Results 121 to 130 of about 384,078 (314)

On the Relentless Pursuit of an Oral Insulin Delivery System: How Far is Too Far?

open access: yesAdvanced Therapeutics, EarlyView.
Injectable insulin preparations have far outpaced oral ones by virtue of adequate bioavailability and are driven by innovations, including insulin pumps, real‐time blood glucose monitoring, and artificial intelligence. In contrast, oral insulin delivery systems, including nanomedicines, continue to struggle and lag due to varied reasons.
Sourav Bhattacharjee
wiley   +1 more source

Genome editing for scalable production of alloantigen‐free lentiviral vectors for in vivo gene therapy

open access: yesEMBO Molecular Medicine, 2017
Lentiviral vectors (LV) are powerful and versatile vehicles for gene therapy. However, their complex biological composition challenges large‐scale manufacturing and raises concerns for in vivo applications, because particle components and contaminants ...
Michela Milani   +12 more
doaj   +1 more source

Excretion of beta 2-glycoprotein I (apolipoprotein H) in renal tubular disease

open access: yesClinical Chemistry, 1991
Abstract beta 2-Glycoprotein I (beta 2GI) was identified as a major urinary protein excreted by patients with several renal tubular diseases, including adult Fanconi syndrome, nephrocalcinosis associated with autoimmune diseases, Lowe's syndrome, and Dent's disease (a familial renal tubular disease).
F. V. Flynn   +3 more
openaire   +3 more sources

Binding of antiphospholipid antibodies to discontinuous epitopes on domain I of human beta(2)-glycoprotein I: mutation studies including residues R39 to R43.

open access: yesArthritis & Rheumatism, 2007
OBJECTIVE Pathogenic antiphospholipid antibodies (aPL) bind the self antigen N-terminal domain (domain I) of beta(2)-glycoprotein I (beta(2)GPI), with residues G40-R43 being important.
Y. Ioannou   +5 more
semanticscholar   +1 more source

Accelerated Bone Healing via Electrical Stimulation

open access: yesAdvanced Science, EarlyView.
Electrical stimulation significantly impacts bone healing by enhancing osteoblast proliferation, differentiation, and vascularization through calmodulin/calcineurin/NFAT signaling. It also boosts macrophage function and cell migration, presenting a comprehensive approach to accelerating bone repair.
Jianfeng Sun   +4 more
wiley   +1 more source

PCSK9 Promotes the Malignancy of Triple‐negative Breast Cancer Cells by Reducing Cholesterol Levels at the Plasma Membrane to Activate EGFR and HER3

open access: yesAdvanced Science, EarlyView.
By decreasing cholesterol and lipid raft levels in the plasma membrane, proprotein convertase subtilisin/kexin type 9 (PCSK9) boosts human epidermal growth factor receptor 1 and 3 (EGFR and HER3) activation, driving tumor growth and metastasis in triple‐negative breast cancer (TNBC).
Tianhong Li, Renfei Wu, Kathy Qian Luo
wiley   +1 more source

The Staphylococcus aureus protein Sbi acts as a complement inhibitor and forms a tripartite complex with host complement Factor H and C3b.

open access: yesPLoS Pathogens, 2008
The Gram-positive bacterium Staphylococcus aureus, similar to other pathogens, binds human complement regulators Factor H and Factor H related protein 1 (FHR-1) from human serum.
Katrin Haupt   +7 more
doaj   +1 more source

Endothelial cells as target for antiphospholipid antibodies. Human polyclonal and monoclonal anti-beta 2-glycoprotein I antibodies react in vitro with endothelial cells through adherent beta 2-glycoprotein I and induce endothelial activation.

open access: yesArthritis & Rheumatism, 1997
OBJECTIVE To investigate the ability of human anti-beta 2-glycoprotein I (anti-beta 2 GPI) antibodies to recognize the cofactor adherent on endothelial cells (EC) and to modulate endothelial functions.
N. Papa   +10 more
semanticscholar   +1 more source

α‐Synuclein Pathology Spreads in a Midbrain–Hindbrain Assembloid Model

open access: yesAdvanced Science, EarlyView.
A novel midbrain–hindbrain assembloid model demonstrates the spread of α‐synuclein pathology, a hallmark of Parkinson's disease, mimicking Braak's hypothesis. This model reveals how pathology propagates from the hindbrain to the midbrain, inducing synaptic changes and early signs of neuronal vulnerability. It offers an innovative platform for exploring
Gemma Gomez‐Giro   +14 more
wiley   +1 more source

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