Possible Effects of Synaptic Imbalances on Oligodendrocyte–Axonic Interactions in Schizophrenia: A Hypothetical Model

A model of glial–neuronal interactions is proposed that could be explanatory for the demyelination identified in brains with schizophrenia. It is based on two hypotheses: (1) that glia–neuron systems are functionally viable and important for normal brain function, and (2) that disruption of this postulated function disturbs the glial categorization function, as shown by formal analysis. According to this model, in schizophrenia receptors on astrocytes in glial–neuronal synaptic units are not functional, loosing their modulatory influence on synaptic neurotransmission. Hence, an unconstrained neurotransmission flux occurs that hyperactivates the axon and floods the cognate receptors of neurotransmitters on oligodendrocytes. The excess of neurotransmitters may have a toxic effect on oligodendrocytes and myelin, causing demyelination. In parallel, an increasing impairment of axons may disconnect neuronal networks. It is formally shown how oligodendrocytes normally categorize axonic information processing via their processes. Demyelination decomposes the oligodendrocyte–axonic system making it incapable to generate categories of information. This incoherence may be responsible for symptoms of disorganization in schizophrenia, such as thought disorder, inappropriate affect and incommunicable motor behavior. In parallel, the loss of oligodendrocytes affects gap junctions in the panglial syncytium, presumably responsible for memory impairment in schizophrenia

Diagnostic performance of the Minimal Eating Observation and Nutrition Form - Version II (MEONF-II) and Nutritional Risk Screening 2002 (NRS 2002) among hospital inpatients - a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>The usefulness of the nutritional screening tool Minimal Eating Observation and Nutrition Form - Version II (MEONF-II) relative to Nutritional Risk Screening 2002 (NRS 2002) remains untested. Here we attempted to fill this gap by testing the diagnostic performance and user-friendliness of the MEONF-II and the NRS 2002 in relation to the Mini Nutritional Assessment (MNA) among hospital inpatients.</p> <p>Methods</p> <p>Eighty seven hospital inpatients were assessed for nutritional status with the 18-item MNA (considered as the gold standard), and screened with the NRS 2002 and the MEONF-II.</p> <p>Results</p> <p>The MEONF-II sensitivity (0.61), specificity (0.79), and accuracy (0.68) were acceptable. The corresponding figures for NRS 2002 were 0.37, 0.82 and 0.55, respectively. MEONF-II and NRS 2002 took five minutes each to complete. Assessors considered MEONF-II instructions and items to be easy to understand and complete (96-99%), and the items to be relevant (87%). For NRS 2002, the corresponding figures were 75-93% and 79%, respectively.</p> <p>Conclusions</p> <p>The MEONF-II is an easy to use, relatively quick and sensitive screening tool to assess risk of undernutrition among hospital inpatients. With respect to user-friendliness and sensitivity the MEONF-II seems to perform better than the NRS 2002, although larger studies are needed for firm conclusions. The different scoring systems for undernutrition appear to identify overlapping but not identical patient groups. A potential limitation with the study is that the MNA was used as gold standard among patients younger than 65 years.</p

Study circles improve the precision in nutritional care in special accommodations

Background: Disease-related malnutrition is a major health problem in the elderly population, but it has until recently received very little attention, especially are management issues under-explored. By identifying residents at the risk of undernutrition, appropriate nutritional care can be provided. Objectives: Do study circles and policy documents improve the precision in nutritional care and decrease the prevalence of low or high BMI? Design: Pre and post intervention study. Setting: Special accommodations (nursing homes) within six municipalities were involved. Participants: In 2005, 1726 (90.4%) out of 1910 residents agreed to participate and in 2007, 1526 (81.8%) out of 1866 residents participated. Intervention: Study circles in one municipality, having a policy document in one municipality and no intervention in four municipalities. Measurements: Risk of undernutrition was defined as involving any of: involuntary weight loss, low BMI, and/or eating difficulties. Overweight was defined as high BMI. Results: In 2005 and 2007, 64% of 1726 and 66% of 1526 residents respectively were at the risk of undernutrition. In 2007 significantly more patients in the study circle municipality were accurately provided protein and energy enriched food compared to in the no intervention municipalities. There was a decrease in the prevalence of low BMI in the study circle municipality and the prevalence of overweight increased in the policy document municipality between 2005 and 2007

