Bibliometric analysis and visualization of quorum sensing research over the last two decade.

Background: Quorum sensing (QS) research stands as a pivotal and multifaceted domain within microbiology, holding profound implications across various scientific disciplines. This bibliometric analysis seeks to offer an extensive overview of QS research, covering the period from 2004 to 2023. It aims to elucidate the hotspots, trends, and the evolving dynamics within this research domain. Methods: We conducted an exhaustive review of the literature, employing meticulous data curation from the Science Citation Index Extension (SCI-E) within the Web of Science (WOS) database. Subsequently, our survey delves into evolving publication trends, the constellation of influential authors and institutions, key journals shaping the discourse, global collaborative networks, and thematic hotspots that define the QS research field. Results: The findings demonstrate a consistent and growing interest in QS research throughout the years, encompassing a substantial dataset of 4,849 analyzed articles. Journals such as Frontiers in Microbiology have emerged as significant contributor to the QS literature, highlighting the increasing recognition of QS's importance across various research fields. Influential research in the realm of QS often centers on microbial communication, biofilm formation, and the development of QS inhibitors. Notably, leading countries engaged in QS research include the United States, China, and India. Moreover, the analysis identifies research focal points spanning diverse domains, including pharmacological properties, genetics and metabolic pathways, as well as physiological and signal transduction mechanisms, reaffirming the multidisciplinary character of QS research. Conclusion: This bibliometric exploration provides a panoramic overview of the current state of QS research. The data portrays a consistent trend of expansion and advancement within this domain, signaling numerous prospects for forthcoming research and development. Scholars and stakeholders engaged in the QS field can harness these findings to navigate the evolving terrain with precision and speed, thereby enhancing our comprehension and utilization of QS in various scientific and clinical domains.

Clinical features and surgical treatments of scoliosis in neurofibromatosis type 1: a systemic review and meta-analysis.

BACKGROUND: Neurofibromatosis type 1 (NF 1) is an autosomal-dominant tumor predisposition genetic disease affecting approximately 1 in 3000 live births. The condition could present various manifestations ranging from skin abnormalities to neurological tumors. The musculoskeletal system could also be frequently affected, and scoliosis is the most common orthopedic manifestation. Characterized by the early-onset and rapid progression tendency, NF 1-related dystrophic scoliosis presented discrepancies from idiopathic scoliosis in terms of natural history, clinical features, and management outcomes and thus required special attention. In the current study, the authors conducted a systemic review to outline the body of evidence of the natural history, clinical characteristics, surgical outcomes, and surgical complications of NF 1-induced scoliosis, aiming to provide an elucidative insight into this condition. METHOD: Systemic review and meta-analysis were conducted according to the latest Preferred Reporting Items for Systematic Reviews Meta-Analyses (PRISMA) guidelines. The search was performed in Medline, Embase, and Web of Science Core Collection up to December 27, 2022, using related keywords. Clinical features such as frequencies, segmental involvement, and hereditary information were summarized and described qualitatively. Meta-analysis was conducted using R software and the 'meta' package to yield an overall outcome of efficacy and safety of surgical management, precisely, spinal fusion procedure and growing rods procedure. Corrective rate of Cobb angle, sagittal kyphosis angle, and T1-S1 length post-operative and at the last follow-up was used to evaluate the efficacy, and the occurrence of surgery-related complications was used to evaluate the safety. RESULT: A total of 37 articles involving 1023 patients were included. Approximately 26.6% of the NF 1 patients would present with scoliosis. Patients tend to develop scoliosis at an earlier age. The thoracic part turned out to be the most affected segment. No obvious correlation between scoliosis and genotype or hereditary type was observed. Both spinal fusion and growing rod surgery have shown acceptable treatment outcomes, with spinal fusion demonstrating better performance in terms of effectiveness and safety. The growing rods technique seemed to allow a better lengthening of the spine. The mainstay post-operative complications were implant-related complications but could be managed with limited revision surgery. Severe neurological deficits were rarely reported. CONCLUSION: Scoliosis, especially the subtype characterized by dystrophic bony changes, is a significant orthopedic manifestation of NF1. It has an early onset, a tendency to persistently and rapidly progress, and is challenging to deal with. The current review outlines the available evidence from the perspective of natural history, clinical features, and the treatment efficacy and safety of the mainstay surgical options. Patients with NF1 scoliosis will benefit from a better understanding of the disease and evidence based treatment strategies.

