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截至目前，引用Bioss產品發表的文獻共39,620篇，總影響因子203,085.07分，發表在Nature, Science, Cell, Cancer Cell以及Immunity等頂級期刊的文獻共142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上百所國際研究機構。我們每月收集引用Bioss產品發表的文獻。若您在當月已發表SCI文章，但未被我公司收集，請致電Bioss，我們將贈予現金鼓勵，金額標準請參考“發文章 領獎金"活動頁面。
本文主要分享10篇IF≥20的文獻，它們引用了Bioss產品，分別發表在Advanced Materials、Nature Biomedical Engineering、Immunity、Exploration、Materials Today、Advanced Fiber Materials、Cell Stem Cell、Bioactive Materials、Nature Neuroscience期刊上，讓我們一起學習吧。
Advanced Materials [IF=26.8]
文獻引用產品：
bs-1363R-Cy5 | AIF1 / Iba1 Rabbit pAb, Cy5 conjugated | IF
作者單位：福州大學
摘要：A growing understanding of the pathophysiological evolution of Alzheimer's disease (AD) underscores the heterogeneity in its progression as a critical factor undermining the success of various candidate interventions and complicating the establishment of effective pharmacotherapeutic regimens. Here, we introduce the development of a hierarchical-responsive therapeutic agent self-assembled from phenylboronate ester-linked Tjernberg's KLVFF peptide-curcumin conjugates (CPKNAs), which is designed to dynamically track the spatiotemporal coordinates of biomarkers associated with AD heterogeneity in progression. The dynamic covalent phenylboronate ester bond undergoes varying degrees of dissociation in response to the temporal evolution patterns of amyloid-β, reactive oxygen species, and glucose, three key indicators for staging AD progression, enabling self-adaptive regulation of drug distribution and dosing tailored to specific phenotypes. Employing seven cellular models and three types of transgenic mice simulating different AD stages, we demonstrate that CPKNAs effectively minimize the risks of under- or overtreatment, achieving consistent therapeutic outcomes in mitigating cellular damage and improving brain dysfunction.
文獻引用產品：
bsm-1698M | ox-LDL Mouse mAb | IF
作者單位：北京協和醫學院
摘要：Cardiovascular and cerebrovascular events due to atherosclerosis (AS) are the leading causes of mortality worldwide. Current therapeutic strategies failed to simultaneously target lipid deposition, chronic inflammation, and endothelial dysfunction. Herein, we developed BIFD, a conformationally variable peptide targeting lysophosphatidylcholine (LPC) on oxidized low-density lipoproteins (ox-LDL), which binds ox-LDL to form nanoaggregates, blocking ox-LDL toxicity, reducing inflammation, promoting metabolism/excretion of ox-LDL in macrophage. In addition, both ox-LDL specifically distributed in plaque sites and the targetability of BIFD to ox-LDL enable the BIFD targetability to plaque of AS. Therefore, rapamycin (Rapa), an anti-inflammatory drug, is designed to be encapsulated into BIFD to form Rapa@BIFD nanoparticles (NPs). Rapa@BIFD may target plaque, enhancing accumulation and retention of Rapa@BIFD on the AS lesion. Consequently, Rapa@BIFD demonstrated high efficacy against AS with minimal side effects. In vitro and in vivo studies in apolipoprotein E-knockout murine and canine models revealed that Rapa@BIFD effectively reduced oxidative damage, and inflammatory responses, while promoting lipid metabolism and excretion. Rapa@BIFD mitigated side effects of Rapa, such as hyperlipidemia and splenic toxicity. These findings present a transformative multitarget for AS, combining efficacy with minimal side effects and enhanced clinical translatability.
Nature Biomedical Engineering [IF=26.6]
文獻引用產品：
作者單位：美國萊斯大學
摘要：Wounds can become chronic if the biological processes that coordinate tissue repair, including immune cell activity and matrix remodelling, become dysregulated. Current treatments mainly focus on a wound’s physical properties, such as moisture and pressure, and do not restore the disrupted molecular pathways. Here we show a removable patch containing engineered human cells that continuously release native cytokines and that can accelerate healing in rodent and porcine full-thickness wounds. The patch is a polydimethylsiloxane structure that houses alginate-encapsulated human retinal epithelial cells engineered to secrete individual cytokines relevant to tissue repair. Once placed on the wound bed, the cells remain viable and locally release the cytokines over several days. Delivery of interleukin 10, interleukin 12 and transforming growth factor-beta accelerates wound healing in mice and pigs, with accompanying changes in gene expression linked to tissue repair, including pathways involved in skin development and collagen organization. This work suggests that localized, cell-based cytokine delivery may enable future wound treatments that directly modulate the cellular programs governing tissue repair.
