Exact Solutions of the Saturable Discrete Nonlinear Schrodinger Equation

Exact solutions to a nonlinear Schr{\"o}dinger lattice with a saturable nonlinearity are reported. For finite lattices we find two different standing-wave-like solutions, and for an infinite lattice we find a localized soliton-like solution. The existence requirements and stability of these solutions are discussed, and we find that our solutions are linearly stable in most cases. We also show that the effective Peierls-Nabarro barrier potential is nonzero thereby indicating that this discrete model is quite likely nonintegrable

Inflammation as a potential mediator for the association between periodontal disease and Alzheimer’s disease

This is the publisher's version, also available electronically from http://www.dovepress.com/inflammation-as-a-potential-mediator-for-the-association-between-perio-peer-reviewed-article-NDT.Periodontal disease (PDD) is associated with increased risk of cardiovascular disease, cerebrovascular disease, and mortality in many studies, while other studies have begun to suggest an association of PDD with Alzheimer’s disease (AD). This paper discusses how infectious pathogens and systemic infection may play a role in AD. The roles of infection and inflammation are addressed specifically with regard to known AD pathologic lesions including senile plaques, neuron death, neurofibrillary tangles, and cerebrovascular changes. A testable model of proposed pathways between periodontal infection and AD is presented including three possible mechanisms: a) direct effects of infectious pathogens, b) inflammatory response to pathogens, and c) the effects on vascular integrity. The role of gene polymorphisms is discussed, including apolipoprotein (APOE) ε4 as a pro-inflammatory and pro-infection genotype

Inflammation as a potential mediator for the association between periodontal disease and Alzheimer’s disease

Periodontal disease (PDD) is associated with increased risk of cardiovascular disease, cerebrovascular disease, and mortality in many studies, while other studies have begun to suggest an association of PDD with Alzheimer’s disease (AD). This paper discusses how infectious pathogens and systemic infection may play a role in AD. The roles of infection and inflammation are addressed specifically with regard to known AD pathologic lesions including senile plaques, neuron death, neurofibrillary tangles, and cerebrovascular changes. A testable model of proposed pathways between periodontal infection and AD is presented including three possible mechanisms: a) direct effects of infectious pathogens, b) inflammatory response to pathogens, and c) the effects on vascular integrity. The role of gene polymorphisms is discussed, including apolipoprotein (APOE) ɛ4 as a pro-inflammatory and pro-infection genotype

Requirement for DNA Ligase IV during Embryonic Neuronal Development

The embryonic ventricular and subventricular zones (VZ/SVZ) contain the neuronal stem and progenitor cells and undergo rapid proliferation. The intermediate zone (IZ) contains nonreplicating, differentiated cells. The VZ/SVZ is hypersensitive to radiation-induced apoptosis. Ablation of DNA non-homologous end-joining (NHEJ) proteins, XRCC4 or DNA ligase IV (LigIV), confers ataxia telangiectasia mutated (ATM)-dependent apoptosis predominantly in the IZ. We examine the mechanistic basis underlying these distinct sensitivities using a viable LigIV (Lig4(Y288C)) mouse, which permits an examination of the DNA damage responses in the embryonic and adult brain. Via combined analysis of DNA breakage, apoptosis, and cell-cycle checkpoint control in tissues, we show that apoptosis in the VZ/SVZ and IZ is activated by low numbers of DNA double-strand breaks (DSBs). Unexpectedly, high sensitivity in the VZ/SVZ arises from sensitive activation of ATM-dependent apoptosis plus an ATM-independent process. In contrast, the IZ appears to be hypersensitive to persistent DSBs. NHEJ functions efficiently in both compartments. The VZ/SVZ and IZ regions incur high endogenous DNA breakage, which correlates with VZ proliferation. We demonstrate a functional G(2)/M checkpoint in VZ/SVZ cells and show that it is not activated by low numbers of DSBs, allowing damaged VZ/SVZ cells to transit into the IZ. We propose a novel model in which microcephaly in LIG4 syndrome arises from sensitive apoptotic induction from persisting DSBs in the IZ, which arise from high endogenous breakage in the VZ/SVZ and transit of damaged cells to the IZ. The VZ/SVZ, in contrast, is highly sensitive to acute radiation-induced DSB formation

