95 research outputs found

    The Litigation Financing Industry: Regulation to Protect and Inform Consumers

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    Litigation financing companies ( LFCs ) provide nonrecourse cash advances to plaintiffs in exchange for a portion of their lawsuits\u27 potential future proceeds. While this arrangement allows individuals to continue to litigate without having to accept unjust settlement offers, desperate consumers are often forced to pay inequitable interest rates for the cases they finance. Because there is no absolute obligation to repay the LFC, the industry manages to avoid regulation under state interest rate ceilings for consumer loans. The few existing litigation financing laws do not restrict the interest rates that LFCs may charge, and even if some courts are willing to strike down egregiously unfair litigation financing agreements on a case-by-case basis, existing regulation fails to sufficiently protect consumers. On the other hand, overly strict interest rate ceilings on litigation financing agreements may foreclose the practice altogether. In order to preserve the benefits of litigation financing while protecting those who are desperate enough to need it, this Comment prescribes measures that would prevent predatory behavior and ensure reasonable profits for LFCs. Express statutory restrictions would prevent LFCs from reaping unreasonable profits, especially for the financing of lawsuits that practically guarantee sufficient settlements. States should also develop an online litigation financing marketplace that would offer updated business information, interest rate data, and customer reviews for each LFC. With transparent access to the industry, this centralized resource would promote consumer choice, expand access to litigation financing, and organically stimulate market competitio

    CCL4 induces inflammatory signalling and barrier disruption in the neurovascular endothelium

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    Background: During neuroinflammation many chemokines alter the function of the blood-brain barrier (BBB) that regulates the entry of macromolecules and immune cells into the brain. As the milieu of the brain is altered, biochemical and structural changes contribute to the pathogenesis of neuroinflammation and may impact on neurogenesis. The chemokine CCL4, previously known as MIP-1β, is upregulated in a wide variety of central nervous system disorders, including multiple sclerosis, where it is thought to play a key role in the neuroinflammatory process. However, the effect of CCL4 on BBB endothelial cells (ECs) is unknown. Materials and methods: Expression and distribution of CCR5, phosphorylated p38, F-actin, zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) were analysed in the human BBB EC line hCMEC/D3 by Western blot and/or immunofluorescence in the presence and absence of CCL4. Barrier modulation in response to CCL4 using hCMEC/D3 monolayers was assessed by measuring molecular flux of 70 ​kDa RITC-dextran and transendothelial lymphocyte migration. Permeability changes in response to CCL4 in vivo were measured by an occlusion technique in pial microvessels of Wistar rats and by fluorescein angiography in mouse retinae. Results: CCR5, the receptor for CCL4, was expressed in hCMEC/D3 cells. CCL4 stimulation led to phosphorylation of p38 and the formation of actin stress fibres, both indicative of intracellular chemokine signalling. The distribution of junctional proteins was also altered in response to CCL4: junctional ZO-1 was reduced by circa 60% within 60 ​min. In addition, surface VE-cadherin was redistributed through internalisation. Consistent with these changes, CCL4 induced hyperpermeability in vitro and in vivo and increased transmigration of lymphocytes across monolayers of hCMEC/D3 cells. Conclusion: These results show that CCL4 can modify BBB function and may contribute to disease pathogenesis

    Complex network model for COVID-19: human behavior, pseudo-periodic solutions and multiple epidemic waves

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    We propose a mathematical model for the transmission dynamics of SARS-CoV-2 in a homogeneously mixing non constant population, and generalize it to a model where the parameters are given by piecewise constant functions. This allows us to model the human behavior and the impact of public health policies on the dynamics of the curve of active infected individuals during a COVID-19 epidemic outbreak. After proving the existence and global asymptotic stability of the disease-free and endemic equilibrium points of the model with constant parameters, we consider a family of Cauchy problems, with piecewise constant parameters, and prove the existence of pseudo-oscillations between a neighborhood of the disease-free equilibrium and a neighborhood of the endemic equilibrium, in a biologically feasible region. In the context of the COVID-19 pandemic, this pseudo-periodic solutions are related to the emergence of epidemic waves. Then, to capture the impact of mobility in the dynamics of COVID-19 epidemics, we propose a complex network with six distinct regions based on COVID-19 real data from Portugal. We perform numerical simulations for the complex network model, where the objective is to determine a topology that minimizes the level of active infected individuals and the existence of topologies that are likely to worsen the level of infection. We claim that this methodology is a tool with enormous potential in the current pandemic context, and can be applied in the management of outbreaks (in regional terms) but also to manage the opening/closing of borders.Comment: 23 pages, 10 figures, submitted 5-Oct-202

