Literatura académica sobre el tema "Endogenous P2P market"

This paper investigates the interrelationship between urbanization, structural transformation, and the post-2000 Chinese housing boom through the lens of a dynamic spatial equilibrium model that features migration and a rich housing market structure with mortgages. Urbanization and structural transformation emerge as key drivers of China's house price boom, while at the same time rising house prices impede these forces of economic transition. Policies to boost urbanization can be undone by the endogenous price response. Land supply expansion ameliorates this negative feedback. Overall, housing markets powerfully shape the path of economic development. (JEL E23, O18, P23, P25, R23, R31, R58)

Abstract Hematopoietic stem cells are resistant to HIV-1 infection. We have identified a novel mechanism by which the cyclin-dependent kinase inhibitor, p21Waf1/Cip1/Sdi1 (p21), known for its regulation of stem cell pool size (1,2), restricts HIV-1 infection of primitive hematopoietic cells in a non-cell cycle dependent manner. Knocking down p21 by siRNA increased HIV-1 infection and induction of p21 expression by phorbol ester (TPA) blocked HIV-1 replication. P21 did not affect the overall levels of cDNA synthesis, but significantly blocked viral integration and resulted in marked increase in 2-LTR circles, a surrogate marker of abortive integration. Consistent with these observations, p21 coimmunoprecipitated with viral integrase and both were detected in the preintegration complex (PIC). Furthermore, silencing p27Kip1 and p18INK4C, cyclin dependent kinase inhibitors related to p21 that affect cell cycle, revealed no impact on viral DNA integration. A closely related dual-tropic lentivirus with a distinct integrase, SIVmac-251 and the other cell-intrinsic inhibitors of HIV-1, Trim5a, PML, Murr1, and IFN-a were unaffected by p21. These results indicate a new function for p21, participating in prevention of HIV integration into the cellular genome. Therefore p21 is an endogenous cellular component in stem cells that provides a unique molecular barrier to HIV-1 infection and may explain the basis for these cells being an uninfected ‘sanctuary’ in HIV disease.

ABSTRACT Cellular differentiation entails the coordination of cell cycle arrest and tissue-specific gene expression. We investigated the involvement of basic helix-loop-helix (bHLH) factors in differentiation of osteoblasts using the human osteoblastic cell line MG63. Serum starvation induced growth arrest at G1 phase, accompanied by expression of cyclin-dependent kinase inhibitor p21WAF1/Cip1. Reporter assays with the p21 gene promoter demonstrated that the combination of E2A (E12 or E47) and coactivator CBP was responsible for p21 induction independent of p53. Twist inhibited E2A-CBP-dependent activation of the exogenous and endogenous p21 promoters. Ids similarly inhibited the exogenously transfected p21 promoter; however less antagonistic effect on the endogenous p21 promoter was observed. Twist was predominantly present in nuclei in MG63 cells growing in complete medium, while it localized mainly in the cytoplasm after serum starvation. The fibroblast growth factor receptor 3 gene (FGFR3), which generates signals leading to differentiation of osteoblasts, was found to be controlled by the same transcriptional regulation as the p21 gene. E2A and Twist influenced alkaline phosphatase expression, a consensus marker of osteoblast differentiation. Expression of E2A and FGFR3 was seen at the location of osteoblast differentiation in the calvaria of mouse embryos, implicating bHLH molecules in physiological osteoblast differentiation. These results demonstrate that a common regulatory system is involved in at least two distinct steps in osteoblastic differentiation. Our results also provide the molecular basis of Saethre-Chotzen syndrome, caused by mutations of the TWISTand FGFR3 genes.

