Evaluating seabed habitat representativeness across a diverse set of marine protected areas on the Mid-Atlantic Ridge

Marine ecosystem-based management requires good spatial information on the distribution of marine species and habitats. Often, such information is limited to a few sampled locations, but modelling techniques can be applied to produce predictive distribution maps. A harmonized broad-scale seabed habitat map was recently produced for the archipelagos of Macaronesia under the EMODnet Seabed Habitats Programme. We use this new information to produce an extent-based evaluation of the representativeness and level of protection conferred by the current set of marine protected areas (MPAs) in the Azores to the variety of benthic marine habitats found in this oceanic region. A more objective assessment of the protection effectively provided to the habitats is obtained by applying a scoring system to the MPAs based on the number of allowed extractive and non-extractive human activities and their potential impact on marine biodiversity and habitats. Results show that Azorean habitats within the MPAs are nearly entirely classified as highly protected. In total, 26 habitats (7 of which are endangered and 2 are rare) have at least 10% of their extent in the Azores EEZ protected by MPAs, but another 29 fail to meet this target (4 on-shelf habitats and 25 deep-sea habitats), highlighting the need to extend current protection of bathyal and abyssal habitats and applying adequate ecological coherence criteria. This approach sets a standard that can be used wherever similar information is available, be it in other European regions or beyond.info:eu-repo/semantics/publishedVersio

Un estudi sobre interdisciplinarietat, professions socials i acció socioeducativa

Aquest article és el relat d'un seguit d'accions encetades per donar resposta a una serie de preguntes referides a l'àmbit de la intervenció socioeducativa. El que volíem era conèixer I'estat de la interdisciplinarietat en I'àmbit de les accions socioeducatives professionals. En quin grau i de quina manera conflueixen les diferents disc iplines en I'acció social o socioeducativa? Quines professions i professionals d'alló social van desenvolupant aquestes accions? Quines relacions -de col·laboració; de confrontació; d'aïllament, etc.- es produeixen entre elles? I, per últim, ens preguntàvem: existeix una consciència entre els i les professionals sobre la necessitat -o no- d'aquesta interdisciplinarietat

ISUOG Practice Guidelines: diagnosis and management of small-for-gestational-age fetus and fetal growth restriction

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The Preclinical discovery and development of opicapone for the treatment of Parkinson's Disease

Introduction: Opicapone (OPC) is a well-established catechol-O-methyltransferase (COMT) inhibitor that is approved for the treatment of Parkinson's disease (PD) associated with L-DOPA / L-amino acid decarboxylase inhibitor (DDI) therapy allowing for prolonged activity due to a more continuous supply of L-DOPA in the brain. Thus, OPC decreases fluctuation in L-DOPA plasma levels and favours more constant central dopaminergic receptor stimulation, thus improving PD symptomatology. Areas covered: This review evaluates the preclinical development, pharmacology, pharmacokinetics and safety profile of OPC. Data were extracted from published preclinical and clinical studies published on PUBMED and SCOPUS (Search period: 2000-2019). Clinical and post-marketing data were also evaluated. Expert opinion: OPC is a third generation COMT inhibitor with a novel structure. It has an efficacy and tolerability superior to its predecessors, tolcapone (TOL) and entacapone (ENT). It also provides a safe and simplified drug regimen that allows neurologists to individually adjust the existing daily administration of L-DOPA. OPC is indicated as an adjunctive therapy to L-DOPA/DDI in patients with PD and end-of-dose motor fluctuations who cannot be stabilised on those combinations. Abbreviations: 3-OMD, 3-O-methyldopa; 6-OHDA, 6-hydroxydopamine; BG, basal ganglia; COMT, Catechol-O-methyltransferase; DDI, decarboxylase inhibitors; ENT, Entacapone; FDA, Food and Drug Administration; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; OPC, Opicapone; PD, Parkinson's disease; TOL, Tolcapone; GDNF, Glial cell-line-derived neurotrophic factor; NTN, neurturin; ICV, Intracerebroventricular; PDUFA, Prescription Drug User Fees Act; EMA, European Medicine Administration; AE, Adverse event BG, Basal ganglia. QD, once a day

Dexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways.

The aim of the present study is to elucidate the neuronal pathways associated to NSAIDs causing a reduction of the risk and progression of Alzheimer's disease. The research was developed administering the active enantiomer of ibuprofen, dexibuprofen (DXI), in order to reduce associated gastric toxicity. DXI was administered from three to six-month-old female APPswe/PS1dE9 mice as a model of familial Alzheimer's disease. DXI treatment reduced the activation of glial cells and the cytokine release involved in the neurodegenerative process, especially TNFα. Moreover, DXI reduced soluble β-amyloid (Aβ1-42) plaque deposition by decreasing APP, BACE1 and facilitating Aβ degradation by enhancing insulin-degrading enzyme. DXI also decreased TAU hyperphosphorylation inhibiting c-Abl/CABLES/p-CDK5 activation signal pathway and prevented spatial learning and memory impairment in transgenic mice. Therefore, chronic DXI treatment could constitute a potential AD-modifying drug, both restoring cognitive functions and reversing multiple brain neuropathological hallmarks

Ultrasensitive mass sensor fully integrated with complementary metal-oxide-semiconductor circuitry

Nanomechanical resonators have been monolithically integrated on preprocessed complementary metal-oxide-semiconductor(CMOS) chips. Fabricatedresonatorsystems have been designed to have resonance frequencies up to 1.5 MHz. The systems have been characterized in ambient air and vacuum conditions and display ultrasensitive mass detection in air. A mass sensitivity of 4ag/Hz has been determined in air by placing a single glycerine drop, having a measured weight of 57 fg, at the apex of a cantilever and subsequently measuring a frequency shift of 14.8 kHz. CMOS integration enables electrostatic excitation, capacitive detection, and amplification of the resonance signal directly on the chip

Benzodiazepines and Related Drugs as a Risk Factor in Alzheimer's Disease Dementia.

