Kortversion av "Den kulturella våtmarken - rapport 2008:51"

Kulturmiljön är skapad av mänsklig aktivitet under lång tid och kommer att fortsätta formas av kommande generationer. Odlingslandskapets kulturmiljövärden måste synliggöras och bevaras i samband med våtmarker anläggs. När man nyanlägger en våtmark är detta ett stort ingrepp i odlingslandskapet men den kan också bli ett viktigt tillskott i kulturmiljön. Viktiga aspekter för ett lyckat resultat är placering, utformning och inte minst framtida skötsel.Regionala inventeringsrapporter import från MDP 2015-05</p

Hur påverkade är Friaåns och Tidans åmynningar och finns naturvärdena kvar? - en studie av två vattendrag vid Vänerns sydöstra strandlinje 2006

I projektet har Tidan och Friaåns nedre delar, till första definitiva vandringshindret, undersökts. Åarna mynnar ut i sydöstra Vänern och båda är kraftigt artificiellt påverkade. De ligger i en jordbruksbygd och är därmed naturligt näringsrika och vattnet är grumligt. Båda vattendragen är påverkade av vattenkraftverksutbyggnad. Friaån har rätats på en sträcka strax nedströms Lyrestad och Tidans mynning har successivt fyllts ut. Vattendragen är också muddrade på olika sträckor i åkerlandskapet. Åarna har här tvära, djupa kanter och bottenmaterialet består mest av lera. I åkerlandskapet har åarna ofta inga skyddszoner med skyddande vegetation, möjligen finns några enstaka träd. Förekomsten av död ved är nästan obefintlig. Kan Tidan och Friaån verkligen ha några naturvärden?Regionala inventeringsrapporter import från MDP 2015-05</p

Åtgärdsidéer för några sandstränder och strandängar. Vänerskärgården i Götene, Lidköpings och Mariestads kommuner

Länsstyrelsen i Västra Götalands län är en av sju länsstyrelser som har fått i uppdrag av regeringen att testa regionala landskapsstrategier för att nå miljömålet ”Ett rikt växt- och djurliv”. Detta delprojekt omfattar Vänerskärgården med Kinnekulle i Götene, Lidköpings, och Mariestads kommuner. I rapporten föreslås sandstränder och strandängar som har höga biologiska värden eller som kan få det om de röjs. Åtgärder föreslås som gynnar växt- och djurlivet, samt friluftslivet.Regionala inventeringsrapporter import från MDP 2015-05</p

Mechanisms involved in the regulation of secretory phospholipase A2 Type IIA expression in human arterial smooth muscle cells. Potential role in atherogenesis

Experimental and clinical evidence indicates that secretory phospholipase A2 group IIA (sPLA2-IIA) contributes to atherogenesis. Activity of sPLA2-IIA may be pro-atherogenic both in the circulation leading to altered lipoprotein profile and/or locally in the artery wall where it contributes to lipid accumulation both intra and extra cellularly. Smooth muscle cells (SMC) are the main source for sPLA2-IIA in the artery wall. However, knowledge about the regulation of the enzyme in this cell type is very limited. The general purpose of this thesis was to establish an in vitro model to investigate the signaling pathways involved in the regulation of sPLA2-IIA expression in human arterial SMC (HASMC). We show that sPLA2-IIA is regulated on three different levels in HASMC in vitro. Expression of sPLA2-IIA in HASMC was induced after prolonged culture periods resulting in cell differentiation, measured by the expression of, p21, p27, heavy caldesmon and smoothelin. Basal sPLA2-IIA secretion and/or transcription were further modulated by different pro- and anti-inflammatory cytokines among which IFNg had the most pronounced effect. IFNg induction was accompanied by phosphorylation, nuclear translocation and binding of the transcription factor STAT3 to the sPLA2-IIA promoter, as measured by western blot and electrophoretic mobility shift assay (EMSA) respectively. Binding of STAT3 was inhibited by the PPARa activator fenofibrate, followed by a decrease in sPLA2-IIA expression. Moreover, IFNg activation was accompanied by increased accumulation of diacylglycerol a potent endogenous activator of protein kinase C (PKC). However, based on the results with PKC inhibitors this pathway did not appear to be essential for IFNg induction of sPLA2-IIA in HASMC. Furthermore, IFNg induced sPLA2-IIA secretion was independent on endogenous production of eicosanoids and was not accompanied by increased eicosanoid secretion by HASMC. The third level of sPLA2-IIA expression was IFNg primed cells that were found to be sensitized to further stimulation by AA or prostaglandin E2. This effect was associated with intracellular accumulation of cyclic AMP and nuclear translocation and binding of cJun/CREB2 to the sPLA2-IIA promoter measured by EMSA. Using different inhibitors we found that the upstream signals for cJun/CREB2 involve both PKC and protein kinase A. In conclusion, changes in the balance of pro- and anti-inflammatory cytokines towards a pro-inflammatory state result in accumulation of cytokines including IFNg, IL1b and TNFa that induces sPLA2-IIA secretion by HASMC. This may contribute to the increased amount of extracellular enzyme identified in the arterial intima and/or increased serum levels observed in atherosclerosis. Extracellular sPLA2-IIA in the atherosclerotic plaque may play an important role to sustain chronic inflammation and contribute to the local accumulation of intracellular and extracellular lipoprotein deposits in the artery wall. Moreover increased serum sPLA2-IIA alters the lipoprotein profile rendering it more atherogenic. Furthermore we provide evidence that the regulation of sPLA2-IIA is cell and species specific. This property is extremely important especially when drawing conclusions relevant to human physiology and patophysiology

Yellow fluorescent protein-based assay to measure GABA(A) channel activation and allosteric modulation in CHO-K1 cells.

