In this work we study classical bouncing solutions in the context of Formula omitted gravity in a flat FLRW background using a perfect fluid as the only matter content. Our investigation is based on ...introducing an effective fluid through defining effective energy density and pressure; we call this reformulation as the "effective picture". These definitions have been already introduced to study the energy conditions in Formula omitted gravity. We examine various models to which different effective equations of state, corresponding to different Formula omitted functions, can be attributed. It is also discussed that one can link between an assumed Formula omitted model in the effective picture and the theories with generalized equation of state (EoS). We obtain cosmological scenarios exhibiting a nonsingular bounce before and after which the Universe lives within a de-Sitter phase. We then proceed to find general solutions for matter bounce and investigate their properties. We show that the properties of bouncing solution in the effective picture of Formula omitted gravity are as follows: for a specific form of the Formula omitted function, these solutions are without any future singularities. Moreover, stability analysis of the nonsingular solutions through matter density perturbations revealed that except two of the models, the parameters of scalar-type perturbations for the other ones have a slight transient fluctuation around the bounce point and damp to zero or a finite value at late times. Hence these bouncing solutions are stable against scalar-type perturbations. It is possible that all energy conditions be respected by the real perfect fluid, however, the null and the strong energy conditions can be violated by the effective fluid near the bounce event. These solutions always correspond to a maximum in the real matter energy density and a vanishing minimum in the effective density. The effective pressure varies between negative values and may show either a minimum or a maximum.
The theorems at the core of density functional theory (DFT) state that the energy of a many-electron system in its ground state is fully defined by its electron density distribution. This connection ...is made via the exact functional for the energy, which minimizes at the exact density. For years, DFT development focused on energies, implicitly assuming that functionals producing better energies become better approximations of the exact functional. We examined the other side of the coin: the energy-minimizing electron densities for atomic species, as produced by 128 historical and modern DFT functionals. We found that these densities became closer to the exact ones, reflecting theoretical advances, until the early 2000s, when this trend was reversed by unconstrained functionals sacrificing physical rigor for the flexibility of empirical fitting.
Among postmenopausal women with osteoporosis and a high risk of fracture, treatment with the monoclonal antibody romosozumab for 12 months followed by alendronate resulted in a significantly lower ...risk of fracture than alendronate for 12 months followed by alendronate.
This study shows that in postmenopausal women with low bone mineral density, the monoclonal antibody romosozumab, which binds to sclerostin, an osteoblast-activity inhibitor, was associated with ...increased bone mineral density and bone formation and decreased bone resorption.
Osteoporosis is characterized by low bone mass and defects in microarchitecture that are responsible for decreased bone strength and increased risk of fracture.
1
Antiresorptive drugs for osteoporosis increase bone mineral density and prevent the progression of structural damage but may not restore bone structure. Stimulation of bone formation is necessary to achieve improvements in bone mass, architecture, and strength.
Sclerostin, encoded by the gene
SOST,
is an osteocyte-secreted glycoprotein that has been identified as a pivotal regulator of bone formation. By inhibiting the Wnt and bone morphogenetic protein signaling pathways, sclerostin impedes osteoblast proliferation and function, thereby decreasing bone formation. . . .
Ionospheric F2 region peak densities (NmF2) are expected to have a positive correlation with total electron content (TEC), and electron densities usually show an anticorrelation with electron ...temperatures near the ionospheric F2 peak. However, during the 17 March 2015 great storm, the observed TEC, NmF2, and electron temperatures of the storm‐enhanced density (SED) over Millstone Hill (42.6°N, 71.5°W, 72° dip angle) show a quiet different picture. Compared with the quiet time ionosphere, TEC, the F2 region electron density peak height (hmF2), and electron temperatures above ~220 km increased, but NmF2 decreased significantly within the SED. This SED occurred where there was a negative ionospheric storm effect near the F2 peak and below it, but a positive storm effect in the topside ionosphere. Thus, this SED event was a SED in TEC but not in NmF2. The very low ionospheric densities below the F2 peak resulted in a much reduced downward heat conduction for the electrons, trapping the heat in the topside in the presence of heat source above. This, in turn, increased the topside scale height so that even though electron densities at the F2 peak were depleted, TEC increased in the SED. The depletion in NmF2 was probably caused by an increase in the density of the molecular neutrals, resulting in enhanced recombination. In addition, the storm time topside ionospheric electron density profiles were much closer to diffusive equilibrium than the nonstorm time profiles, indicating less daytime plasma flow between the ionosphere and the plasmasphere.
