截止目前，引用Bioss產(chǎn)品發(fā)表的文獻共30160篇，總影響因子147590.23分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共76篇，合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等國際知名研究機構(gòu)上百所。
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圖一
圖二
本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Nature, Immunity, Cancer Cell等期刊的10篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。
Nature [IF=64.8]
bs-6982R | Neutrophil Elastase Rabbit pAb | IF
作者單位：麻省理工大學
摘要：Implanted biomaterials and devices face compromised functionality and efficacy in the long term owing to foreign body reactions and subsequent formation of fibrous capsules at the implant–tissue interfaces1,2,3,4. Here we demonstrate that an adhesive implant–tissue interface can mitigate fibrous capsule formation in diverse animal models, including rats, mice, humanized mice and pigs, by reducing the level of infiltration of inflammatory cells into the adhesive implant–tissue interface compared to the non-adhesive implant–tissue interface. Histological analysis shows that the adhesive implant–tissue interface does not form observable fibrous capsules on diverse organs, including the abdominal wall, colon, stomach, lung and heart, over 12 weeks in vivo. In vitro protein adsorption, multiplex Luminex assays, quantitative PCR, immunofluorescence analysis and RNA sequencing are additionally carried out to validate the hypothesis. We further demonstrate long-term bidirectional electrical communication enabled by implantable electrodes with an adhesive interface over 12 weeks in a rat model in vivo. These findings may offer a promising strategy for long-term anti-fibrotic implant–tissue interfaces.
Cancer Cell [IF=50.3]
bs-24627R | MYCL Rabbit pAb | WB
作者單位：中國醫(yī)學科學院腫瘤醫(yī)院
摘要：Neuroendocrine carcinomas (NECs) are extremely lethal malignancies that can arise at almost any anatomic site. Characterization of NECs is hindered by their rarity and significant inter- and intra-tissue heterogeneity. Herein, through an integrative analysis of over 1,000 NECs originating from 31 various tissues, we reveal their tissue-independent convergence and further unveil molecular divergence driven by distinct transcriptional regulators. Pan-tissue NECs are therefore categorized into five intrinsic subtypes defined by ASCL1, NEUROD1, HNF4A, POU2F3, and YAP1. A comprehensive portrait of these subtypes is depicted, highlighting subtype-specific transcriptional programs, genomic alterations, evolution trajectories, therapeutic vulnerabilities, and clinicopathological presentations. Notably, the newly discovered HNF4A-dominated subtype-H exhibits a gastrointestinal-like signature, wild-type RB1, unique neuroendocrine differentiation, poor chemotherapeutic response, and prevalent large-cell morphology. The proposal of uniform classification paradigm illuminates transcriptional basis of NEC heterogeneity and bridges the gap across different lineages and cytomorphological variants, in which context-dependent prevalence of subtypes underlies their phenotypic disparities.
Immunity [IF=32.4]
bs-5355R | phospho-GFAP (Ser8) Rabbit pAb | WB
作者單位：廣東省人民醫(yī)院
摘要：Recent evidence reveals hyper T follicular helper (Tfh) cell responses in systemic lupus erythematosus (SLE); however, molecular mechanisms responsible for hyper Tfh cell responses and whether they cause SLE are unclear. We found that SLE patients downregulated both ubiquitin ligases, casitas B-lineage lymphoma (CBL) and CBLB (CBLs), in CD4+ T cells. T cell-specific CBLs-deficient mice developed hyper Tfh cell responses and SLE, whereas blockade of Tfh cell development in the mutant mice was sufficient to prevent SLE. ICOS was upregulated in SLE Tfh cells, whose signaling increased BCL6 by attenuating BCL6 degradation via chaperone-mediated autophagy (CMA). Conversely, CBLs restrained BCL6 expression by ubiquitinating ICOS. Blockade of BCL6 degradation was sufficient to enhance Tfh cell responses. Thus, the compromised expression of CBLs is a prevalent risk trait shared by SLE patients and causative to hyper Tfh cell responses and SLE. The ICOS-CBLs axis may be a target to treat SLE.
Nature Neuroscience [IF=25.0]
文獻引用產(chǎn)品：
bs-6316R | PTGER1 Rabbit pAb | IF
作者單位：蘇黎世大學
摘要：Oligodendrocyte-lineage cells, including NG2 glia, undergo prominent changes in various neurodegenerative disorders. Here, we identify a neuroprotective role for NG2 glia against prion toxicity. NG2 glia were activated after prion infection in cerebellar organotypic cultured slices (COCS) and in brains of prion-inoculated mice. In both model systems, depletion of NG2 glia exacerbated prion-induced neurodegeneration and accelerated prion pathology. Loss of NG2 glia enhanced the biosynthesis of prostaglandin E2 (PGE2) by microglia, which augmented prion neurotoxicity through binding to the EP4 receptor. Pharmacological or genetic inhibition of PGE2 biosynthesis attenuated prion-induced neurodegeneration in COCS and mice, reduced the enhanced neurodegeneration in NG2-glia-depleted COCS after prion infection, and dampened the acceleration of prion disease in NG2-glia-depleted mice. These data unveil a non-cell-autonomous interaction between NG2 glia and microglia in prion disease and suggest that PGE2 signaling may represent an actionable target against prion diseases.