Optimizing lifestyle profiles is potential for preventing nonalcoholic fatty liver disease and enhancing its survival.

The aim of this study was to evaluate the association between lifestyle profile and disease incidence/mortality in patients with non-alcoholic fatty liver disease (NAFLD). Lifestyle profiles ascertainment was based on the latent profile analysis. The associations of lifestyle profile and outcomes were analyzed by multivariate logistic or Cox regressions. Four lifestyle profiles (profile 1 and 2 for male, profile 3 and 4 for female) were established for all participants. Compared to profile 1, profile 2 (P = 0.042) and profile 3 (P = 0.013) had lower incidence for NAFLD. In contrast, profile 4 showed similar NAFLD prevalence compared to profile 1 (P = 0.756). Individuals with NAFLD within profile 3 had the best long-term survival, and the HR was 0.55 (95% CI 0.40-0.76) for all-cause mortality (compared to profile 1). Profile 4 (P = 0.098) and profile 2 (P = 0.546) had similar all-cause survival compared to profile 1. We explored the associations of healthy lifestyle score with mortality and incidence of NAFLD stratified by lifestyle profiles. We observed that with the increase of healthy lifestyle score, participants within profile 2 did not display lower NAFLD incidence and better long-term survival in NAFLD cases. In this study, lifestyle profiles were constructed in NHANES participants. The distinct lifestyle profiles may help optimize decision-making regarding lifestyle management in preventing NAFLD development, as well as selection of a more personalized approach for improving NAFLD survival.

Bisphenol S induces brown adipose tissue whitening and aggravates diet-induced obesity in an estrogen-dependent manner.

Bisphenol S (BPS) exposure has been implied epidemiologically to increase obesity risk, but the underlying mechanism is unclear. Here, we propose that BPS exposure at an environmentally relevant dose aggravates diet-induced obesity in female mice by inducing brown adipose tissue (BAT) whitening. We explored the underlying mechanism by which KDM5A-associated demethylation of the trimethylation of lysine 4 on histone H3 (H3K4me3) in thermogenic genes is overactivated in BAT upon BPS exposure, leading to the reduced expression of thermogenic genes. Further studies have suggested that BPS activates KDM5A transcription in BAT by binding to glucocorticoid receptor (GR) in an estrogen-dependent manner. Estrogen-estrogen receptors facilitate the accessibility of the KDM5A gene promoter to BPS-activated GR by recruiting the activator protein 1 (AP-1) complex. These results indicate that BAT is another important target of BPS and that targeting KDM5A-related signals may serve as an approach to counteract the BPS-induced susceptivity to obesity.

Activation of P2Y1R impedes intestinal mucosa repair during colitis.

Delayed intestinal mucosal healing is one of the pathogenic bases for the recurrence of inflammatory bowel disease (IBD), but how the IBD inflammatory environment impedes intestinal mucosa repair remains unclear. Adenosine diphosphate (ADP) is an endogenous ligand of P2Y1R that is highly produced at sites of inflammation. We herein identify a novel role of ADP to directly facilitate inflammation-induced epithelial permeability, delay wound healing, and disrupt tight junction integrity, and we found that P2Y1R, a receptor preferentially activated by ADP, was significantly upregulated in the colonic mucosa of ulcerative colitis (UC) patients and in colonic epithelial cells of colitis mice. Inhibition of P2Y1R significantly increased the epithelial permeability, decreased the wound healing capacity, and impaired the tight junction integrity in TNF-α-challenged Caco-2 cells. In parallel, the same effects in promoting intestinal mucosa repair were observed in DSS-induced colitis in P2Y1R-/- mice. Mechanistic investigation revealed that P2Y1R inhibition facilitated epithelial AMP-activated protein kinase (AMPK) phosphorylation and gut microbiota homeostasis reconstruction. Taken together, these findings highlight that P2Y1R activation plays an important role in impeding intestinal mucosa repair during colitis, and that P2Y1R is an attractive target for the therapy of IBD.

Improved Deep Residual Shrinkage Network for Intelligent Interference Recognition with Unknown Interference.

