截止目前，引用Bioss產品發(fā)表的文獻共23452篇，總影響因子107756.664分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共55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2023年1月引用Bioss產品發(fā)表的文獻共295篇（圖一，綠色柱），文章影響因子(IF) 總和高達2000.977，其中，10分以上文獻37篇（圖二）。
圖一
圖二
本文主要分享引用Bioss產品發(fā)表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的5篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。
NATURE [IF=69.504]
Anti-Aquaporin 4 /PE pAb | FCM
作者單位：美國馬薩諸塞州波士頓哈佛大學醫(yī)學院布里格姆婦女醫(yī)院安·羅姆尼神經疾病中心
ADVANCED MATERIALS [IF=32.086]
文獻引用抗體：
bs-1563R; Anti-E.coli O157:H7 pAb
bs-2033R; Anti-E.coli DH-5 Alpha pAb
作者單位：CAS化學研究院分子科學研究所綠色印刷卓越研究教育中心重點實驗室
摘要：Fast and accurate detection of microbial cells in clinical samples is highly valuable but remains a challenge. Here, a simple, culture-free diagnostic system is developed for direct detection of pathogenic bacteria in water, urine and serum samples using an optical colorimetric biosensor. It consists of printed nanoarrays chemically conjugated with specific antibodies that exhibits distinct color changes after capturing target pathogens. By utilizing the internal capillarity inside an evaporating droplet, target preconcentration is achieved within a few minutes to enable rapid identification and more efficient detection of bacterial pathogens. More importantly, the scattering signals of bacteria can be significantly amplified by the nanoarrays due to strong near-field localization, which supports a visualizable analysis of the growth, reproduction and cell activity of bacteria at the single-cell level. Finally, in addition to high selectivity, this nanoarray-based biosensor is also capable of accurate quantification and continuous monitoring of bacterial load on food over a broad linear range, with a detection limit of 10 CFU mL?1. This work provides an accessible and user-friendly tool for point-of-care testing of pathogens in many clinical and environmental applications, and possibly enables a breakthrough in early prevention and treatment.
NATURE IMMUNOLOGY [IF=31.25]
文獻引用抗體：bs-6480R
Anti-CH25H pAb | WB作者單位：美國馬薩諸塞州伍斯特市馬薩諸塞大學陳醫(yī)學院病理科
NATURE CELL BIOLOGY [IF=28.213]
作者單位：中國廣州中山大學中山醫(yī)學院中山紀念醫(yī)院RNA生物醫(yī)學研究所
摘要：T?cell acute lymphoblastic leukaemia (T-ALL) is an aggressive malignancy with poor prognosis, but a decisive marker and effective treatment for leukaemia stem cells (LSCs) remain unclear. Here, using lineage tracing, limiting dilution assays and in vivo live imaging approaches, we identify rare inhibitory receptor programmed cell death?1 (PD-1)-expressing cells that reside at the apex of leukaemia hierarchy for initiation and relapse in T-ALL. Ablation of PD-1-expressing cells, deletion of PD-1 in T-ALL cells or blockade of PD-1 or PD-1 ligand?1 significantly eradicated LSCs and suppressed disease progression. Combination therapy using PD-1 blockade and chemotherapy substantially extended the survival of mice engrafted with mouse or human T-ALL cells. Mechanistically, PD-1+ LSCs had high NOTCH1–MYC activity for disease initiation. Furthermore, PD-1 signalling maintained quiescence and protected LSCs against T?cell receptor-signal-induced apoptosis. Overall, our data highlight the hierarchy of leukaemia by identifying PD-1+ LSCs and provide a therapeutic approach for the elimination of LSCs through PD-1 blockade in T-ALL.
BRAIN BEHAVIOR AND IMMUNITY [IF=19.227]
文獻引用抗體：
bs-2455R;Anti-CLEC7A pAb | WB
bs-3393R;Anti-Phospho-SIRT1 (Ser47) pAb | WB
作者單位：西班牙巴塞羅那大學神經科學研究所醫(yī)學院生物醫(yī)學系
摘要：In the last two decades, microglia have emerged as key contributors to disease progression in many neurological disorders, not only by exerting their classical immunological functions but also as extremely dynamic cells with the ability to modulate synaptic and neural activity. This dynamic behavior, together with their heterogeneous roles and response to diverse perturbations in the brain parenchyma has raised the idea that microglia activation is more diverse than anticipated and that understanding the molecular mechanisms underlying microglial states is essential to unravel their role in health and disease from development to aging. The Ikzf1 (a.k.a. Ikaros) gene plays crucial roles in modulating the function and maturation of circulating monocytes and lymphocytes, but whether it regulates microglial functions and states is unknown. Using genetic tools, here we describe that Ikzf1 is specifically expressed in the adult microglia in brain regions such as cortex and hippocampus. By characterizing the Ikzf1 deficient mice, we observed that these mice displayed spatial learning deficits, impaired hippocampal CA3-CA1 long-term potentiation, and decreased spine density in pyramidal neurons of the CA1, which correlates with an increased expression of synaptic markers within microglia. Additionally, these Ikzf1 deficient microglia exhibited a severe abnormal morphology in the hippocampus, which is accompanied by astrogliosis, an aberrant composition of the inflammasome, and an altered expression of disease-associated microglia molecules. Interestingly, the lack of Ikzf1 induced changes on histone 3 acetylation and methylation levels in the hippocampus. Since the lack of Ikzf1 in mice appears to induce the internalization of synaptic markers within microglia, and severe gliosis we then analyzed hippocampal Ikzf1 levels in several models of neurological disorders. Ikzf1 levels were increased in the hippocampus of these neurological models, as well as in postmortem hippocampal samples from Alzheimer’s disease patients. Finally, over-expressing Ikzf1 in cultured microglia made these cells hyporeactive upon treatment with lipopolysaccharide, and less phagocytic compared to control microglia. Altogether, these results suggest that altered Ikzf1 levels in the adult hippocampus are sufficient to induce synaptic plasticity and memory deficits via altering microglial state and function.
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