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截至目前，引用Bioss產(chǎn)品發(fā)表的文獻共36,344篇，總影響因子182,030.01分，發(fā)表在Nature, Science, Cell, Cancer Cell以及Immunity等頂級期刊的文獻共129篇，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)等上百所國際研究機構(gòu)。
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本文主要分享12篇IF≥15的文獻，它們引用了Bioss產(chǎn)品，分別發(fā)表在Nature Immunology、Advanced Materials、Nature Biomedical Engineering、Nature Aging、Nature Microbiology、ACS Nano、Nature Communications、Cell Death & Differentiation期刊上，讓我們一起學(xué)習(xí)吧。
Nature Immunology [IF=27.6]
bsk12015 | Mouse IL-1? ELISA Kit | ELISA
作者單位：軍醫(yī)大學(xué)大坪醫(yī)院
摘要：The formation of membrane pores by cleaved N-terminal gasdermin D (GSDMD-NT) results in the release of cytokines and inflammatory cell death, known as pyroptosis. Blocking GSDMD-NT pores is an attractive and promising strategy for mitigating inflammation. Here we demonstrate that SK56, an artificial intelligence-screened peptide, effectively obstructs GSDMD-NT pores and inhibits pyroptosis and cytokine release in macrophages and human peripheral blood leukocyte-induced pyroptosis. SK56 prevents septic death induced by lipopolysaccharide or cecal ligation and puncture surgery in mice. SK56 does not influence cleavage of interleukin-1β or GSDMD. Instead, SK56 inhibits the release of cytokines from pyroptotic macrophages, mitigates the activation of primary mouse dendritic cells triggered by incubation with pyroptotic cytomembranes and prevents widespread cell death of human alveolar organoids in an organoid–macrophage coculture model. SK56 blocks GSDMD-NT pores on lipid-bilayer nanoparticles and enters pyroptotic macrophages to inhibit mitochondrial damage. SK56 presents new therapeutic possibilities for counteracting inflammation, which is implicated in numerous diseases.
Advanced Materials [IF=26.8]
文獻引用產(chǎn)品：
bs-1074R | Nrf2 Rabbit pAb | WB
bs-2075R | Heme Oxygenase 1 Rabbit pAb | WB
bsm-41327R | ZO-1 Recombinant Rabbit mAb | WB, IF
bsm-60763M | Occludin Mouse mAb | WB, IF
bs-0061R | beta-Actin Rabbit pAb, Loading Control | WB
作者單位：中國科學(xué)院長春應(yīng)用化學(xué)研究所
Nature Biomedical
Engineering [IF=26.6]
文獻引用產(chǎn)品：
作者單位：北京大學(xué)
摘要：Immunoassays using affinity binders such as antibodies and aptamers are crucial for molecular biology. However, the advancement of analytical methods based on these affinity probes is often hampered by complex operational steps that can introduce errors, particularly in intricate environments such as intracellular settings and microfluidic systems. There is growing interest in developing molecular probes for wash-free assays that activate signals upon target detection. Here we report a systematic functional screening platform for switchable aptamer beacon probes that can achieve target-responsive detection. A stem–loop, hairpin-shaped beacon library was constructed on microbeads and screened using target-responsive fluorescence-activated sorting. The selected aptamer beacons exhibit strong affinities, triggering fluorescence only upon binding, thus enabling wash-free immunoassays for the detection of intracellular and membrane proteins. Computational modelling offers insights into aptamer binding and structural switching mechanisms, revealing how specific protein–aptamer interactions drive stem–loop unwinding and postbinding conformational changes critical for functional activation. This approach establishes a standardized platform for generating switchable aptameric tools, supporting their potential in advanced diagnostics and research.