Abstract Fc fragment-, subfragment-, and p23-induced polyclonal antibody production are regulated by endogenous and exogenous PGE. Addition of the PG synthetase inhibitor indomethacin (IM) to murine spleen cell cultures resulted in a significant increase in the amount of Ig secreted. Moreover, addition of exogenous PGE to culture resulted in a marked suppression of IgM and IgG secretion. Splenic adherent macrophages and P388D1 cells release PGE upon stimulation with Fc fragments, subfragments, and p23. The inclusion of IM or aspirin in culture was found to abrogate the ability of Fc fragments to induce PGE release from adherent cells. These results suggest a role for PG in immune complex mediated regulation of immune responses.

We model the equilibrium sex ratio when parents can choose the sex of their child. With intrinsic son preference, sex selection results in a male-biased sex ratio. This is inefficient due to a marriage market congestion externality. Medical innovations that facilitate selection aggravate the inefficiency. If son preference arises endogenously, due to population growth causing an excess supply of women on the marriage market, selection may improve welfare. Empirically, sex selection causes an excess of males and reduces welfare in China. In most parts of India, cohort sizes are growing, implying an excess supply of women. (JEL J12, J13, J16, O15, P23)

Accelerated cell apoptosis with dysregulated long noncoding RNAs is the crucial pathogenesis in lupus nephritis (LN). Pro-apoptotic lincRNA-p21 was studied in LN patients, cell lines with lentivirus-mediated overexpression and CRISPR interference (CRISPRi)-conducted repression, and a mouse model. Clinical samples were from patients and age/sex-matched controls. Expression of lincRNA-p21 and endogenous RNA target miR-181a, were examined in mononuclear and urine cells. Guide RNA sequences targeting lincRNA-p21 were cloned into CRISPRi with dCas9/ Krüppel-associated box (KRAB) domain. LincRNA-p21-silened transfectants were investigated for apoptosis and miR-181a expression. LincRNA-p21-overexpressed cells were evaluated for apoptosis and p53-related down-stream molecules. Balb/C mice were injected with pristane to induce LN and examined for apoptosis and lincRNA-p21. Higher lincRNA-p21 levels were found in LN mononuclear and urine cells, positively correlated with activity. There were lower miR-181a levels in LN mononuclear cells, negatively correlated with activity. Doxorubicin-induced apoptotic cells had up-regulated lincRNA-p21 levels. CRISPRi with dCas9/KARA domain showed efficient repression ability on transcription initiation/elongation. CRISPRi-conducted lincRNA-p21-silenced transfectants displayed reduced apoptosis with up-regulated miR-181a levels, whereas lentivirus-mediated lincRNA-p21-overexpressed cells revealed enhanced apoptosis with up-regulated downstream PUMA/Bax expression. LN mice had glomerular apoptosis with progressive increased lincRNA-p21 levels. Our results demonstrate up-regulated lincRNA-p21 expression in LN, implicating a potential diagnostic marker and therapeutic target.

Hyperactivation of the GHRH receptor or downstream signaling components is associated with hyperplasia of the pituitary somatotrope population, in which adenomas form relatively late in life, with less than 100% penetrance. Hyperplastic and adenomatous pituitaries of metallothionein promoter-human GHRH transgenic (Tg) mice (4 and > 10 months, respectively) were used to identify mechanisms that may prevent or delay adenoma formation in the presence of excess GHRH. In hyperplastic pituitaries, expression of the late G1/G2 marker Ki67 increased, whereas the proportion of 5-bromo-2′-deoxyuridine-labeled cells (S phase marker) did not differ from age-matched controls. These results indicate cell cycle progression is blocked, with further evidence suggesting that enhanced p27 activity may contribute to this process. For adenomas, formation was associated with loss of p27 activity (nuclear localization and mRNA). Increased endogenous somatostatin (SST) tone may also slow the conversion from hyperplastic to adenomatous state because mRNA levels for SST receptors, sst2 and sst5, were elevated in hyperplastic pituitaries, whereas adenomas were associated with a decline in sst1 and sst5 mRNA. Also, SST-knockout Tg pituitaries were larger and adenomas formed earlier compared with those of SST-intact Tg mice. Unexpectedly, these changes were independent of changes in proliferation rate within the hyperplastic tissue, suggesting that endogenous SST controls GHRH-induced adenoma formation primarily via modulation of apoptotic and/or cellular senescence pathways, consistent with the predicted function of some of the most differentially expressed genes (Casp1, MAP2K1, TNFR2) identified by membrane arrays and confirmed by quantitative real-time RT-PCR.

