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截止目前，引用Bioss產品發表的文獻共35,336篇，總影響因子176,219.79分，發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共126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上百所國際研究機構。
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本文主要分享11篇IF＞16的文獻，它們引用了Bioss產品，分別發表在CELL、Nature Biomedical Engineering、Advanced Fiber Materials、Nature Metabolism、Bioactive Materials、Advanced Functional Materials、ACS Nano期刊上，讓我們一起學習吧。
CELL [IF=42.5]
文獻引用產品：
bs-0297P | Human IgG | IF
作者單位：首都醫科大學宣武醫院
摘要：Exercise has well-established health benefits, yet its molecular underpinnings remain incompletely understood. We conducted an integrated multi-omics analysis to compare the effects of acute vs. long-term exercise in healthy males. Acute exercise induced transient responses, whereas repeated exercise triggered adaptive changes, notably reducing cellular senescence and inflammation and enhancing betaine metabolism. Exercise-driven betaine enrichment, partly mediated by renal biosynthesis, exerts geroprotective effects and rescues age-related health decline in mice. Betaine binds to and inhibits TANK-binding kinase 1(TBK1), retarding the kinetics of aging. These findings systematically elucidate the molecular benefits of exercise and position betaine as an exercise mimetic for healthy aging.
Nature Biomedical
Engineering [IF=26.6]
文獻引用產品：
bs-20316R | QPRT/QAPRTase Rabbit pAb | IF, WB
bs-2713R | HAVCR1 Rabbit pAb | IF
bs-0189R | alpha smooth muscle Actin Rabbit pAb | IF, WB
bs-10423R | Collagen I Rabbit pAb | IF, WB
bsm-33033M | GAPDH Mouse mAb, Loading Control | WB
bs-0295G-HRP | Goat Anti-Rabbit IgG H&L, HRP conjugated | WB
bs-0296G-HRP | Goat Anti-Mouse IgG H&L, HRP conjugated | WB
作者單位：北京大學
Advanced Fiber
Materials [IF=21.3]
文獻引用產品：
bs-10802R | TNF alpha Rabbit pAb | IHC
作者單位：浙江大學
摘要：Traditional antibiotic-based therapies for treating infectious wounds often face challenges in balancing long-term biosafety, promoting wound healing, and effectivelyeradicating bacteria. Herein, we introduce an innovative "top-down" approach to fabricating one-dimensional(1D) pristine silk nanofibers(SNFs) by the gradual exfoliation of silk fibers, preserving their inherent semi-crystalline structure. These SNFs functioned as a robust template for the in situ growth of two-dimensional(2D) plum blossom-like bismuth nanosheets(BiNS), whose anisotropic morphology enhances bactericidal contact efficiency. The resulting BiNS-equipped SNFs(SNF@Bi) are assembled into membranes(SNFM@Bi) via vacuum filtration, showing superior biocompatibility, photothermal efficiency, and photodynamic activity. Furthermore, the acidic wound microenvironment or near-infrared(NIR) irradiation triggered the release of Bi3+, exhibiting nanoenzyme-mediated catalytic activity. This multimodal mechanism allows SNFM@Bi to eliminate over 99% of Staphylococcus aureus and 100% of Escherichia coli by disrupting biofilms, inducing lysis, and causing oxidative damage. In vivo evaluations demonstrated significant bacteria clearance, accelerated angiogenesis, and enhanced collagen deposition, contributing to rapid wound healing without systemic toxicity. Notably, SNFM@Bi detaches spontaneously after healing, avoiding chronic nanomaterial retention risks. This multifunctional antimicrobial platform offers a controllable, effective, and biocompatible therapeutic strategy for antimicrobial dressing design, with potential applications in biomedicine, environmental protection, and public health.
