SIP-based mobility management in next generation networks

The ITU-T definition of next generation networks includes the ability to make use of multiple broadband transport technologies and to support generalized mobility. Next generation networks must integrate several IP-based access technologies in a seamless way. In this article, we first describe the requirements of a mobility management scheme for multimedia real-time communication services; then, we report a survey of the mobility management schemes proposed in the recent literature to perform vertical handovers between heterogeneous networks. Based on this analysis, we propose an application-layer solution for mobility management that is based on the SIP protocol and satisfies the most important requirements for a proper implementation of vertical handovers. We also implemented our proposed solution, testing it in the field, and proving its overall feasibility and its interoperability with different terminals and SIP servers

Modulation by chronic stress and ketamine of ionotropic AMPA/NMDA and metabotropic glutamate receptors in the rat hippocampus

Converging clinical and preclinical evidence has shown that dysfunction of the glutamate system is a core feature of major depressive disorder. In this context, the N-methyl-d-aspartate (NMDA) receptor antagonist ketamine has raised growing interest as fast acting antidepressant. Using the chronic mild stress (CMS) rat model of depression, performed in male rats, we aimed at analyzing whether hippocampal specific changes in subunit expression and regulation of \u3b1-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) or NMDA ionotropic receptors and in metabotropic glutamate receptors could be associated with behavioral vulnerability/resilience to CMS. We also assessed whether acute ketamine (10 mg/kg) was able to dampen the alterations in CMS vulnerable animals. Although chronic stress and ketamine had no effect on ionotropic glutamate receptors mRNAs (expression, RNA editing and splicing), we found selective modulations in their protein expression, phosphorylation and localization at synaptic membranes. AMPA GluA2 expression at synaptic membranes was significantly increased only in CMS resilient rats (although a trend was found also in vulnerable animals), while its phosphorylation at Ser880 was higher in both CMS resilient and vulnerable rats, a change partially dampened by ketamine. In the hippocampus from all stressed groups, despite NMDA receptor expression levels were reduced in total extract, the levels of GluN2B-containing NMDA receptors were remarkably increased in synaptic membranes. Finally, mGlu2 underwent a selective downregulation in stress vulnerable animals, which was completely restored by acute ketamine. Overall, these results are in line with a hypofunction of activity-dependent glutamatergic synaptic transmission induced by chronic stress exposure in all the animals, as suggested by the alterations of ionotropic glutamate receptors expression and localization at synaptic level. At the same time, the selective modulation of mGlu2 receptor, confirms its previously hypothesized functional role in regulating stress vulnerability and, for the first time here, suggests a mGlu2 involvement in the fast antidepressant effect of ketamine

Depression as a determinant of frailty in late life

Objectives Accumulating evidence shows depression as a risk factor for frailty, but studies are mainly population-based and widely differ in their assessment of either depression or frailty. We investigated the association between depression and frailty among geriatric outpatients using different assessment instruments for both conditions. Method Among 315 geriatric outpatients (mean age 72.1 years, 68.3% female sex) participating the MiMiCS-FRAIL cohort study, major and subthreshold depression were measured with psychiatric diagnostic interview according to DSM-5 criteria (SCID-5) as well as with instruments to screen and measure severity of depressive symptoms (GDS-15 and PHQ-9). Frailty was assessed according to a screening instrument (FRAIL-BR) and a multidimensional Frailty Index (FI-36 items). Multiple logistic and linear regression were performed to assess the association between depression (independent variable) and frailty (dependent variable) adjusted for confounders. Results Frailty prevalence in patients with no, subthreshold or major depressive disorder increases from either 14.5%, 46.5% to 65.1% when using the FRAIL-BR questionnaire, and from 10.2%, 20.9%, to 30.2% when using the FI-36 index. These association remain nearly the same when adjusted for covariates. Both the FRAIL-BR and the FI-36 were strongly associated with major depressive disorder, subthreshold depression, and depressive symptoms by PHQ-9 and GDS-15. Conclusion Late life depression and frailty are associated in a dose-dependent manner, irrespective of the used definitions. Nonetheless, to avoid residual confounding, future research on underlying biological mechanisms should preferably be based on formal psychiatric diagnoses and objectively assessment frailty status

Functional and Molecular Changes in the Prefrontal Cortex of the Chronic Mild Stress Rat Model of Depression and Modulation by Acute Ketamine

Stress is a primary risk factor in the onset of neuropsychiatric disorders, including major depressive disorder (MDD). We have previously used the chronic mild stress (CMS) model of depression in male rats to show that CMS induces morphological, functional, and molecular changes in the hippocampus of vulnerable animals, the majority of which were recovered using acute subanesthetic ketamine in just 24 h. Here, we focused our attention on the medial prefrontal cortex (mPFC), a brain area regulating emotional and cognitive functions, and asked whether vulnerability/resilience to CMS and ketamine antidepressant effects were associated with molecular and functional changes in the mPFC of rats. We found that most alterations induced by CMS in the mPFC were selectively observed in stress-vulnerable animals and were rescued by acute subanesthetic ketamine, while others were found only in resilient animals or were induced by ketamine treatment. Importantly, only a few of these modifications were also previously demonstrated in the hippocampus, while most are specific to mPFC. Overall, our results suggest that acute antidepressant ketamine rescues brain-area-specific glutamatergic changes induced by chronic stress