The harmful habit of smoking is an urgent and important socio-medical problem that has become an epidemic, including in Ukraine. It is a matter of concern that more than 500,000 young people join this bad habit every year. Today, smoking is a modified risk factor for the formation and progression of many diseases, including dental pathology among different age groups, especially among teenagers and young adults. The oral cavity is the first barrier to tobacco smoke with toxins and carcinogens that are part of it. It is known that the pathogenesis of many diseases is accompanied by a nonspecific generalized response of the organism in the form of endogenous intoxication (EI) syndrome, the severity of which may be a criterion for the severity of the pathological process and affect its course. Medium-weight molecules (MWM) are a common marker of EI in biological fluids among metabolites that can be used to assess the severity of disease. The universally accepted marker of EI in biological liquids among metabolites, which gives a possibility to assess the severity of the disease, is medium-weight molecules (MWM) - a class, which combines chemically differently structured components with a mass between 500 and 5000 Da and pronounced biologic activity. Purpose - to determine the degree of EI in the oral fluid by the level of MWM in teenagers and young adults who smoke. Materials and methods. It is studied the dental status of 114 teenagers and young adults aged 15 to 24 years, which was divided into groups: group I included 26 people who regularly smoke traditional cigarettes; group II - 22 people who regularly smoke electronic cigarettes (Vapes); group III - 23 people who regularly smoke tobacco heating devices (IQOS); group IV - 43 people without a bad habit of smoking. The degree of EI was determined by the rate of MWM in oral fluid by the express method according to a modified method Gabrielyan NI et al., 1984. Results. The analyze of the rate in the oral fluid of peptide residues (MWM254) in persons of the group I was exhibited 1.4 times more than in persons of the group IV (p<0.001). There was a similar tendency in the other groups - the group I and the group II had 1.3 times more MWM254 (p<0.05) and 1.2 times more (p<0.001). There was also a difference in the nucleotide fillings (MWM280) in oral fluid of the study groups. Thus, in persons of the group I it was found MWM280 1.6 times more than in persons of the group IV (p<0.001) and 1.3 times more (p<0.05) in persons of the groups II and III respectively. The increase of nucleotide-peptide index was determined depending on the presence and type of malodorous behavior in the study participants. Conclusions. The obtained results indicate the development of EI in teenagers and young adults who smoke, as indicated by the increase in the level of MWM in the oral fluid in the subjects, a marker of endotoxicosis. It was found that the degree of endogenous intoxication depends on the type of smoking, as well as the degree of development of the pathological process. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of the participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors. Keywords: teenagers and young adults, endogenous intoxication, medium weight molecules, smoking.

