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近期收录2023年6月引用Bioss产品发表的文献共305篇（图一，绿色柱），文章影响因子 (IF) 总和高达1742.4，其中，10分以上34篇（图二）。

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本文主要分享引用Bioss产品发表文章至Nature Nanotechnology / Immunity / Cancer Cell等期刊的7篇IF＞15的文献摘要，让我们一起欣赏吧

文献 1

[IF=18.2] ACS Central Science

DOI:10.1021/acscentsci.3c00377

文献引用抗体：

bs-0737R | Anti-HIF-1 Alpha pAb | WB,IHC

bs-3494R | Anti-Phospho-mTOR (Ser2448) pAb | IHC,FCM

Institution:河南大学药学院天然药物与免疫工程重点实验室

Abstract:

Changes in the cerebral microenvironment caused by

acute ischemic stroke-reperfusion are the main obstacle to the recovery of

neurological function and an important cause of stroke recurrence after

thrombolytic therapy. The intracerebral microenvironment after

ischemia-reperfusion reduces the neuroplasticity of the penumbra and ultimately

leads to permanent neurological damage. To overcome this challenge, we

developed a triple-targeted self-assembled nanodelivery system, which combines

the neuroprotective drug rutin with hyaluronic acid through esterification to

form a conjugate, and then connected SS-31, a small peptide that can penetrate

the blood brain barrier and target mitochondria. Brain targeting, CD44-mediated

endocytosis, hyaluronidase 1-mediated degradation, and the acidic environment

synergistically promoted the enrichment of nanoparticles and drug release in

the injured area. Results demonstrate that rutin has a high affinity for ACE2

receptors on the cell membrane and can directly activate ACE2/Ang1-7 signaling,

maintain neuroinflammation, and promote penumbra angiogenesis and normal

neovascularization. Importantly, this delivery system enhanced the overall

plasticity of the injured area and significantly reduced neurological damage

after stroke. The relevant mechanism was expounded from the aspects of

behavior, histology, and molecular cytology. All results suggest that our

delivery system may be an effective and safe strategy for the treatment of

acute ischemic stroke-reperfusion injury.

文献 2

[IF=16.6] Nature Communications

DOI:10.1038/s41467-023-38849-z

文献引用抗体：bs-2527R-Cy5.5 | Anti-CD163/Cy5.5 pAb | FCM

Institution:美国圣路易斯华盛顿大学医学院医学系

 Abstract:

Environmental factors may alter the fetal genome to

cause metabolic diseases. It is unknown whether embryonic immune cell

programming impacts the risk of type 2 diabetes in later life. We demonstrate

that transplantation of fetal hematopoietic stem cells (HSCs) made vitamin D

deficient in utero induce diabetes in vitamin D-sufficient mice. Vitamin D

deficiency epigenetically suppresses Jarid2 expression and activates the Mef2/PGC1a pathway in

HSCs, which persists in recipient bone marrow, resulting in adipose macrophage

infiltration. These macrophages secrete miR106-5p, which promotes adipose

insulin resistance by repressing PIK3 catalytic and regulatory subunits and

down-regulating AKT signaling. Vitamin D-deficient monocytes from human cord

blood have comparable Jarid2/Mef2/PGC1a

expression changes and secrete miR-106b-5p, causing adipocyte insulin

resistance. These findings suggest that vitamin D deficiency during development

has epigenetic consequences impacting the systemic metabolic milieu.

文献 3

[IF=15.1] BRAIN BEHAVIOR AND IMMUNITY

DOI:10.1016/j.bbi.2023.06.020

文献引用抗体：bs-0947R-FITC| Anti-ADRB2/FITC pAb | FCM

Institution:以色列特拉维夫大学萨克勒医学院临床微生物学与免疫学系

 Abstract:

Stress-induced β2-adrenergic receptor (β2AR)

activation in B cells increases IgG secretion; however, the impact of this

activation on antibody affinity and the underlying mechanisms remains unclear.

In the current study, we demonstrate that stress in mice following ovalbumin

(OVA) or SARS-CoV-2 RBD immunization significantly increases both serum and

surface-expressed IgG binding to the immunogen, while concurrently reducing

surface IgG expression and B cell clonal expansion. These effects were

abolished by pharmacological β2AR blocking or when the experiments were

conducted in β2AR -/- mice. In the second part of our study, we used single B

cell sorting to characterize the monoclonal antibodies (mAbs) generated

following β2AR activation in cultured RBD-stimulated B cells from convalescent

SARS-CoV-2 donors. Ex vivo β2AR activation increased the affinities of the

produced anti-RBD mAbs by 100-fold compared to mAbs produced by the same donor

control cultures. Consistent with the mouse experiments, β2AR activation

reduced both surface IgG levels and the frequency of expanded clones. mRNA

sequencing revealed a β2AR-dependent upregulation of the PI3K pathway and B

cell receptor (BCR) signaling through AKT phosphorylation, as well as an

increased B cell motility. Overall, our study demonstrates that stress-mediated

β2AR activation drives changes in B cells associated with BCR activation and

higher affinity antibodies.