Materials Today [IF=24.2]
文獻引用產(chǎn)品：
bs-10423R | Collagen I Rabbit pAb | IF
作者單位：中國藥科大學
摘要：Despite great success of chimeric antigen receptor T (CAR-T) cells in hematological cancers, the efficacy in solid tumors is extremely restricted. Transforming growth factor-β (TGF-β) and hypoxia are key processes in the development of solid tumors, including the formation of neo-vasculature, dense extracellular matrix (ECM), and immunosuppression. TGF-β inhibition and hypoxia alleviation may be promising approaches to enhance activity of CAR-T cells in solid tumors. Therefore, a self-reinforcing nano-spearhead (BM/LPsiTGF-β NPs) is developed to collaboratively remodel tumor microenvironment (TME) through albumin-mediated tumor targeted delivery of TGF-β siRNA and the nano enzyme MnO2. BM/LPsiTGF-β NPs efficiently eliminates ECM by down-regulation of TGF-β. Additionally, BM/LPsiTGF-β NPs also produces abundant O2 and down-regulates HIF-α, leading to normalized vasculature and improved tumor immunosuppression. More importantly, the ECM degradation induced by BM/LPsiTGF-β NPs forms a self-reinforcing loop, further promoting greater tumor penetration of BM/LPsiTGF-β NPs and CAR-T cells. Due to robust TME remodeling capacity of BM/LPsiTGF-β NPs, the therapeutic efficacy of Mesothelin (MSLN) CAR-T cells against triple negative breast cancer (TNBC) are enhanced both in vitro and in vivo. This nano-spearhead provides a good regimen for potent TME remodeling and gives rise to enhanced CAR-T cell efficacy in TNBC treatment.
ADVANCED FUNCTIONAL MATERIALS [IF=19.0]
文獻引用產(chǎn)品：
bs-23679R | FGF21 Rabbit pAb | IHC
作者單位：江蘇大學
摘要：Efforts to develop advanced bone substitutes for effective bone regeneration in substantial defects have led to the fabrication of tissue-engineered scaffolds. These scaffolds, featuring hierarchical structures, specific chemical compositions, and functional qualities, are essential in mimicking native bone tissue. Inspired by the biomineralization process, hydrothermal treatment is used to synthesize micro-/nano-hydroxyapatite bioceramics functionalized with tea polyphenols (TP-nwHA), closely resembling the structure of bone-like apatite induced by hydroxyapatite bioceramics in vivo. The in vitro results demonstrate TP-nwHA's superior biocompatibility, enhancing cell proliferation and adhesion. Furthermore, TP-nwHA scaffolds significantly influence mesenchymal stem cells, promoting osteogenic differentiation while inhibiting osteoclastogenic differentiation. The upregulation of osteogenic proteins BMP2 and ITGB1, along with the downregulation of osteoclastic proteins FGF21 and IGFBP1, demonstrate the synergistic effect of the biomimetic structure and polyphenols on the activation of the MAPK signaling pathway. In vivo, TP-nwHA showe early angiogenic capabilities, leading to improved bone regeneration in critical-size femoral bone defects in osteoporotic rats. Histological staining confirms the complete bridging of defects with new bone tissue in the TP-nwHA group, and nanoindentation tests indicate the formation of mature mineralized bone tissue. Collectively, these findings suggest a novel strategy for fabricating bone-mimicking constructs with potential applications in disease modeling.
ADVANCED FUNCTIONAL MATERIALS [IF=19.0]
文獻引用產(chǎn)品：
bs-20403R | CD68 Rabbit pAb | IF
bs-20601R | iNos/Nos-2 Rabbit pAb | IF
ADVANCED FUNCTIONAL MATERIALS [IF=19.0]
文獻引用產(chǎn)品：
bs-0295G | Goat Anti-Rabbit IgG H&L | WB
作者單位：成均館大學
摘要：Chemodynamic therapy (CDT) has emerged as a novel approach to overcome cancer resistance and enhance anticancer efficacy. Despite the considerable effort devoted to current chemodynamic therapeutic agents, developing efficient delivery systems to induce ferroptosis remains demanding due to their limited efficacy and lack of selectivity. Herein, an iron-based single-atom upconversion photocatalyst (UmFe-OA@hPM) mimicking natural horseradish peroxidases has been developed. This nanoformulation not only targets tumors via the existence of a hybrid platelet membrane (hPM) coating but also generates excessive hydroxyl radicals in response to both tumor microenvironment and external laser irradiation. This nanoenzyme overcomes the low tissue penetration of UV light, which sensitizes the iron-doped graphitic carbon nitride network, attributed to the unique anti-Stokes shift from infrared to UV displayed by upconversion nanoparticles. Together with an increase in intracellular polyunsaturated fatty acid accumulation induced by oleanolic acid (OA), lipid peroxidation is significantly elevated, leading to the enhancement of CDT. UmFe-OA@hPM is demonstrated to induce significant ferroptosis in vitro, superior antitumor efficacy in breast cancer mouse models, and suppression of metastasis status when incorporated with an immune checkpoint blockade. These findings provide a potential strategy for developing a precisely controlled CDT to deal with aggressive cancers, especially in combination with immunotherapy.