    CCL4 induces inflammatory signalling and barrier disruption in the neurovascular endothelium

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    Background: During neuroinflammation many chemokines alter the function of the blood-brain barrier (BBB) that regulates the entry of macromolecules and immune cells into the brain. As the milieu of the brain is altered, biochemical and structural changes contribute to the pathogenesis of neuroinflammation and may impact on neurogenesis. The chemokine CCL4, previously known as MIP-1β, is upregulated in a wide variety of central nervous system disorders, including multiple sclerosis, where it is thought to play a key role in the neuroinflammatory process. However, the effect of CCL4 on BBB endothelial cells (ECs) is unknown. Materials and methods: Expression and distribution of CCR5, phosphorylated p38, F-actin, zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) were analysed in the human BBB EC line hCMEC/D3 by Western blot and/or immunofluorescence in the presence and absence of CCL4. Barrier modulation in response to CCL4 using hCMEC/D3 monolayers was assessed by measuring molecular flux of 70 ​kDa RITC-dextran and transendothelial lymphocyte migration. Permeability changes in response to CCL4 in vivo were measured by an occlusion technique in pial microvessels of Wistar rats and by fluorescein angiography in mouse retinae. Results: CCR5, the receptor for CCL4, was expressed in hCMEC/D3 cells. CCL4 stimulation led to phosphorylation of p38 and the formation of actin stress fibres, both indicative of intracellular chemokine signalling. The distribution of junctional proteins was also altered in response to CCL4: junctional ZO-1 was reduced by circa 60% within 60 ​min. In addition, surface VE-cadherin was redistributed through internalisation. Consistent with these changes, CCL4 induced hyperpermeability in vitro and in vivo and increased transmigration of lymphocytes across monolayers of hCMEC/D3 cells. Conclusion: These results show that CCL4 can modify BBB function and may contribute to disease pathogenesis

    Surface Analysis of 4-Aminothiophenol Adsorption at Polycrystalline Platinum Electrodes

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    Formation of self-assembled monolayer (SAM) of 4-aminothiophenol (4-ATP) on polycrystalline platinum electrodes has been studied by surface analysis and electrochemistry techniques. The 4-ATP monolayer was characterized by cyclic voltammetry (CV), Raman spectroscopy, reflection absorption infrared (RAIR) spectroscopy, and X-ray photoelectron spectroscopy (XPS). Cyclic voltammetry (CV) experiments give an idea about the packing quality of the monolayer. RAIR and Raman spectra for 4-ATP modified platinum electrodes showed the characteristic adsorption bands for neat 4-ATP indicating the adsorption of 4-ATP molecules on platinum surface. The adsorption on platinum was also evidenced by the presence of sulfur and nitrogen peaks by XPS survey spectra of the modified platinum electrodes. High resolution XPS studies and RAIR spectrum for platinum electrodes modified with 4-ATP indicate that molecules are sulfur-bonded to the platinum surface. The formation of S-Pt bond suggests that ATP adsorption gives up an amino terminated SAM. Thickness of the monolayer was evaluated via angle-resolved XPS (AR-XPS) analyses. Derivatization of 4-ATP SAM was performed using 16-Br hexadecanoic acid

    A Protocol to Understand the Implementation and Experiences of an Online Community-Based Performance Arts Programme Through and Beyond the COVID-19 Pandemic, Brain Waves.

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    INTRODUCTION: Individuals living with acquired brain injury experience numerous psychological, physical, and social challenges. Since the COVID-19 pandemic, many have experienced additional isolation, mental health issues and have had limited access to social and physical activities otherwise available in the community. MATERIALS AND METHODS: Brain Waves is a 12-week online performance arts programme developed during the COVID-19 pandemic, for people with acquired brain injury (ABI). The research component of Brain Waves is a qualitative study, using Interpretative Phenomenological Analysis (IPA) and ethnographic methods (Observations and Interviews). The study will recruit two distinct populations: individuals living with acquired brain injury (including people who have experienced traumatic brain injury and stroke who are participating in the programme) and stakeholders (facilitators, involved in the delivery of Brain Waves). This paper presents the protocol for a project which aims to gain an understanding of the implementation and experiences of creating and participating in an online community-based performance arts programme
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