In complex battlefield environments, flying ad-hoc network (FANET) faces challenges in manually extracting communication interference signal features, a low recognition rate in strong noise environments, and an inability to recognize unknown interference types. To solve these problems, one simple non-local correction shrinkage (SNCS) module is constructed. The SNCS module modifies the soft threshold function in the traditional denoising method and embeds it into the neural network, so that the threshold can be adjusted adaptively. Local importance-based pooling (LIP) is introduced to enhance the useful features of interference signals and reduce noise in the downsampling process. Moreover, the joint loss function is constructed by combining the cross-entropy loss and center loss to jointly train the model. To distinguish unknown class interference signals, the acceptance factor is proposed. Meanwhile, the acceptance factor-based unknown class recognition simplified non-local residual shrinkage network (AFUCR-SNRSN) model with the capacity for both known and unknown class recognition is constructed by combining AFUCR and SNRSN. Experimental results show that the recognition accuracy of the AFUCR-SNRSN model is the highest in the scenario of a low jamming to noise ratio (JNR). The accuracy is increased by approximately 4-9% compared with other methods on known class interference signal datasets, and the recognition accuracy reaches 99% when the JNR is -6 dB. At the same time, compared with other methods, the false positive rate (FPR) in recognizing unknown class interference signals drops to 9%.

Gut microbiota-derived tryptamine and phenethylamine impair insulin sensitivity in metabolic syndrome and irritable bowel syndrome.

The incidence of metabolic syndrome is significantly higher in patients with irritable bowel syndrome (IBS), but the mechanisms involved remain unclear. Gut microbiota is causatively linked with the development of both metabolic dysfunctions and gastrointestinal disorders, thus gut dysbiosis in IBS may contribute to the development of metabolic syndrome. Here, we show that human gut bacterium Ruminococcus gnavus-derived tryptamine and phenethylamine play a pathogenic role in gut dysbiosis-induced insulin resistance in type 2 diabetes (T2D) and IBS. We show levels of R. gnavus, tryptamine, and phenethylamine are positively associated with insulin resistance in T2D patients and IBS patients. Monoassociation of R. gnavus impairs insulin sensitivity and glucose control in germ-free mice. Mechanistically, treatment of R. gnavus-derived metabolites tryptamine and phenethylamine directly impair insulin signaling in major metabolic tissues of healthy mice and monkeys and this effect is mediated by the trace amine-associated receptor 1 (TAAR1)-extracellular signal-regulated kinase (ERK) signaling axis. Our findings suggest a causal role for tryptamine/phenethylamine-producers in the development of insulin resistance, provide molecular mechanisms for the increased prevalence of metabolic syndrome in IBS, and highlight the TAAR1 signaling axis as a potential therapeutic target for the management of metabolic syndrome induced by gut dysbiosis.

Research hotspot and trend of chronic wounds: A bibliometric analysis from 2013 to 2022.

Chronic wounds have been confirmed as a vital health problem facing people in the global population aging process. While significant progress has been achieved in the study of chronic wounds, the treatment effect should be further improved. The number of publications regarding chronic wounds has been rising rapidly. In this study, bibliometric analysis was conducted to explore the hotspots and trends in the research on chronic wounds. All relevant studies on chronic wounds between 2013 and 2022 were collected from the PubMed database of the Web of Science (WOS) and the National Center for Biotechnology Information (NCBI). The data were processed and visualised using a series of software. On that basis, more insights can be gained into hotspots and trends of this research field. Wound Repair and Regeneration has the highest academic achievement in the field of chronic wound research. The United States has been confirmed as the most productive country, and the University of California System ranks high among other institutions. Augustin, M. is the author of the most published study, and Frykberg, RG et al. published the most cited study. Furthermore, the hotspots of wound research over the last decade were identified (e.g., bandages, infection and biofilms, pathophysiology and therapy). This study will help researchers gain insights into chronic wound research's hotspots and trends accurately and quickly. Moreover, the exploration of bacterial biofilm and the pathophysiological mechanism of the chronic wound will lay a solid foundation and clear direction for treating chronic wounds.

Bibliometric analysis and visualization of transdermal drug delivery research in the last decade: global research trends and hotspots.

