Sensing the Same Space – Spatial Understanding and Engagement in Higher Education

The aim of this theoretically oriented review is to examine the role of space and spatial thinking in the changing teaching and learning environments in higher education. The starting point is that educational space is not a pre-set institution or only a physical space but a social construction. As such, space is a crucial element in the learning process and student engagement. In the paper, basic concepts of educational space and spatiality are discussed. The complexity of the relations between spatial understanding and student engagement is demonstrated by referring to a specific drama and theatre course as a case example. The case was a joint master-level course between two European universities (in UK and Finland) where multiple online platforms were used. By the means of the learning space in the case, we discuss the nexus of spaces, comprising a dynamic spatial plurality across the learning environments. Blurring boundaries between formal and informal spaces seems to give room for meaningful and embodied experiences - social, situational and emotional connectedness with students in different places. Formal ICT solutions of digital learning do not automatically pay enough attention to spatial aspects of learning and engagement. Understanding the connections between spatial thinking and the meanings of engagement and senses of belonging brings vital elements to the development of digital learning and learning environments. Parallel with the discussions of the distinctive role of interaction and communication in digital environments, spatial understanding can offer an important contribution to increase understanding of personal meanings of learning. Based on the theoretical reflections of the presented case, bodily experiences of the sense of “sharing a space” appears to interrelate with the feelings of belonging and ownership in learning

Environmental Characteristics and Anthropogenic Impact Jointly Modify Aquatic Macrophyte Species Diversity

Species richness and spatial variation in community composition (i.e., beta diversity) are key measures of biodiversity. They are largely determined by natural factors, but also increasingly affected by anthropogenic factors. Thus, there is a need for a clear understanding of the human impact on species richness and beta diversity, the underlying mechanisms, and whether human-induced changes can override natural patterns. Here, we dissect the patterns of species richness, community composition and beta diversity in relation to different environmental factors as well as human impact in one framework: aquatic macrophytes in 66 boreal lakes in Eastern Finland. The lakes had been classified as having high, good or moderate status (according to ecological classification of surface waters in Finland) reflecting multifaceted human impact. We used generalized least square models to study the association between different environmental variables (Secchi depth, irregularity of the shoreline, total phosphorus, pH, alkalinity, conductivity) and species richness. We tested the null hypothesis that the observed community composition can be explained by random distribution of species. We used multivariate distance matrix regression to test the effect of each environmental variable on community composition, and distance-based test for homogeneity of multivariate dispersion to test whether lakes classified as high, good or moderate status have different beta diversity. We showed that environmental drivers of species richness and community composition were largely similar, although dependent on the particular life-form group studied. The most important ones were characteristics of water quality (pH, alkalinity, conductivity) and irregularity of the shoreline. Differences in community composition were related to environmental variables independently of species richness. Species richness was higher in lakes with higher levels of human impact. Lakes with different levels of human impact had different community composition. Between-lake beta diversity did not differ in high, good or moderate status groups. However, the variation in environmental variables shaping community composition was larger in lakes with moderate status compared to other lakes. Hence, beta diversity in lakes with moderate status was smaller than what could be expected on the basis of these environmental characteristics. This could be interpreted as homogenization

Systemic Inflammation Induced Changes in Protein Expression of ABC Transporters and Ionotropic Glutamate Receptor Subunit 1 in the Cerebral Cortex of Familial Alzheimer`s Disease Mouse Model

Alzheimer's disease (AD) is an incurable disease, with complex pathophysiology and a myriad of proteins involved in its development. In this study, we applied quantitative targeted absolute proteomic analysis for investigation of changes in potential AD drug targets, biomarkers, and transporters in cerebral cortices of lipopolysaccharide (LPS)-induced neuroinflammation mouse model, familial AD mice (APdE9) with and without LPS treatment as compared to age-matched wild type (WT) mice. The ABCB1, ABCG2 and GluN1 protein expression ratios between LPS treated APdE9 and WT control mice were 0.58 (95% CI 0.44-0.72), 0.65 (95% CI 0.53-0.77) and 0.61 (95% CI 0.52-0.69), respectively. The protein expression levels of other proteins such as MGLL, COX-2, CytC, ABCC1, ABCC4, SLC2A1 and SLC7A5 did not differ between the study groups. Overall, the study revealed that systemic inflammation can alter ABCB1 and ABCG2 protein expression in brain in AD, which can affect intra-brain drug distribution and play a role in AD development. Moreover, the inflammatory insult caused by peripheral infection in AD may be important factor triggering changes in GluN1 protein expression. However, more studies need to be performed in order to confirm these findings. The quantitative information about the expression of selected proteins provides important knowledge, which may help in the optimal use of the mouse models in AD drug development and better translation of preclinical data to humans. (c) 2021 American Pharmacists Association. Published by Elsevier Inc. All rights reserved.Peer reviewe