Striatal Hypodensities, Not White Matter Hypodensities on CT, Are Associated with Late-Onset Depression in Alzheimer's Disease

This study examined whether there were neuroanatomical differences evident on CT scans of individuals with dementia who differed on depression history. Neuroanatomical variables consisted of visual ratings of frontal lobe deep white matter, subcortical white matter, and subcortical gray matter hypodensities in the CT scans of 182 individuals from the Study of Dementia in Swedish Twins who were diagnosed with dementia and had information on depression history. Compared to individuals with Alzheimer's disease and no depression, individuals with Alzheimer's disease and late-onset depression (first depressive episode at age 60 or over) had a greater number of striatal hypodensities (gray matter hypodensities in the caudate nucleus and lentiform nucleus). There were no significant differences in frontal lobe deep white matter or subcortical white matter. These findings suggest that late-onset depression may be a process that is distinct from the neurodegenerative changes caused by Alzheimer's disease

Mid- and Late-Life Diabetes in Relation to the Risk of Dementia: A Population-Based Twin Study

OBJECTIVE—We aimed to verify the association between diabetes and the risk of dementia, Alzheimer's disease, and vascular dementia in twins and to explore whether genetic and early-life environmental factors could contribute to this association

Dementia in Swedish Twins: Predicting Incident Cases

Thirty same-sex twin pairs were identified in which both members were assessed at baseline and one twin subsequently developed dementia, at least 3 years subsequent to the baseline measurement, while the partner remained cognitively intact for at least three additional years. Eighteen of the 30 cases were diagnosed with Alzheimer’s disease. Baseline assessments, conducted when twins’ average age was 70.6 (SD = 6.8), included a mailed questionnaire and in-person testing. Which twin would develop dementia was predicted by less favorable lipid values (higher apoB, ratio of apoB to apoA1, and total cholesterol), poorer grip strength, and—to a lesser extent—higher emotionality on the EAS Temperament Scale. Given the long preclinical period that characterizes Alzheimer’s disease, these findings may suggest late life risk factors for dementia, or may reflect changes that are part of preclinical disease

Solitons in nonlocal nonlinear media: exact results

We investigate the propagation of one-dimensional bright and dark spatial solitons in a nonlocal Kerr-like media, in which the nonlocality is of general form. We find an exact analytical solution to the nonlinear propagation equation in the case of weak nonlocality. We study the properties of these solitons and show their stability.Comment: 9 figures, submitted to Phys. Rev.

Bistable Helmholtz bright solitons in saturable materials

We present, to the best of our knowledge, the first exact analytical solitons of a nonlinear Helmholtz equation with a saturable refractive-index model. These new two-dimensional spatial solitons have a bistable characteristic in some parameter regimes, and they capture oblique (arbitrary-angle) beam propagation in both the forward and backward directions. New conservation laws are reported, and the classic paraxial solution is recovered in an appropriate multiple limit. Analysis and simulations examine the stability of both solution branches, and stationary Helmholtz solitons are found to emerge from a range of perturbed input beams

Gene-environment interplay in depressive symptoms:Moderation by age, sex, and physical illness

BackgroundNumerous factors influence late-life depressive symptoms in adults, many not thoroughly characterized. We addressed whether genetic and environmental influences on depressive symptoms differed by age, sex, and physical illness.MethodThe analysis sample included 24 436 twins aged 40–90 years drawn from the Interplay of Genes and Environment across Multiple Studies (IGEMS) Consortium. Biometric analyses tested age, sex, and physical illness moderation of genetic and environmental variance in depressive symptoms.ResultsWomen reported greater depressive symptoms than men. After age 60, there was an accelerating increase in depressive symptom scores with age, but this did not appreciably affect genetic and environmental variances. Overlap in genetic influences between physical illness and depressive symptoms was greater in men than in women. Additionally, in men extent of overlap was greater with worse physical illness (the genetic correlation ranged from near 0.00 for the least physical illness to nearly 0.60 with physical illness 2s.d.above the mean). For men and women, the same environmental factors that influenced depressive symptoms also influenced physical illness.ConclusionsFindings suggested that genetic factors play a larger part in the association between depressive symptoms and physical illness for men than for women. For both sexes, across all ages, physical illness may similarly trigger social and health limitations that contribute to depressive symptoms.</jats:sec