Life Sciences Commons^™

Manganese Chloride Effects Chondrogenesis Of Atdc5 Cells, Isabella Somera

Seton Hall University Dissertations and Theses (ETDs)

Manganese is an essential trace element found in humans, which aids in several processes including brain and nerve function, glucose metabolism, calcium absorption, and bone formation and homeostasis. Specifically, bone homeostasis utilizes osteoblasts and osteoclasts, cells which function to build and reabsorb bone respectively, as well as chondrocytes, cells which aid in endochondral ossification. Chondrocytes deposit extracellular matrix components, such as aggrecan, collagen, and proteoglycans, that provide the necessary scaffold for osteoblasts to synthesize and mineralize bone. Activation of the rapamycin (mTOR) pathway influences the regulation of several cellular processes, such as skeletal development and bone homeostasis. In this study, …

Investigation Of The Effect Of Trace Element, Copper Chloride, On Chondrogenic Cell Line, Atdc5 Function, Alexandra Bambrick

Seton Hall University Dissertations and Theses (ETDs)

Copper chloride (CuCl₂) is an essential trace element found in humans, which helps to aid in brain and nerve function, glucose metabolism, calcium absorption, and bone formation. Bone formation utilizes a variety of cell types, including, osteoblasts, osteoclasts, and chondrocytes. Chondrocytes deposit cartilage components like collagen and proteoglycans that provide the necessary scaffold for osteoblasts to synthesize and mineralize bone. Copper chloride is known to aid in osteogenesis, maintain bone metabolism, and regulate bone mineral density, but its role in chondrogenesis is still unclear (15).

In this study, it is hypothesized that CuCl₂ treatments would enhance chondrogenic …

Human Neuroblastoma Adaptation To Cobalt Chloride-Induced Hypoxia, Conor Mcauliffe

Seton Hall University Dissertations and Theses (ETDs)

Hypoxia is a frequent characteristic of the solid tumor microenvironment, which occurs when cancer cells lack adequate access to oxygen. By selecting for cells that can adapt to and grow in low oxygen conditions, tumor hypoxia contributes to a more aggressive and invasive cancer phenotype that portends a poor clinical outcome. While many aspects of the cellular response to hypoxia have been explored, the roles of some factors have not been fully explained. Cell signaling factors, including signal transducer and activator of transcription 3 (STAT3), the mu opioid receptor (MOR), and the delta opioid receptor (DOR), as well as changes …

Endotoxin-Induced Inflammation & Morphine-Induced Conditioned Place Preference In The Hiv-1 Transgenic Rat, Natasha F. Homji-Mishra

Seton Hall University Dissertations and Theses (ETDs)

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Somatostatin Regulates Raw 264.7 Cell Cytokine Release, Shilpa Swarup

Seton Hall University Dissertations and Theses (ETDs)

Immigrant monocytes and resident macrophages propagate the vertebrate innate immune response through cell migration and cytokine production. Monocytes responding to inflammatory challenge migrate into tissues, and as resident macrophages, release a major pro-inflammatory cytokine, tumor necrosis factor a (TNF-a). Macrophge cytokine synthesis is known to be under both negative and positive regulatory control. Recent studies have shown that somatostatin (SRIF) regulates monocyte and peritoneal macrophages. However, the effects of SRIF on RAW 264.7 cells, a transformed monocyte/macrophage cell line, have not been investigated. In the present study, SRIF effect on cytokine release in LPS stimulated RAW 264. 7 cells was …

Lipopolysaccharide Induced Septicemia In Chronic Morphine Treated Rats, Frank Ocasio

Seton Hall University Dissertations and Theses (ETDs)

Opiate-addicts have been known to show increased susceptibility to bacterial infection. Lipopolysaccharide (LPS), which is a cell wall component in gram-negative bacterial, is a potent stimulator of inflammation. We investigated how treatment with morphine alters LPS-induced inflammatory responses in the rat. Chronic morphine exposure alone elevated serum endotoxin levels. Animals treated with morphine and LPS (250 µglkg) developed hypothermia, decreased mean arterial pressure (MAP), increased plasma thrombin anti-thrombin III (TAT) complex, and approximately 67% exhibited progressive intramicrovascular coagulation. Morphine also enhanced LPS­ induced leukocyte endothelial adhesion (LEA), suppressed leukocyte flux and corticosterone production, and elevated interleukin- I�, tumor necrotic factor-a, …

Morphine Enhances The Permeability Across Vascular Endothelial Cell Barriers, Jenine Anday

Seton Hall University Dissertations and Theses (ETDs)

Using three types of in vitro endothelial cell barrier models, we investigated the direct effects and mechanisms of morphine on vascular permeability. Our current studies illustrate LPS induces permeability across these VEC barriers, and is significantly enhanced when co-treated with morphine, displayed using the [ 14 CJ-inulin paracellular marker. Incubation with morphine alone induces permeability in a concentration­ depeodent manner, and is not blocked by the addition of naloxone. Morphine enhances the detrimental effects of LPS on cell viability and alone also decreases endothelial cell viability, concentration-dependently, which is also not affected by naloxone, as demonstrated by the trypan blue …