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In late December 2019, a cluster of cases with 2019 Novel Coronavirus pneumonia (SARS-CoV-2) in Wuhan, China, aroused worldwide concern. Previous studies have reported epidemiological and clinical characteristics of coronavirus disease 2019 (COVID-19). The purpose of this brief review is to summarize those published studies as of late February 2020 on the clinical features, symptoms, complications, and treatments of COVID-19 and help provide guidance for frontline medical staff in the clinical management of this outbreak.

The family Toxoderidae (Mantodea) contains an ecologically diverse group of praying mantis species that have in common greatly elongated bodies. In this study, we sequenced and compared the complete mitochondrial genomes of two Toxoderidae species, Paratoxodera polyacantha and Toxodera hauseri , and compared their mitochondrial genome characteristics with another member of the Toxoderidae, Stenotoxodera porioni ( KY689118 ) . The lengths of the mitogenomes of T. hauseri and P. polyacantha were 15,616 bp and 15,999 bp, respectively, which is similar to that of S. porioni (15,846 bp). The size of each gene as well as the A+T-rich region and the A+T content of the whole genome were also very similar among the three species as were the protein-coding genes, the A+T content and the codon usages. The mitogenome of T. hauseri had the typical 22 tRNAs, whereas that of P. polyacantha had 26 tRNAs including an extra two copies of trnA - trnR . Intergenic regions of 67 bp and 76 bp were found in T. hauseri and P. polyacantha , respectively, between COX2 and trnK ; these can be explained as residues of a tandem duplication/random loss of trnK and trnD. This non-coding region may be synapomorphic for Toxoderidae. In BI and ML analyses, the monophyly of Toxoderidae was supported and P. polyacantha was the sister clade to T. hauseri and S. porioni .

We determined 15 complete and two nearly complete mitogenomes of Heptageniidae belonging to three subfamilies (Heptageniinae, Rhithrogeninae, and Ecdyonurinae) and six genera (Afronurus, Epeorus, Leucrocuta, Maccaffertium, Stenacron, and Stenonema). Species of Rhithrogeninae and Ecdyonurinae had the same gene rearrangement of CR-I-M-Q-M-ND2, whereas a novel gene rearrangement of CR-I-M-Q-NCR-ND2 was found in Heptageniinae. Non-coding regions (NCRs) of 25–47 bp located between trnA and trnR were observed in all mayflies of Heptageniidae, which may be a synapomorphy for Heptageniidae. Both the BI and ML phylogenetic analyses supported the monophyly of Heptageniidae and its subfamilies (Heptageniinae, Rhithrogeninae, and Ecdyonurinae). The phylogenetic results combined with gene rearrangements and NCR locations confirmed the relationship of the subfamilies as (Heptageniinae + (Rhithrogeninae + Ecdyonurinae)). To assess the effects of low-temperature stress on Heptageniidae species from Ottawa, Canada, we found 27 positive selection sites in eight protein-coding genes (PCGs) using the branch-site model. The selection pressure analyses suggested that mitochondrial PCGs underwent positive selection to meet the energy requirements under low-temperature stress.

Gene tagging with fluorescent proteins is essential for investigations of the dynamic properties of cellular proteins. CRISPR-Cas9 technology is a powerful tool for inserting fluorescent markers into all alleles of the gene of interest (GOI) and allows functionality and physiological expression of the fusion protein. It is essential to evaluate such genome-edited cell lines carefully in order to preclude off-target effects caused by (i) incorrect insertion of the fluorescent protein, (ii) perturbation of the fusion protein by the fluorescent proteins or (iii) nonspecific genomic DNA damage by CRISPR-Cas9. In this protocol, we provide a step-by-step description of our systematic pipeline to generate and validate homozygous fluorescent knock-in cell lines.We have used the paired Cas9D10A nickase approach to efficiently insert tags into specific genomic loci via homology-directed repair (HDR) with minimal off-target effects. It is time-consuming and costly to perform whole-genome sequencing of each cell clone to check for spontaneous genetic variations occurring in mammalian cell lines. Therefore, we have developed an efficient validation pipeline of the generated cell lines consisting of junction PCR, Southern blotting analysis, Sanger sequencing, microscopy, western blotting analysis and live-cell imaging for cell-cycle dynamics. This protocol takes between 6 and 9 weeks. With this protocol, up to 70% of the targeted genes can be tagged homozygously with fluorescent proteins, thus resulting in physiological levels and phenotypically functional expression of the fusion proteins.