Acute Ketamine Facilitates Fear Memory Extinction in a Rat Model of PTSD Along With Restoring Glutamatergic Alterations and Dendritic Atrophy in the Prefrontal Cortex

Stress represents a major risk factor for psychiatric disorders, including post-traumatic stress disorder (PTSD). Recently, we dissected the destabilizing effects of acute stress on the excitatory glutamate system in the prefrontal cortex (PFC). Here, we assessed the effects of single subanesthetic administration of ketamine (10 mg/kg) on glutamate transmission and dendritic arborization in the PFC of footshock (FS)-stressed rats, along with changes in depressive, anxious, and fear extinction behaviors. We found that ketamine, while inducing a mild increase of glutamate release in the PFC of na\uefve rats, blocked the acute stress-induced enhancement of glutamate release when administered 24 or 72 h before or 6 h after FS. Accordingly, the treatment with ketamine 6 h after FS also reduced the stress-dependent increase of spontaneous excitatory postsynaptic current (sEPSC) amplitude in prelimbic (PL)-PFC. At the same time, ketamine injection 6 h after FS was found to rescue apical dendritic retraction of pyramidal neurons induced by acute stress in PL-PFC and facilitated contextual fear extinction. These results show rapid effects of ketamine in animals subjected to acute FS, in line with previous studies suggesting a therapeutic action of the drug in PTSD models. Our data are consistent with a mechanism of ketamine involving re-establishment of synaptic homeostasis, through restoration of glutamate release, and structural remodeling of dendrites

Intravenous C.E.R.A. maintains stable haemoglobin levels in patients on dialysis previously treated with darbepoetin alfa: results from STRIATA, a randomized phase III study

Background. Extending the administration interval of erythropoiesis-stimulating agents (ESAs) represents an opportunity to improve the efficiency of anaemia management in patients with chronic kidney disease (CKD). However, effective haemoglobin (Hb) maintenance can be challenging with epoetin alfa and epoetin beta administered at extended intervals. C.E.R.A., a continuous erythropoietin receptor activator, has a unique pharmacologic profile and long half-life (∼130 h), allowing administration at extended intervals. Phase III results have demonstrated that C.E.R.A. administered once every 4 weeks effectively maintains stable Hb levels in patients with CKD on dialysis

Criminalidade organizada nas prisões e os ataques do PCC

The advent of organized crime in Brazilian prisons, especially in the state of São Paulo, constitutes the object of this article. The waves of attack unleashed by the Capital's First Command (PCC - Primeiro Comando da Capital), in May 2006, which resulted in countless deaths, brought cities to a halt, and cornered authorities in charge preventing them from applying law and order are the starting as well as reference points taken. The advent of organized criminality is analyzed under the light of determined axes: the international scenario and the Brazilian context, the historical antecedents, the taking root of crime in society and the role of penitentiary public policies.A emergência da criminalidade organizada nas prisões brasileiras, em especial no Estado de São Paulo, constitui objeto deste artigo. Tomam-se como ponto de partida e referência para análise as ondas de ataques desencadeadas pelo Primeiro Comando da Capital (PCC), de maio a agosto de 2006, que resultaram em inúmeros mortos, paralisaram cidades e acuaram as autoridades encarregadas de aplicar lei e ordem. A emergência da criminalidade organizada é analisada sob eixos determinados: cenário internacional e contexto brasileiro, antecedentes históricos, enraizamento do crime na sociedade e papel das políticas públicas penitenciárias

Reflections on the entrepreneurial state, innovation and social justice

The state and its role in technological innovation and social justice have become, once again, fashionable topics of political and economic debate. A number of innovation theorists argue that never more than today, it is necessary to rethink the state’s entrepreneurial role in society and welfare. Their argument provides justification for the existence of the state, going beyond classical political theory and especially contractarian accounts of legitimacy and obligation. It emphasises the ability and willingness of the state to take risks and reduce uncertainty of economic agents for the sake of innovation that can make everyone better off. This paper insists that although the risk-taking argument of innovation theorists deserves further attention and analysis, it should not be abstracted from a holistic politico-theoretical approach to the state. Such an approach is necessary for a critical understanding of the complex set of predominantly political institutions which compose the state and which have been historically developed to guarantee social evolution. Any risk-taking for innovative enterprise and mission-oriented investment ought to be justified and legitimised on the grounds of principled democratic procedures. This implies that innovation itself is a value-laden political process, requiring participation in the decision-making and standards of fairness