Spatial division multiplexing for optical data center networks

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Cumbersome but desirable – Breaking the code of everyday cycling

publishedVersio

Altered fibroblast proteoglycan production in COPD

<p>Abstract</p> <p>Background</p> <p>Airway remodeling in COPD includes reorganization of the extracellular matrix. Proteoglycans play a crucial role in this process as regulators of the integrity of the extracellular matrix. Altered proteoglycan immunostaining has been demonstrated in COPD lungs and this has been suggested to contribute to the pathogenesis. The major cell type responsible for production and maintenance of ECM constituents, such as proteoglycans, are fibroblasts. Interestingly, it has been proposed that central airways and alveolar lung parenchyma contain distinct fibroblast populations. This study explores the hypothesis that altered depositions of proteoglycans in COPD lungs, and in particular versican and perlecan, is a result of dysregulated fibroblast proteoglycan production.</p> <p>Methods</p> <p>Proliferation, proteoglycan production and the response to TGF-β₁were examined <it>in vitro </it>in centrally and distally derived fibroblasts isolated from COPD patients (GOLD stage IV) and from control subjects.</p> <p>Results</p> <p>Phenotypically different fibroblast populations were identified in central airways and in the lung parenchyma. Versican production was higher in distal fibroblasts from COPD patients than from control subjects (p < 0.01). In addition, perlecan production was lower in centrally derived fibroblasts from COPD patients than from control subjects (p < 0.01). TGF-β₁triggered similar increases in proteoglycan production in distally derived fibroblasts from COPD patients and control subjects. In contrast, centrally derived fibroblasts from COPD patients were less responsive to TGF-β₁than those from control subjects.</p> <p>Conclusions</p> <p>The results show that fibroblasts from COPD patients have alterations in proteoglycan production that may contribute to disease development. Distally derived fibroblasts from COPD patients have enhanced production of versican that may have a negative influence on the elastic recoil. In addition, a lower perlecan production in centrally derived fibroblasts from COPD patients may indicate alterations in bronchial basement membrane integrity in severe COPD.</p

Two centuries of masting data for European beech and Norway spruce across the European continent

Tree masting is one of the most intensively studied ecological processes. It affects nutrient fluxes of trees, regeneration dynamics in forests, animal population densities, and ultimately influences ecosystem services. Despite a large volume of research focused on masting, its evolutionary ecology, spatial and temporal variability and environmental drivers are still matter of debate. Understanding the proximate and ultimate causes of masting at broad spatial and temporal scales will enable us to predict tree reproductive strategies and their response to changing environment. Here we provide broad spatial (distribution range-wide) and temporal (century) masting data for the two main masting tree species in Europe, European beech (Fagus sylvatica L.) and Norway spruce (Picea abies (L.) H. Karst.). We collected masting data from a total of 359 sources through an extensive literature review and from unpublished surveys. The dataset has a total of 1747 series and 18348 yearly observations from 28 countries and covering a time span of years 1677-2016 and 1791-2016 for beech and spruce, respectively. For each record, the following information is available: identification code; species; year of observation; proxy of masting (flower, pollen, fruit, seed, dendrochronological reconstructions); statistical data type (ordinal, continuous); data value; unit of measurement (only in case of continuous data); geographical location (country, Nomenclature of Units for Territorial Statistics NUTS-1 level, municipality, coordinates); first and last record year and related length; type of data source (field survey, peer reviewed scientific literature, grey literature, personal observation); source identification code; date when data were added to the database; comments. To provide a ready-to-use masting index we harmonized ordinal data into five classes. Furthermore, we computed an additional field where continuous series with length >4 years where converted into a five classes ordinal index. To our knowledge, this is the most comprehensive published database on species-specific masting behaviour. It is useful to study spatial and temporal patterns of masting and its proximate and ultimate causes, to refine studies based on tree-ring chronologies, to understand dynamics of animal species and pests vectored by these animals affecting human health, and it may serve as calibration-validation data for dynamic forest models.The paper was partly funded by the “Fondo di Ricerca Locale 2015-2016” of the University of Torino and by the Stiftelsen Stina Werners fond (grant SSWF 10-1/29-3 to I.D.)