截止目前，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等頂級期刊的文獻共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知名研究機構上百所。
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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
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]
作者單位：中國人民解放軍總醫(yī)院第五醫(yī)療中心腫瘤內(nèi)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
JOURNAL OF CLINICAL INVESTIGATION [IF=19.456]
文獻引用抗體：bs-3195R；Anti-Phospho-IRF3 (Ser396) pAb; WB
JOURNAL OF CLINICAL INVESTIGATION [IF=19.456]
文獻引用抗體：bs-4089R；Anti-phospho-AKT2 (Ser474) pAb; IF
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.
