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<section> <section> <section> <section> <section> <p>截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共<span style="color: #007aaa;"><strong>29281篇</strong></span>，總影響因子<span style="color: #007aaa;"><strong>141751.15分</strong></span>，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共<span style="color: #007aaa;"><strong>68篇</strong></span>，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(guó)際知名研究機(jī)構(gòu)上百所。</p> <p>我們每月收集引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)。若您在當(dāng)月已發(fā)表SCI文章，但未被我公司收集，請(qǐng)致電Bioss，我們將贈(zèng)予現(xiàn)金鼓勵(lì)，金額標(biāo)準(zhǔn)請(qǐng)參考<a style="color: #0052ff;" href="http://mp.weixin.qq.com/s?__biz=MzA4OTQ5MTQ5Ng==&mid=2247501137&idx=2&sn=f97d64e7cf85b9bd3f985e2b468a66d0&chksm=90189416a76f1d0088cd957568d3b6acbcd0aa7631cce01a92358def01ac9fce47a30fd32d3c&scene=21#wechat_redirect" target="_blank" rel="noopener">“發(fā)文章 領(lǐng)獎(jiǎng)金”</a>活動(dòng)頁(yè)面。</p> <p>近期收錄2024年2月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共<span style="color: #007aaa;"><strong>363篇</strong></span>（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)<span style="color: #007aaa;"><strong>2298.3</strong></span>，其中，10分以上文獻(xiàn)<span style="color: #007aaa;"><strong>45篇</strong></span>（圖二）。</p> <p style="color: #ffe4c2;"><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/3f50df4d0879a3da08919d380ffc0644.png" alt="" width="600" height="366" /></p> <p style="color: #ffe4c2; text-align: center;"><span style="color: #000000;">圖一</span></p> <p style="text-align: center;"><img title="" src="https://admin.biosschina.com/uploads/images/20240527/a9a2a7ff4400c1aed673d2333c78a7cf.png" alt="" width="600" height="429" /></p> <p style="text-align: center;"><span style="color: #000000;">圖二</span></p> </section> </section> </section> </section> </section> <p style="color: #3e3e3e;"><span style="color: #000000;">本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Nature, Immunity, Cancer Cell等期刊的<strong>5篇 </strong><strong>IF＞15 </strong><strong>的文獻(xiàn)摘要</strong>，讓我們一起欣賞吧。</span></p> <p style="color: #3e3e3e;"> </p> <section> <section> <section> <section> <section> <section> <section> <p style="color: #a9cd07; text-align: center;"><span style="color: #000000;"><strong>Molecular Cancer [IF=37.3]</strong></span></p> </section> </section> </section> <section> <section> <p><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/e34233982e538b45edcf72765a8aa119.png" alt="" width="600" height="190" /></p> <p><strong>文獻(xiàn)引用產(chǎn)品：</strong><a class="" href="https://www.biosschina.com/#/productDetail?goods_id=12968" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bsm-33070M</strong></span></a></p> <p>Ki-67 Mouse mA | IHC</p> <p><strong>作者單位：</strong>重慶醫(yī)科大學(xué)</p> <section> <section> <section> <p><strong>摘要：</strong><span style="color: #222222;">CircPDHK1 was upregulated in ccRCC tissues and closely related to WHO/ISUP stage, T stage, distant metastasis, VHL mutation and Ki-67 levels. CircPDHK1 had a functional internal ribosome entry site (IRES) and encoded a novel peptide PDHK1-241aa. Functionally, we confirmed that PDHK1-241aa and not the circPDHK1 promoted the proliferation, migration and invasion of ccRCC. Mechanistically, circPDHK1 was activated by HIF-2A at the transcriptional level. PDHK1-241aa was upregulated and interacted with PPP1CA, causing the relocation of PPP1CA to the nucleus. This thereby inhibited AKT dephosphorylation and activated the AKT-mTOR signaling pathway.</span></p> </section> </section> </section> </section> </section> </section> </section> </section> </section> <section> <section> <section> <section> <section></section> <section> <p style="text-align: center;"><strong>Cellular & Molecular </strong><strong>Imm</strong><strong>unology [IF=24.1]</strong></p> </section> </section> </section> <section> <section> <p><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/8b3267f72fc904e5d7798fbd433f58eb.png" alt="" width="600" height="166" /></p> <p style="color: #606060;"><span style="color: #000000;"><strong>文獻(xiàn)引用產(chǎn)品：</strong></span></p> <p style="color: #606060;"><a href="https://www.biosschina.com/#/productDetail?goods_id=26527" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bs-2789R</strong></span></a>; <span style="color: #000000;">Tap1 Rabbit pAb | FC</span></p> <p style="color: #606060;"><a href="https://www.biosschina.com/#/productDetail?goods_id=22767" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bs-2374</strong></span><span style="color: #a9cd07;"><strong>R</strong></span></a>; <span style="color: #000000;">TAP2 Rabbit pAb | FC</span></p> <p style="color: #676b70;"><span style="color: #000000;"><strong>作者單位<span style="color: #000000;">：</span></strong>北京大學(xué)</span></p> <section> <section> <section> <p><strong>摘</strong><strong>要：</strong><span