Nano Today [IF=17.4]
BA00207 | Annexin V PE/7-AAD Apoptosis assay Kit
BA00204 | Cell Cycle Analysis Kit
作者單位：北京大學
摘要：KRAS gene is mutated in 40% of colorectal cancers (CRC), which induces malignant proliferation by regulating cellular nutrient metabolism and biosynthesis. It has been found that malignant proliferation of KRAS-mutant colorectal cancer relies on the upregulation of SLC25A22 protein expression, suggesting that inhibition the expression of both KRAS and SLC25A22 is a potential CRC therapeutics. Stably knocking down the oncogenic KRAS-G12V gene can achieve long-term gene therapy effects, while transient downregulation of SLC25A22, a normal functional gene most of the time, is preferred to kill tumor cells and minimize the side impact on normal cells. Here, two lipid nanoparticles (LNP) were designed to encapsulate KRAS-G12V CRISPR/Cas9 gene editing plasmids (pKRAS-LNPs) and SLC25A22 siRNA (siSLC-LNPs), respectively. Therapeutic effects of both nanoparticles alone and in combination on KRAS-G12V mutant colorectal cancer cells in vitro were first examined. The result showed that delivery of pKRAS-LNPs or siSLC-LNPs alone could effectively achieve KRAS-G12V gene editing or SLC25A22 gene silencing and inhibit tumor cell proliferation, while co-delivery of both LNPs could achieve stronger inhibition of tumor cell proliferation by inducing stronger apoptosis. Furthermore, we found that co-delivery of pKRAS-LNPs and siSLC-LNPs induced stronger apoptosis and cell proliferation inhibition compared to pKRAS&siSLC-LNPs that were constructed by pre-mixing pKRAS and siSLC and then encapsulating them. Finally, we validated that co-delivery of pKRAS-LNPs and siSLC-LNPs can achieve KRAS-G12V colorectal cancer treatment in vivo with a tumor inhibition rate of 61.15%. In summary, the delivery vectors constructed for nucleic acids targeting KRAS and SLC25A22 achieved therapeutic targeting of KRAS-G12V colorectal cancer in vitro and in vivo.
Nano Today [IF=17.4]
文獻引用產(chǎn)品：
bs-20689R-FITC | CD11c Rabbit pAb, FITC conjugated | FCM
bsm-41815M-PE | CD80 Mouse mAb, PE conjugated | FCM
bsm-30162A-APC | Mouse CD86 Rat mAb, APC conjugated | FCM
bs-4790R-APC | CD8 Rabbit pAb, APC conjugated | FCM
bsm-30149A-FITC | Mouse CD3 Rat mAb, FITC conjugated | FCM
bsm-30152A-APC | Mouse CD4 Rat mAb, APC conjugated | FCM
bs-0647R-FITC | CD4 Rabbit pAb, FITC conjugated | FCM
bs-10211R-PE | FOXP3 Rabbit pAb, PE conjugated | FCM
作者單位：沈陽藥科大學
摘要：Cancer immunotherapy emerges as a promising therapeutic modality, while its clinical application remains constrained by low tumor immunogenicity and immunosuppressive microenvironments. Herein, we report a unique superdimeric nanoassembly pattern by elaborately integrating cyclodextrin inclusion with dimeric prodrug, enabling spatio-temporally self-adaptive drug delivery and multimodal photo-immunotherapy. Specifically, it is precisely engineered through host-guest inclusion between a GSH-sensitive cyclodextrin-photosensitizer conjugate and an oxidation-responsive homodimer prodrug of NLG919. Notably, on-demand photosensitizer activation and aggregation-caused quenching relief significantly facilitates photodynamic induction of ICD. Meanwhile, photodynamic ROS together with the endogenous ROS collaboratively facilitate on-demand NLG919 activation and release, efficiently reversing the immunosuppressive microenvironments. As such, the superdimeric nanoassembly allows spatio-temporally cascade-potentiated photo-immunotherapy, starting from photosensitizer activation to ICD induction, NLG919 release and IDO inhibition. Finally, it exerts intense antitumor efficacy, abscopal effect and synergy with PD-L1 antibody in two mouse models. This study presents new insights into the design of nanomedicines for multimodal photo-immunotherapy.
