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Reactive oxygen species (ROS) produced by NADPH oxidase promote contraction of peripheral arteries, which is especially pronounced in early postnatal period in comparison to adulthood, but the mechanisms of such vasomotor influence are poorly understood. We tested the hypothesis that Rho-kinase and protein kinase C (PKC) mediate procontractile influence of NADPH oxidase derived ROS in peripheral artery of early postnatal rats. In addition, we evaluated the involvement Src-kinase and L-type voltage-gated Ca channels (LTCC) into procontractile influence of ROS, produced by NADPH oxidase, because of their known interplay with Rho-kinase and PKC pathways.

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As the main inhibitory neurotransmission system, the GABAergic system poses an interesting yet underutilized target for molecular brain imaging. While PET imaging of postsynaptic GABAergic neurons has been accomplished using radiolabeled benzodiazepines targeting the GABA receptor, the development of presynaptic radioligands targeting GABA transporter 1 (GAT1) has been unsuccessful thus far. Therefore, we developed a novel GAT1-addressing radioligand and investigated its applicability as a PET tracer in rodents.

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Type 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.

Burns Trauma

January 2025

Department of Critical Care Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No. 321 Zhongshan Road, Gulou District, Nanjing, Jiangsu 210008, China.

Background: Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.

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Effect of Low-Dose Methylprednisolone in Promoting Neurological Function Recovery after Spinal Cord Injury: Clinical and Animal Studies.

Spine (Phila Pa 1976)

January 2025

Department of Orthopedics, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.

Study Design: Subgroup analysis of a retrospective clinical and animal trial [Study of different doses of methylprednisolone on functional recovery of spinal cord injury].

Objective: The aimed to investigate the efficacy of low-dose methylprednisolone regimens in promoting neural repair after SCI.

Summary Of Background Data: Spinal cord injury (SCI) can result in sensory, motor, and autonomic nerve dysfunction, often leading to disability or death.

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Chewing-Activated TRPV4/PIEZO1--Zn Axes in a Rat Periodontal Complex.

J Dent Res

January 2025

Department of Preventive and Restorative Dental Sciences, School of Dentistry, University of California, San Francisco, CA, USA.

The upstream mechanobiological pathways that regulate the downstream mineralization rates in periodontal tissues are limitedly understood. Herein, we spatially colocalized and correlated compression and tension strain profiles with the expressions of mechanosensory ion channels (MS-ion) TRPV4 and PIEZO1, biometal zinc, mitochondrial function marker (), cell senescence indicator (), and oxygen status marker hypoxia-inducible factor-1α () in rats fed hard and soft foods. The observed zinc and related cellular homeostasis in vivo were ascertained by TRPV4 and PIEZO1 agonists and antagonists on human periodontal ligament fibroblasts ex vivo.

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