Ranskalaisten ylijohdon tiedustelun järjestely ja sen tuottamat tulokset ennen saksalaisten hyökkäystä vuonna 1940

Sotilastiedustelun merkitystä ei voi korostaa liikaa. Yksikään sotilaallinen operaatio tai niihin johtava suunnitelma ei ole riittävän hyvä ilman tiedustelun antamaa arviota eri vaihtoehtojen mahdollisuuksista verrattuna vihollisen toimintaan. Kapteeni (myöhemmin kenraaliluutnantti) Ermei Kanninen on vuoden 1954 Sotakorkeakoulun diplomityössään omien sanojensa mukaan tutkinut suomalaisista upseereista ensimmäisenä vieraan valtion tiedustelupalvelun toimintaa. Kannisen diplomityössä nimeltään Ranskalaisten ylijohdon tiedustelun järjestely ja sen tuottamat tulokset ennen saksalaisten hyökkäystä v 1940 tulevat hyvin esille tuon aikaiset, ja mikseivät myös nykyisetkin ylimmän tason tiedustelun tehtävät. Niitä ovat sotateknisen kehityksen seuraaminen, eri valtioiden sotilaallisen voiman selvittäminen, sotilaallisesti tärkeiden raaka-aineiden jakaantumisen selvittäminen sekä geo- ja säätiedustelu. Yksittäistä tiedustelu-upseeria hän kuvaa työssään itsenäiseksi toimijaksi, jonka tulee kantaa komentajan tahdosta riippumattomana henkilökohtaista vastuuta sekä omata runsaasti mielikuvitusta. Tiedustelutieto on juuri niin käyttökelpoinen kuin sotilaallinen johto haluaa sen olevan. Kannisen työssä useampaan kertaan tuodaan ilmi, että sodanjohto ei ollut saanut, ei ollut huomioinut tai ei ollut uskonut tiedustelutietoon. Lähes väistämättä tällainen johtaa vääristyneeseen tilannekuvaan ja jopa virhearviointeihin. Tiedustelutiedon osalta pelkästään oikean tiedon tuottaminen ei riitä, vaan tiedon eheys ja käytettävyys eli jakaminen tulee varmistaa. Nykyaikaisia esimerkkejä tiedustelutiedon sivuuttamisesta tai sen vääristymistä lienevät terrori-iskut Yhdysvalloissa 2001 ja Afganistanin liukuminen talibanien hallintaan 2021. Sotilasdiplomatian eli puolustusasiamiestoiminnan, josta tutkija itse sai myöhemmin uransa varrella omakohtaistakin kokemusta, Kanninen esittää yhtenä kolmesta rauhan ajan tiedustelun tavasta. Kaksi muuta ovat asiakirjatiedustelu sekä salainen asiamiestiedustelu eli vakoilu. Sodan syttyessä hän lisää tiedustelutapoihin lentotiedustelun, tähystystiedustelun, vankitietojen keräämisen, kuuntelutiedustelun sekä asiakirjasieppaukset. Kaikki nämä muodot ovat käytössä edelleenkin. Johtopäätöksissään hän kuitenkin pitää asiamiestiedustelua ranskalaisten tehokkaimpana yksittäisenä tiedonhankinnan keinona

Increased Expression and Activity of Brain Cortical cPLA2 Due to Chronic Lipopolysaccharide Administration in Mouse Model of Familial Alzheimer’s Disease

Cytosolic phospholipase A2 (cPLA2) is an enzyme regulating membrane phospholipid homeostasis and the release of arachidonic acid utilized in inflammatory responses. It represents an attractive target for the treatment of Alzheimer’s disease (AD). Previously, we showed that lipopolysaccharide (LPS)-induced systemic inflammation caused abnormal lipid metabolism in the brain of a transgenic AD mouse model (APdE9), which might be associated with potential changes in cPLA2 activity. Here, we investigated changes in cPLA2 expression and activity, as well as the molecular mechanisms underlying these alterations due to chronic LPS administration in the cerebral cortex of female APdE9 mice as compared to saline- and LPS-treated female wild-type mice and saline-treated APdE9 mice. The study revealed the significant effects of genotype LPS treatment on cortical cPLA2 protein expression and activity in APdE9 mice. LPS treatment resulted in nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) activation in the cortex of APdE9 mice. The gene expressions of inflammation markers Il1b and Tnfa were significantly elevated in the cortex of both APdE9 groups compared to the wild-type groups. The study provides evidence of the elevated expression and activity of cPLA2 in the brain cortex of APdE9 mice after chronic LPS treatment, which could be associated with NFkB activation

Intracerebral overexpression of miR-669c is protective in mouse ischemic stroke model by targeting MyD88 and inducing alternative microglial/macrophage activation