Nature Aging [IF=19.4]
文獻引用產(chǎn)品：
摘要：Aging is a major risk factor for various neurological disorders, including Alzheimer’s disease, and is associated with the accumulation of senescent cells, which can themselves propagate the senescence process through paracrine signaling. Migrasomes are organelles that form during cellular migration, detach from parent cells and mediate intercellular communication. Here we demonstrate that border-associated macrophages (BAMs) acquire senescence-associated properties during early brain aging, possibly due to prolonged exposure to amyloid beta. Senescent-like BAMs show elevated production of migrasomes, which convey senescence-associated signals including the apoptosis inhibitor of macrophage to neighboring cells. We show that microglia are prominent recipients of senescent-like BAM-derived migrasomes, and that through activation of CD16 in recipient cells, the apoptosis inhibitor of macrophage inhibits apoptosis and promotes senescence induction. Blocking migrasome induction in senescent-like BAMs through treatment with Tspan4-targeting siRNA-encapsulated liposomes ameliorates cognitive deficits in aged mice. Our findings suggest that migrasomes are potent vehicles of senescence-regulatory signals and represent a promising target for senomorphic therapy.
Nature Microbiology [IF=19.4]
文獻引用產(chǎn)品：
摘要：The human microbiome has a pronounced impact on human physiology and behaviour. Despite its unique anatomical connection to the brain, the role of the nasal microbiome in neurological diseases is understudied. Here, using human data and experiments in mice, we show that nasal Staphylococcus aureus is linked to depression. Nasal microbiome analyses revealed a positive correlation between depression scores and S. aureus abundance among patients with depression and healthy controls. Metabolomics of the nasal cavity showed decreased sex hormones, estradiol and testosterone in patients with depression versus controls. Nasal microbiota transplants from patients reproduced depression-like behaviour in mice with differential abundance of S. aureus. Further homology and mutational analysis uncovered an S. aureus sex hormone-degrading enzyme, 17b-hydroxysteroid dehydrogenase (Hsd12), which degraded testosterone and estradiol in mice, leading to lower levels of dopamine and serotonin in the murine brain. These findings reveal a nasal commensal that influences depressive behaviour and provides insights into the nose–brain axis.
文獻引用產(chǎn)品：
bs-0743R | CTGF Rabbit pAb | IHC
作者單位：韓國成均館大學(xué)
摘要：Vagus nerve stimulation (VNS) is a promising therapy for neurological and inflammatory disorders across multiple organ systems. However, conventional rigid interfaces fail to accommodate dynamic mechanical environments, leading to mechanical mismatches, tissue irritation, and unstable long-term interfaces. Although soft neural interfaces address these limitations, maintaining mechanical durability and stable electrical performance remains challenging. Herein, we introduce a self-bondable and strain-durable electroceutical (SSE) as an effective platform for VNS. The SSE self-bonds around the vagus nerve without fixation tools, ensuring stable interfacing through the intrinsic self-bonding property of the self-healing polymer (SHP), while the stress relaxation properties minimize strain and tissue damage. The trilayer-structured electrode enhances the wiring capability and electrical durability under cyclic mechanical stress through interactions between the SHP matrix, conductive silver (Ag) flakes, and a carbon nanotube (CNT) network. Additionally, the synergistic combination of poly (3,4-ethylenedioxythiophene) polystyrenesulfonate and the CNT network improves the electrochemical stability and prevents leakage of Ag ions, thereby addressing cytotoxicity concerns. To evaluate the therapeutic potential, the SSE was applied in a drug-induced seizure rodent model, and electroencephalogram (EEG) monitoring was performed to distinguish between normal, seizure, and post-VNS states. Quantitative EEG analysis demonstrated significant modulation of the power spectra and peak frequencies, confirming the therapeutic efficacy of VNS. Histological analysis revealed minimal inflammation, thus validating the biocompatibility of the electrodes. These findings establish SSE as a robust and adaptable electroceutical platform for the treatment of epilepsy and for broader neuromodulation applications.
