截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共23200篇，總影響因子106190.49分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻(xiàn)共54篇，合作單位覆蓋了清華、北大、復(fù)旦、華盛頓大學(xué)、麻省理工學(xué)院、東京大學(xué)以及紐約大學(xué)等國際知名研究機(jī)構(gòu)上百所。
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近期收錄2022年12月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共273篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1724.643，其中，10分以上文獻(xiàn)29篇（圖二）。
圖一
圖二
本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的6篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。
IMMUNITY [IF=43.474]
文獻(xiàn)引用抗體：
bs-6197R；Anti-TIM4 pAb
作者單位：美國德克薩斯大學(xué)西南醫(yī)學(xué)中心免疫學(xué)系
ADVANCED MATERIALS
[IF=32.086]
文獻(xiàn)引用抗體：
bs-0162R；Anti-iNOS pAb
作者單位：香港大學(xué)李嘉誠醫(yī)學(xué)院骨科及創(chuàng)傷科
摘要：Conferring catalytic defects in sonosensitizers is of paramount importance in reinforcing sonodynamic therapy. However, the formation of such 0D defects is governed by the Schottky defect principle. Herein, 2D catalytic planar defects are designed within Ti3C2 sheets to address this challenge. These specific planar slip dislocations with abundant Ti3+ species (Ti3C2-SD(Ti3+)) can yield surface-bound O due to the effective activation of O2, thus resulting in a substantial amount of1O2 generation and the 99.72% ± 0.03% bactericidal capability subject to ultrasound (US) stimulation. It is discovered that the 2D catalytic planar defects can intervene in electron transfer through the phonon drag effect—a coupling effect between surface electrons and US-triggered phonons—that simultaneously contributes to a dramatic decrease in O2 activation energy from 1.65 to 0.06 eV. This design has achieved a qualitative leap in which the US catalytic site has transformed from 0D to 2D. Moreover, it is revealed that the electron origin, electron transfer, and visible O2 activation pathway triggered by US can be attributed to the phonon–electron coupling effect. After coating with neutrophil membrane (NM) proteins, the NM-Ti3C2-SD(Ti3+) sheets further demonstrate a 6-log10 reduction in methicillin-resistant Staphylococcus aureus burden in the infected bony tissue.
ADVANCED MATERIALS
[IF=32.086]
文獻(xiàn)引用抗體：
bs-0812R; Anti-IL-1 Beta pAb
bsm-33207M; Anti-TNF alpha mAb
作者單位：溫州醫(yī)科大學(xué)眼科醫(yī)院眼科視光學(xué)院
This article is protected by copyright. All rights reserved
JOURNAL OF MEDICAL VIROLOGY
[IF=20.693]
文獻(xiàn)引用抗體：
bs-1264R; Anti-RSV G pAbbs-6670R; Anti-IGF2R/M6PR pAb
bs-0227R; Anti-IGF1R pAb
作者單位：中南大學(xué)湘雅醫(yī)學(xué)院醫(yī)學(xué)微生物學(xué)系
ACS Nano [IF=18.027]
文獻(xiàn)引用抗體：bs-4947R
Anti-IL-1 Alpha pAb
作者單位：湖南長沙中南大學(xué)湘雅醫(yī)院眼科中心
摘要：Glaucoma is the leading cause of irreversible blindness worldwide, characterized by progressive vision loss due to the selective damage to retinal ganglion cells (RGCs) and their axons. Oxidative stress is generally believed as one key factor of RGCs death. Recently, necroptosis was identified to play a key role in glaucomatous injury. Therefore, depletion of reactive oxygen species (ROS) and inhibition of necroptosis in RGCs has become one of treatment strategies for glaucoma. However, existing drugs without efficient drug enter into the retina and have controlled release due to a short drug retention. Herein, we designed a glaucomatous microenvironment-responsive drug carrier polymer, which is characterized by the presence of thioketal bonds and 1,4-dithiane unit in the main chain for depleting ROS as well as the pendant cholesterols for targeting cell membranes. This polymer was adopted to encapsulate an inhibitor of necroptosis, necrostatin-1, into nanoparticles (designated as NP1). NP1 with superior biosafety could scavenge ROS in RGCs both in vitro and in vivo of an acute pathological glaucomatous injury model. Further, NP1 was found to effectively inhibit the upregulation of the necroptosis pathway, reducing the death of RGCs. The findings in this study exemplified the use of nanomaterials as potential strategies to treat glaucoma.
ACS Nano [IF=18.027]
文獻(xiàn)引用抗體：
bs-0061R; Anti-beta-Actin (Loading Control) pAbbs-5913R; Anti-Calreticulin pAb
bs-0295G-HRP; Goat Anti-Rabbit IgG H&L / HRP作者單位：韓國成均館大學(xué)藥學(xué)院
摘要：As an emerging anticancer strategy, ferroptosis has recently been developed in combination with current therapeutic modalities to overcome the existing limitations of conventional therapies. Herein, an ultraviolet (UV) upconversion luminescence-fueled nanoreactor is explored to combine ferroptosis and apoptosis through the UV-catalyzed Fenton reaction of an iron supplement (ferric ammonium citrate) loaded in a mesoporous silica layer in addition to the support of a chemotherapeutic agent (cisplatin) attached on the functionalized silica surface for the treatment of triple negative breast cancer (TNBC). The nanoplatform can circumvent the low penetration depth typical of UV light by upconverting near-infrared irradiation and emitting UV photons that convert Fe3+ to Fe2+ to boost the generation of hydroxyl radicals (·OH), causing devastating lipid peroxidation. Apart from DNA damage-induced apoptosis, cisplatin can also catalyze Fenton-based therapy by its abundant production of hydrogen peroxide (H2O2). As a bioinspired lipid membrane, the folate receptor-targeted liposome as the coating layer offers high biocompatibility and colloidal stability for the upconversion nanoparticles, in addition to prevention of the premature release of encapsulated hydrophilic compounds, before driving the nanoformulation to the target tumor site. As a result, superior antitumor efficacy has been observed in a 4T1 tumor-bearing mouse model with negligible side effects, suggesting that such a nanoformulation could play a pivotal role in effective apoptosis-strengthened ferroptosis TNBC therapy.
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