281 research outputs found
Dieterici gas as a Unified Model for Dark Matter and Dark Energy
The dominance of dark energy in the universe has necessitated the
introduction of a repulsive gravity source to make q0 negative. The models for
dark energy range from a simple lambda-term to quintessence, Chaplygin gas,
etc. We look at the possibility of how change of behaviour of missing energy
density, from DM to DE, may be determined by the change in the equation of
state of a background fluid instead of a form of potential. The question of
cosmic acceleration can be discussed within the framework of theories which do
not necessarily include scalar fields.Comment: 9 pages, 38 equation
Combining Gene Transfer and Nonhuman Primates to Better Understand and Treat Parkinson’s Disease
Parkinson's disease (PD) is a progressive CNS disorder that is primarily associated with impaired movement. PD develops over decades and is linked to the gradual loss of dopamine delivery to the striatum, via the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). While the administration of L-dopa and deep brain stimulation are potent therapies, their costs, side effects and gradual loss of efficacy underlines the need to develop other approaches. Unfortunately, the lack of pertinent animal models that reproduce DA neuron loss and behavior deficits-in a timeline that mimics PD progression-has hindered the identification of alternative therapies. A complementary approach to transgenic animals is the use of nonhuman primates (NHPs) combined with the overexpression of disease-related genes using viral vectors. This approach may induce phenotypes that are not influenced by developmental compensation mechanisms, and that take into account the personality of animals. In this review article, we discuss the combination of gene transfer and NHPs to develop "genetic" models of PD that are suitable for testing therapeutic approaches
Легочная гипертензия при диастолической дисфункции левого желудочка у больных с ишемической кардиомиопатией
На основании данных эхокардиографического исследования выявлена взаимосвязь между степенью легочной гипертензии и тяжестью диастолической дисфункции левого желудочка у больных с ишемической кардиомиопатией. Показано, что рестриктиное наполнение левого желудочка наблюдается в основном при выраженной легочной гипертензии.The findings of echocardiography were used to reveal interrelation between the degree of pulmonary hypertension and severity of diastolic dysfunction of the left ventricle in patients with ischemic cardiomyopathy. Restrictive filling of the left ventricle is shown to be observed in marked pulmonary hypertension
Cosmic coincidence problem and variable constants of physics
The standard model of cosmology is investigated using time dependent
cosmological constant and Newton's gravitational constant . The
total energy content is described by the modified Chaplygin gas equation of
state. It is found that the time dependent constants coupled with the modified
Chaplygin gas interpolate between the earlier matter to the later dark energy
dominated phase of the universe. We also achieve a convergence of parameter
, with minute fluctuations, showing an evolving . Thus our
model fairly alleviates the cosmic coincidence problem which demands
at present time.Comment: 27 pages, 15 figure
Despite the presence of UVB-induced DNA damage, HLA-DR+ cells from ex vivo UVB-exposed human skin are able to migrate and show no impaired allostimulatory capacity
In this study, we investigated the effect of ultraviolet B radiation on human Langerhans cell function. Normal human skin was irradiated ex vivo with single doses of ultraviolet B. For assessment of T-cell stimulatory function, cells that spontaneously migrated from epidermal sheets were used, whereas full-thickness skin biopsies were used to investigate alterations in migratory properties. The cells migrating from ultraviolet B-exposed epidermal sheets demonstrated a decrease in the percentage of HLA-DR positive Langerhans cells, as well as a reduced capacity to induce proliferation of allogeneic T cells, when compared with cells migrating from nonexposed sheets. When a correction was made for the decreased number of HLA-DR positive Langerhans cells migrating from ultraviolet B-exposed epidermis, however, it appeared that the capacity to induce T-cell proliferation was identical for Langerhans cells migrating from ultraviolet B-exposed and nonexposed epidermis. The presence of ultraviolet B-induced DNA damage could be demonstrated in the Langerhans cells from ultraviolet B-treated skin, indicating that the cells had received significant doses of ultraviolet B. As regards the effect of ultraviolet B on migratory properties of Langerhans cells, we found not only that reduced numbers of CD1a-positive Langerhans cells migrated from the ultraviolet B-exposed full-thickness skin, but also that there was a reduction in CD1a-positive Langerhans cells in the epidermis. This implies that ultraviolet B induces death of Langerhans cells as well as loss of cell surface molecules rather than altering Langerhans cells migration, whereas the Langerhans cells that were still able to migrate fully retained the capacity to activate allogeneic T cells
Constraints on coupling constant between dark energy and dark matter
We have investigated constraints on the coupling between dark matter and the
interacting Chaplygin gas. Our results indicate that the coupling constant
between these two entities can take arbitrary values, which can be either
positive or negative, thus giving arbitrary freedom to the inter-conversion
between Chaplygin gas and dark matter. Thus our results indicate that the
restriction on the coupling constant occurs as a very special case. Our
analysis also supports the existence of phantom energy under certain conditions
on the coupling constant.Comment: 16 Pages, 3 figure
Interacting new generalized Chaplygin gas
We have presented a model in which the new generalized Chaplygin gas
interacts with matter. We find that there exists a stable scaling solution at
late times in the evolution of the universe. Moreover, the phantom crossing
scenario is observed in this model.Comment: 16 pages, 6 figures, accepted for publication in Int. J. Theor. Phy
Simulations of the Static Friction Due to Adsorbed Molecules
The static friction between crystalline surfaces separated by a molecularly
thin layer of adsorbed molecules is calculated using molecular dynamics
simulations. These molecules naturally lead to a finite static friction that is
consistent with macroscopic friction laws. Crystalline alignment, sliding
direction, and the number of adsorbed molecules are not controlled in most
experiments and are shown to have little effect on the friction. Temperature,
molecular geometry and interaction potentials can have larger effects on
friction. The observed trends in friction can be understood in terms of a
simple hard sphere model.Comment: 13 pages, 13 figure
Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1
Excitotoxicity, a critical process in neurodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown. Since oxidative stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity. Unexpectedly, we find that excitotoxicity provokes an early inactivation of PKD1 through a dephosphorylation-dependent mechanism mediated by protein phosphatase-1 (PP1) and dual specificity phosphatase-1 (DUSP1). This step turns off the IKK/NF-κB/SOD2 antioxidant pathway. Neuronal PKD1 inactivation by pharmacological inhibition or lentiviral silencing in vitro, or by genetic inactivation in neurons in vivo, strongly enhances excitotoxic neuronal death. In contrast, expression of an active dephosphorylation-resistant PKD1 mutant potentiates the IKK/NF-κB/SOD2 oxidative stress detoxification pathway and confers neuroprotection from in vitro and in vivo excitotoxicity. Our results indicate that PKD1 inactivation underlies excitotoxicity-induced neuronal death and suggest that PKD1 inactivation may be critical for the accumulation of oxidation-induced neuronal damage during aging and in neurodegenerative disorders
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