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發表者：北京博奧森生物      發表時間：2023-1-12

截止目前，引用Bioss產品發表的文獻共23200篇，總影響因子106190.49分，發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共54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2022年12月引用Bioss產品發表的文獻共273篇（圖一，綠色柱），文章影響因子(IF) 總和高達1724.643，其中，10分以上文獻29篇（圖二）。

圖一

圖二

本文主要分享引用Bioss產品發表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的6篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。

IMMUNITY [IF=43.474]

文獻引用抗體：

bs-6197R；Anti-TIM4 pAb

作者單位：美國德克薩斯大學西南醫學中心免疫學系

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]

文獻引用抗體：

bs-0162R；Anti-iNOS pAb

作者單位：香港大學李嘉誠醫學院骨科及創傷科

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]

文獻引用抗體：

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

bsm-33207M; Anti-TNF alpha mAb

作者單位：溫州醫科大學眼科醫院眼科視光學院

摘要：Photodynamic therapy (PDT) is commonly used in choroidal neovascularization (CNV) treatment due to the superior light transmittance of the eye. However, PDT often leads to surrounding tissue damage and further microenvironmental deterioration, including exacerbated hypoxia, inflammation, and secondary neovascularization. Herein, Pt nanoparticles (NPs) and Au NPs decorated zeolitic imidazolate framework-8 (ZIF-8) nanoplatform is developed to load indocyanine green (ICG) for precise PDT and microenvironment amelioration, which can penetrate the internal limiting membrane through Müller cells endocytosis and target to CNV by surface grafted cyclo(Arg-Gly-Asp-d-Phe-Lys) after intravitreal injection. The excessive H₂O₂ in the CNV microenvironment is catalyzed by catalase-like Pt NPs for hypoxia relief and enhanced PDT occlusion of neovascular. Meanwhile, Au NPs show significant anti-inflammatory and anti-angiogenesis properties in regulating macrophages and blocking vascular endothelial growth factor (VEGF). Compared with verteporfin treatment, the mRNA expressions of hypoxia-inducible factor-1α and VEGF in the nanoplatform group are downregulated by 90.2% and 81.7%, respectively. Therefore, the nanoplatform realizes a comprehensive CNV treatment effect based on the high drug loading capacity and biosafety. The CNV treatment mode developed in this work provides a valuable reference for treating other diseases with similar physiological barriers that limit drug delivery and similar microenvironment.

This article is protected by copyright. All rights reserved

JOURNAL OF MEDICAL VIROLOGY

[IF=20.693]

文獻引用抗體：

bs-1264R; Anti-RSV G pAb

bs-6670R; Anti-IGF2R/M6PR pAb

bs-0227R; Anti-IGF1R pAb

作者單位：中南大學湘雅醫學院醫學微生物學系

摘要：Respiratory syncytial virus (RSV) is one of the main pathogens of viral pneumonia and bronchiolitis in infants and young children and life-threatening diseases among infants and young children. GTPases of the immune-associated protein family (GIMAP) are new family members of immune-associated GTPases. In recent years, much attention has been paid to the function of the GIMAP family in coping with infection and stress. Gimap5 is a member of the GIMAP family, which may be correlated with anti-infectious immunity. RT-qPCR, Western blot, and indirect immunofluorescence (IFA) were used to detect the expression of Gimap5, M6PR and IGF1R(the major RSV receptor). Transmission electron microscopy (TEM) was used to detect the degradation of RSV in Gimap5-overexpressed or -silent cell lines. Computer virtual screening was used to screen small molecule compounds targeting Gimap5 and the anti-RSV effects were explored through in vivo and in vitro experiments. GIMAP5 and M6PR were significantly downregulated after RSV infection. Gimap5 accelerated RSV degradation in lysosomes by interacting with M6PR, and further prevented RSV invasion by downregulating the expression of RSV surface receptor IGF1R. Three small molecule compounds targeting Gimap5 were confirmed to be the agonists of Gimap5. The three compounds effectively inhibited RSV infection and RSV-induced complications. Gimap5 promotes the degradation of RSV and its receptor through interacting with M6PR. Gimap5 agonists can effectively reduce RSV infection and RSV-induced complication in vivo and in vitro, which provides a new choice for the treatment of RSV.

ACS Nano [IF=18.027]

文獻引用抗體：bs-4947R

Anti-IL-1 Alpha pAb

作者單位：湖南長沙中南大學湘雅醫院眼科中心

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]

文獻引用抗體：

bs-0061R; Anti-beta-Actin (Loading Control) pAb

bs-5913R; Anti-Calreticulin pAb

bs-0295G-HRP; Goat Anti-Rabbit IgG H&L / HRP

作者單位：韓國成均館大學藥學院

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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