Results 181 to 190 of about 294,536 (285)

Human Atlas of Tooth Decay Progression: Identification of Cellular Mechanisms Driving the Switch from Dental Pulp Repair Toward Irreversible Pulpitis

open access: yesAdvanced Science, EarlyView.
Tooth decay progression transforms the dental pulp response from repair to fibrosis. At early stages, stromal cells reprogram to repair the extra cellular matrix (ECM), blood vessels, and nerves, remodel and grow, keeping repair possible. In advanced decay, hypoxia, and vessel regression, in complement with an immune switch, fuel nerve degeneration and
Hoang Thai Ha   +12 more
wiley   +1 more source

HRS Degradation‐Induced Nicotinamide Deficiency in Placental Extracellular Vesicles Triggers Preeclampsia by Disrupting Maternal‐Fetal Immune Homeostasis

open access: yesAdvanced Science, EarlyView.
This study shows that lower NAM levels in PE‐derived pEVs correlate with disease severity. NAM‐deficient pEVs reduce Th1 and Th17 inhibition, leading to PE‐like symptoms. NAM in pEVs inhibits Th1 via SIRT1 and Th17 via macrophages. Reduced NAM in PE‐EVs is due to decreased HRS expression in trophoblasts, resulting from elevated HSP27.
Haiyi Fei   +10 more
wiley   +1 more source

Alkyltriphenylphosphonium Binding to Cardiolipin Triggers Oncosis in Cancer Cells

open access: yesAdvanced Science, EarlyView.
Alkyltriphenylphosphonium, exemplified by TPP+‐C14, preferentially accumulates in mitochondria and selectively binds to cardiolipin, a key phospholipid of the inner mitochondrial membrane, causing loss of mitochondrial membrane potential, severe cellular ATP depletion, and calcium imbalance.
Jin Li   +8 more
wiley   +1 more source

CHB‐Induced Immune Zonation Chaos Elicited LXRα‐mediated Lipid Metabolism Disorders in Kupffer Cells to Induce Cancer Stem Cell Formation

open access: yesAdvanced Science, EarlyView.
By profiling the spatiotemporal hepatic landscape of CHB mouse models, the originally peri‐portal localized KCs migrated to the peri‐central in a CXCL9‐CXCR3‐dependent manner, facilitating their interaction with HBV+ hepatocytes. The interaction promoted LMD in KCs through ASGR1‐induced LXRα degradation, which, in turn, induced CSC formation via Stat3 ...
Jingqi Shi   +18 more
wiley   +1 more source

Single‐Nucleus Multi‐Omics Reveals Hypoxia‐Driven Angiogenic Programs and Their Epigenetic Control in Sinonasal Squamous Cell Carcinoma

open access: yesAdvanced Science, EarlyView.
Single‐nucleus multi‐omics profiling of sinonasal squamous cell carcinoma unveils a hypoxia‐driven angiogenic axis. A specific hypoxic tumor subpopulation orchestrates endothelial tip cell differentiation via epigenetically regulated ADM and VEGFA secretion.
Chaelin You   +12 more
wiley   +1 more source

Development of Germline-Humanized Antibodies Neutralizing Botulinum Neurotoxin A and B. [PDF]

open access: yesPLoS One, 2016
Miethe S   +13 more
europepmc   +1 more source

Skeletal Muscle HSF1 Alleviates Age‐Associated Sarcopenia and Mitochondrial Function Decline via SIRT3‐PGC1α Axis

open access: yesAdvanced Science, EarlyView.
Aged HSF1 muscle‐specific knockout mice show deteriorated muscle atrophy and metabolic dysfunction, while active HSF1 overexpression improves muscle function via activating SIRT3 to deacetylate both PGC1α1 and PGC1α4, which boosts mitochondrial function and muscle hypertrophy in a fiber‐type specific manner, and induces FNDC5/Irisin for tissue ...
Jun Zhang   +18 more
wiley   +1 more source

Antibody and complement-dependent viral neutralization [PDF]

open access: yesSpringer Seminars in Immunopathology, 1979
Cooper, Neil R., Welsh, Raymond M.
openaire   +2 more sources

PARPi Combining Nanoparticle LIN28B siRNA for the Management of Malignant Ascites

open access: yesAdvanced Science, EarlyView.
This study demonstrates that co‐inhibition of LIN28B and PARP using siLin28b/DSSP@lip‐PEG‐FA nanoparticles in combination with the PARP inhibitor BMN673 effectively suppresses the accumulation of malignant ascites associated with advanced cancers.
Yan Fang   +13 more
wiley   +1 more source

Targeting Itga8 Mitigates Neurogenic Bladder Fibrosis Driven by Trem2⁺ Macrophage‐Derived Fn1 via FAK/RhoA/ROCK Signaling

open access: yesAdvanced Science, EarlyView.
Normal bladders exhibit quiescent fibroblasts/macrophages, whereas neurogenic bladders show acute‐phase Itga8⁺ fibroblast expansion driven by Trem2⁺ macrophage‐secreted Fn1, which activates FAK/RhoA/ROCK signaling, promotes cytoskeletal remodeling, and upregulates pro‐fibrotic genes.
Jiaxin Wang   +9 more
wiley   +1 more source

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