The γ-aminobutyric acid A (GABA(A)) ion channels are important drug targets for treatment of neurological and psychiatric disorders. Finding GABA(A) channel subtype selective allosteric modulators could lead to new improved treatments. However, the progress in this area has been obstructed by the challenging task of developing functional assays to support screening efforts and the generation of cells expressing functional GABA(A) ion channels with the desired subtype composition. To address these challenges, we developed a yellow fluorescent protein (YFP)-based assay to be able to study allosteric modulation of the GABA(A) ion channel using cryopreserved, transiently transfected, assay-ready cells. We show for the first time how the MaxCyte STX electroporation instrument can be used to generate CHO-K1 cells expressing functional GABA(A) α2β3γ2 along with a halide sensing YFP-H148Q/I152L (YFP-GABA(A2) cells). As a basis for a cell-based assay capable of detecting allosteric modulators, experiments with antagonist, ion channel blocker and modulators were used to verify GABA(A) subunit composition and functionality. We found that the I(-) concentration used in the YFP assay affected both basal quench of YFP and potency of GABA. For the first time the assay was used to study modulation of GABA with 7 known modulators where statistical analysis showed that the assay can distinguish modulatory pEC50 differences of 0.15. In conclusion, the YFP assay proved to be a robust, reproducible and inexpensive assay. These data provide evidence that the assay is suitable for high throughput screening (HTS) and could be used to discover novel modulators acting on GABA(A) ion channels

Resilience in the face of pelvic pain: A pilot study in males and females affected by urologic chronic pelvic pain

Aims Resilience represents a fundamental element in the experience of pain, as it allows adaptation to suffering and increases psychological social well-being and quality of life (QoL). We investigated resilience in patients affected by urologic chronic pelvic pain (UCPP) and the relationships with pain severity and distribution, catastrophizing and psychological distress.Methods Forty-eight consecutive UCPP patients were classified on a pain body map as being affected by pelvic pain only or widespread pain (WP), and underwent the evaluation of resilience with the 14-item Resilience Scale (RS-14), with higher scores indicating high resilience levels; scores &lt; 56 denote very poor resilience. Pelvic and nonpelvic pain intensity and the bother of urinary symptoms on QoL were measured by means of Pain Numerical Rating Scale (PNRS) and Visual Analog Scale (VAS). Pain Catastrophizing Scale (PCS) and Depression Anxiety Stress Scales (DASS-21) investigated catastrophizing and psychological conditions.Results Overall, RS-14 mean +/- SD total score was 50.2 +/- 12.5 in patients with pelvic pain only and 40.2 +/- 10.2 in those with WP. Significant relationships were observed between low resilience levels and high scores of pelvic and nonpelvic PNRS, VAS, pain catastrophizing scale and depression and anxiety, stress scale (for all: p &lt; 0.001). Significantly lower RS-14 scores were detected in females and in patients with WP.Conclusions A very poor resilience has been identified in UCPP patients, particularly in those with greater catastrophizing and mood alterations. WP and female gender were mostly affected. In UCPP patients, low resilience appears as a crucial factor in pain experience

Modulation of GABA signal with Diazepam (Dia) and TPA-023.

<p>YFP-GABA_A2 cells were exposed to EC₂₀ of GABA alone or in the presence of 1 µM of modulator. Data at 1–10 s was adjusted to a baseline of 100%. Representative time-courses of fluorescent quench at basal (10 mM I⁻) and maximum GABA response (GABA_max). A) Modulation of GABA EC₂₀ quench showing a significant increase in the presence of Diazepam. B) No significant change of GABA EC₂₀ quench in the presence of TPA-023. The experiment was repeated three times with similar results.</p

Modulation of GABA Signal with Allosteric Modulators.

<p>Modulator pEC₅₀ values were calculated from GABA concentration-response curves in the presence of 1 µM modulator. pEC₅₀ differences were calculated from [Log (EC₅₀ GABA alone) – Log (EC₅₀ GABA with modulator)] and stated as statistically significant or non-significant at p<0.05. A pooled estimate of variability was used to calculate the standard error of the difference between two compounds' average of 3 occasions pEC₅₀. The 95% confidence interval was calculated as 2× this standard error. Taking the anti-log converts this to a fold change (ratio) between two EC₅₀ values.</p

Basal I⁻ Permeability at Different I⁻ Concentrations.

<p>YFP-GABA_A2 cells were exposed to different concentrations of I⁻ in the absence or presence of GABA. Data at 1–10 s was adjusted to a baseline of 100%. A) Representative time-courses of fluorescent quench showing basal I⁻ permeability and maximum GABA response (GABA_max) of cells exposed to 5 mM, 10 mM, 20 mM and 40 mM NaI buffer. 0 mM NaI buffer is included in each graph as a reference. B) Concentration-responses of GABA with 0 mM, 5 mM, 10 mM, 20 mM and 40 mM NaI buffer showing I⁻ concentration-dependent baseline shift. The data represented are mean ± SD of quadruplicate wells. The experiment was repeated twice with similar results.</p