Background Ischemic stroke is a devastating disease without a cure. The available treatments for ischemic stroke, thrombolysis by tissue plasminogen activator, and thrombectomy are suitable only to a fraction of patients and thus novel therapeutic approaches are urgently needed. The neuroinflammatory responses elicited secondary to the ischemic attack further aggravate the stroke-induced neuronal damage. It has been demonstrated that these responses are regulated at the level of non-coding RNAs, especially miRNAs. Methods We utilized lentiviral vectors to overexpress miR-669c in BV2 microglial cells in order to modulate their polarization. To detect whether the modulation of microglial activation by miR-669c provides protection in a mouse model of transient focal ischemic stroke, miR-669c overexpression was driven by a lentiviral vector injected into the striatum prior to induction of ischemic stroke. Results Here, we demonstrate that miR-669c-3p, a member of chromosome 2 miRNA cluster (C2MC), is induced upon hypoxic and excitotoxic conditions in vitro and in two different in vivo models of stroke. Rather than directly regulating the neuronal survival in vitro, miR-669c is capable of attenuating the microglial proinflammatory activation in vitro and inducing the expression of microglial alternative activation markers arginase 1 (Arg1), chitinase-like 3 (Ym1), and peroxisome proliferator-activated receptor gamma (PPAR-gamma). Intracerebral overexpression of miR-669c significantly decreased the ischemia-induced cell death and ameliorated the stroke-induced neurological deficits both at 1 and 3 days post injury (dpi). Albeit miR-669c overexpression failed to alter the overall Iba1 protein immunoreactivity, it significantly elevated Arg1 levels in the ischemic brain and increased colocalization of Arg1 and Iba1. Moreover, miR-669c overexpression under cerebral ischemia influenced several morphological characteristics of Iba1 positive cells. We further demonstrate the myeloid differentiation primary response gene 88 (MyD88) transcript as a direct target for miR-669c-3p in vitro and show reduced levels of MyD88 in miR-669c overexpressing ischemic brains in vivo. Conclusions Collectively, our data provide the evidence that miR-669c-3p is protective in a mouse model of ischemic stroke through enhancement of the alternative microglial/macrophage activation and inhibition of MyD88 signaling. Our results accentuate the importance of controlling miRNA-regulated responses for the therapeutic benefit in conditions of stroke and neuroinflammation.Peer reviewe

Intracerebral overexpression of miR-669c is protective in mouse ischemic stroke model by targeting MyD88 and inducing alternative microglial/macrophage activation

Background Ischemic stroke is a devastating disease without a cure. The available treatments for ischemic stroke, thrombolysis by tissue plasminogen activator, and thrombectomy are suitable only to a fraction of patients and thus novel therapeutic approaches are urgently needed. The neuroinflammatory responses elicited secondary to the ischemic attack further aggravate the stroke-induced neuronal damage. It has been demonstrated that these responses are regulated at the level of non-coding RNAs, especially miRNAs. Methods We utilized lentiviral vectors to overexpress miR-669c in BV2 microglial cells in order to modulate their polarization. To detect whether the modulation of microglial activation by miR-669c provides protection in a mouse model of transient focal ischemic stroke, miR-669c overexpression was driven by a lentiviral vector injected into the striatum prior to induction of ischemic stroke. Results Here, we demonstrate that miR-669c-3p, a member of chromosome 2 miRNA cluster (C2MC), is induced upon hypoxic and excitotoxic conditions in vitro and in two different in vivo models of stroke. Rather than directly regulating the neuronal survival in vitro, miR-669c is capable of attenuating the microglial proinflammatory activation in vitro and inducing the expression of microglial alternative activation markers arginase 1 (Arg1), chitinase-like 3 (Ym1), and peroxisome proliferator-activated receptor gamma (PPAR-gamma). Intracerebral overexpression of miR-669c significantly decreased the ischemia-induced cell death and ameliorated the stroke-induced neurological deficits both at 1 and 3 days post injury (dpi). Albeit miR-669c overexpression failed to alter the overall Iba1 protein immunoreactivity, it significantly elevated Arg1 levels in the ischemic brain and increased colocalization of Arg1 and Iba1. Moreover, miR-669c overexpression under cerebral ischemia influenced several morphological characteristics of Iba1 positive cells. We further demonstrate the myeloid differentiation primary response gene 88 (MyD88) transcript as a direct target for miR-669c-3p in vitro and show reduced levels of MyD88 in miR-669c overexpressing ischemic brains in vivo. Conclusions Collectively, our data provide the evidence that miR-669c-3p is protective in a mouse model of ischemic stroke through enhancement of the alternative microglial/macrophage activation and inhibition of MyD88 signaling. Our results accentuate the importance of controlling miRNA-regulated responses for the therapeutic benefit in conditions of stroke and neuroinflammation.Peer reviewe