 文献 4

[IF=15.1] BRAIN BEHAVIOR AND IMMUNITY

DOI:10.1016/j.bbi.2023.06.003

文献引用抗体：

bs-20649R | Anti-PSD95 pAb | WB

bs-2723R | Anti-TREM2 pAb | FCM

Institution:国家药监局麻醉药品与精神药品研究与评价重点实验室

 Abstract:

Inflammatory bowel disease (IBD) is a chronic

condition with a high recurrence rate. To date, the clinical treatment of IBD

mainly focuses on inflammation and gastrointestinal symptoms while ignoring the

accompanying visceral pain, anxiety, depression, and other emotional symptoms.

Evidence is accumulating that bi-directional communication between the gut and

the brain is indispensable in the pathophysiology of IBD and its comorbidities.

Increasing efforts have been focused on elucidating the central immune

mechanisms in visceral hypersensitivity and depression following colitis. The

triggering receptors expressed on myeloid cells-1/2 (TREM-1/2) are newly

identified receptors that can be expressed on microglia. In particular, TREM-1

acts as an immune and inflammatory response amplifier, while TREM-2 may

function as a molecule with a putative antagonist role to TREM-1. In the

present study, using the dextran sulfate sodium (DSS)-induced colitis model, we

found that peripheral inflammation induced microglial and glutamatergic

neuronal activation in the anterior cingulate cortex (ACC). Microglial ablation

mitigated visceral hypersensitivity in the inflammation phase rather than in

the remission phase, subsequently preventing the emergence of depressive-like

behaviors in the remission phase. Moreover, a further mechanistic study

revealed that overexpression of TREM-1 and TREM-2 remarkably aggravated DSS-induced

neuropathology. The improved outcome was achieved by modifying the balance of

TREM-1 and TREM-2 via genetic and pharmacological means. Specifically, a

deficiency of TREM-1 attenuated visceral hyperpathia in the inflammatory phase,

and a TREM-2 deficiency improved depression-like symptoms in the remission

phase. Taken together, our findings provide insights into mechanism-based

therapy for inflammatory disorders and establish that microglial innate immune

receptors TREM-1 and TREM-2 may represent a therapeutic target for the

treatment of pain and psychological comorbidities associated with chronic

inflammatory diseases by modulating neuroinflammatory responses.

文献 5

[IF=15.1] CHEMICAL ENGINEERING JOURNAL

DOI:10.1016/j.cej.2023.144360

文献引用抗体：bs-5913R | Anti-Calreticulin pAb | IF

Institution:东南大学化学化工学院

 Abstract:

Ferroptosis is an emerging antitumor treatment

modality with the superiority for evading apoptotic cell death pathway.

However, how to elevate catalytic efficacy of Fe²⁺-mediated Fenton reaction and

efficiently elicit ferroptosis remain enormously challenging. Herein, inspired

by hyperthermia-enhanced Fenton reaction kinetics, we firstly designed

iron-polyphenol-aspirin-coordinated nanochelates for photothermal-enhanced

ferroptosis antitumor immunotherapy. Specifically, we modulated optimal mass

feeding ratio of gallic acid (GA), aspirin (ASA), Fe (II) and

polyvinylpyrrolidone (PVP) to construct novel nanofibrous GA-ASA-Fe (II)

metalchelates named GAFs. The variations in size and structure allowed the

nanomedicines to avoid the risk of premature renal clearance in vivo, compared

with the reported ultrasmall GA-Fe (II) nanocomplexes (GFs). Under NIR laser

irradiation, GAFs could constantly amplify toxic hydroxyl radicals (radical

dotOH) generation and deplete excessive GSH to induce more accumulation of lethal

lipid peroxidation (LPO), thereby triggering ferroptosis pathway in vitro and

in vivo. Besides, the introduction of ASA could inhibit cyclooxygenase-2

(COX-2) and prostaglandin E₂

(PGE₂),

in combination with photothermal-enhanced ferroptosis tumor therapy to induce

immunogenic cell death (ICD), promote maturation of dendritic cells (DCs) and

activate cytotoxic T cells for synergistic antitumor immunotherapy. GAFs with

laser irradiation exhibited the capacity of inhibition of pulmonary metastasis.

