Data-precoded algorithm for multiple-relay-assisted systems

A data-precoded relay-assisted (RA) scheme is proposed for a system cooperating with multiple relay nodes (RNs), each equipped with either a single-antenna or a two-antenna array. The classical RA systems using distributed space-time/frequency coding algorithms, because of the half-duplex constraint at the relays, require the use of a higher order constellation than in the case of a continuous link transmission from the base station to the user terminal. This implies a penalty in the power efficiency. The proposed precoding algorithm exploits the relation between QPSK and 4 L -QAM, by alternately transmitting through L relays, achieving full diversity, while significantly reducing power penalty. This algorithm explores the situations where a direct path (DP) is not available or has poor quality, and it is a promising solution to extend coverage or increase system capacity. We present the analytical derivation of the gain obtained with the data-precoded algorithm in comparison with distributed space-frequency block code (SFBC) ones. Furthermore, analysis of the pairwise error probability of the proposed algorithm is derived and confirmed with numerical results. We evaluate the performance of the proposed scheme and compare it relatively to the equivalent distributed SFBC scheme employing 16-QAM and non-cooperative schemes, for several link quality scenarios and scheme configurations, highlighting the advantages of the proposed scheme

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Functional cognitive disorder: dementia's blind spot

An increasing proportion of cognitive difficulties are recognized to have a functional cause, the chief clinical indicator of which is internal inconsistency. When these symptoms are impairing or distressing, and not better explained by other disorders, this can be conceptualized as a cognitive variant of functional neurological disorder, termed functional cognitive disorder (FCD). FCD is likely very common in clinical practice but may be under-diagnosed. Clinicians in many settings make liberal use of the descriptive term mild cognitive impairment (MCI) for those with cognitive difficulties not impairing enough to qualify as dementia. However, MCI is an aetiology-neutral description, which therefore includes patients with a wide range of underlying causes. Consequently, a proportion of MCI cases are due to non-neurodegenerative processes, including FCD. Indeed, significant numbers of patients diagnosed with MCI do not 'convert' to dementia. The lack of diagnostic specificity for MCI 'non-progressors' is a weakness inherent in framing MCI primarily within a deterministic neurodegenerative pathway. It is recognized that depression, anxiety and behavioural changes can represent a prodrome to neurodegeneration; empirical data are required to explore whether the same might hold for subsets of individuals with FCD. Clinicians and researchers can improve study efficacy and patient outcomes by viewing MCI as a descriptive term with a wide differential diagnosis, including potentially reversible components such as FCD. We present a preliminary definition of functional neurological disorder-cognitive subtype, explain its position in relation to other cognitive diagnoses and emerging biomarkers, highlight clinical features that can lead to positive diagnosis (as opposed to a diagnosis of exclusion), and red flags that should prompt consideration of alternative diagnoses. In the research setting, positive identifiers of FCD will enhance our recognition of individuals who are not in a neurodegenerative prodrome, while greater use of this diagnosis in clinical practice will facilitate personalised interventions

Using death to one's advantage: HIV modulation of apoptosis

Infection by human immunodeficiency virus (HIV) is associated with an early immune dysfunction and progressive destruction of CD4+ T lymphocytes. This progressive disappearance of T cells leads to a lack of immune control of HIV replication and to the development of immune deficiency resulting in the increased occurrence of opportunistic infections associated with acquired immune deficiency syndrome (AIDS). The HIV-induced, premature destruction of lymphocytes is associated with the continuous production of HIV viral proteins that modulate apoptotic pathways. The viral proteins, such as Tat, Env, and Nef, are associated with chronic immune activation and the continuous induction of apoptotic factors. Viral protein expression predisposes lymphocytes, particularly CD4+ T cells, CD8+ T cells, and antigen-presenting cells, to evolve into effectors of apoptosis and as a result, to lead to the destruction of healthy, non-infected T cells. Tat and Nef, along with Vpu, can also protect HIV-infected cells from apoptosis by increasing anti-apoptotic proteins and down- regulating cell surface receptors recognized by immune system cells. This review will discuss the validity of the apoptosis hypothesis in HIV disease and the potential mechanism(s) that HIV proteins perform in the progressive T cell depletion observed in AIDS pathogenesis. Originally published Leukemia, Vol. 15, No. 3, Mar 200

Bioavailable Trace Metals in Neurological Diseases

Medical treatment in Wilson’s disease includes chelators (d-penicillamine and trientine) or zinc salts that have to be maintain all the lifelong. This pharmacological treatment is categorised into two phases; the first being a de-coppering phase and the second a maintenance one. The best therapeutic approach remains controversial, as only a few non-controlled trials have compared these treatments. During the initial phase, progressive increase of chelators’ doses adjusted to exchangeable copper and urinary copper might help to avoid neurological deterioration. Liver transplantation is indicated in acute fulminant liver failure and decompensated cirrhosis; in cases of neurologic deterioration, it must be individually discussed. During the maintenance phase, the most important challenge is to obtain a good adherence to lifelong medical therapy. Neurodegenerative diseases that lead to a mislocalisation of iron can be caused by a culmination of localised overload (pro-oxidant siderosis) and localised deficiency (metabolic distress). A new therapeutic concept with conservative iron chelation rescues iron-overloaded neurons by scavenging labile iron and, by delivering this chelated metal to endogenous apo-transferrin, allows iron redistribution to avoid systemic loss of iron

Effectiveness and cost-effectiveness of transmural collaborative care with consultation letter (TCCCL) and duloxetine for major depressive disorder (MDD) and (sub)chronic pain in collaboration with primary care: design of a randomized placebo-controlled multi-Centre trial: TCC:PAINDIP

__Abstract__ Background: The comorbidity of pain and depression is associated with high disease burden for patients in terms of disability, wellbeing, and use of medical care. Patients with major and minor depression often present themselves with pain to a general practitioner and recognition of depression in such cases is low, but evolving. Also, physical symptoms, including pain, in major depressive disorder, predict a poorer response to treatment. A multi-faceted, patient-tailored treatment programme, like collaborative care, is promising. However, treatment of chronic pain conditions in depressive patients has, so far, received limited attention in research. Cost effectiveness of an integrated approach of pain in depressed patients has not been studied. This article describes the aims and design of a study to evaluate effects and costs of collaborative care with the antidepressant duloxetine for patients with pain symptoms and a depressive disorder, compared to collaborative care with placebo and compared to duloxetine alone