Background: Transdermal delivery has become a crucial field in pharmaceutical research. There has been a proliferation of innovative methods for transdermal drug delivery. In recent years, the number of publications regarding transdermal drug delivery has been rising rapidly. To investigate the current research trends and hotspots in transdermal drug delivery, a comprehensive bibliometric analysis was performed. Methods: An extensive literature review was conducted to gather information on transdermal drug delivery that had been published between 2003 and 2022. The articles were obtained from the Web of Science (WOS) and the National Center for Biotechnology Information (NCBI) databases. Subsequently, the collected data underwent analysis and visualization using a variety of software tools. This approach enables a deeper exploration of the hotspots and emerging trends within this particular research domain. Results: The results showed that the number of articles published on transdermal delivery has increased steadily over the years, with a total of 2,555 articles being analyzed. The most frequently cited articles were related to the optimization of drug delivery and the use of nanotechnology in transdermal drug delivery. The most active countries in the field of transdermal delivery research were the China, United States, and India. Furthermore, the hotspots over the past 2 decades were identified (e.g., drug therapy, drug delivery, and pharmaceutical preparations and drug design). The shift in research focus reflects an increasing emphasis on drug delivery and control release, rather than simply absorption and penetration, and suggests a growing interest in engineering approaches to transdermal drug delivery. Conclusion: This study provided a comprehensive overview of transdermal delivery research. The research indicated that transdermal delivery would be a rapidly evolving field with many opportunities for future research and development. Moreover, this bibliometric analysis will help researchers gain insights into transdermal drug delivery research's hotspots and trends accurately and quickly.

Nf1 in heart development: a potential causative gene for congenital heart disease: a narrative review.

Congenital heart disease is the most frequent congenital disorder, affecting a significant number of live births. Gaining insights into its genetic etiology could lead to a deeper understanding of this condition. Although the Nf1 gene has been identified as a potential causative gene, its role in congenital heart disease has not been thoroughly clarified. We searched and summarized evidence from cohort-based and experimental studies on the issue of Nf1 and heart development in congenital heart diseases from various databases. Available evidence demonstrates a correlation between Nf1 and congenital heart diseases, mainly pulmonary valvar stenosis. The mechanism underlying this correlation may involve dysregulation of epithelial-mesenchymal transition (EMT). The Nf1 gene affects the EMT process via multiple pathways, including directly regulating the expression of EMT-related transcription factors and indirectly regulating the EMT process by regulating the MAPK pathway. This narrative review provides a comprehensive account of the Nf1 involvement in heart development and congenital cardiovascular diseases in terms of epidemiology and potential mechanisms. RAS signaling may contribute to congenital heart disease independently or in cooperation with other signaling pathways. Efficient management of both NF1 and cardiovascular disease patients would benefit from further research into these issues.

Saffron Petal, an Edible Byproduct of Saffron, Alleviates Dextran Sulfate Sodium-Induced Colitis by Inhibiting Macrophage Activation and Regulating Gut Microbiota.

Saffron petal (SP) is an agricultural byproduct in the process of the crude drug saffron, accounting for 90% of the dry weight of saffron flowers. To promote the utilization of SP in the food and pharmaceutical industries, its anti-inflammatory activities were evaluated on LPS-activated RAW 264.7 cells and DSS-challenged colitic mice. The results indicated that the SP extract had a notable effect in alleviating the clinical manifestations of colitis, such as reduction in body weight, improvement in disease activity index, mitigation of colon shortening, and alleviation of colon tissue damage. Moreover, SP extract significantly suppressed macrophage infiltration and activation, evidenced by a decrease in colonic F4/80 macrophages and suppression of the transcription and secretion of colonic tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) in DSS-challenged colitic mice. In vitro, SP extract also significantly suppressed nitric oxide production, COX-2 and iNOS expressions, and TNF-α and IL-1ß transcription of activated RAW 264.7 cells. Network pharmacology-guided research identified that SP extract significantly downregulated Akt, p38, ERK, and JNK phosphorylation in vivo and in vitro. In parallel, SP extract also effectively corrected microbial dysbiosis by increasing the abundance of Bacteroides acidifaciens, Bacteroides vulgatus, Lactobacillus murinus, and Lactobacillus gasseri. These findings indicate that the effectiveness of SP extract in treating colitis is demonstrated by its ability to reduce macrophage activation, inhibit the PI3K/Akt and MAPK pathways, and regulate gut microbiota, suggesting that SP extract holds great potential as a therapeutic option for colitis.

