截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共20043篇，總影響因子89696.086分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共53篇，合作單位覆蓋了清華、北大、復(fù)旦、華盛頓大學(xué)、麻省理工學(xué)院、東京大學(xué)以及紐約大學(xué)等國(guó)際知名研究機(jī)構(gòu)上百所。
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近期收錄2022年8月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共236篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1302.467，其中，10分以上文獻(xiàn)22篇（圖二）。
圖一
圖二
JOURNAL OF MEDICAL VIROLOGY
[IF=20.693]
作者單位：中南大學(xué)醫(yī)學(xué)微生物學(xué)系
摘要：The lung–brain axis is an emerging area of study that got its basis from the gut–brain axis biological pathway. Using Respiratory Synctial Virus (RSV) as the model of respiratory viral pathogen, this study aims to establish some biological pathways. After establishing the mice model, the inflammation in lung and brain were assayed using Hematoxylin-eosin staining, indirect immunofluorescence (IFA), and quantitative reverse-transcription polymerase chain reaction. The biological pathways between lung and brain were detected through metabolomics analysis. In lung, RSV infection promoted epithelial shedding and infiltration of inflammatory cells. Also, RSV immunofluorescence and titerss were significantly increased. Moreover, interleukin (IL)-1, IL-6 and tumor necrosis factor-α (TNF-α) were also significantly increased after RSV infection. In brain, the cell structure of hippocampal CA1 area was loose and disordered. Inflammatory cytokines IL-6 and IL-1β expression in the brain also increased, however, TNF-α expression showed no differences among the control and RSV group. We observed an increased expression of microglia biomarker IBA-1 and decreased neuronal biomarker NeuN. In addition, RSV mRNA expression levels were also increased in the brains. 15 metabolites were found upregulated in the RSV group including nerve-injuring metabolite glutaric acid, hydroxyglutaric acid and Spermine. ɑ-Estradiol increased significantly while normorphine decreased significantly at Day 7 of infection among the RSV group. This study established a mouse model for exploring the pathological changes in lungs and brains. There are many biological pathways between lung and brain, including direct translocation of RSV and metabolite pathway.
Emerging Microbes & Infections
[IF=19.568]
作者單位：韓國(guó)忠南國(guó)立大學(xué)獸醫(yī)學(xué)院獸醫(yī)公共衛(wèi)生實(shí)驗(yàn)室
摘要：Swine acute diarrhea syndrome coronavirus (SADS-CoV) was reported in China in 2017 and is a causative agent of porcine enteric disease. Recent studies indicate that cells from various hosts are susceptible to SADS-CoV, suggesting the zoonotic potential of this virus. However, little is known about the mechanisms through which this virus enters cells. In this study, we investigated the role of furin in SADS-CoV spike (S)-mediated cell–cell fusion and entry. We found that the SADS-CoV S protein induced the fusion of various cells. Cell–cell fusion was inhibited by the proprotein convertase inhibitor dec-RVKR-cmk, and between cells transfected with mutant S proteins resistant to furin cleavage. These findings revealed that furin-induced cleavage of the SADS-CoV S protein is required for cell–cell fusion. Using mutagenesis analysis, we demonstrated that furin cleaves the SADS-CoV S protein near the S1/S2 cleavage site, 446RYVR449 and 543AVRR546. We used pseudotyped viruses to determine whether furin-induced S cleavage is also required for viral entry. Pseudotyped viruses expressing S proteins with a mutated furin cleavage site could be transduced into target cells, indicating that furin-induced cleavage is not required for pseudotyped virus entry. Our data indicate that S cleavage is critical for SADS-CoV S-mediated cell–cell fusion and suggest that furin might be a host target for SADS-CoV antivirals.
