the research outputs of MDD-related systematic reviews and meta-analyses (SR/MA) from a bibliometric perspective. Methods: Relevant data were retrieved with search terms on MDD, systematic review and meta-analysis. Results: A total of 4,870 papers with 365,402 citations published from 1983 to 2022 were included in the analysis. The publication output has grown steadily over time with the most publications originating from the USA (1,020; 20.94%), the UK (516; 10.60%) and China (448; 9.20%). The research collaborations between countries were most frequent between the USA and UK (266; 5.46%). Journal of Affective Disorders (379; 7.78%) was the most productive journal, while Cuijpers P was the most productive author (121; 2.48%), and University of Toronto (569; 11.78%) was the most productive institution. The top 10 most cited articles on MDD-related SR/MA had citations ranging from 1,806 to 3,448. The high-frequency keywords were mainly clustered into four themes, including psychiatric comorbidities, clinical trials, treatment, and brain stimulation in MDD. Conclusion: The rapid increase in the number of SR/MA of MDD in recent years highlights the importance of this research field. Psychiatric comorbidities, clinical interventions, and treatment of MDD have been identified as hot topics, while biological mechanisms in MDD are likely to be an emerging research priority.

Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression.

This study is to determine the regulation of nitric oxide synthase 3 (NOS3) by edaravone in mice with hypoxic pulmonary hypertension (HPH). C57BL/6J mice were reared in a hypoxic chamber. HPH mice were treated with edaravone or edaravone + L-NMMA (a NOS inhibitor). Lung tissue was collected for histological assessment, apoptosis analysis, and detection of malondialdehyde, superoxide dismutase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and NOS3. The levels of serum TNF-α and IL-6 were also measured. Immunohistochemistry was used to visualize the expression of α-smooth muscle actin (SMA) in pulmonary arterioles. Edaravone treatment improved hemodynamics, inhibited right ventricular hypertrophy, increased NOS3 expression, and reduced pathological changes, pulmonary artery wall thickness, apoptotic pulmonary cells, oxidative stress, and the expression of TNF-α, IL-6, and α-SMA in HPH mice. L-NMMA treatment counteracted the lung protective effects of edaravone. In conclusion, edaravone might reduce lung damage in HPH mice by increasing the expression of NOS3.

SMALPs Are Not Simply Nanodiscs: The Polymer-to-Lipid Ratios of Fractionated SMALPs Underline Their Heterogeneous Nature.

Amphipathic styrene-maleic acid (SMA) copolymers directly solubilize biomembranes into SMA-lipid particles, or SMALPs, that are often regarded as nanodiscs and hailed as a native membrane platform. The promising outlook of SMALPs inspires the discovery of many SMA-like copolymers that also solubilize biomembranes into putative nanodiscs, but a fundamental question remains on how much the SMALPs or SMALP analogues truly resemble the bilayer structure of nanodiscs. This unfortunate ambiguity undermines the utility of SMA or SMA-like copolymers in membrane biology because the structure and function of many membrane proteins depend critically on their surrounding matrices. Here, we report the structural heterogeneity of SMALPs revealed through fractionating SMALPs comprised of lipids and well-defined SMAs via size-exclusion chromatography followed by quantitative determination of the polymer-to-lipid (P/L) stoichiometric ratios in individual fractions. Through the lens of P/L stoichiometric ratios, different self-assembled polymer-lipid nanostructures are inferred, such as polymer-remodeled liposomes, polymer-encased nanodiscs, polymer-lipid mixed micelles, and lipid-doped polymer micellar aggregates. We attribute the structural heterogeneity of SMALPs to the microstructure variations amongst individual polymer chains that give rise to their polydisperse detergency. As an example, we demonstrate that SMAs with a similar S/MA ratio but different chain sizes participate preferentially in different polymer-lipid nanostructures. We further demonstrate that proteorhodopsin, a light-driven proton pump solubilized within the same SMALPs is distributed amongst different self-assembled nanostructures to display different photocycle kinetics. Our discovery challenges the native nanodisc notion of SMALPs or SMALP analogues and highlights the necessity to separate and identify the structurally dissimilar polymer-lipid particles in membrane biology studies.

Schizophrenia and oxidative stress from the perspective of bibliometric analysis.

Background: A growing number of studies has implicated oxidative stress in the pathophysiology of psychiatric disorders including schizophrenia. The aim of this study was to explore the field of schizophrenia and oxidative stress-related research from a bibliometric perspective. Methods: All relevant publications on schizophrenia and oxidative stress were obtained from Web of Science Core Collection (WOSCC) database from its inception date to November 8, 2022. VOSviewer software was used to examine co-authorships and co-occurring keywords. R software was used to present the main characteristics of publications and cooperation frequency among countries. CiteSpace was used to investigate keywords with the strongest citation bursts. Results: A total of 3,510 publications on schizophrenia and oxidative stress were included. The United States had the largest number of publications (26.1%), and international collaborations. University of Melbourne was the most productive institution, while Schizophrenia Research was the most productive journal in this field. Apart from "schizophrenia" and "oxidative stress", the terms "prefrontal cortex", "brain" and "nitric oxide" were among the most frequently used keywords. Conclusions: In conclusion, research on the association between oxidative stress and schizophrenia has received growing attention in the academic literature that is expected to continue its upward trajectory during the next two decades. Existing research suggests there has been a transition from research focused on pathways to animal models, and subsequently to clinical applications. Intervention studies on oxidative stress and schizophrenia are likely to be an important focus of related work in the near future.

Targeted modulation of gut microbiota by traditional Chinese medicine and natural products for liver disease therapy.

The gut microbiota not only constitutes intestinal microenvironment homeostasis and human health but also exerts indispensable roles in the occurrence and progression of multiple liver diseases, including alcohol-related liver disease, nonalcoholic fatty liver disease, autoimmune liver disease and liver cancer. Given the therapeutic status of these diseases, their prevention and early therapy are crucial, and the detailed mechanism of gut microbiota in liver disease urgently needs to be explored. Meanwhile, multiple studies have shown that various traditional Chinese medicines, such as Si Miao Formula, Jiangzhi Granules, Liushen Capsules, Chaihu-Shugan Power, Cassiae Semen and Gynostemma, as well as some natural products, including Costunolide, Coprinus comatus polysaccharide, Antarctic krill oil, Oridonin and Berberine, can repair liver injury, improve fatty liver, regulate liver immunity, and even inhibit liver cancer through multiple targets, links, and pathways. Intriguingly, the aforementioned effects demonstrated by these traditional Chinese medicines and natural products have been shown to be closely related to the gut microbiota, directly driving the strategy of traditional Chinese medicines and natural products to regulate the gut microbiota as one of the breakthroughs in the treatment of liver diseases. Based on this, this review comprehensively summarizes and discusses the characteristics, functions and potential mechanisms of these medicines targeting gut microbiota during liver disease treatment. Research on the potential effects on gut microbiota and the regulatory mechanisms of traditional Chinese medicine and natural products provides novel insights and significant references for developing liver disease treatment strategies. In parallel, such explorations will enhance the comprehension of traditional Chinese medicine and natural products modulating gut microbiota during disease treatment, thus facilitating their clinical investigation and application.