Population Models with Diffusion and Constant Yield Harvesting

In this paper we discuss reaction-diffusion equations arising in population dynamics with constant yield harvesting in one dimension. We focus on the mathematical models of the logistic growth, the strong Allee effect, and the weak Allee effect and their influence on the existence of positive steady states as well as global bifurcation diagrams. We analyze the equations using the quadrature method and the method of sub-super solutions

Environmentally Persistent Free Radicals (EPFRs). 3. Free versus Bound Hydroxyl Radicals in EPFR Aqueous Solutions

Additional experimental evidence is presented for in vitro generation of hydroxyl radicals because of redox cycling of environmentally persistent free radicals (EPFRs) produced after adsorption of 2-monochlorophenol at 230 °C (2-MCP-230) on copper oxide supported by silica, 5% Cu(II)O/silica (3.9% Cu). A chemical spin trapping agent, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), in conjunction with electron paramagnetic resonance (EPR) spectroscopy was employed. Experiments in spiked O17 water have shown that ∼15% of hydroxyl radicals formed as a result of redox cycling. This amount of hydroxyl radicals arises from an exogenous Fenton reaction and may stay either partially trapped on the surface of particulate matter (physisorbed or chemisorbed) or transferred into solution as free OH. Computational work confirms the highly stable nature of the DMPO–OH adduct, as an intermediate produced by interaction of DMPO with physisorbed/chemisorbed OH (at the interface of solid catalyst/solution). All reaction pathways have been supported by ab initio calculations

A Novel Peptide Derived from Human Apolipoprotein E Is an Inhibitor of Tumor Growth and Ocular Angiogenesis

Angiogenesis is a hallmark of tumor development and metastasis and now a validated target for cancer treatment. We previously reported that a novel dimer peptide (apoEdp) derived from the receptor binding region of human apolipoprotein E (apoE) inhibits virus-induced angiogenesis. However, its role in tumor anti-angiogenesis is unknown. This study demonstrates that apoEdp has anti-angiogenic property in vivo through reduction of tumor growth in a mouse model and ocular angiogenesis in a rabbit eye model. Our in vitro studies show that apoEdp inhibits human umbilical vein endothelial cell proliferation, migration, invasion and capillary tube formation. We document that apoEdp inhibits vascular endothelial growth factor-induced Flk-1 activation as well as downstream signaling pathways that involve c-Src, Akt, eNOS, FAK, and ERK1/2. These in vitro data suggest potential sites of the apoE dipeptide inhibition that could occur in vivo

Kaposi\u27s Sarcoma-Associated Herpesvirus G-protein Coupled Receptor Activates the Canonical Wnt/β-catenin Signaling Pathway.

Abstract Background: KSHV is a tumorigenic γ-herpesvirus that has been identified as the etiologic agent of Kaposi\u27s sarcoma (KS), a multifocal highly vascularized neoplasm that is the most common malignancy associated with acquired immunodeficiency syndrome (AIDS). The virus encodes a constitutively active chemokine receptor homologue, vGPCR that possesses potent angiogenic and tumorigenic properties, and is critical for KSHV pathobiology. To date, a number of signaling pathways have been identified as key in mediating vGPCR oncogenic potential. Findings: In this study, we identify a novel pathway, the Wnt/β-catenin pathway, which is dysregulated by vGPCR expression in endothelial cells. Expression of vGPCR in endothelial cells enhances the nuclear accumulation of β-catenin, that correlates with an increase in β-catenin transcriptional activity. Activation of β-catenin signaling by vGPCR is dependent on the PI3K/Akt pathway, as treatment of vGPCR-expressing cells with a pharmacological inhibitor of PI3K, leads to a decreased activation of a β-catenin-driven reporter, a significant decrease in expression of β-catenin target genes, and reduced endothelial tube formation. Conclusions: Given the critical role of Wnt/β-catenin signaling in angiogenesis and tumorigenesis, the findings from this study suggest a novel mechanism in KSHV-induced malignancies

Transthyretin Val122Ile, accumulated Aβ, and inclusion-body myositis aspects in cultured muscle

Cultured muscle fibers (CMF) from a patient with inclusion-body myositis (IBM) and cardiac amyloidosis associated with the transthyretin (TTR) Val122Ile mutation contained aspects of the IBM phenotype: vacuolation, congophilic inclusions, and clusters of immunocolocalizing amyloid β-peptide (Aβ) and TTR accumulations. These abnormalities are never present in normal human CMF. These perturbations were greatly increased after Aβ precursor protein gene transfer. The TTR mutation may be a genetic predisposition factor for the patient's IBM

Cystatin C colocalizes with amyloid-beta and coimmunoprecipitates with amyloid-beta precursor protein in sporadic inclusion-body myositis muscles

Cystatin C (CC), an endogenous cysteine protease inhibitor, is accumulated within amyloid-\u3b2 (A\u3b2) amyloid deposits in Alzheimer's disease (AD) brain and was proposed to play a role in the AD pathogenesis. Because the chemo-morphologic muscle phenotype of sporadic inclusion-body myositis (s-IBM) has several similarities with the phenotype of AD brain, including abnormal accumulation of A\u3b2 deposits, we studied expression and localization of CC in muscle biopsies of 10 s-IBM, and 16 disease- and five normal-control muscle biopsies. Physical interaction of CC with amyloid-\u3b2 precursor protein (A\u3b2PP) was studied by a combined immunoprecipitation/immunoblotting technique in the s-IBM muscle biopsies and in A\u3b2PP-overexpressing cultured human muscle fibers. In all s-IBM muscle biopsies, CC-immunoreactivity either colocalized with, or was adjacent to, the A\u3b2-immunoreactive inclusions in 80-90% of the vacuolated muscle fibers, mostly in non-vacuolated regions of their cytoplasm. Ultrastructurally, CC immunoreactivity-colocalized with A\u3b2 on 6-10 nm amyloid-like fibrils and floccular material. By immunoblotting, CC expression was strongly increased in IBM muscle as compared to the controls. By immunoprecipitation/immunoblotting experiments, CC coimmunoprecipitated with A\u3b2PP, both in s-IBM muscle and in A\u3b2PP-overexpressing cultured normal human muscle fibers. Our studies (i) demonstrate for the first time that CC physically associates with A\u3b2PP, and (ii) suggest that CC may play a novel role in the s-IBM pathogenesis, possibly by influencing A\u3b2PP processing and A\u3b2 deposition