The prevalence of cardiomyopathy is higher in diabetic patients than those without diabetes. Diabetic cardiomyopathy (DCM) is defined as a clinical condition of abnormal myocardial structure and performance in diabetic patients without other cardiac risk factors, such as coronary artery disease, hypertension, and significant valvular disease. Multiple molecular events contribute to the development of DCM, which include the alterations in energy metabolism (fatty acid, glucose, ketone and branched chain amino acids) and the abnormalities of subcellular components in the heart, such as impaired insulin signaling, increased oxidative stress, calcium mishandling and inflammation. There are no specific drugs in treating DCM despite of decades of basic and clinical investigations. This is, in part, due to the lack of our understanding as to how heart failure initiates and develops, especially in diabetic patients without an underlying ischemic cause. Some of the traditional anti-diabetic or lipid-lowering agents aimed at shifting the balance of cardiac metabolism from utilizing fat to glucose have been shown inadequately targeting multiple aspects of the conditions. Peroxisome proliferator-activated receptor α (PPARα), a transcription factor, plays an important role in mediating DCM-related molecular events. Pharmacological targeting of PPARα activation has been demonstrated to be one of the important strategies for patients with diabetes, metabolic syndrome, and atherosclerotic cardiovascular diseases. The aim of this review is to provide a contemporary view of PPARα in association with the underlying pathophysiological changes in DCM. We discuss the PPARα-related drugs in clinical applications and facts related to the drugs that may be considered as risky (such as fenofibrate, bezafibrate, clofibrate) or safe (pemafibrate, metformin and glucagon-like peptide 1-receptor agonists) or having the potential (sodium–glucose co-transporter 2 inhibitor) in treating DCM.

In industry, the task of defect classification and defect localization is an important part of defect detection system. However, existing studies only focus on one task and it is difficult to ensure the accuracy of both tasks. This paper proposes a defect detection system based on improved Yolo_v4, which greatly improves the detection ability of minor defects. For K_Means algorithm clustering prianchors question with strong subjectivity, the paper proposes the Density Based Spatial Clustering of Applications with Noise (DBSCAN) algorithm to determine the number of Anchors. To solve the problem of low detection rate of small targets caused by insufficient reuse rate of low-level features in CSPDarknet53 feature extraction network, this paper proposes an ECA-DenseNet-BC-121 feature extraction network to improve it. And the Dual Channel Feature Enhancement (DCFE) module is proposed to improve the local information loss and gradient propagation obstruction caused by quad chain convolution in PANet networks to improve the robustness of the model. The experimental results on the fabric surface defect detection datasets show that the mAP of the improved Yolo_v4 is 98.97%, which is 7.67% higher than SSD, 3.75% higher than Faster_RCNN, 10.82% higher than Yolo_v4 tiny, and 5.35% higher than Yolo_v4, and the detection speed reaches 39.4 fps. It can meet the real-time monitoring needs of industrial sites.

Background The high prevalence of diabetic kidney disease (DKD) in the United States necessitates further investigation into its impact on complications associated with total hip arthroplasty (THA). This study utilizes a large nationwide database to explore risk factors in DKD cases undergoing THA. Methods This research utilized a case–control design, leveraging data from the national inpatient sample for the years 2016 to 2019. Employing propensity score matching (PSM), patients diagnosed with DKD were paired on a 1:1 basis with individuals free of DKD, ensuring equivalent age, sex, race, Elixhauser Comorbidity Index (ECI), and insurance coverage. Subsequently, comparisons were drawn between these PSM-matched cohorts, examining their characteristics and the incidence of post-THA complications. Multivariate logistic regression analysis was then employed to evaluate the risk of early complications after surgery. Results DKD's prevalence in the THA cohort was 2.38%. A 7-year age gap separated DKD and non-DKD patients (74 vs. 67 years, P  < 0.0001). Additionally, individuals aged above 75 exhibited a substantial 22.58% increase in DKD risk (49.16% vs. 26.58%, P  < 0.0001). Notably, linear regression analysis yielded a significant association between DKD and postoperative acute kidney injury (AKI), with DKD patients demonstrating 2.274-fold greater odds of AKI in contrast with non-DKD individuals (95% CI: 2.091–2.473). Conclusions This study demonstrates that DKD is a significant risk factor for AKI in patients undergoing total hip arthroplasty. Optimizing preoperative kidney function through appropriate interventions might decrease the risk of poor prognosis in this population. More prospective research is warranted to investigate the potential of targeted kidney function improvement strategies in reducing AKI rates after THA. The findings of this study hold promise for enhancing preoperative counseling by surgeons, enabling them to provide DKD patients undergoing THA with more precise information regarding the risks associated with their condition.