The mechanisms through which the small GTPases Rac1 and Cdc42 regulate the formation of membrane ruffles, lamellipodia, and filopodia are currently unknown. The p21-activated kinases (PAKs) are direct targets of active Rac and Cdc42 which can induce the assembly of polarized cytoskeletal structures when expressed in fibroblasts, suggesting that they may play a role in mediating the effects of these GTPases on cytoskeletal dynamics. We have examined the subcellular localization of endogenous PAK1 in fibroblast cell lines using specific PAK1 antibodies. PAK1 is detected in submembranous vesicles in both unstimulated and stimulated fibroblasts that colocalize with a marker for fluid-phase uptake. In cells stimulated with PDGF, in v-Src–transformed fibroblasts, and in wounded cells, PAK1 redistributed into dorsal and membrane ruffles and into the edges of lamellipodia, where it colocalizes with polymerized actin. PAK1 was also colocalized with F-actin in membrane ruffles extended as a response to constitutive activation of Rac1. PAK1 appears to precede F-actin in translocating to cytoskeletal structures formed at the cell periphery. The association of PAK1 with the actin cytoskeleton is prevented by the actin filament-disrupting agent cytochalasin D and by the phosphatidylinositol 3-kinase inhibitor wortmannin. Co-immunoprecipitation experiments demonstrate an in vivo interaction of PAK1 with filamentous (F)-actin in stimulated cells. Microinjection of a constitutively active PAK1 mutant into Rat-1 fibroblasts overexpressing the insulin receptor (HIRcB cells) induced the formation of F-actin- and PAK1-containing structures reminiscent of dorsal ruffles. These data indicate a close correlation between the subcellular distribution of endogenous PAK1 and the formation of Rac/Cdc42-dependent cytoskeletal structures and support an active role for PAK1 in regulating cortical actin rearrangements.

L'augmentation de la production renouvelable décentralisée nécessaire à la transition énergétique complexifiera la gestion du réseau électrique.Une riche littérature propose de décentraliser la gestion pour éviter la surcharge de l'opérateur central pendant la gestion réelle. Cependant la décentralisation exacerbe les problèmes de passage à l'échelle lors des simulations préliminaires permettant de valider les performances, la robustesse de la gestion ou le dimensionnement du futur réseau. Une démarche Adéquation Algorithme Architecture a été suivie dans cette thèse pour un marché pair à pair pour résoudre le problème de passage à l'échelle lors de la simulation sur une architecture matérielle de calcul unique.L'influence des agents sur le réseau en grande dimension ne pouvant plus être négligée, l'étude a porté sur un marché endogène pair à pair.Nous avons étudié la complexité calculatoire de différents algorithmes. Des méthodes d'optimisation de temps de traitements sur des architectures type GPU ont été développées. L'évaluation des performances, en termes de temps de traitement et de convergence, a été réalisée.Ainsi, un modèle de calcul parallèle sur une architecture GPU a apporté une accélération substantielle lorsque la précision n'est pas critique. Une implémentation optimisée sur une architecture GPU a permis de réduire de plus de 98% les temps de simulation d'un marché sans contraintes réseau. Comparé à un modèle de calcul sur une architecture conventionnelle type PC, la démarche d'adéquation algorithme-architecture a permis de définir un modèle de calcul sur GPU 1000 fois plus rapide lors de la simulation d'un DC-marché endogène et 10 fois plus rapide sur un marché AC-endogène sur un réseau radial. Les résultats de cette thèse ont permis de consolider l'étude menée sur les aspects algorithmiques comme sur les aspects d'architectures matérielles pour l'accélération des simulations de réseaux électriques sur des architectures parallèles
The growth of distributed energy resources raises the challenge of scaling up network management algorithms. This difficulty may be overcome in operating conditions with the help of a rich literature that frequently calls upon the distribution of computations. However, this issue persists during preliminary simulations validating the performances, the operation's safety, and the infrastructure's sizing. A hardware-software co-design approach is conducted here for a Peer-to-Peer market to address this scaling issue while computing simulations on a single machine. With the increasing number of distributed agents, the impact on the grid cannot be neglected anymore. Thus, this work will focus on an endogenous market. The mapping between several algorithms and different partitioning models on Central and Graphic Processing Units (CPU-GPU) has been conducted. The complexity and performance of these algorithms have been analyzed on CPU and GPU. The implementations have shown that the GPU is more numerically unstable than the CPU. Nevertheless, when precision is not critical, GPU gives substantial speedup. Thus, markets without grid constraints are 98% faster on GPU. Even with the grid constraints, the GPU is 1000 times faster with the DC hypothesis and ten times faster on the AC radial grid. This dimension-dependent acceleration increases with the grid size and the agent's count