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當前位置：首頁  >  新聞資訊  >  【9月文獻戰(zhàn)報】Bioss抗體新增高分文獻精彩呈現(xiàn)

【9月文獻戰(zhàn)報】Bioss抗體新增高分文獻精彩呈現(xiàn)

更新時間：2022-11-10  |  點擊率：877

 


截至目前，引用Bioss產(chǎn)品發(fā)表的文獻共20640篇，總影響因子93542.19分，發(fā)表在Nature, Science, Cell以及Immunity等期刊的文獻共53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研究機構上百所。

我們每月收集引用Bioss產(chǎn)品發(fā)表的文獻。若您在當月已發(fā)表SCI文章，但未被我公司收集，請致電Bioss，我們將贈予現(xiàn)金鼓勵，金額標準請參考“發(fā)文章 領獎金”活動頁面。

近期收錄2022年9月引用Bioss產(chǎn)品發(fā)表的文獻共291篇（圖一，綠色柱），文章影響因子(IF) 總和高達1897.06，其中，10分以上文獻34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7篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。

 

NATURE METHODS

 [IF=47.99]



文獻引用抗體：bs-6970R

Anti-FOXN1 pAb; IF

作者單位：美國賓夕法尼亞州匹茲堡，阿勒格尼健康網(wǎng)絡，細胞治療研究所

摘要：Hematopoietic humanized (hu) mice are powerful tools for modeling the action of human immune system and are widely used for preclinical studies and drug discovery. However, generating a functional human T cell compartment in hu mice remains challenging, primarily due to the species-related differences between human and mouse thymus. While engrafting human fetal thymic tissues can support robust T cell development in hu mice, tissue scarcity and ethical concerns limit their wide use. Here, we describe the tissue engineering of human thymus organoids from inducible pluripotent stem cells (iPSC-thymus) that can support the de novo generation of a diverse population of functional human T cells. T cells of iPSC-thymus-engrafted hu mice could mediate both cellular and humoral immune responses, including mounting robust proinflammatory responses on T cell receptor engagement, inhibiting allogeneic tumor graft growth and facilitating efficient Ig class switching. Our findings indicate that hu mice engrafted with iPSC-thymus can serve as a new animal model to study human T cell-mediated immunity and accelerate the translation of findings from animal studies into the clinic.

 

Military Medical Research

 [IF=34.915]


文獻引用抗體：bs-9267R
Anti-USP10 pAb; IHC

作者單位：總醫(yī)院第五醫(yī)療中心腫瘤內科、高級腫瘤科

摘要：Background

Melatonin, a natural hormone secreted by the pineal gland, has been reported to exhibit antitumor properties through diverse mechanisms of action. However, the oncostatic function of melatonin on esophageal squamous cell carcinoma (ESCC) remains elusive. This study was conducted to investigate the potential effect and underlying molecular mechanism of melatonin as single anticancer agent against ESCC cells.

Methods

ESCC cell lines treated with or without melatonin were used in this study. In vitro colony formation and EdU incorporation assays, and nude mice tumor xenograft model were used to confirm the proliferative capacities of ESCC cells. RNA-seq, qPCR, Western blotting, recombinant lentivirus-mediated target gene overexpression or knockdown, plasmids transfection and co-IP were applied to investigate the underlying molecular mechanism by which melatonin inhibited ESCC cell growth.

 

 

 


ADVANCED MATERIALS

 [IF=32.086]


文獻引用抗體：bs-0666R

Anti-Fibronectin/FN1 pAb; IF

作者單位：德國肺研究中心，亥姆霍茲慕尼黑，肺健康與免疫研究所和綜合肺病學中心

摘要：Lung fibrosis, one of the major post-COVID complications, is a progressive and ultimately fatal disease without a cure. Here, an organ- and disease-specific in vitro mini-lung fibrosis model equipped with noninvasive real-time monitoring of cell mechanics is introduced as a functional readout. To establish an intricate multiculture model under physiologic conditions, a biomimetic ultrathin basement (biphasic elastic thin for air–liquid culture conditions, BETA) membrane (<1 µm) is developed with unique properties, including biocompatibility, permeability, and high elasticity (<10 kPa) for cell culturing under air–liquid interface and cyclic mechanical stretch conditions. The human-based triple coculture fibrosis model, which includes epithelial and endothelial cell lines combined with primary fibroblasts from idiopathic pulmonary fibrosis patients established on the BETA membrane, is integrated into a millifluidic bioreactor system (cyclic in vitro cell-stretch, CIVIC) with dose-controlled aerosolized drug delivery, mimicking inhalation therapy. The real-time measurement of cell/tissue stiffness (and compliance) is shown as a clinical biomarker of the progression/attenuation of fibrosis upon drug treatment, which is confirmed for inhaled Nintedanib—an antifibrosis drug. The mini-lung fibrosis model allows the combined longitudinal testing of pharmacodynamics and pharmacokinetics of drugs, which is expected to enhance the predictive capacity of preclinical models and hence facilitate the development of approved therapies for lung fibrosis.

