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      发表者:北京博奥森生物      发表时间:2023-1-6

      截止目前,引用Bioss产品发表的文献共23073篇总影响因子105342.2分,发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共54篇,合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等国际知名研究机构上百所。

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      本文主要分享引用Bioss产品发表文章至Nature NanotechnologyImmunityCancer Cell等期刊的6篇 IF>15 的文献摘要让我们一起欣赏吧。




      bs-0199R; Anti-GFAP pAb; IF

      bs-1363R; Anti-AIF1/Iba1 pAb; IF

      bs-0296G-FITC; Goat Anti-Mouse IgG H&L / FITC antibody; IF

      bs-0295G-Cy3; Goat Anti-Rabbit IgG H&L / Cy3 antibody; IF


      摘要:Flexible microelectronics capable of straightforward implantation, remotely controlled navigation, and stable long-term recording hold great promise in diverse medical applications, particularly in deciphering complex functions of neural circuits in the brain. Existing flexible electronics, however, are often limited in bending and buckling during implantation, and unable to access a large brain region. Here, an injectable class of electronics with stable recording, omnidirectional steering, and precise navigating capabilities based on magnetic actuation is presented. After simple transcriptional injection, the rigid coatings are biodegraded quickly and the bundles of magnetic-nanoparticles-coated microelectrodes become separated, ultra-flexible, and magnetic actuated for further minimally invasive three-dimensional interpenetration in the brain. As proof of concept, this paradigm-shifting approach is demonstrated for selective and multiplexed neural activities recording across distant regions in the deep rodent brains. Coupling with optogenetic neural stimulation, the unique capabilities of this platform in electrophysiological readouts of projection dynamics in vivo are also demonstrated. The ability of these miniaturized, remotely controllable, and biocompatible ferromagnetic flexible electronics to afford minimally invasive manipulations in the soft tissues of the mammalian brain foreshadows applications in other organ systems, with great potential for broad utility in biomedical science and engineering.




      bs-0271R; Anti-HCMV pp65 pAb; IF

      bsk11014; Human TNF-α ELISA KIT; ELISA

      bsk11007; Human IL-6 ELISA KIT; ELISA


      摘要:Lots of epidemiological and clinical studies have shown that human cytomegalovirus (HCMV) is related to the pathogenesis of atherosclerosis. Released by inflammatory cells and vascular smooth muscle cell (VSMCs), metalloproteinases are observed in many pathological vessel conditions, including atherosclerosis and restenosis. This study was designed to investigate the effect of HCMV infection on the expression of metalloproteinases and their involvements in the HCMV-induced functional changes of VSMCs. Differential metalloproteinase after HCMV infection was assayed using reverse transcription-polymerase chain reaction (RT-PCR) microarray. 




      Anti-MDH1 pAb; WB


      摘要:Inhibition of the electron transport chain (ETC) prevents the regeneration of mitochondrial NAD+, resulting in cessation of the oxidative tricarboxylic acid (TCA) cycle and a consequent dependence upon reductive carboxylation for aspartate synthesis. NAD+ regeneration alone in the cytosol can rescue the viability of ETC-deficient cells. Yet, how this occurs and whether transfer of oxidative equivalents to the mitochondrion is required remain unknown. Here, we show that inhibition of the ETC drives reversal of the mitochondrial aspartate transaminase (GOT2) as well as malate and succinate dehydrogenases (MDH2 and SDH) to transfer oxidative NAD+ equivalents into the mitochondrion. This supports the NAD+-dependent activity of the mitochondrial glutamate dehydrogenase (GDH) and thereby enables anaplerosis—the entry of glutamine-derived carbon into the TCA cycle and connected biosynthetic pathways. Thus, under impaired ETC function, the cytosolic redox state is communicated into the mitochondrion and acts as a rheostat to support GDH activity and cell viability.

      Nature Communications



      Anti-BCAS1 pAb; IF


      摘要:Oligovascular coupling contributes to white matter vascular homeostasis. However, little is known about the effects of oligovascular interaction on oligodendrocyte precursor cell (OPC) changes in chronic cerebral ischemia. Here, using a mouse of bilateral carotid artery stenosis, we show a gradual accumulation of OPCs on vasculature with impaired oligodendrogenesis. Mechanistically, chronic ischemia induces a substantial loss of endothelial caveolin-1 (Cav-1), leading to vascular secretion of heat shock protein 90α (HSP90α). Endothelial-specific over-expression of Cav-1 or genetic knockdown of vascular HSP90α restores normal vascular-OPC interaction, promotes oligodendrogenesis and attenuates ischemic myelin damage. miR-3074(?1)?3p is identified as a direct inducer of Cav-1 reduction in mice and humans. Endothelial uptake of nanoparticle-antagomir improves myelin damage and cognitive deficits dependent on Cav-1. In summary, our findings demonstrate that vascular abnormality may compromise oligodendrogenesis and myelin regeneration through endothelial Cav-1, which may provide an intercellular mechanism in ischemic demyelination.

      Nature Communications



      bs-0296G-FITCGoat Anti-Mouse IgG H&L / FITC antibody; IF

      bs-0521R-FITCAnti-CD44/FITC pAb;IF

      C05-07004BiossECL Plus WB Substrate


      摘要:Cancer vaccine, which can promote tumor-specific immunostimulation, is one of the most important immunotherapeutic strategies and holds tremendous potential for cancer treatment/prevention. Here, we prepare a series of nanoparticles composed of doxorubicin- and tyrosine kinase inhibitor-loaded and hyaluronic acid-coated dendritic polymers (termed HDDT nanoparticles) and find that the HDDT nanoparticles can convert various cancer cells to micrometer-sized vesicles (1.6?3.2?μm; termed HMVs) with ~100% cell-to-HMV conversion efficiency. We confirm in two tumor-bearing mouse models that the nanoparticles can restrain tumor growth, induce robust immunogenic cell death, and convert the primary tumor into an antigen depot by producing HMVs in situ to serve as personalized vaccines for cancer immunotherapy. Furthermore, the HDDT-healed mice show a strong immune memory effect and the HDDT treatment can realize long-term protection against tumor rechallenge. Collectively, the present work provides a general strategy for the preparation of tumor-associated antigen-containing vesicles and the development of personalized cancer vaccines.

      Nature Communications



      Streptavidin / AF555


      摘要:RIG-I/DDX58 plays a key role in host innate immunity. However, its therapeutic potential for inflammation-related cancers remains to be explored. Here we identify frameshift germline mutations of RIG-I occurring in patients with colon cancer. Accordingly, Rig-ifs/fs mice bearing a frameshift mutant Rig-i exhibit increased susceptibility to colitis-related colon cancer as well as enhanced inflammatory response to chemical, virus or bacteria. In addition to interruption of Rig-i mRNA translation, the Rig-i mutation changes the secondary structure of Rig-i pre-mRNA and impairs its association with DHX9, consequently inducing a circular RNA generation from Rig-i transcript, thereby, designated as circRIG-I. CircRIG-I is frequently upregulated in colon cancers and its upregulation predicts poor outcome of colon cancer. Mechanistically, circRIG-I interacts with DDX3X, which in turn stimulates MAVS/TRAF5/TBK1 signaling cascade, eventually activating IRF3-mediated type I IFN transcription and aggravating inflammatory damage. Reciprocally, all-trans retinoic acid acts as a DHX9 agonist, ameliorates immunopathology through suppression of circRIG-I biogenesis. Collectively, our results provide insight into mutant RIG-I action and propose a potential strategy for the treatment of colon cancer.

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