[Transconjunctival lower eyelid blepharoplasty with "super released" orbital fat in correction of tear trough and palpebromalar groove depression].

Objective: To investigate effectiveness of transconjunctival lower eyelid blepharoplasty with "super released" orbital fat in correction of lower eyelid pouch protrusion and tear trough and palpebromalar groove depression. Methods: A clinical data of 82 patients (164 sides) with lower eyelid pouch protrusion and tear trough and palpebromalar groove depression, who met the selection criteria between September 2021 and May 2022, was retrospectively analyzed. Of the included patients, 3 were males and 79 were females, with an average age of 34.5 years (range, 22-46 years). All patients had varying degrees of eyelid pouch protrusion and tear trough and palpebromalar groove depression. The deformities were graded by the Barton grading system as gradeⅠ in 64 sides, grade Ⅱ in 72 sides, and grade Ⅲ in 28 sides. The orbital fat transpositions were performed through the lower eyelid conjunctival approach. The membrane surrounding the orbital fat was completely released, allowing the orbital fat to fully herniate until the herniated orbital fat did not retract significantly in a resting and relaxed state, which is regarded as the "super released" standard. The released fat strip was spread into the anterior zygomatic space and the anterior maxillary space, and percutaneous fixed to the middle face. The suture that penetrates the skin was externally fixed by adhesive tape pasting without knotted. Results: There were 3 sides with chemosis after operation, 1 side with facial skin numbness, 1 side with mild lower eyelid retraction at the early stage after operation, and 5 sides with slight pouch residue. No hematoma, infection, or diplopia occurred. All patients were followed up 4-8 months, with an average of 6.2 months. The eyelid pouch protrusion, tear trough, and palpebromalar groove depression were significantly corrected. At last follow-up, the deformity was graded by Barton grading system as grade 0 in 158 sides and grade Ⅰ in 6 sides, with a significant difference compared to the preoperative score ( P<0.001). Patient's self-evaluation satisfaction reached very satisfied in 67 cases (81.7%), satisfied in 10 cases (12.2%), generally satisfied in 4 cases (4.8%), and dissatisfied in 1 case (1.2%). Conclusion: The "super released" orbital fat can effectively prevent the retraction of orbital fat, reduce the probability of residual or recurrence of eyelid pouches, and improve the correction effect.

Emerging role of GCN5 in human diseases and its therapeutic potential.

As the first histone acetyltransferase to be cloned and identified in yeast, general control non-depressible 5 (GCN5) plays a crucial role in epigenetic and chromatin modifications. It has been extensively studied for its essential role in regulating and causing various diseases. There is mounting evidence to suggest that GCN5 plays an emerging role in human diseases and its therapeutic potential is promising. In this paper, we begin by providing an introduction GCN5 including its structure, catalytic mechanism, and regulation, followed by a review of the current research progress on the role of GCN5 in regulating various diseases, such as cancer, diabetes, osteoporosis. Thus, we delve into the various aspects of GCN5 inhibitors, including their types, characteristics, means of discovery, activities, and limitations from a medicinal chemistry perspective. Our analysis highlights the importance of identifying and creating inhibitors that are both highly selective and effective inhibitors, for the future development of novel therapeutic agents aimed at treating GCN5-related diseases.

Network Pharmacology Study of Bioactive Components and Molecular Mechanisms of the Glycoside Fraction from Picrorhiza scrophulariiflora Against Experimental Colitis.