 

JOURNAL OF CLINICAL 

INVESTIGATION [IF=19.456]


文獻引用抗體：bs-3195R

Anti-Phospho-IRF3 (Ser396) pAb; WB

作者單位：臺北醫(yī)科大學醫(yī)學科學研究所

摘要：Diabetes mellitus (DM) is highly comorbid with severe dengue diseases; however, the underlying mechanisms are unclear. Patients with DM have a 1.61-fold increased risk of developing dengue hemorrhagic fever. In search of host factors involved in dengue virus (DENV) infection, we used high-glucose (HG) treatment and showed that HG increased viral protein expression and virion release but had no effects on the early stages of viral infection. After HG stimulation, DENV–firefly luciferase–transfected assay and cellular replicon–based assay indicated increased viral translation, whereas using the glucose uptake inhibitor phloretin blocked this effect. HG treatment increased the translational factor poly(A)-binding protein (PABP) in a glucose transporter–associated, PI3K/AKT-regulated manner. Silencing PABP significantly decreased HG-prompted virion production. HG enhanced the formation of the PABP–eukaryotic translation initiation factor 4G complex, which is regulated by protein–disulfide isomerase. Hyperglycemia increased PABP expression, mortality rate, viral protein expression, and viral loads in streptozotocin-induced DM mice. Overall, hyperglycemic stress facilitates DENV infection by strengthening PABP-mediated viral translation.

 

JOURNAL OF CLINICAL 

INVESTIGATION [IF=19.456]


文獻引用抗體：bs-4089R

Anti-phospho-AKT2 (Ser474) pAb; IF

作者單位：北京大學口腔醫(yī)學院和口腔醫(yī)院和口腔疼痛中心

摘要：Early-stage temporomandibular joint osteoarthritis (TMJOA) is characterized by excessive subchondral bone loss. Emerging evidence suggests that TMJ disc displacement is involved, but the pathogenic mechanism remains unclear. Here, we established a rat model of TMJOA that simulated disc displacement with a capacitance-based force-sensing system to directly measure articular surface pressure in vivo. Micro-CT, histological staining, immunofluorescence staining, IHC staining, and Western blot were used to assess pathological changes and underlying mechanisms of TMJOA in the rat model in vivo as well as in RAW264.7 cells in vitro. We found that disc displacement led to significantly higher pressure on the articular surface, which caused rapid subchondral bone loss via activation of the RANTES–chemokine receptors–Akt2 (RANTES-CCRs-Akt2) axis. Inhibition of RANTES or Akt2 attenuated subchondral bone loss and resulted in improved subchondral bone microstructure. Cytological studies substantiated that RANTES regulated osteoclast formation by binding to its receptor CCRs and activating the Akt2 pathway. The clinical evidence further supported that RANTES was a potential biomarker for predicting subchondral bone loss in early-stage TMJOA. Taken together, this study demonstrates important functions of the RANTES-CCRs-Akt2 axis in the regulation of subchondral bone remodeling and provides further knowledge of how disc displacement causes TMJOA.


 

Advanced Science 

[IF=17.521]


文獻引用抗體：

bs-0397R; Anti-MMP9 pAb

bs-1313R; Anti-VEGFA pAb

bs-10802R; Anti-TNF alpha pAb

bs-1407R; Anti-HIF1 beta pAb

bs-4593R; Anti-MMP9 pAb

bs-0782R; Anti-IL-6 pAb

bs-6761R; Anti-IL-10 pAb

bsm-33188M; Mouse Anti-alpha smooth muscle Actin mAb
作者單位：西北大學研究院陜西省可降解生物醫(yī)用材料重點實驗室陜西省生物材料與發(fā)酵工程生物技術研發(fā)中心

摘要：In addition to oxidative stress and impaired angiogenesis, the overexpression of metalloproteinases (MMPs) and proinflammatory cytokines, which are promoted by hyperglycemia, causes chronic inflammation in diabetic wounds. Herein, TA-siRNA nanogels are prepared for the first time on the basis of the self-assembling interaction between tannic acid (TA) and short interfering RNA (siRNA). The efficient, biodegradable nanogels are cross-linked with poly(vinyl alcohol) (PVA), human-like collagen (HLC), TA, and borax to prepare adaptive, conductive PHTB (TA-siRNA) hydrogels. In response to high levels of reactive oxygen species (ROS), the ROS-responsive borate ester bonds in the hydrogels are oxidized and broken, and TA-siRNA nanogels are released into cells to reduce the expression of the MMP-9. Moreover, the TA and HLC promote collagen expression, reduce inflammation, and ROS level. It is found that electrical stimulation (ES) promotes the in vivo release of TA-siRNA nanogels from PHTB (TA-siRNA) hydrogels and endocytosis of the nanogels. The combination therapy using ES and PHTB (TA-siRNA) hydrogels accelerates the healing of diabetic wounds by reducing the levels of ROS and MMP-9 and promoting the polarization of macrophages, production of collagen, and angiogenesis. This study provides insights on the design of functional gene-delivery and efficient therapeutic strategies to promote the repair of diabetic chronic wounds.


 

CHEMICAL ENGINEERING 

JOURNAL [IF=16.744]


文獻引用抗體：bs-0470R
Anti-Osteocalcin pAb; IHC

作者單位：上海交通大學醫(yī)學院,上海市第九人民醫(yī)院口腔種植科

摘要：Metabolic energy to steer osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) could be a promising therapeutic target for bone tissue engineering (BTE), but prior knowledge of this issue is limited. To address bone defects with BTE, we customized a three-dimensional (3D)-printed composite scaffold (Cur@MS) to allow the controlled release of curcumin, which could facilitate the “switch-on” mode of Glucose transporter 1 (GLUT1) in BMSCs. Consequently, bioenergetic channels, i.e. glucose uptake, were “switched on” to activate GLUT1-RUNX2 crosstalk, which was closely orchestrated with bone regeneration. Furthermore, curcumin-induced cholesterol/lipid raft (Cho/LR) was a “sensor” to trigger the “switch” (GLUT1) by directing its spatial distribution into clusters. In contrast, selective inhibition of Cho/LR and GLUT1 led to a “switch-off” mode and compromised bone regeneration in vivo. Overall, the results suggest Cho/LR is a potential target to steer BMSCs and Cur@MS is an ideal BTE material for stimulating rapid bone regeneration.
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