Immunity [IF=26.3]
文獻引用產品：
bs-7765R-APC | RAB35 Rabbit pAb, APC conjugated | FC,WB摘要：Surface proteins enable T follicular helper (Tfh) cells’ chemotactic migration toward B cells and subsequent functional interactions, underpinning effective humoral immunity. We showed that geranylgeranyl diphosphate (GGPP), a mevalonate (MVA) pathway-derived isoprenoid, was indispensable for Tfh cell function by maintaining surface protein expression. Either pharmacological inhibition or genetic depletion of geranylgeranyl diphosphate synthase (GGPS1), the enzyme responsible for GGPP biosynthesis, impaired Tfh cell generation. Mechanistically, geranylgeranyl transferase Ⅱ (GGTase Ⅱ) utilizes GGPP to geranylgeranylate RAB GTPases for surface protein expression, as exemplified by RAB35-mediated recycling of the chemokine receptor CXCR5 to the cell surface. Notably, the MVA pathway-GGPS1-GGTase Ⅱ-RAB35 axis in Tfh cells was enhanced by T cell receptor signaling and hyperactivated in autoimmunity. Conversely, the potent statin pitavastatin inhibited this axis to suppress pathogenic Tfh cells and alleviate autoimmunity. Thus, GGPP links the MVA pathway to T cell function via surface protein regulation, revealing a therapeutic target for autoimmune diseases.
Exploration [IF=22.5]
文獻引用產品：
摘要：Diabetic foot ulcers (DFUs) present a persistent clinical challenge, posing a significant and ongoing threat to patient health. Current treatment strategies are failing to concurrently address the excessive oxidative stress and impaired angiogenesis during whole-course management of diabetic wounds. To overcome these limitations, this study developed an innovative microneedle (MN)-based drug delivery system incorporating cerium-based metal?organic frameworks (MOFs) loaded with dihydrocapsaicin (DHC). Fabricated from a Gelatin Methacryloyl (GelMA) hydrogel, the resulting MN-MOF@DHC system exhibited a sustained release profile of DHC that nearly covered the whole-course management of diabetic wounds. Our results revealed that the MN-MOF@DHC system effectively reduced the levels of reactive oxygen species (ROS), promoted the transformation of macrophage phenotypes from the pro-inflammatory M1 subtype to the anti-inflammatory M2 subtype, and significantly enhanced endothelial cell angiogenesis. These combined actions markedly accelerated wound closure. Collectively, the advanced MN platform offers a highly promising strategy for the treatment of DFUs.
Materials Today [IF=22]
文獻引用產品：
bs-1278R | 8-OHdG (DNA/RNA Damage) Rabbit pAb | IF
bs-6313R | 4 Hydroxynonenal Rabbit pAb | IF
bs-10211R | FOXP3 Rabbit pAb | IF
作者單位：杭州醫學院
Advanced Fiber Materials [IF=21.3]
文獻引用產品：
作者單位：哈爾濱工業大學
摘要：Parkinson’s disease (PD) affects tens of millions of people globally, yet current clinical management remains fragmented, relying on subjective assessments and episodic laboratory measurements that fail to capture disease dynamics in real-world settings. Here, we present a smart textile-integrated multimodal interface (STMI) that seamlessly combines tremor quantification with real-time therapeutic drug monitoring through a wearable wristband platform. The system integrates an array of enhanced triboelectric nanogenerators with optimized bead-on-string nanofiber architecture for sensitive tremor detection, coupled with fiber-based electrochemical sensors for simultaneous monitoring of levodopa (LD), pH, and sodium levels in sweat. By leveraging deep learning algorithms (bidirectional LSTM), the STMI achieves accurate discrimination between healthy controls, prodromal Parkinson’s patients, and PD patients—including early detection of prodromal stages currently undetectable by standard imaging. Longitudinal tracking in PD patients demonstrates real-time correlation between tremor suppression and LD pharmacokinetics, enabling quantitative assessment of medication efficacy and identification of wearing-off phenomena. The textile-based form factor ensures ergonomic wearability and mechanical robustness for continuous monitoring, while the integrated multimodal sensing paradigm establishes a new standard for personalized PD management. This work demonstrates how intelligent wearable systems can bridge the gap between motor symptom assessment and pharmacological profiling, transforming PD care from episodic clinical visits to continuous, data-driven therapeutic optimization.