Key Points
A SED in TEC but not in NmF2
Storm time topside ionospheric electron density profiles were in diffusive equilibrium
Increase in the topside but decrease in bottom side ionosphere
On the notions of upper and lower density Leonetti, Paolo; Tringali, Salvatore
Proceedings of the Edinburgh Mathematical Society,
02/2020, Volume:
63, Issue:
1
Journal Article
Peer reviewed
Open access
Abstract
Let
$\mathcal {P}(\mathbf{N})$
be the power set of
N
. We say that a function
$\mu ^\ast : \mathcal {P}(\mathbf{N}) \to \mathbf{R}$
is an upper density if, for all
X
,
Y
⊆
N
and
h
,
k
∈
N
+
..., the following hold: (
f1
)
$\mu ^\ast (\mathbf{N}) = 1$
; (
f2
)
$\mu ^\ast (X) \le \mu ^\ast (Y)$
if
X
⊆
Y
; (
f3
)
$\mu ^\ast (X \cup Y) \le \mu ^\ast (X) + \mu ^\ast (Y)$
; (
f4
)
$\mu ^\ast (k\cdot X) = ({1}/{k}) \mu ^\ast (X)$
, where
k
·
X
: = {
kx
:
x
∈
X
}; and (
f5
)
$\mu ^\ast (X + h) = \mu ^\ast (X)$
. We show that the upper asymptotic, upper logarithmic, upper Banach, upper Buck, upper Pólya and upper analytic densities, together with all upper
α
-densities (with
α
a real parameter ≥ −1), are upper densities in the sense of our definition. Moreover, we establish the mutual independence of axioms (
f1
)–(
f5
), and we investigate various properties of upper densities (and related functions) under the assumption that (
f2
) is replaced by the weaker condition that
$\mu ^\ast (X)\le 1$
for every
X
⊆
N
. Overall, this allows us to extend and generalize results so far independently derived for some of the classical upper densities mentioned above, thus introducing a certain amount of unification into the theory.
Elevated LDL-cholesterol (LDLc) levels are a major risk factor for cardiovascular disease and atherosclerosis. LDLc is cleared from circulation by the LDL receptor (LDLR). Proprotein convertase ...subtilisin/kexin 9 (PCSK9) enhances the degradation of the LDLR in endosomes/lysosomes, resulting in increased circulating LDLc. PCSK9 can also mediate the degradation of LDLR lacking its cytosolic tail, suggesting the presence of as yet undefined lysosomal-targeting factor(s). Herein, we confirm this, and also eliminate a role for the transmembrane-domain of the LDLR in mediating its PCSK9-induced internalization and degradation. Recent findings from our laboratory also suggest a role for PCSK9 in enhancing tumor metastasis. We show herein that while the LDLR is insensitive to PCSK9 in murine B16F1 melanoma cells, PCSK9 is able to induce degradation of the low density lipoprotein receptor-related protein 1 (LRP-1), suggesting distinct targeting mechanisms for these receptors. Furthermore, PCSK9 is still capable of acting upon the LDLR in CHO 13-5-1 cells lacking LRP-1. Conversely, PCSK9 also acts on LRP-1 in the absence of the LDLR in CHO-A7 cells, where re-introduction of the LDLR leads to reduced PCSK9-mediated degradation of LRP-1. Thus, while PCSK9 is capable of inducing degradation of LRP-1, the latter is not an essential factor for LDLR regulation, but the LDLR effectively competes with LRP-1 for PCSK9 activity. Identification of PCSK9 targets should allow a better understanding of the consequences of PCSK9 inhibition for lowering LDLc and tumor metastasis.
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