CHEMICAL ENGINEERING JOURNAL
[IF=16.744]
作者單位：中山大學(xué)深圳校區(qū)藥學(xué)院
摘要：Stem cell transplantation has wide application prospects in tissue injury recovery, especially in neurological recovery. However, the low survival rate of stem cells after transplanted to inflammatory lesions seriously limits their therapeutic effect. Here, we reported that the bioactive black phosphorus nanosheets (BPNs) can effectively improve the antioxidant capacity of stem cells and protect stem cells from oxidative stress-induced cell damage. The antioxidant activity of BPNs was found in different types of stem cells, mainly due to the significantly upregulated nuclear factor erythroid 2-like 2 (Nrf2)-dependent antioxidant pathways by BPNs. In addition, compared with natural neural progenitor cells (NPCs), BP-treated NPCs could protect neurons from oxidative damage more effectively in vitro. Further in vivo transplantation results also demonstrated that BP-treated NPCs could significantly increase the survival rate and effectively inhibit lipid peroxidation, inflammatory response and neuronal apoptosis in stroke rats. Our study reveals a novel biological effect of BPNs on stem cells, which expands the biomedical application of BPNs and opens a new way to increase the therapeutic effects of stem cell.
JOURNAL OF THROMBOSIS AND
HAEMOSTASIS [IF=16.036]
文獻(xiàn)引用抗體：bs-0196R
Anti-PDGF-A pAb作者單位：加拿大艾伯塔省埃德蒙頓阿爾伯塔大學(xué)藥學(xué)和藥物科學(xué)學(xué)院藥理學(xué)系Within the vasculature platelets and endothelial cells play crucial roles in hemostasis and thrombosis. Platelets, like endothelial cells, possess intermediate conductance Ca2+-activated K+ (IKCa) channels and generate nitric oxide (NO). Although NO limits platelet aggregation, the role of IKCa channels in platelet function and NO generation has not yet been explored.
Objectives
We investigated whether IKCa channel activation inhibits platelet aggregation, and per endothelial cells, enhances platelet NO production...
BIOMATERIALS
[IF=15.304]
文獻(xiàn)引用抗體：bs-1665R
Anti-VEGFA pAb; IHC作者單位：韓國(guó)大學(xué)組織再生工程研究所
JOURNAL OF AUTOIMMUNITY
[IF=14.511]
文獻(xiàn)引用抗體：
bs-2717R; Anti-TLR9 pAb;IHCbs-7443R; Anti-TGFBI pAb;IHCbs-1316R; Anti-PDGFBB pAb;IHCC02-04004; Hematoxylin-Eosin/HE Staining KitS0074; Masson trichrome stain
作者單位：吉林大學(xué)第一醫(yī)院轉(zhuǎn)化醫(yī)學(xué)科摘要：Lupus nephritis (LN) is the most common cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Currently, immunosuppressive treatments for LN are suboptimal and can induce significant side effects. SB431542 is a selective and potent inhibitor of the TGFβ/Activin/NODAL pathway. Here, we study the effects of SB431542 treatment on LN and discuss the potential mechanisms. SB431542 ameliorated clinical outcomes with a consequent histological improvement in NZB/W mice. A comparative transcriptional profiling analysis revealed 586 differentially expressed genes (247 downregulated genes) in the SB431542 group compared to the control group. We found that the downregulated genes were mainly enriched in the biological processes of B cell activation, B cell proliferation, B cell differentiation, and B cell receptor signaling. Kyoto encyclopedia of genes and genomes pathway analysis revealed that the hematopoietic cell linage pathway was significantly downregulated in the SB431542 group. In addition, we observed that SB431542 reduced the splenic or renal levels of CD20 and the serum levels of anti-dsDNA antibody (IgG) in NZB/W mice. Furthermore, qRT-PCR and immunohistochemistry confirmed that SB431542 inhibits the production of TLR9, TGFβ1, and PDGFB. Thus, due to its immunomodulatory activities, SB431542 could be considered for clinical therapy development for LN.
