【12月文献战报】Bioss抗体新增高分文献精彩呈现-商家动态-资讯-生物在线

【12月文献战报】Bioss抗体新增高分文献精彩呈现

作者:北京博奥森生物技术有限公司 2023-01-12T09:25 (访问量:3293)


截止目前,引用Bioss产品发表的文献共23200篇总影响因子106190.49分,发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共54篇,合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等国际知名研究机构上百所。

我们每月收集引用Bioss产品发表的文献。若您在当月已发表SCI文章,但未被我公司收集,请致电Bioss,我们将赠予现金鼓励,金额标准请参考“发文章 领奖金”活动页面。

近期收录2022年12月引用Bioss产品发表的文献共273篇(图一,绿色柱),文章影响因子(IF) 总和高达1724.643,其中,10分以上文献29篇(图二)。

图一

图二



本文主要分享引用Bioss产品发表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的6IF>15 的文献摘要让我们一起欣赏吧。


IMMUNITY [IF=43.474]



文献引用抗体:bs-6197R

Anti-TIM4 pAb

作者单位:美国德克萨斯大学西南医学中心免疫学系

摘要:Obesity-induced chronic liver inflammation is a hallmark of nonalcoholic steatohepatitis (NASH)—an aggressive form of nonalcoholic fatty liver disease. However, it remains unclear how such a low-grade, yet persistent, inflammation is sustained in the liver. Here, we show that the macrophage phagocytic receptor TREM2, induced by hepatocyte-derived sphingosine-1-phosphate, was required for efferocytosis of lipid-laden apoptotic hepatocytes and thereby maintained liver immune homeostasis. However, prolonged hypernutrition led to the production of proinflammatory cytokines TNF and IL-1β in the liver to induce TREM2 shedding through ADAM17-dependent proteolytic cleavage. Loss of TREM2 resulted in aberrant accumulation of dying hepatocytes, thereby further augmenting proinflammatory cytokine production. This ultimately precipitated a vicious cycle that licensed chronic inflammation to drive simple steatosis transition to NASH. Therefore, impaired macrophage efferocytosis is a previously unrecognized key pathogenic event that enables chronic liver inflammation in obesity. Blocking TREM2 cleavage to restore efferocytosis may represent an effective strategy to treat NASH.

ADVANCED MATERIALS

[IF=32.086]


文献引用抗体:bs-0162R

Anti-iNOS pAb
作者单位:香港大学李嘉诚医学院骨科及创伤科

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]


文献引用抗体:

bs-0812R; Anti-IL-1 Beta pAb

bsm-33207M; Anti-TNF alpha mAb
作者单位:温州医科大学眼科医院眼科视光学院
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