787 research outputs found

    A shooting argument approach to a sharp type solution for nonlinear degenerate Fisher-KPP equations

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    In this paper we prove the existence and uniqueness of a travelling-wave solution of sharp type for the degenerate (at u = 0) parabolic equation u1=[D(u)ux]x+g(u)u_1 = [D(u)u_x]_x + g(u) where D is a strictly increasing function and g is a function which generalizes the kinetic part of the classical Fisher-KPP equation. The original problem is transformed into the proper travelling-wave variables, and then a shooting argument is used to show the existence of a saddle-saddle heteroclinic trajectory for a critical value, c*>0, of the speed c of an autonomous system of ordinary differential equations. Associated with this connection is a sharp-type solution of the nonlinear partial differential equation

    A review on travelling wave solutions of one-dimensional reaction diffusion equations with non-linear diffusion term

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    In this paper we review the existence of different types of travelling wave solutions u(x,t)=ϕ(xct)u(x,t) = \phi(x - ct) of degenerate non-linear reaction-diffusion equations of the form ut=[D(u)ux]x+g(u)u_t = [D(u)u_x]_x + g(u) for different density-dependent diffusion coefficients D and kinetic part g. These include the non-linear degenerate generalized Fisher-KPP and the Nagumo equations. Also, we consider an equation whose diffusion coefficient changes sign as the diffusive substance increases. This describes a diffusive-aggregative process. In this case the travelling wave solutions are explored and the ill-posedness of two boundary-value problems associated with the above equation is stated

    The effect of interferon beta-1b treatment on MRI measures of cerebral atrophy in secondary progressive multiple sclerosis.

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    The recently completed European trial of interferon beta-1b (IFN beta -1b) in patients with secondary progressive multiple sclerosis (SP multiple sclerosis) has given an opportunity to assess the impact of treatment on cerebral atrophy using serial MRI. Unenhanced T-1-weighted brain imaging was acquired in a subgroup of 95 patients from five of the European centres; imaging was performed at 6-month intervals from month 0 to month 36. A blinded observer measured cerebral volume on four contiguous 5 mm cerebral hemisphere slices at each time point, using an algorithm with a high level of reproducibility and automation. There was a significant and progressive reduction in cerebral volume in both placebo and treated groups, with a mean reduction of 3.9 and 2.9%, respectively, by month 36 (P = 0.34 between groups). Exploratory subgroup analyses indicated that patients without gadolinium (Gd) enhancement at the baseline had a greater reduction of cerebral volume in the placebo group (mean reduction at month 36: placebo 5.1%, IFN beta -1b 1.8%, P < 0.05) whereas those with Gd-enhancing lesions showed a trend to greater reduction of cerebral volume if the patient was on IFN<beta>-1b (placebo 2.6%, IFN beta -1b, 3.7%; P > 0.05). These results are consistent with ongoing tissue loss in both arms of this study of secondary progressive multiple sclerosis. This finding is concordant with previous observations that disease progression, although delayed, is not halted by IFN beta. The different pattern seen in patients with and without baseline gadolinium enhancement suggests that part of the cerebral volume reduction observed in IFN beta -treated patients may be due to the anti-inflammatory/antioedematous effect of the drug. Longer periods of observation and larger groups of patients may be needed to detect the effects of treatment on cerebral atrophy in this population of patients with advanced disease

    No evidence of disease activity status in patients treated with early vs. delayed subcutaneous interferon β-1a.

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    Abstract Background Clinically isolated syndrome (CIS) is defined as a monophasic clinical episode highly suggestive of multiple sclerosis (MS). Regardless, studies have shown that treatment at this early stage of MS can delay a second event and prolong the transition to clinically diagnosed MS. The objective of this post-hoc analysis was to determine the effect of early CIS treatment with once weekly (qw) or three times weekly (tiw) subcutaneous interferon (scIFN) β-1a vs. delayed treatment (DT) on the composite endpoint of no evidence of disease activity (NEDA)-3. Methods In REFLEX, patients with CIS were randomized to double-blind scIFN β-1a 44 µg tiw, qw, or placebo for 24 months. Upon clinically-definite MS, patients switched to open-label scIFN β-1a tiw. Patients who completed REFLEX entered an extension (REFLEXION). Patients initially randomized to placebo switched to tiw (DT); scIFN β-1a patients continued their initial qw/tiw regimen for up to 60-months post-randomization. This post-hoc analysis was conducted in the integrated intent-to-treat REFLEX plus REFLEXION population (tiw, n = =171; qw, n = =175; DT, n = =171). All p values are nominal. CIS was defined using the McDonald 2010 criteria. Results Patients receiving early treatment (ET) with scIFN β-1a tiw and qw were more likely to achieve NEDA-3 than DT at year 2 (tiw vs. DT: OR 4.26, 95% CI 2.02–8.98, p = =0.0001; qw vs. DT: OR 2.99, 95% CI 1.39–6.43, p = =0.005). Compared with DT, ET with scIFN β-1a tiw was more likely to achieve NEDA-3 at year 3 (OR 3.73, 95% CI 1.63–8.55, p = =0.002) and year 5 (OR 12.96, 95% CI 1.66–101.04, p = =0.015). Between ET regimens, the odds of achieving NEDA-3 were not significantly improved by scIFN β-1a 44 µg tiw at year 2 (OR 1.42, 95% CI 0.81–2.50, p = =0.22) but were at year 3 (OR 2.26, 95% CI 1.11–4.60, p = =0.024) and year 5 (OR 3.22, 95% CI 1.01–10.22, p = =0.048), indicating that the beneficial effects of more frequent scIFN β-1a dosing become more apparent over time in patients with CIS. In the subgroup of patients with Gd+ lesions at baseline the odds for achieving NEDA-3 were higher for ET up to year 2 compared with DT (tiw: OR 10.21, 95% CI 1.23–84.82, p = =0.03; qw: OR 8.97, 95% CI 1.08–74.28, p = =0.04). In patients without Gd+ lesions at baseline, those receiving ET were more likely to achieve NEDA-3 at year 2 (OR 3.56, 95% CI 1.56–8.10, p = =0.003), year 3 (OR 2.54, 95% CI 1.05–6.18, p = =0.04) and year 5 (OR 9.63, 95% CI 1.19–77.79, p = =0.034) than patients who received DT. Conclusions ET with scIFN β-1a tiw was associated with a higher likelihood of achieving NEDA-3 not only at 2 but also at 3 and 5 years
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