Purpose: To explore the potential mechanism of glycosidic fraction of Picrorhiza scrophulariiflora Pennell (GPS) extract for the treatment of colitis using UPLC-QTOF-MS analysis, network pharmacology and experimental research. Methods: The active components of GPS extract were identified by UPLC-QTOF-MS analysis and extracted their targets from the databases, which was used for network pharmacology analysis. Kyoto Encyclopedia of genes and genomes (KEGG) pathway analysis was performed to discover potential therapeutic mechanisms, and the network pharmacology results were then validated by in vivo and in vitro experiments. Results: The results showed that GPS extract significantly alleviated the clinical signs of colitis, including body weight, disease activity index, colon shortening, and colon tissue damage, and inhibited the transcription and production of colonic IL-1ß and IL-6 in DSS-induced colitis mice. In vitro, GPS extract also significantly suppressed nitric oxide (NO) production, iNOS expression, IL-1ß and IL-6 transcription of LPS-activated RAW 264.7 cells. Network pharmacology integrated with experimental validation identified that GPS extract significantly suppressed Akt, p38, ERK, and JNK phosphorylation in vivo and in vitro, and luteolin, apocynin, caffeic acid, caffeic acid methyl ester, luteoloside, picroside II, aucubin, cinnamic acid, vanillic acid, and sweroside were the main components responsible for the anti-inflammatory effect of GPS. These findings demonstrate that the potential anti-inflammatory effect of GPS extract against colitis is achieved through suppressing PI3K/Akt and MAPK pathways, and that the abovementioned active components mainly exerted its anti-inflammatory effect. Conclusion: The therapeutic effect of GPS extract on colitis is related to PI3K/Akt and MAPK pathways, which is a promising remedy for colitis therapy.

Picroside III, an Active Ingredient of Picrorhiza scrophulariiflora, Ameliorates Experimental Colitis by Protecting Intestinal Barrier Integrity.

This study aims to explore the protective effects of Picroside III, an active ingredient of Picrorhiza scrophulariiflora, on the intestinal epithelial barrier in tumor necrosis factor-α (TNF-α) induced Caco-2 cells and dextran sulfate sodium (DSS) induced colitis in mice. Results show that Picroside III significantly alleviated clinical signs of colitis including body weight loss, disease activity index increase, colon shortening, and colon tissue damage. It also increased claudin-3, ZO-1 and occludin expressions and decreased claudin-2 expression in the colon tissues of mice with colitis. In vitro, Picroside III also significantly promoted wound healing, decreased the permeability of cell monolayer, upregulated the expressions of claudin-3, ZO-1 and occludin and downregulated the expression of claudin-2 in TNF-α treated Caco-2 cells. Mechanism studies show that Picroside III significantly promoted AMP-activated protein kinase (AMPK) phosphorylation in vitro and in vivo, and blockade with AMPK could significantly attenuate the upregulation of Picroside III in ZO-1 and occludin expressions and the downregulation of claudin-2 expression in TNF-α treated Caco-2 cells. In conclusion, this study demonstrates that Picroside III attenuated DSS-induced colitis by promoting colonic mucosal wound healing and epithelial barrier function recovery via the activation of AMPK.

Circ_0000566 contributes oxygen-glucose deprivation and reoxygenation (OGD/R)-induced human brain microvascular endothelial cell injury via regulating miR-18a-5p/ACVR2B axis.

Circular RNAs (circRNAs) exert regulatory roles in cerebrovascular disease. Human brain microvascular endothelial cells (HBMECs) participated in brain vascular dysfunction in ischemic stroke. Herein, the functions of circ_0000566 in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced HBMECs were investigated. The expression of circ_0000566, miR-18a-5p, and Activin receptor type 2B (ACVR2B) was measured via quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8) and flow cytometry assays were utilized to detect cell viability and cell apoptosis. Western blot assay was employed to measure the levels of apoptotic-related proteins and ACVR2B. The secretion of IL-1ß, IL-6, and TNF-α was detected via corresponding kits. The relationship between miR-18a-5p and circ_0000566 or ACVR2B was examined via dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Circ_0000566 and ACVR2B were highly expressed, while miR-18a-5p was down-regulated in OGD/R-treated HBMECs. OGD/R treatment promoted HBMECs apoptosis and inflammation and suppressed cell viability, which could be attenuated by silencing of circ_0000566. Circ_0000566 acted as a miR-18a-5p sponge to contribute to OGD/R-induced HBMECs injury. ACVR2B served as a direct target of miR-18a-5p, and ACVR2B overexpression might abolish the inhibitory role of miR-18a-5p on OGD/R-treated HBMEC injury. Circ_0000566 sponged miR-18a-5p to regulate OGD/R-induced HBMECs injury via regulating ACVR2B expression.

Adversarial Auxiliary Weighted Subdomain Adaptation for Open-Set Deep Transfer Bridge Damage Diagnosis.