JOURNAL OF CONTROLLED RELEASE
[IF=11.467]
文獻(xiàn)引用抗體：bs-0560R
Anti-IL13 pAb; IHC,IF
作者單位：溫州醫(yī)科大學(xué)藥學(xué)院藥劑學(xué)系摘要：Diabetic foot ulcer (DFU) is a devastating complication in diabetes patients, imposing a high risk of amputation and economic burden on patients. Sustained inflammation and angiogenesis hindrance are thought to be two key drivers of the pathogenesis of such ulcers. Nitric oxide (NO) has been proven to accelerate the healing of acute or chronic wounds by modulating inflammation and angiogenesis. However, the use of gas-based therapeutics is difficult for skin wounds. Herein, therapeutic NO gas was first prepared as stable microbubbles, followed by incorporation into a cold Poloxamer-407 (P407) solution. Exposed to the DFU wound, the cold P407 solution would rapidly be transformed into a semisolid hydrogel under body temperature and accordingly capture NO microbubbles. The NO microbubble-captured hydrogel (PNO) was expected to accelerate wound healing in diabetic feet. The NO microbubbles had an average diameter of 0.8 ± 0.4 μm, and most of which were captured by the in situ P407 hydrogel. Moreover, the NO microbubbles were evenly distributed inside the hydrogel and kept for a longer time. In addition, the gelling temperature of 30% (w/v) P407 polymer (21 °C) was adjusted to 31 °C for the PNO gel, which was near the temperature of the skin surface. Rheologic studies showed that the PNO gel had mechanical strength comparable with that of the P407 hydrogel. The cold PNO solution was conveniently sprayed or smeared on the wound of DFU and rapidly gelled. In vivo studies showed that PNO remarkably accelerated wound healing in rats with DFU. Moreover, the sustained inflammation at the DFU wound was largely reversed by PNO, as reflected by the decreased levels of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and the increased levels of anti-inflammatory cytokines (IL-10, IL-22 and IL-13). Meanwhile, angiogenesis was significantly promoted by PNO, resulting in rich blood perfusion at the DFU wounds. The therapeutic mechanism of PNO was highly associated with polarizing macrophages and maintaining the homeostasis of the extracellular matrix. Collectively, PNO gel may be a promising vehicle of therapeutic NO gas for DFU treatment.
Redox Biology [IF=10.787]
Mouse Anti-GAPDH mAb; WB
作者單位：北京大學(xué)健康科學(xué)中心基礎(chǔ)醫(yī)學(xué)院人體解剖學(xué)、組織學(xué)和胚胎學(xué)系
摘要：As a novel type of non-coding RNAs, covalently closed circular RNAs (circRNAs) are ubiquitously expressed in eukaryotes. Emerging studies have indicated that dysregulation of circRNAs was related to neurological diseases. However, the biogenesis, regulation, function, and mechanism of circRNAs in Parkinson's disease (PD) remain largely unclear. In this study, thirty-three differentially expressed circRNAs (DECs) were detected by RNA-sequencing between the MPTP-induced PD mice model and the wild-type mice. Quantitative real-time PCR was used to determine the RNA level of DECs in the striatum (STR), substantia nigra pars compacta (SNpc), and serum exosomes, and it was found that circSV2b was downregulated in PD mice. Then, functional experiments in vivo were employed to explore the effect of circSV2b in PD. For the mechanism study, dual-luciferase reporter, fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP), RNA pull-down, gene editing, and CUT & Tag were performed in vitro to confirm that circSV2b directly sponged miR-5107-5p and alleviated the suppression of the expression of the target gene Foxk1, and then positively regulated Akt1 transcription. In vivo, the mechanistic analysis demonstrated that circSV2b overexpression resisted oxidative stress damage through the ceRNA-Akt1 axis in PD models. Taken together, these findings suggested that the miR-5107-5p-Foxk1-Akt1 axis might serve as a key target of circSV2b overexpression in PD treatment, and highlighted the significant change of circSV2b in serum exosomes. Therefore, circSV2b might be a novel biomarker for the diagnosis and treatment of PD.