Nature Metabolism [IF=20.8]
文獻引用產品：
bs-6313R | 4 Hydroxynonenal Rabbit pAb | IHC
摘要：Increased reactive oxygen species(ROS) levels are a hallmark of inflammatory bowel disease(IBD) and constitute a major mechanism of epithelial cell death. Approaches to broadly inhibit ROS have had limited efficacy in treating IBD. Here we show that lipid peroxidation contributes to the pathophysiology of IBD by promoting ferroptosis, an iron-dependent form of programmed cell death. Mechanistically, we provide evidence of heterocellular crosstalk between intestinal fibroblasts and epithelial cells. In IBD tissues and mouse models of chronic colitis, acyl-CoA synthetase long-chain family 4(ACSL4) is overexpressed in fibroblasts. ACSL4 in fibroblasts reprograms lipid metabolism and mediates intestinal epithelial cell sensitivity to ferroptosis. In mouse models, overexpressing ACSL4 in fibroblasts results in increased intestinal epithelial ferroptosis and worsened colitis, while pharmacological inhibition or deletion of fibroblast ACSL4 ameliorates colitis. Our work provides a targeted approach to therapeutic antioxidant treatments for IBD.
Bioactive Materials [IF=20.3]
文獻引用產品：
bsm-33112M | CD41/ITGA2B Mouse mAb | WB
摘要：Chronic nephritis management remains challenging due to the compromised therapeutic efficacy and severe systemic complications of conventional glucocorticoid therapy. Here, we developed a bioinspired platelet-mediated delivery system(LN-DEX@PLT) that leverages platelet tropism toward injured glomeruli for precision drug delivery. This system integrates lipid nanoemulsion encapsulation with platelet-mediated hitchhiking delivery to achieve three key functionalities:(1) enhanced renal targeting demonstrated by 2.2-fold higher glomerular accumulation compared to free dexamethasone via In vivo imaging, (2) effective mitigation of glucocorticoid-induced metabolic toxicity evidenced by reduced fasting plasma glucose(5.2 ± 0.3 vs 8.3 ± 0.7 mmol/L in free DEX), suppression of hepatic gluconeogenic enzymes(PEPCK expression decreased by 43 %, G-6 Pase by 51 %, both p < 0.001), and suppressed body weight (?23.1 % versus free DEX group), and(3) dual-pathway therapeutic effects through IL-6/TNF-α suppression and p53-p21Cip1-mediated senescence delay. In Adriamycin-based chronic nephritis models, LN-DEX@PLT demonstrated superior renal protection with 81 % reduction in proteinuria (vs 33 % for free DEX). In LPS-induced and Adriamycin-based chronic nephritis models, LN-DEX@PLT demonstrated suppression of renal inflammation markers(IL-6 expression decreased to 68 %, TNF-α to 51 %) and macrophage infiltration (F4/80+ cells decreased 5.3-fold). This platelet-biohybrid system provides a clinically translatable paradigm for precision glucocorticoid therapy with reduced dosing frequency.
Bioactive Materials [IF=20.3]
文獻引用產品：
bs-10900R | GAPDH Rabbit pAb, Loading Control | WB
作者單位：中山大學
摘要：The ligamentization process of the tendon graft in anterior cruciate ligament(ACL) reconstruction is crucial for graft healing quality, thereby affecting knee joint function. Excessive scar tissue, caused by activation of trans-differentiation of fibroblasts to myofibroblasts, rather than orientated collagen fibers with normal composition and structure in the graft mid-substance seriously impacts ligamentization. The elucidation of the underlying mechanism behind the graft fibrosis may facilitate modulation of tendon graft ligamentization. Here, we show that transforming growth factor beta 1(TGF-β1) was significantly upregulated with ligamentization process, contributing to fibroblast to myofibroblast trans-differentiation and thereby leading to impaired collagen orientation with overproduction of collagen type III. Of note, we verified that prostaglandin E2(PGE2), a principal mediator of inflammation secreted by macrophages, significantly reversed TGF-β1-induced trans-differentiation of fibroblasts to myofibroblasts. Importantly, magnesium(Mg) ions were found to upregulate PGE2 production in macrophages, ultimately favoring inhibition of scar tissue formation and promoting expression of ligament-like phenotype in the graft mid-substance in rats. Consistently, the rats, with injection of the sodium alginate containing Mg ions into knee joint cavity, exhibited significantly improved gait performance and failure load relative to the control group. These results demonstrate the feasibility of using Mg ions to modulate tendon ligamentization in patients after ACL reconstruction.
