Open Access. Powered by Scholars. Published by Universities.®
- Keyword
-
- ALD (1)
- AMPs (1)
- Acute tubular necrosis (1)
- Apoptosis (1)
- Arsenic (1)
-
- Aryl hydrocarbon receptor (1)
- Biological modeling and simulation (1)
- Cadmium (1)
- Cancer (1)
- Cathelicidin (1)
- Chemotherapy (1)
- Cisplatin (1)
- Cisplatin nephrotoxicity (1)
- ER stress (1)
- Gender differences (1)
- Gut microbiota (1)
- Hepatokine (1)
- Hepatoxicity (1)
- In utero (1)
- Inflammasome (1)
- Liver disease (1)
- Liver-pancreas axis (1)
- Metabolic syndrome (1)
- NAFLD (1)
- Nanoparticle (1)
- Nanotherapy (1)
- Non-alcoholic fatty liver disease (1)
- Organochlorine (1)
- Polychlorinated biphenyls (1)
- Relative potency values (1)
Articles 1 - 6 of 6
Full-Text Articles in Life Sciences
The Role Of Cathelicidin In The Regulation Of Gut Microbiota And Inflammasome Activation In Alcoholic Liver Disease., Fengyuan Li
The Role Of Cathelicidin In The Regulation Of Gut Microbiota And Inflammasome Activation In Alcoholic Liver Disease., Fengyuan Li
Electronic Theses and Dissertations
Alcoholic liver disease (ALD) is characterized by gut dysbiosis and hepatic and intestinal inflammation. Gut microbiota is critically maintained by antimicrobial peptides (AMPs) expressed in the epithelial and immune cells. AMPs are also identified as immune-regulators in various diseases. Previous studies demonstrated that deficiency of AMPs REG3 lectins exacerbated alcoholic steatohepatitis. LL-37 is the sole member of human cathelicidin AMP family, named CRAMP in mouse. Despite of the extensive studies in infectious diseases and in gut-microbiota-related inflammatory bowel disease, the role of LL-37/CRAMP in ALD is yet unknown. Our previous studies showed a decreased intestinal CRAMP in a mouse model …
Evaluation Of Drug-Loaded Gold Nanoparticle Cytotoxicity As A Function Of Tumor Tissue Heterogeneity., Hunter Allan Miller
Evaluation Of Drug-Loaded Gold Nanoparticle Cytotoxicity As A Function Of Tumor Tissue Heterogeneity., Hunter Allan Miller
Electronic Theses and Dissertations
The inherent heterogeneity of tumor tissue presents a major challenge to nanoparticle-medicated drug delivery. This heterogeneity spans from the molecular to the cellular (cell types) and to the tissue (vasculature, extra-cellular matrix) scales. Here we employ computational modeling to evaluate therapeutic response as a function of vascular-induced tumor tissue heterogeneity. Using data with three-layered gold nanoparticles loaded with cisplatin, nanotherapy is simulated with different levels of tissue heterogeneity, and the treatment response is measured in terms of tumor regression. The results show that tumor vascular density non-trivially influences the nanoparticle uptake and washout, and the associated tissue response. The drug …
Loss Of The Na+/H+ Exchange Regulatory Factor 1 Results In Increased Susceptibility To Cisplatin-Induced Acute Kidney Injury., Adrienne M. Bushau-Sprinkle
Loss Of The Na+/H+ Exchange Regulatory Factor 1 Results In Increased Susceptibility To Cisplatin-Induced Acute Kidney Injury., Adrienne M. Bushau-Sprinkle
Electronic Theses and Dissertations
Background. Acute kidney injury (AKI), an abrupt loss of kidney function which carries a high mortality and confers an increased risk of chronic kidney disease, develops in 30% of patients who receive cisplatin, a widely used chemotherapeutic agent [1], [2], [3]. The sodium hydrogen exchange regulatory factor isoform 1 (NHERF1) is a scaffolding protein that anchors multiple membrane proteins, in renal proximal tubules [4]. NHERF-1 deficient mice have aberrant localization of BBM proteins in intracellular compartments [5]. The investigators have recently demonstrated NHERF1 deficient proximal tubule cells have an underlying …
The Effects Of Polychlorinated Biphenyls Exposure On Non-Alcoholic Fatty Liver Disease : Role Of Aryl Hydrocarbon Receptor., Hongxue Shi
Electronic Theses and Dissertations
Polychlorinated biphenyls (PCBs) are detectable in serum of 100% of adults in US, and has been associated with fatty liver disease in epidemiological studies. PCBs are classified as either dioxin-like (DL) or non-dioxin-like (NDL) PCB based on their ability to activate the aryl hydrocarbon receptor (AhR). We used exposures that reflect human bioaccumulation patterns, which resembles Aroclor 1260 with a low level of the DL-PCB, PCB 126. Our aim was to determine if this exposure will activate the human and mouse AhR and examine if receptor activation influences these steatotic responses due to PCB exposures. DL-PCBs exposure-induced AhR activation in …
A Model To Study The Effects Of Whole Life Chronic Exposure To Arsenic Or Cadmium On The Development Of Adult Metabolic Syndrome : Initial Characterization Of Hepatic Changes., Jamie L. Young
Electronic Theses and Dissertations
Metabolic syndrome (MetS) is a group of diseases affecting < 30% of adults. Although obesity is a major risk for the development of MetS, it does not account for all cases, suggesting contribution of other risk factors. We hypothesized that early life exposure to arsenic (As) or cadmium (Cd) may represent such a risk. The purpose of this study was to characterize a model to discern the effects of early life exposures to Cd and As on high fat diet (HFD)-induced MetS. Adult C57BL/6J mice were exposed to control or metals containing drinking water. Pregnant dams and offspring were continuously exposed to the same toxicants as their parents. At weaning, offspring were fed LFD or HFD and sacrificed 10 or 24 weeks later. Metal exposure caused time- and sex-dependent alterations in HFD-induced variables of liver damage. The initial results suggest that these toxicants enhanced obesity-induced liver injury.
Vinyl Chloride Enhances Diet-Induced Liver Injury Via Metabolic Dyshomeostasis : Critical Role Of Mitochondria., Anna L. Lang
Vinyl Chloride Enhances Diet-Induced Liver Injury Via Metabolic Dyshomeostasis : Critical Role Of Mitochondria., Anna L. Lang
Electronic Theses and Dissertations
Background. Vinyl chloride (VC) is an environmental toxicant and has been shown to be directly hepatotoxic at high exposures. However, recent studies suggest low-level toxicant exposure can cause subtle changes to the liver. Given the high prevalence of non-alcoholic fatty liver disease (NAFLD) in the United States, it is important to determine the impact of low-level toxicant exposure on the progression of underlying liver injury when combined with other factors. Therefore, the overarching goal of this dissertation was to develop a model of VC co-exposure with high-fat diet (HFD) and to determine the mechanisms by which VC contributes to the …