Results 221 to 230 of about 5,053,091 (357)

Proton therapy of cancer: Potential clinical advantages and cost-effectiveness [PDF]

open access: bronze, 2005
Jonas Lundkvist   +4 more
openalex   +1 more source

Proton Beam Therapy [PDF]

open access: yesEuropean Oncology & Haematology, 2018
openaire   +2 more sources

UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage‐to‐Myofibroblast Transition in Chronic Pancreatitis

open access: yesAdvanced Science, EarlyView.
These findings suggest that UCP2 promotes LD formation and release in acinar cells by upregulating ACSL3 expression. This alteration in the local lipid metabolic environment indirectly drives the MMT process. Additionally, UCP2 may regulate the acetylation of Smad3 through Sirt1, enhancing its nuclear activity and activating the TGF‐β/ Smad3 signaling ...
Kunpeng Wang   +9 more
wiley   +1 more source

Proton-pump inhibitor therapy for acetylsalicylic acid associated upper gastrointestinal symptoms, a randomised clinical trial

open access: bronze, 2003
Robert J.F. Laheij   +3 more
openalex   +1 more source

Intensity modulated proton therapy (IMPT) - The future of IMRT for head and neck cancer.

open access: yesOral Oncology, 2019
A. Moreno   +11 more
semanticscholar   +1 more source

Cathepsin K Aggravates Pulmonary Fibrosis Through Promoting Fibroblast Glutamine Metabolism and Collagen Synthesis

open access: yesAdvanced Science, EarlyView.
CTSK plays a critical role in pulmonary fibrosis. Excessive CTSK accumulation interacts with SNX9 to enhance TGF‐β1‐induced SMAD3 activation and GLS1 expression in fibroblasts, driving glutamine metabolism for collagen biosynthesis and exacerbating pulmonary fibrosis.
Mengting Chen   +10 more
wiley   +1 more source

The research beamlines at the Dresden proton therapy facility: available infrastructure and experimental capabilities. [PDF]

open access: yesFront Oncol
Horst F   +12 more
europepmc   +1 more source

Dynein‐Dependent Endo‐Lysosomal Degradation Drives Lewy Body Disorders Accompanied by Aβ Pathology

open access: yesAdvanced Science, EarlyView.
This study investigates the impact of Aβ plaques on α‐synuclein (αSyn) pathologies in dementia with Lewy bodies (DLB). Co‐culturing primary neurons with AD mouse brain slices reveals impaired dynein‐dependent organelle trafficking, affecting αSyn degradation. Activating Rab7 restores this process, reducing αSyn inclusions.
Linlin Zhou   +14 more
wiley   +1 more source

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