Results 111 to 120 of about 96,616 (241)

Pathological Mechanism‐Inspired Biomimetic Nano‐Senotherapy for Reversing Experimental Atherosclerosis in ApoE−/− Mice

open access: yesAdvanced Science, EarlyView.
The biomimetic self‐assembly nanomedicine reversing atherosclerosis via senotherapy strategy. ABSTRACT The greatest challenge in atherosclerosis (AS) management lies in achieving lesion reversal, not merely slowing progression. Senescent cell accumulation—driven by continuous generation and apoptotic resistance—perpetuates plaque pathology and ...
Yuhan Tian   +9 more
wiley   +1 more source

Alemtuzumab in the treatment of multiple sclerosis

open access: yesJournal of Inflammation Research, 2014
Óscar Fernandez Institute of Clinical Neuroscience, Neurology Department, Hospital Regional Universitario Carlos Haya, FIMABIS, Malaga, Spain Abstract: Alemtuzumab (formerly known as Campath-1H) has recently been approved by the European ...
Fernandez Ó
doaj  

Epidermal METTL1‐Mediated m7G Modification Drives Psoriatic Inflammation by Stabilizing Bdkrb1 and Orchestrating Neutrophil Recruitment

open access: yesAdvanced Science, EarlyView.
This study unveils an unrecognized pro‐inflammatory epitranscriptomic checkpoint in psoriasis. By installing m7G modifications on the 5′ UTR of Bdkrb1 mRNA, METTL1 enhances receptor stability to orchestrate keratinocyte‐driven neutrophil recruitment via p38 MAPK signaling.
Chang Zhang   +10 more
wiley   +1 more source

PRMT9 Aggravated Dopaminergic Neurodegeneration in Parkinson's Disease Model by Facilitating the Degradation of DUSP26 and Inducing Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
In the pathological state of PD induced by MPP+, the upregulated PRMT9 in dopaminergic neurons translocates into mitochondrion and interacts with DUSP26 and catalyzes its arginine methylation, leading to the ubiquitin‐proteasomal degradation of DUSP26 mediated by Trim32.
Tengfei Liu   +13 more
wiley   +1 more source

Review of teriflunomide and its potential in the treatment of multiple sclerosis

open access: yesNeuropsychiatric Disease and Treatment, 2009
Clemens Warnke1, Gerd Meyer zu Hörste1, Hans-Peter Hartung1, Olaf Stüve2,3,4, Bernd C Kieseier11Department of Neurology, Heinrich-Heine-University Düsseldorf, Germany; 2Neurology Section, VA North Texas Health Care System ...
Clemens Warnke   +4 more
doaj  

Microplastics‐Induced Gut Microbiota Dysbiosis Accelerates Alzheimer's‐Like Pathology and Cognitive Decline via the Gut–Brain Axis

open access: yesAdvanced Science, EarlyView.
Microplastics (MPs) breach the gut‐brain axis by triggering taurine‐depleting microbiota dysbiosis that accelerates Alzheimer‐like pathology in 5XFAD mice. Taurine supplementation normalizes autophagy, microglial quiescence, and cognition, and plasma taurine inversely tracks cognitive decline in ADNI participants, revealing a readily translatable ...
Zifeng Wu   +8 more
wiley   +1 more source

Long-term safety and efficacy of natalizumab in relapsing-remitting multiple sclerosis: impact on quality of life

open access: yesPatient Related Outcome Measures, 2014
Raquel Planas, Roland Martin, Mireia Sospedra Neuroimmunology and MS Research, Department of Neurology, University of Zurich, Zurich, Switzerland Abstract: Natalizumab was the first monoclonal antibody to be approved for the treatment of relapsing ...
Planas R, Martin R, Sospedra M
doaj  

Safety of Disease-Modifying Therapies for Highly Active Relapsing-Remitting Multiple Sclerosis

open access: yes, 2022
MS-tautia eli pesäkekovettumatautia hoidetaan taudinkulkua muuntavilla lääkehoidoilla. Näiden hoitojen tarkoitus on vähentää MS-taudin tulehduksellista tautiaktiivisuutta ja sitä kautta estää toimintakyvyn heikkenemistä. Osalla MS-tautia sairastavista henkilöistä tauti on kuitenkin poikkeuksellisen aktiivinen, jolloin usein turvaudutaan kaikista ...
openaire   +1 more source

Mechanical Activation of Piezo1 Drives Osteoarthritis Through Kdm5c‐Mediated Epigenetic Silencing

open access: yesAdvanced Science, EarlyView.
Excessive mechanical stress activates Piezo1, triggering Ca2+‐dependent cytoskeletal forces that deform the nucleus and reduce H3K4me3. Kdm5c demethylates H3K4me3 at Col2a1 and Runx3 promoters. Kdm5c knockout rescues degradation. Repurposed telmisartan directly inhibits Kdm5c, blocking this axis and showing disease‐modifying efficacy in mouse OA models
Tianyou Kan   +13 more
wiley   +1 more source

Subcutaneously delivered natalizumab for the treatment of highly active relapsing-remitting multiple sclerosis

open access: yesČeská a slovenská neurologie a neurochirurgie, 2022
Simona Halúsková, Martin Vališ
openaire   +1 more source

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