BackgroundCigarette smoking is a common risk factor for diseases and cancers. Oral microbiota is also associated with diseases and cancers. However, little is known about the impact of cigarette smoking on the oral microbiota, especially among ethnic minority populations.MethodsWe investigated cigarette smoking in relationship with the oral microbiota in a large population of predominately low-income and African-American participants. Mouth rinse samples were collected from 1616 participants within the Southern Community Cohort Study, including 592 current-smokers, 477 former-smokers and 547 never-smokers. Oral microbiota was profiled by 16S ribosomal RNA gene deep sequencing.ResultsCurrent-smokers showed a different overall microbial composition from former-smokers (p=6.62×10−7) and never-smokers (p=6.00×10−8). The two probiotic genera, Bifidobacterium and Lactobacillus, were enriched among current-smokers when compared with never-smokers, with Bonferroni-corrected p values (PBonferroni ) of 1.28×10−4 and 5.89×10−7, respectively. The phylum Actinobacteria was also enriched in current-smokers when compared with never-smokers, with a median relative abundance of 12.35% versus 9.36%, respectively, and with a PBonferroni =9.11×10−11. In contrast, the phylum Proteobacteria was depleted in current smokers (PBonferroni =5.57×10−13), with the relative abundance being almost three times that of never-smokers (7.22%) when compared with that of current-smokers (2.47%). Multiple taxa within these two phyla showed differences in abundance/prevalence between current-smokers and never-smokers at PBonferroni <0.05. The differences in the overall microbial composition and abundance/prevalence of most taxa were observed among both African-Americans and European-Americans. Meanwhile, such differences were not observed between former-smokers and never-smokers.ConclusionSmoking has strong impacts on oral microbial community, which was recovered after smoking cessation.

Diabetic neuropathy is one of the clinical syndromes characterized by pain and substantial morbidity primarily due to a lesion of the somatosensory nervous system. The burden of diabetic neuropathy is related not only to the complexity of diabetes but also to the poor outcomes and difficult treatment options. There is no specific treatment for diabetic neuropathy other than glycemic control and diligent foot care. Although various metabolic pathways are impaired in diabetic neuropathy, enhanced cellular oxidative stress is proposed as a common initiator. A mechanism-based treatment of diabetic neuropathy is challenging; a better understanding of the pathophysiology of diabetic neuropathy will help to develop strategies for the new and correct diagnostic procedures and personalized interventions. Thus, we review the current knowledge of the pathophysiology in diabetic neuropathy. We focus on discussing how the defects in metabolic and vascular pathways converge to enhance oxidative stress and how they produce the onset and progression of nerve injury present in diabetic neuropathy. We discuss if the mechanisms underlying neuropathy are similarly operated in type I and type II diabetes and the progression of antioxidants in treating diabetic neuropathy.

