Results 101 to 110 of about 3,675,695 (304)

Increased gene copy number of DEFA1/DEFA3 worsens sepsis by inducing endothelial pyroptosis. [PDF]

open access: yes, 2019
Sepsis claims an estimated 30 million episodes and 6 million deaths per year, and treatment options are rather limited. Human neutrophil peptides 1-3 (HNP1-3) are the most abundant neutrophil granule proteins but their neutrophil content varies because ...
Chen, QiXing   +12 more
core   +1 more source

Prospects for transgenesis in the chick [PDF]

open access: yes, 2004
Research to develop a useful method for genetic modification of the chick has been on-going since the first demonstrations in the mouse in the 1980s that genetic modification is an invaluable tool for the study of gene function. Manipulation of the chick
Bosselman   +52 more
core   +1 more source

Materials and System Design for Self‐Decision Bioelectronic Systems

open access: yesAdvanced Materials, EarlyView.
This review highlights how self‐decision bioelectronic systems integrate sensing, computation, and therapy into autonomous, closed‐loop platforms that continuously monitor and treat diseases, marking a major step toward intelligent, self‐regulating healthcare technologies.
Qiankun Zeng   +9 more
wiley   +1 more source

Renal phenotype of Et-1 transgenic mice is modulated by androgens

open access: yesEuropean Journal of Medical Research, 2009
Introduction Activation of the endothelin (ET) system promotes inflammation and fibrosis in various tissues including the kidney. Male ET-1 transgenic mice are characterized by chronic kidney inflammation and renal scarring.
Kalk P   +6 more
doaj   +1 more source

Depopulation of dense α-synuclein aggregates is associated with rescue of dopamine neuron dysfunction and death in a new Parkinson's disease model.

open access: yes, 2019
Parkinson's disease (PD) is characterized by the presence of α-synuclein aggregates known as Lewy bodies and Lewy neurites, whose formation is linked to disease development. The causal relation between α-synuclein aggregates and PD is not well understood.
Anichtchik, O.   +12 more
core   +1 more source

Increased risk for T cell autoreactivity to ß-cell antigens in the mice expressing the Avy obesity-associated gene. [PDF]

open access: yes, 2019
There has been considerable debate as to whether obesity can act as an accelerator of type 1 diabetes (T1D). We assessed this possibility using transgenic mice (MIP-TF mice) whose ß-cells express enhanced green fluorescent protein (EGFP). Infecting these
Atkinson, Mark A   +6 more
core   +2 more sources

NARFL Knockout Triggers Ferroptosis‐Driven Vascular Endothelial Dysfunction

open access: yesAdvanced Science, EarlyView.
NARFL is vital for CIA and oxidative stress resistance. NARFL deletion in HPMEC cells, zebrafish, and mice is lethal and rescued by a Ferroptosis inhibitor. NARFL deficiency disrupted its interaction with CIA proteins, decreased aconitase activity, increased IRP1 activity, induced Fe overload, and led to ferroptosis and oxidative stress, resulting in ...
Hui Hu   +15 more
wiley   +1 more source

HDAC inhibitor sodium butyrate reverses transcriptional downregulation and ameliorates ataxic symptoms in a transgenic mouse model of SCA3

open access: yesNeurobiology of Disease, 2011
Spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant neurodegenerative disease caused by polyglutamine-expanded ataxin-3. Previously, we prepared a SCA3 animal model by generating transgenic mice expressing disease-causing ataxin-3-Q79.
An-Hsun Chou   +4 more
doaj   +1 more source

Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites [PDF]

open access: yes, 2016
Autoantibodies to insulin are a harbinger of autoimmunity in type 1 diabetes in humans and in non-obese diabetic mice. To understand the genesis of these autoantibodies, we investigated the interactions of insulin-specific T and B lymphocytes using T ...
Acevedo-Suárez   +59 more
core   +2 more sources

Mettl3‐Mediated m6A Modification Represents a Novel Therapeutic Target for FSGS

open access: yesAdvanced Science, EarlyView.
This study explores the roles of Mettl3‐induced N6‐methyladenosine (m6A) modifications in Focal segmental glomerulosclerosis (FSGS). The findings reveal that inhibition of Mettl3 results in podocyte injury by modulating the TJP1CDC42 pathway. Moreover, Administration of N6‐methyladenosine attenuates the FSGS phenotype in WT mice induced by Adriamycin ...
Fubin Zhu   +14 more
wiley   +1 more source

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