截止目前，引用Bioss產品發表的文獻共28637篇，總影響因子137867.7分，發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共67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上百所。
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近期收錄2024年1月引用Bioss產品發表的文獻共317篇（圖一，綠色柱），文章影響因子(IF) 總和高達2010.8，其中，10分以上文獻35篇（圖二）。
圖一
圖二
本文主要分享引用Bioss產品發表文章至Nature, Immunity, Cancer Cell等期刊的5篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。
ACS Nano [IF=17.1]
文獻引用產品：
bs-1035R; CD86 Rabbit pAb | IF
bs-2527R; CD163 Rabbit pAb | IF
作者單位：第三軍醫大學
摘要： The administration of drugs resident to counteract fluid washout has received considerable attention. However, the fabrication of a biocompatible system with adequate adhesion and tissue penetration capability remains challenging. This study presents a cell membrane-inspired carrier at the subcellular scale that facilitates interfacial adhesion and tissue penetration to improve drug delivery efficiency. Both chitosan oligosaccharide (COS) and oleic acid (OA) modified membranes exhibit a high affinity for interacting with the negatively charged glycosaminoglycan layer, demonstrating that the zeta potential of the carrier is the key to determining spontaneous penetration and accumulation within the bladder tissue. In vivo modeling has shown that a high surface charge significantly improves the retention of the drug carrier in the presence of urine washout. Possibly due to charge distribution, electric field gradients, and lipid membrane softening, the high positive surface charge enabled the carriers to penetrate the urinary bladder barrier and/or enter the cell interior. Overall, this study represents a practical and effective delivery strategy for tissue binders.
Nature Communications [IF=16.6]
文獻引用抗體：bs-1035R
CD86 Rabbit pAb | IF
作者單位：四川大學
摘要：Drug-eluting stent implantation suppresses the excessive proliferation of smooth muscle cells to reduce in-stent restenosis. However, the efficacy of drug-eluting stents remains limited due to delayed reendothelialization, impaired intimal remodeling, and potentially increased late restenosis. Here, we show that a drug-free coating formulation functionalized with tailored recombinant humanized type III collagen exerts one-produces-multi effects in response to injured tissue following stent implantation. We demonstrate that the one-produces-multi coating possesses anticoagulation, anti-inflammatory, and intimal hyperplasia suppression properties. We perform transcriptome analysis to indicate that the drug-free coating favors the endothelialization process and induces the conversion of smooth muscle cells to a contractile phenotype. We find that compared to drug-eluting stents, our drug-free stent reduces in-stent restenosis in rabbit and porcine models and improves vascular neointimal healing in a rabbit model. Collectively, the one-produces-multi drug-free system represents a promising strategy for the next-generation of stents.
Nature Communications [IF=16.6]
文獻引用抗體：bs-3337R
Phospho-PKR (Thr446 + Thr451) Rabbit pAb | FC
作者單位：俄亥俄州立大學
摘要：Adipose stem cells (ASCs) have attracted considerable attention as potential therapeutic agents due to their ability to promote tissue regeneration. However, their limited tissue repair capability has posed a challenge in achieving optimal therapeutic outcomes. Herein, we conceive a series of lipid nanoparticles to reprogram ASCs with durable protein secretion capacity for enhanced tissue engineering and regeneration. In vitro studies identify that the isomannide-derived lipid nanoparticles (DIM1T LNP) efficiently deliver RNAs to ASCs. Co-delivery of self-amplifying RNA (saRNA) and E3 mRNA complex (the combination of saRNA and E3 mRNA is named SEC) using DIM1T LNP modulates host immune responses against saRNAs and facilitates the durable production of proteins of interest in ASCs. The DIM1T LNP-SEC engineered ASCs (DS-ASCs) prolong expression of hepatocyte growth factor (HGF) and C-X-C motif chemokine ligand 12 (CXCL12), which show superior wound healing efficacy over their wild-type and DIM1T LNP-mRNA counterparts in the diabetic cutaneous wound model. Overall, this work suggests LNPs as an effective platform to engineer ASCs with enhanced protein generation ability, expediting the development of ASCs-based cell therapies.
Nature Communications [IF=16.6]
文獻引用產品：bs-0335R
Rabbit Anti-Monkey IgG H&L
作者單位：中國科學院腦科學與智能技術卓越創新中心
摘要：Somatic cell nuclear transfer (SCNT) successfully clones cynomolgus monkeys, but the efficiency remains low due to a limited understanding of the reprogramming mechanism. Notably, no rhesus monkey has been cloned through SCNT so far. Our study conducts a comparative analysis of multi-omics datasets, comparing embryos resulting from intracytoplasmic sperm injection (ICSI) with those from SCNT. Our findings reveal a widespread decrease in DNA methylation and the loss of imprinting in maternally imprinted genes within SCNT monkey blastocysts. This loss of imprinting persists in SCNT embryos cultured in-vitro until E17 and in full-term SCNT placentas. Additionally, histological examination of SCNT placentas shows noticeable hyperplasia and calcification. To address these defects, we develop a trophoblast replacement method, ultimately leading to the successful cloning of a healthy male rhesus monkey. These discoveries provide valuable insights into the reprogramming mechanism of monkey SCNT and introduce a promising strategy for primate cloning.
BRAIN BEHAVIOR AND IMMUNITY [IF=15.1]
文獻引用產品：bs-2527R-AF680
CD163/AF680 Rabbit pAb | FC
作者單位：杜蘭大學醫學院
摘要：Risk factors contributing to dementia are multifactorial. Accumulating evidence suggests a role for pathogens as risk factors, but data is largely correlative with few causal relationships. Here, we demonstrate that intermittent murine cytomegalovirus (MCMV) infection of mice, alters blood brain barrier (BBB) permeability and metabolic pathways. Increased basal mitochondrial function is observed in brain microvessels cells (BMV) exposed to intermittent MCMV infection and is accompanied by elevated levels of superoxide. Further, mice score lower in cognitive assays compared to age-matched controls who were never administered MCMV. Our data show that repeated systemic infection with MCMV, increases markers of neuroinflammation, alters mitochondrial function, increases markers of oxidative stress and impacts cognition. Together, this suggests that viral burden may be a risk factor for dementia. These observations provide possible mechanistic insights through which pathogens may contribute to the progression or exacerbation of dementia.