Traditionally, the nervous system has been perceived primarily as a complex network predominantly composed of neurons. Nevertheless, ongoing developments in the field of neuroscience have brought to light the significant contributions of non-neuronal cells, highlighting their importance 1,2 . Getting a profound insight into their functional traits and the mechanisms that govern them is essential for developing innovative approaches to treating and preventing neurological disorders.Recently, there has been significant progress in the investigation of non-neuronal cells within the nervous system. The primary emphasis lies in uncovering the intricate network of interactions that connect these cells to neurons and to each other. As an illustration, recent studies in the field of neurovascular coupling have begun to elucidate the intricate relationship between brain activity and the modulation of blood flow within the cerebral system [3][4][5][6] . Investigations into neuroimmunology have introduced novel insights into the critical roles that immune cells play in both inflammatory response in the nervous system and the progression of neurodegenerative disorders 7,8 . Investigating the interactions between glial cells serves as a burgeoning area of study, focusing on unraveling the complexities of communication and the exchange of information among astrocytes, other glial cells, and neurons, along with their significant influence on neural operations 2,9,10 .Microglia, the primary resident immune cells found within the nervous system, act as the initial barrier against invasive pathogens and play an essential role in upholding the immune balance of the neural environment 11 . These cells play a significant part in essential processes such as the elimination of excess synapses throughout neural maturation and are capable of rapidly triggering protective immune mechanisms when faced with injury or pathological conditions in the nervous system [12][13][14] . Astrocytes play a vital role not only in offering critical structural support for neurons but also in expertly managing the intricate balance of neurotransmitter absorption and release 15,16 , meticulously maintaining ion equilibrium 17,18 , and influencing synaptic adaptability 19 . Cells within the neurovascular unit, including the endothelial and pericyte populations, are essential for maintaining the stability and integrity of the blood-brain barrier while ensuring the accurate and suitable regulation of cerebral perfusion 20,21 .In the field of neurological disorders, the unnormal functioning of glial cells is commonly identified. In conditions such as Alzheimer's and Parkinson's diseases, the involvement of immune cells and astrocytes in the inflammatory response has become a characteristic feature of these disorders [22][23][24] . Additionally, impairments in the mechanisms that link neural function with vascular responses and disruptions to the integrity of the neural barrier are also critical factors in the development of numerous neurological disorders, including stroke and multiple sclerosis [25][26][27] . Consequently, a thorough exploration of the functions and mechanisms of non-neuronal cells throughout the disease progression is anticipated to yield novel perspectives and strategic avenues for identifying new therapeutic targets.This special issue provides an examination of important aspects regarding non-neuronal cells within the nervous system. Non-neuronal cells (mainly glial cells) play roles in supporting, protecting, and nourishing neurons in the nervous system. Their ability to divide makes them prone to mutation and malignant transformation. Most of malignant tumors in the central nervous system originate from non-neuronal cells. Ji et al reported the discovery of Gap Junction Protein, Gamma 1(GJC1) as a prognostic biomarker in glioma cells 28 . GJC1 is located on human chromosome 17 and encodes the gap junction gamma -1 protein (connexin 45, Cx45), which participates in intercellular communication. The expression of Cx45 is decreased in colorectal cancer and has a tumor-suppressive role in melanoma cells, but its function in gliomas remains unclear. The study of Ji et al systematically investigated the influence of clinicopathological features, molecular subclasses, and prognosis of gliomas on GJC1 expression patterns. They analyzed the biological processes and markers associated with GJC1 in tumor cells and further performed drug correlation analysis. Moreover, all the specific mechanisms of drug action obtained from the drug correlation analysis were related to the cell cycle, further supporting the influence of GJC1 on cell-cycle regulation.The review article of Zhao et al comprehensively stated olfactory system's complexity and the pivotal roles glial cells play in both health and disease conditions 29 . This review discussed the diverse functions and dynamics of glial cells in the mammalian olfactory bulb, mainly focused on astrocytes, microglia, oligodendrocytes, olfactory ensheathing cells, and radial glia cells. Each type of glial contributes uniquely to the olfactory bulb 's functionality, influencing many processes from synaptic modulation and neuronal survival to immune defense and axonal guidance. The review features their roles in maintaining neural health, their involvement in neurodegenerative diseases, and their potential therapeutic applications for neuroregeneration.Traumatic brain injury (TBI) is a critical global health concern characterized by elevated rates of both morbidity and mortality. The pathological and physiological changes after TBI are closely related to microglia. Microglia, the primary immune cells in the brain, are closely linked to the mechanisms and treatment of TBI. Zhang et al published a bibliometric analysis and visualization study to identify current research hotspots and predict future 30 . In this study, the authors meticulously discussed the mechanism of action of non-neuronal cells in ischemic stroke from two aspects: the repair of the blood-brain barrier and the immune infiltration following TBI and post-TBI peripheral immunosuppression and inflammation.Ischemic stroke accounts for 75% to 80% of all stroke events, making it the leading cause of cerebrovascular diseases and related deaths worldwide 31 . Following ischemic stroke, non-neuronal cells within the nervous system play a crucial role in maintaining neurovascular unit functions, regulating metabolic and inflammatory processes of the nervous system. Wang et al. systemically explored the global research trends and prospects of immune-related therapy in ischemic stroke 32 .To summarize, the field of research focused on non-neuronal cells within the nervous system is currently experiencing a significant growth. This dedicated Research Topic is intended to significantly support the advancement of this area by establishing a platform for academic discussions and for the demonstration of research achievements.