Benzodiazepines (BZDs) and Z-drugs are compounds widely prescribed in medical practice due to their anxiolytic, hypnotic, and muscle relaxant properties. Yet, their chronic use is associated with cases of abuse, dependence, and relapse in many patients. Furthermore, elderly people are susceptible to alterations in pharmacodynamics, pharmacokinetics as well as to drug interaction due to polypharmacy. These situations increase the risk for the appearance of cognitive affectations and the development of pathologies like Alzheimer's disease (AD). In the present work, there is a summary of some clinical studies that have evaluated the effect of BZDs and Z-drugs in the adult population with and without AD, focusing on the relationship between their use and the loss of cognitive function. Additionally, there is an assessment of preclinical studies focused on finding molecular proof on the pathways by which these drugs could be involved in AD pathogenesis. Moreover, available data (1990-2019) on BZD and Z-drug use among elderly patients, with and without AD, was compiled in this work. Finally, the relationship between the use of BZD and Z-drugs for the treatment of insomnia and the appearance of AD biomarkers was analyzed. Results pointed to a vicious circle that would worsen the condition of patients over time. Likewise, it put into relevance the need for close monitoring of those patients using BZDs that also suffer from AD. Consequently, future studies should focus on optimizing strategies for insomnia treatment in the elderly by using other substances like melatonin agonists, which is described to have a much more significant safety profile

The Implication of the Brain Insulin Receptor in Late Onset Alzheimer's Disease Dementia

Alzheimer's disease (AD) is progressive neurodegenerative disorder characterized by brain accumulation of the amyloid β peptide (Aβ), which form senile plaques, neurofibrillary tangles (NFT) and, eventually, neurodegeneration and cognitive impairment. Interestingly, epidemiological studies have described a relationship between type 2 diabetes mellitus (T2DM) and this pathology, being one of the risk factors for the development of AD pathogenesis. Information as it is, it would point out that, impairment in insulin signalling and glucose metabolism, in central as well as peripheral systems, would be one of the reasons for the cognitive decline. Brain insulin resistance, also known as Type 3 diabetes, leads to the increase of Aβ production and TAU phosphorylation, mitochondrial dysfunction, oxidative stress, protein misfolding, and cognitive impairment, which are all hallmarks of AD. Moreover, given the complexity of interlocking mechanisms found in late onset AD (LOAD) pathogenesis, more data is being obtained. Recent evidence showed that Aβ42 generated in the brain would impact negatively on the hypothalamus, accelerating the 'peripheral' symptomatology of AD. In this situation, Aβ42 production would induce hypothalamic dysfunction that would favour peripheral hyperglycaemia due to down regulation of the liver insulin receptor. The objective of this review is to discuss the existing evidence supporting the concept that brain insulin resistance and altered glucose metabolism play an important role in pathogenesis of LOAD. Furthermore, we discuss AD treatment approaches targeting insulin signalling using anti-diabetic drugs and mTOR inhibitors

A metabolic perspective of late onset Alzheimer's disease

After decades of research, the molecular neuropathology of Alzheimer's disease (AD) is still one of the hot topics in biomedical sciences. Some studies suggest that soluble amyloid β (Aβ) oligomers act as causative agents in the development of AD and could be initiators of its complex neurodegenerative cascade. On the other hand, there is also evidence pointing to Aβ oligomers as mere aggravators, with an arguable role in the origin of the disease. In this line of research, the relative contribution of soluble Aβ oligomers to neuronal damage associated with metabolic disorders such as Type 2 Diabetes Mellitus (T2DM) and obesity is being actively investigated. Some authors have proposed the endoplasmic reticulum (ER) stress and the induction of the unfolded protein response (UPR) as important mechanisms leading to an increase in Aβ production and the activation of neuroinflammatory processes. Following this line of thought, these mechanisms could also cause cognitive impairment. The present review summarizes the current understanding on the neuropathological role of Aβ associated with metabolic alterations induced by an obesogenic high fat diet (HFD) intake. It is believed that the combination of these two elements has a synergic effect, leading to the impairement of ER and mitochondrial functions, glial reactivity status alteration and inhibition of insulin receptor (IR) signalling. All these metabolic alterations would favour neuronal malfunction and, eventually, neuronal death by apoptosis, hence causing cognitive impairment and laying the foundations for late-onset AD (LOAD). Moreover, since drugs enhancing the activation of cerebral insulin pathway can constitute a suitable strategy for the prevention of AD, we also discuss the scope of therapeutic approaches such as intranasal administration of insulin in clinical trials with AD patients

Strategies against β-amyloid protein as therapeutics in Alzheimer's disease

Podeu consultar el llibre complet a: http://hdl.handle.net/2445/12071