Cell Stem Cell [IF=20.4]
文獻引用產品：
bs-0252R | Glucocorticoid receptor Rabbit pAb | IF
作者單位：美國耶魯大學
摘要：Human emotional and stress responses are orchestrated by subcortical limbic circuits, with the amygdala playing a central role in integrating affective, sensory, and endocrine signals. Despite the urgent need to understand how these circuits develop and contribute to anxiety and stress-related disorders, progress has been hindered by lack of ex vivo human models. Here, we generated human amygdala-like telencephalic organoids (hATOs) that recapitulate cellular composition, region-specific development, and key features of the amygdala. By assembling hATOs with a hypothalamic organoid (hypoTO) with paraventricular nucleus (PVN)-like features, we modeled the amygdala-hypothalamus-like interaction, which enabled circuit-level analysis of stress-responsive signaling. Exposure to cortisol led to robust upregulation of BCYRN1, a primate-specific retrotransposon-derived noncoding RNA, which uncovered a previously unrecognized mechanism of stress hormone signaling to retrotransposon biology and human-specific synaptic regulation. These findings highlight the potential of hATOs to understand molecular features of affective circuitry underlying emotion and the stress response and neuropsychiatric disorders.
Bioactive Materials [IF=20.3]
文獻引用產品：
bsm-33187M | alpha smooth muscle Actin Mouse mAb | IF
bs-0296G-BF647 | Goat Anti-Mouse IgG H&L, BF647 conjugated | IF
作者單位：南方醫科大學第十附屬醫院
摘要：Reconstruction of a healthy endothelium following stent implantation is critical for enhancing vascular healing process. Surface engineering of stents with endothelial cell (EC)-selective molecules represents one of the most effective strategies to promote re-endothelialization. However, the adsorption of blood components accompanied by stenting inevitably mask the surface-modified bioactive molecules, leading to a reduction or alteration in the EC selectivity. Herein, we develop a serum albumin (SA)-armed, extracellular-matrix-derived, EC-selective peptide (i.e., REDV) (REDV-SA) self-assembling amyloid-like coating to address this issue. Our results show that the intrinsic biological properties of SA endow the REDV-SA-functionalized stents with immune escape capabilities and resistance to the adsorption of blood components, thereby creating a favorable microenvironment for REDV to exhibit its high EC selectivity. Of particular significance is the adaptive synergy between SA and REDV, which significantly reinforces EC selectivity by inhibiting smooth muscle cell (SMC) adhesion and preferentially promoting EC over SMC migration. Owing to its high EC selectivity, the stent functionalized with REDV-SA coating achieves nearly complete endothelial coverage within one weekin vivo, markedly reduces inflammation, and effectively inhibits neointimal hyperplasia, implying great application potential in vascular implants.
Nature Neuroscience [IF=20]
文獻引用產品：
C-0010 | DAB kit (20×) | Other
作者單位：復旦大學
摘要：Synaptic inputs onto the dendrites and cell body integrate and trigger action potentials (APs) at the axon initial segment (AIS). The AIS receives GABAergic synaptic inputs; however, the structure and function of glutamatergic synapses at the AIS remain poorly understood. Here, we show that, in adult mice, the AIS exhibits axonic spines in about half of the neurons examined in three brain regions: the dorsal lateral septum (dLS), bed nucleus of the stria terminalis and striatum. In the dLS, axonic spines express ionotropic glutamate receptors and undergo structural plasticity. Voltage-gated Na+ channels at the AIS boost the synaptic responses of axonic spines and thus AP generation. Although hippocampal dorsal CA3 neurons synapse onto both axonic spine neurons (ASNs) and non-ASNs, they preferentially activate ASNs and subsequently inhibit non-ASNs through feedforward inhibition. Together, these results indicate that axonic spines jump-start APs in dLS neurons and route information flow from the hippocampus to downstream brain regions.
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