Deep learning models have been widely used in data-driven bridge structural damage diagnosis methods in recent years. However, these methods require training and test datasets to satisfy the same distribution, which is difficult to satisfy in practice. Domain adaptation transfer learning is an efficient method to solve this problem. Most of the current domain adaptation methods focus on close-set scenarios with the same classes in the source and target domains. However, in practical applications, new damage caused by long-term degradation often makes the target and source domains dissimilar in the class space. For such challenging open-set scenarios, existing domain adaptation methods will be powerless. To effectively solve the above problems, an adversarial auxiliary weighted subdomain adaptation algorithm is proposed for open-set scenarios. Adversarial learning is introduced to proposed an adversarial auxiliary weighting scheme to reflect the similarity of target samples with source classes. It effectively distinguishes unknown damage from known states. This paper further proposes a multi-channel multi-kernel weighted local maximum mean discrepancy metric (MCMK-WLMMD) to capture the fine-grained transferable information for conditional distribution alignment (sub-domain alignment). Extensive experiments on transfer tasks between three bridges verify the effectiveness of the algorithm in open-set scenarios.

Efficient extraction of phycobiliproteins from dry biomass of Spirulina platensis using sodium chloride as extraction enhancer.

An efficient strategy for phycobiliprotein extraction from Spirulina platensis dry biomass has been developed by using NaCl as an enhancer. Different sodium ion and chloride ion salts were screened, and NaCl was selected as the most appropriate solvent for phycobiliprotein extraction. The extraction parameters with NaCl were optimized using response surface methodology. Under optimal operating conditions, a phycobiliprotein extraction rate of 74.8 % and a phycocyanin extraction yield of 102.4 mg/g with a purity of 74.0 % were achieved. Adding NaCl resulted in smaller fragments and destroyed the cell integrity of S. platensis, facilitating phycobiliprotein exudation. The secondary structure and antioxidant activity of phycobiliproteins were not affected by NaCl extraction. The stability of the phycobiliproteins was improved by adding NaCl. This study provides a potential method for phycobiliprotein extraction with high efficiency and good quality using an inexpensive extraction enhancer.

Ruminococcus gnavus plays a pathogenic role in diarrhea-predominant irritable bowel syndrome by increasing serotonin biosynthesis.

Diarrhea-predominant irritable bowel syndrome (IBS-D), a globally prevalent functional gastrointestinal (GI) disorder, is associated with elevated serotonin that increases gut motility. While anecdotal evidence suggests that the gut microbiota contributes to serotonin biosynthesis, mechanistic insights are limited. We determined that the bacterium Ruminococcus gnavus plays a pathogenic role in IBS-D. Monocolonization of germ-free mice with R. gnavus induced IBS-D-like symptoms, including increased GI transit and colonic secretion, by stimulating the production of peripheral serotonin. R. gnavus-mediated catabolism of dietary phenylalanine and tryptophan generated phenethylamine and tryptamine that directly stimulated serotonin biosynthesis in intestinal enterochromaffin cells via a mechanism involving activation of trace amine-associated receptor 1 (TAAR1). This R. gnavus-driven increase in serotonin levels elevated GI transit and colonic secretion but was abrogated upon TAAR1 inhibition. Collectively, our study provides molecular and pathogenetic insights into how gut microbial metabolites derived from dietary essential amino acids affect serotonin-dependent control of gut motility.

Advancing targeted protein degradation for metabolic diseases therapy.

The development and application of traditional drugs represented by small molecule chemical drugs and biological agents, especially inhibitors, have become the mainstream drug development. In recent years, targeted protein degradation (TPD) technology has become one of the most promising methods to remove specific disease-related proteins using cell self-destruction mechanisms. Many different TPD strategies are emerging based on the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP), including but not limited to proteolysis-targeting chimeras (PROTAC), molecular glues (MG), lysosome targeting chimeras (LYTAC), chaperone-mediated autophagy (CMA)-targeting chimeras, autophagy-targeting chimera (AUTAC), autophagosome-tethering compound (ATTEC), and autophagy-targeting chimera (AUTOTAC). The advent of targeted degradation technology can change most protein targets in human cells from undruggable to druggable, greatly expanding the therapeutic prospect of refractory diseases such as metabolic syndrome. Here, we summarize the latest progress of major TPD technologies, especially in metabolic syndrome and look forward to providing new insights for drug discovery.