style="color: #1f1f1f;">CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells can "help” or "license” conventional type 1 dendritic cells (cDC1s) to induce CD8</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> cytotoxic T lymphocyte (CTL) anticancer responses, as proven in mouse models. We recently identified cDC1s with a transcriptomic imprint of CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T-cell help, specifically in T-cell-infiltrated human cancers, and these cells were associated with a good prognosis and response to PD-1-targeting immunotherapy. Here, we delineate the mechanism of cDC1 licensing by CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells in humans. Activated CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells produce IFNβ via the STING pathway, which promotes MHC-I antigen (cross-)presentation by cDC1s and thereby improves their ability to induce CTL anticancer responses. In cooperation with CD40 ligand (L), IFNβ also optimizes the costimulatory and other functions of cDC1s required for CTL response induction. IFN-I-producing CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells are present in diverse T-cell-infiltrated cancers and likely deliver “help” signals to CTLs locally, according to their transcriptomic profile and colocalization with “helped/licensed” cDCs and tumor-reactive CD8</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells. In agreement with this scenario, the presence of IFN-I-producing CD4</span><sup style="color: #1f1f1f;">+</sup><span style="color: #1f1f1f;"> T cells in the TME is associated with overall survival and the response to PD-1 checkpoint blockade in cancer patients.</span></p> </section> </section> </section> </section> </section> </section> </section> <section> <section> <section> <section> <section> <p><strong> </strong></p> <p style="text-align: center;"><strong>ADVANCE</strong><strong>D FUNCTIONAL </strong><strong>MATERIALS [IF=19.0]</strong></p> </section> <section><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/c35637053d9dae2a44208e4c333e35a0.png" alt="" width="600" height="166" /></section> </section> </section> <section> <section> <p style="color: #606060;"><strong><span style="color: #000000;">文獻(xiàn)引用產(chǎn)品：</span></strong><a href="https://www.biosschina.com/#/productDetail?goods_id=5530" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bs-4917R</strong></span></a></p> <p style="color: #606060;"><span style="color: #000000;">Osteocalcin Rabbit pAb | IF</span></p> <p><strong><span style="color: #000000;">作者單位：</span></strong>北京大學(xué)口腔醫(yī)院</p> <section><strong>摘要：</strong><span style="color: #1f1f1f;">Utilization of electro-responsive biomaterials with antibacterial properties is advantageous for facilitating septic wound healing and tissue regeneration. However, the dose-response effects of electrical stimuli from these materials against bacteria are not rigorously characterized, and achieving synergy of bactericidal and pro-regenerative effects of biomaterials remains a major challenge. Here, a graded series of flexible BaTiO</span><span style="color: #1f1f1f;"><sub>3</sub></span><span style="color: #1f1f1f;">/P(VDF-TrFE) electroactive nanocomposite membranes (EMs) are developed with varying surface charge intensities, to serve as antibacterial dressing for septic wound healing. EMs display broad-spectrum antibacterial effects against both Gram-positive and Gram-negative bacteria in a dose-dependent manner, depending on the magnitude of their surface electrical potential. Mechanistically, the surface charge of EMs increase intracellular levels of reactive oxygen species within bacteria cells, which in turn caused oxidative damage to the bacterial membrane, thereby suppressing bacterial activity and biofilm formation. Moreover, in vivo studies demonstrated that EMs effectively inhibited S. aureus infection and accelerated wound healing in a mouse skin defect model, as well as ameliorated P. gingivalis-mediated periodontal inflammation in a mouse periodontitis model. Hence, this study optimizes the antibacterial properties of electroactive materials and characterizes the dose-response effects of surface electrical charge against bacteria, thus validating the therapeutic applications of electroactive biomaterials in combating bacterial infection.