ACS Nano [IF=16]
文獻引用產(chǎn)品：
bs-17270R-Cy3 | SCARA3 Rabbit pAb, Cy3 conjugated | IF
作者單位：上海中醫(yī)藥大學(xué)附屬龍華醫(yī)院
摘要：Sepsis still remains the leading cause of morbidity and mortality in clinical settings, characterized by pyroptosis-induced cytokine release syndrome, multiple organ dysfunction, and gut microbiota disturbances. Inhibiting the pyroptosis pathway by nanosystems represents a potential therapeutic strategy for the treatment of sepsis. However, current pharmacological interventions primarily focus on blocking reactive oxygen species (ROS)/NOD-like receptor pyrin domain-containing 3 (NLRP3)/Caspase-1-based pyroptosis rather than lipopolysaccharide (LPS)-triggered pyroptosis. Besides, given the importance of microbiota disturbances in a second wave of cytokine storms, the assessment of the composition of intestinal flora after treatment was also missing. Herein, picroside II-encapsulated, palmitic acid-modified nanoformulations were prepared as a pyroptosis modulator to inhibit cytokine release syndrome, accompanied by reprogramming the composition of intestinal flora. Results demonstrated that the modification of palmitic acid on nanoformulations promotes the cellular uptake of nanoparticles via Toll-like receptor-mediated specific recognition. The sustained release of picroside II scavenged the massive reactive oxygen species, reduced the levels of inflammatory factors, and downregulated the pyroptosis-related proteins. Furthermore, the interaction between palmitic acid and Toll receptors reduced the combination site of LPS, providing a positive loop in drug delivery and inhibiting pyroptosis. Consequently, the obtained nanoformulations exerted a better antioxidant, anti-inflammatory, and antiproptosis activity than other treatment groups, thereby alleviating LPS-stimulated multiorgan damage, especially the kidney and colon. Interestingly, it also improved the abundance of intestinal flora, contributing to enhanced intestinal barrier function and improved immune system. Thus, palmitic acid-anchored, picroside II-encapsulated nanoformulations potentiated a systematic and desirable therapeutic outcome in sepsis treatment.
Nature Communications
[IF=15.7]
文獻引用產(chǎn)品：
作者單位：意大利佛羅倫薩大學(xué)
摘要：Analgesia by non-steroidal anti-inflammatory drugs (NSAIDs) is ascribed to inhibition of prostaglandin (PG) biosynthesis and ensuing inflammation. However, NSAIDs have life-threatening side effects, and inhibition of inflammation delays pain resolution. Decoupling the mechanisms underlying PG-evoked pain vs. protective inflammation would facilitate pain treatment. Herein, we reveal that selective silencing of the PGE? receptor 2 (EP2) in Schwann cells via adeno-associated viral vectors abrogates the indomethacin-sensitive component of pain-like responses in mice elicited by inflammatory stimuli without affecting inflammation. In human Schwann cells and in mice, EP2 activation and optogenetic stimulation of adenylyl cyclase evokes a plasma membrane-compartmentalized cyclic adenosine monophosphate (cAMP) signal that, via A-kinase anchor protein-associated protein kinase A, sustains inflammatory pain-like responses, but does not delay their resolution. Thus, an unforeseen and druggable EP2 receptor in Schwann cells, via specific cAMP nanodomains, encodes PGE? -mediated persistent inflammatory pain but not PG-dependent protective inflammation.
Nature Communications
[IF=15.7]
文獻引用產(chǎn)品：
作者單位：南方醫(yī)科大學(xué)南方醫(yī)院
Nature Communications
[IF=15.7]
作者單位：巴塞羅那生物醫(yī)學(xué)研究所
Nature Communications
[IF=15.7]
文獻引用產(chǎn)品：
作者單位：意大利維羅納大學(xué)
Cell Death&
Differentiation [IF=15.4]
文獻引用產(chǎn)品：
作者單位：上海市第九人民醫(yī)院
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