Advanced Functional
Materials [IF=19]
文獻引用產品：
bsm-60761R | CD206 Recombinant Rabbit mAb | IF
作者單位：同濟大學
摘要：Optimal healing of diabetic chronic wound requires a well-organized cascade integration of bacterial death, cell migration and proliferation, and extracellular remodeling. However, such biological progress is usually impaired in chronic diabetic wound and traditional antibacterial hydrogels unmatched for ordered repair needs. Herein, an iron-coordinated glycopeptide hydrogel(Fe-GP gel) that could effectively treat MRSA-infected chronic diabetic wounds within 11 days by reprogramming healing process is developed. This Fe-GP hydrogel is formed based on glucomannan-decorated peptide nanofibers framework and then loaded with tannic acid/Fe nanocomplexes. The burst release of nanocomplexes is achieved to conduct the first healing stage, which could induce the ferroptosis-like death of methicillin-resistant Staphylococcus aureus (MRSA) for eliminating over 98% of MRSA bacteria by metabolism disrupting within 6 h. In the second healing stage, sustained release of glucomannan promotes M2 macrophage polarization(five times higher than control group) through extracellular signal-regulated kinase and signal transducer and activator of transcription 6(ERK/STAT6) pathway within 2 days. After the elimination of MRSA and restoration of immune microenvironment, the remaining 3D peptide nanofibers framework is able to facilitate extracellular remodeling through anchoring fibroblast cells as the third healing stage within weeks. Overall, this glycopeptide hydrogel has demonstrated a promising approach to realize the orderly progression during healing process for enhanced treatment of drug-resistant bacteria-infected chronic wounds.
Advanced Functional
Materials [IF=19]
文獻引用產品：
bs-0061R | beta-Actin Rabbit pAb, Loading Control | WB
作者單位：AIR FORCE MEDICAL CENTER, PLA
摘要：Monoclonal antibodies demonstrate significant potential in the clinical management of Human Epidermal Growth Factor Receptor 2/Estrogen Receptor-positive(HER2/ER+) breast cancer. However, the therapeutic outcomes of antitumor drugs are significantly hampered by challenges such as inter-pathway crosstalk, the restricted efficacy of single-pathway mechanisms, and suboptimal drug targeting. Herein, this study developed a Zr/Fe bimetallic MOF loaded with Cyclin-dependent kinases 4 and 6(CDK4/6) inhibitor ribociclib and surface-functionalized with trastuzumab (Herceptin). Under the acidic tumor microenvironment(TME), this nanomaterial degrades, releasing trastuzumab, ribociclib, and Fe3+. Trastuzumab enhances tumor targeting, reduces normal tissue toxicity, and inhibits Cyclin D1-CDK4/6 activation to decrease retinoblastoma(RB) phosphorylation, while ribociclib suppresses CDK4/6 enzymatic activity, synergistically blocking RB phosphorylation, inducing G1-phase arrest, and halting tumor proliferation. Additionally, Fe3+ catalyzes the conversion of H2O2 into highly cytotoxic hydroxyl radicals (·OH) through the Fenton reaction, leading to oxidative stress-induced cellular damage. Together, these three components synergistically inhibit the proliferation of HER2/ER+ breast cancer cells by disrupting cell cycle progression and cellular homeostasis. In vivo studies demonstrated that Zr-Fe MOF@Ribociclib@Herceptin(ZFRH) not only significantly inhibits the growth of orthotopic tumors but also effectively suppresses the formation of lung-metastatic tumors. These findings suggest a promising strategy for the precision-targeted therapy of HER2/ER+ breast cancer.
ACS Nano [IF=16]
文獻引用產品：
作者單位：中國科學院武漢病毒研究
ACS Nano [IF=16]
D-9110 | DiD perchlorate | Other
作者單位：重慶醫科大學
ACS Nano [IF=16]
文獻引用產品：
作者單位：東南大學
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