This work presented a strategy for incorporating small molecule immunomodulator

into the metal-polyphenolic coordination to ameliorate its deficiencies,

thereby inspiring a new design concept for tumor treatment.

文献 6

[IF=15.1] CHEMICAL ENGINEERING JOURNAL

DOI:10.1016/j.cej.2023.143985

文献引用抗体：bs-2527R | Anti-CD163 pAb | IF,ICC

Institution:南京工业大学材料科学与工程学院

 Abstract:

Smart hydrogel dressings capable of simultaneously

highly effective antimicrobial, anti-inflammatory, and promoting

re-epithelialization and angiogenesis are urgently needed for the management of

diabetic wounds. Herein, a H₂S-releasing

multifunctional hydrogel was developed by utilizing the dynamic Schiff base

reaction between carboxymethyl chitosan (CMC) and polyhexamethylene guanidine

(PHMG)-modified aldehyde F108 (PFC). Diallyl trisulfide (DATS) was encapsulated

into the PFC nanoparticles. Apart from possessing the essential properties

necessary for an idealized hydrogel dressing, such as excellent injectability,

tissue adhesion, self-healing, and stimulus–response degradation, the

DATS@PFC&CMC also utilized the synergistic effect of the PHMG and DATS to

provide an efficient antimicrobial effect; the H₂S was slowly released from the DATS

under the action of GSH and exerted excellent anti-inflammatory effects, by

inhibiting the expression of p-ERK and p-STAT3 in activated macrophages, and

promoting macrophage polarization to the M2 phenotype. Strikingly, following

the completion of the efficient antimicrobial and anti-inflammatory effects,

the continuously generated H₂S

further significantly accelerated the proliferation, migration, and

vascularization of endothelial cells by extending the activation of the p-p38

and p-ERK1/2. Owing to superior performances, DATS@PFC&CMC significantly

promoted the healing of diabetic wounds induced by streptozotocin with good

biocompatibility. This study demonstrates that DATS@PFC&CMC is a versatile

hydrogel dressing with great potential for the management of diabetic wounds.

文献 7

[IF=15.1] CHEMICAL ENGINEERING JOURNAL

DOI:10.1016/j.cej.2023.143844

文献引用抗体：

bs-43042P | Recombinant SARS-Cov-2 Spike S1 protein (L18F, T20N, P26S, D138Y,

R190S, K417T, E484K, N501Y, D614G, H655Y), His (HEK293)

bs-43049P | Recombinant SARS-Cov-2 Spike S1 protein (T19R, G142D, del157/158,

L452R, T478K, D614G, P681R), His (HEK293)

bs-43041P | Recombinant SARS-Cov-2 Spike S1 protein (D80A, D215G, del241/243,

K417N, E484K, N501Y, D614G), His (HEK293)

Institution:哈尔滨医科大学生物医学学院

 Abstract:

Biosensors are rapid and portable detection devices

with great potential for the instant screening of infectious diseases.

Receptors are the critical element of biosensors. They determine the

specificity, sensitivity and stability. However, current receptors are mainly

limited to antibodies and aptamers. Herein, we developed a glycosylated

extracellular vesicle-like receptor (GlycoEVLR) for the rapid detection of

virus antigens, specifically using SARS-CoV-2 as a model. The human

angiotensin-converting enzyme 2 (ACE2)-overexpressed and heparin-functionalized

HEK-293T cell membrane-cloaked Fe₃O₄ nanoparticles (NPs) were prepared as

functionalizing GlycoEVLR. They were characterized as spherical core–shell

structures with a diameter of around 100 nm, which were perfectly comparable to

natural extracellular vesicles. Binding affinities between GlycoEVLR and spike1

(S1) antigen were demonstrated using surface plasmon resonance (SPR). The

GlycoEVLR was fixed on magnetic electrodes to construct electrochemical

biosensors. Using electrochemical impedance spectroscopy (EIS) as a measurement

technique, the S1 antigen was detected down to 1 pg/mL within 20 min and showed

a good linearity range from 1 pg/mL to 1 ng/mL. Also, the GlycoEVLR-based

electrochemical biosensors showed excellent antifouling performance and

stability. Overall, our work provides a useful methodology for developing

extracellular vesicle-like receptors for biosensors. Combining the inherit

natural receptor proteins and antifouling lipids from the host cells with

engineered glycan motifs to target and sense viral antigens will open a new avenue

for biosensors.