</span></section> </section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section> <section> <section></section> <section> <p style="text-align: center;"><strong>ACS </strong><strong>Nano [IF=17.1]</strong></p> <p><strong><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/804ce648a56b5360341440069b6bc022.png" alt="" width="600" height="153" /></strong></p> </section> </section> </section> <section> <section> <p><strong>文獻(xiàn)引用抗體：</strong></p> <p><a href="https://www.biosschina.com/#/productDetail?goods_id=30448" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bs-0292P</strong></span></a>; BSA-V</p> <p><a href="https://www.biosschina.com/#/productDetail?goods_id=53548" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>D-9106</strong></span></a>; DAPI</p> <p><a href="https://www.biosschina.com/#/productDetail?goods_id=12968" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bsm-33070M</strong></span></a>; Ki-67 Mouse mAb | IF</p> <section></section> <section></section> <section></section> <section></section> <p><strong>作者單位：</strong>北京大學(xué)</p> <section> <section> <section><strong>摘要：</strong><span style="color: #222222;">Cancer progression and treatment-associated cellular stress impairs therapeutic outcome by inducing resistance. Endoplasmic reticulum (ER) stress is responsible for core events. Aberrant activation of stress sensors and their downstream components to disrupt homeostasis have emerged as vital regulators of tumor progression as well as response to cancer therapy. Here, an orchestrated nanophotoinducer (ERsNP) results in specific tumor ER-homing, induces hyperthermia and mounting oxidative stress associated reactive oxygen species (ROS), and provokes intense and lethal ER stress upon near-infrared laser irradiation. The strengthened “dying” of ER stress and ROS subsequently induce apoptosis for both primary and abscopal B16F10 and GL261 tumors, and promote damage-associated molecular patterns to evoke stress-dependent immunogenic cell death effects and release “self-antigens”. Thus, there is a cascade to activate maturation of dendritic cells, reprogram myeloid-derived suppressor cells to manipulate immunosuppression, and recruit cytotoxic T lymphocytes and effective antitumor response. The long-term protection against tumor recurrence is realized through cascaded combinatorial preoperative and postoperative photoimmunotherapy including the chemokine (C–C motif) receptor 2 antagonist, ERsNP upon laser irradiation, and an immune checkpoint inhibitor. The results highlight great promise of the orchestrated nanophotoinducer to exert potent immunogenic cell stress and death by reinforcing ER stress and oxidative stress to boost cancer photoimmunotherapy.</span></section> </section> </section> </section> </section> </section> </section> </section> <section> <section> <section> <section></section> <section> <p style="text-align: center;"><strong>Advanced Science [IF=15.1]</strong></p> <p><strong><img style="display: block; margin-left: auto; margin-right: auto;" title="" src="https://admin.biosschina.com/uploads/images/20240527/d370d2bf061c3da2b1223b51ac25767a.png" alt="" width="600" height="176" /></strong></p> </section> </section> </section> <section> <section> <section> <p><strong>文獻(xiàn)引用抗體：</strong></p> <p><a href="https://www.biosschina.com/#/productDetail?goods_id=47027" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bs-0292P-FITC</strong></span></a>; BSA / FITC | IF</p> </section> <p><a href="https://www.biosschina.com/#/productDetail?goods_id=27102" target="_blank" rel="noopener"><span style="color: #a9cd07;"><strong>bsm-60235R</strong></span></a>; Keratin 6 Recombinant Rabbit mAb | IF</p> <p style="color: #676b70;"><span style="color: #000000;"><strong>作者單位：</strong>南方醫(yī)科大學(xué)</span></p> <section> <section> <p><strong>摘要：</strong><span style="color: #222222;">To address current challenges in effectively treating large skin defects caused by trauma in clinical medicine, the fabrication, and evaluation of a novel radially aligned nanofiber scaffold (RAS) with dual growth factor gradients is presented. These aligned nanofibers and the scaffold's spatial design provide many all-around “highways” for cell migration from the edge of the wound to the center area. Besides, the chemotaxis induced by two growth factor gradients further promotes cell migration. Incorporating epidermal growth factor (EGF) aids in the proliferation and differentiation of basal layer cells in the epidermis, augmenting the scaffold's ability to promote epidermal regeneration. Concurrently, the scaffold-bound vascular endothelial growth factor (VEGF) recruits vascular endothelial cells at the wound's center, resulting in angiogenesis and improving blood supply and nutrient delivery, which is critical for granulation tissue regeneration. The RAS+EGF+VEGF group demonstrates superior performance in wound immune regulation, wound closure, hair follicle regeneration, and ECM deposition and remodeling compared to other groups. This study highlights the promising potential of hierarchically assembled nanofiber scaffolds with dual growth factor gradients for wound repair and tissue regeneration applications.</span></p> </section> </section> </section> </section> </section> </section> </section> </section>