Rukiin sakoluku Etelä-Pohjanmaalla

vokKirjasto Aj-

Rakennetut meren rannat 2005

Meren rannikon ja saarten koko rantaviivasta on keskimäärin 41 % sulkeutunutta eli rannan läheisyydessä olevat rakennukset pihapiireineen sulkevat rannan muulta käytöltä. Kun alle hehtaarin saaret, jotka käytännössä eivät sovellu rakentamiseen, jätetään laskelmien ulkopuolelle, tulee mannerrannan ja yli hehtaarin saarten sulkeutuneisuusasteeksi 48 %. Sulkeutuneisuusaste on tällöin 22 rannikkokunnan alueella 60 % tai enemmän ja näistä kuuden kunnan alueella 70 % tai enemmän. Tässä raportissa tarkastellaan sulkeutuneiden ja vapaiden rantojen määrää ja sijaintia sekä vapaiden rantojen laatua, saavutettavuutta ja yhtenäisyyttä

Bebyggda havsstränder 2005

Av hela strandlinjen längs havskusten och kring öarna är i genomsnitt 41 % sluten. Det vill säga att de byggnader med gårdsplaner, som finns i närheten av stranden sluter stranden från övrig användning. Om man utesluter från kalkylerna öar som utgör mindre än 1 ha och därmed i praktiken inte lämpar sig för byggande, blir slutenhetsgraden för strandlinjen på fastlandet och på öar som är större än 1 ha 48 %. Därmed är slutenhetsgraden i 22 kommuner 60 % eller högre och i 6 av dessa kommuner 70 % eller högre. Den här rapporten behandlar mängden slutna stränder och fria stränder och deras läge, samt kvaliteten, tillgängligheten och sammanhängandet hos fria stränder

Suomen maatalous ja maaseutuelinkeinot 1998

vokMTT Taloustutkimus (MTTL

Suomen maatalous ja maaseutuelinkeinot 1999/2000

vokMTT

Etiology of acute respiratory disease in fattening pigs in Finland

Background: The objective of our study was to clinically and etiologically investigate acute outbreaks of respiratory disease in Finland. Our study also aimed to evaluate the clinical use of various methods in diagnosing respiratory infections under field conditions and to describe the antimicrobial resistance profile of the main bacterial pathogen(s) found during the study. Methods: A total of 20 case herds having finishing pigs showing acute respiratory symptoms and eight control herds showing no clinical signs suggesting of respiratory problems were enrolled in the study. Researchers visited each herd twice, examining and bleeding 20 pigs per herd. In addition, nasal swab samples were taken from 20 pigs and three pigs per case herd were necropsied during the first visit. Serology was used to detect Actinobacillus pleuropneumoniae (APP), swine influenza virus (SIV), porcine reproductive and respiratory syndrome virus (PRRSV), porcine respiratory coronavirus (PRCV) and Mycoplasma hyopneumoniae antibodies. Polymerase chain reaction (PCR) was used to investigate the presence of porcine circovirus type 2 (PCV2) in serumand SIV in the nasal and lung samples. Pathology and bacteriology, including antimicrobial resistance determination, were performed on lung samples obtained from the field necropsies. Results: According to the pathology and bacteriology of the lung samples, APP and Ascaris suum were the main causes of respiratory outbreaks in 14 and three herds respectively, while the clinical signs in three other herds had a miscellaneous etiology. SIV, APP and PCV2 caused concurrent infections in certain herds but they were detected serologically or with PCR also in control herds, suggesting possible subclinical infections. APP was isolated from 16 (80%) case herds. Marked resistance was observed against tetracycline for APP, some resistance was detected against trimethoprim/sulfamethoxazole, ampicillin and penicillin, and no resistance against florfenicol, enrofloxacin, tulathromycin or tiamulin was found. Serology, even from paired serum samples, gave inconclusive results for acute APP infection diagnosis. Conclusions: APP was the most common cause for acute respiratory outbreaks in our study. SIV, A. suum, PCV2 and certain opportunistic bacteria were also detected during the outbreaks; however, viral pathogens appeared less important than bacteria. Necropsies supplemented with microbiology were the most efficient diagnostic methods in characterizing the studied outbreaks.Peer reviewe

Amorphous carbon thin film electrodes with intrinsic Pt-gradient for hydrogen peroxide detection

Nanoscale amorphous carbon thin films with intrinsic Pt gradient show great promise as new electrode materials for electrochemical detection of hydrogen peroxide. Embedding the Pt particles in the carbon matrix during the fabrication process allows tighter integration than, for example, adding them after the fabrication on top of the substrate. Especially, this approach can offer excellent electrochemical properties combined with CMOS compatibility, which is crucial for further device development. Here we provide extensive in depth electrochemical and physicochemical characterization of these novel materials by cyclic voltammetry (CV), chronoamperometry (CA), rotating disk electrode (RDE) experiments, transmission electron microscopy (TEM), Raman spectroscopy, x-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). Equipped with these detailed results on these materials we proceed to present some suggestions how the physicochemical properties correlate with the results from electrochemical measurements. (i) It is shown that coarsening of the initially very finely dispersed structure occurs both under electron bombardment during TEM imaging as well as during cyclic voltammetry in H2SO4. (ii) Further, it is shown that OH is adsorbed on small Pt islands much more strongly compared to the bulk Pt, which may heavily influence hydrogen peroxide redox reactions on these Pt-containing amorphous carbon films. (iii) Finally, we proceed to demonstrate that despite these complications, these materials show linear response for hydrogen peroxide reduction in neutral phosphate buffered saline combined with very fast response times.Academy of Finland (E.P. grant #274670, T.L. grants # 285015 and #285526), Biocentrum Helsinki, Finnish Cultural Foundation (N.I. grant #00160331) and Foundation for Aalto University Science and Technology are acknowledged for funding

A B-cell gene signature correlates with the extent of gluten-induced intestinal injury in celiac disease

Background & Aims: Celiac disease (CeD) provides an opportunity to study autoimmunity and the transition in immune cells as dietary gluten induces small intestinal lesions. Methods: Seventy-three celiac disease patients on a long-term, gluten-free diet ingested a known amount of gluten daily for 6 weeks. A peripheral blood sample and intestinal biopsy specimens were taken before and 6 weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus-heightâtoâcrypt-depth ratio to quantify gluten-induced intestinal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained a relatively healthy intestinal mucosa or deteriorated in the face of a gluten challenge. Results: Gluten-dependent intestinal damage from baseline to 6 weeks varied widely across all patients, ranging from no change to extensive damage. Genes differentially expressed in B cells correlated strongly with the extent of intestinal damage. A relative increase in B-cell gene expression correlated with a lack of sensitivity to gluten whereas their relative decrease correlated with gluten-induced mucosal injury. A core B-cell gene module, representing a subset of B-cell genes analyzed, accounted for the correlation with intestinal injury. Conclusions: Genes comprising the core B-cell module showed a net increase in expression from baseline to 6 weeks in patients with little to no intestinal damage, suggesting that these individuals may have mounted a B-cell immune response to maintain mucosal homeostasis and circumvent inflammation. DNA microarray data were deposited at the GEO repository (accession number: GSE87629; available: https://www.ncbi.nlm.nih.gov/geo/). Keywords: Oral Tolerance, Mucosal Immunity, Autoimmunity, Regulatory B Cel