Open Access. Powered by Scholars. Published by Universities.®
Articles 1 - 3 of 3
Full-Text Articles in Medical Physiology
Signaling Induced By Inflammatory Mediators In The Rodent Pulmonary Microvasculature, Rachel Escue Helms
Signaling Induced By Inflammatory Mediators In The Rodent Pulmonary Microvasculature, Rachel Escue Helms
Theses and Dissertations (ETD)
Acute lung inflammation (ALI), stemming from a disproportionate and detrimental immune response, may arise from or complicate other disease states, leading to the often-fatal acute respiratory distress syndrome (ARDS). Because of the many culpable factors and differing points of induction, pinning down the signaling mechanisms involved in the morbidity of this disorder as well as defining an effective treatment has proved problematic. However, the most detrimental characteristic of this condition is seen regardless of the development of the response: increased microvascular permeability. Because of the architecture and the size of the pulmonary microvascular network, the lungs have a resident, sequestered …
Protein Trafficking Of Bk Channel Β1 Subunits In Cerebral Artery Myocytes, Xue Zhai
Protein Trafficking Of Bk Channel Β1 Subunits In Cerebral Artery Myocytes, Xue Zhai
Theses and Dissertations (ETD)
Rationale: Large-conductance calcium (Ca2+)-activated potassium channels (BK) are expressed in arterial myocytes to control arterial contractility. It is composed of pore- forming BKα and auxiliary β1 subunits. Auxiliary β1 subunits associate with BKα which modulate Ca2+ sensitivity of BK channel. Previous data showed that BKα locates at cell membrane, whereas β1 subunits are primarily intracellular which regulated by Rab11A- positive recycling endosomes. Endothelin-1 (ET-1), a vasoconstrictor, induces contraction of myocytes. ET-1 inhibits BK channel but mechanisms are not fully understood. It is unclear that vasoconstrictors regulate the cellular distribution of BK channels. Furthermore, BK channels are involved …
Characterization Of The Hepatotoxicity Of Rifampicin And Isoniazid, Christopher T. Brewer
Characterization Of The Hepatotoxicity Of Rifampicin And Isoniazid, Christopher T. Brewer
Theses and Dissertations (ETD)
In a mouse model, rifampicin and isoniazid combination treatment results in cholestatic liver injury that is associated with an increase of protoporphyrin ix (PPIX), the penultimate heme precursor. Excess PPIX is believed to bind to bile acids, precipitate in bile canaliculi, and form bile plugs leading to cholestasis fol owed by liver injury. Both ferrochelatase (FECH/Fech) and aminolevulinic acid synthase 1 (ALAS1/Alas1) are crucial enzymes in regulating heme biosynthesis. Isoniazid has recently been reported to up-regulate Alas1 but down-regulate Fech protein levels in mice; however the mechanism of isoniazid mediated heme synthesis …