Medarbetarskapet i fokus: En studie om skillnader i små och medelstora organisationer

Syftet med denna studie var att undersöka medarbetarskapet på ett antal butiker inom samma koncern med olika storlek för att se om det förelåg skillnader beroende på organisationernas storlek. Vidare undersöktes också om det förelåg någon skillnad mellan organisationerna i det upplevda medarbetarskapet beroende av arbetsledning med personalansvar, arbetsledning utan personalansvar eller ingen arbetsledning. Med detta ville vi tillföra ny kunskap på medarbetarskapets förhållande till organisationsstorlek då det tidigare finns begränsad forskning inom detta. Studien genomfördes på åtta små och tre medelstora butiker i Malmö stad och Lunds kommun. Materialet om medarbetarskapet samlades in genom frågeformuläret Work-Oriented Relationships and Knowledge-based Investigation Questionnarie (WORK-IQ) (Bertlett & Arvidsson, 2009), vilket innehåller följande åtta dimensioner: Kunskap och färdighet, psykologisk mognad, lärande, inomgruppskommunikation, mellangruppskommunikation, sociala relationer, demokratiska processer och slutligen tillit- lojalitet och respekt. Totalt samlades 115 komplett ifyllda formulär in. Resultaten visar att det finns signifikanta skillnader mellan små och medelstora organisationer i dimensionerna lärande och demokratiska processer men i övrigt verkar inte organisationsstorlek ha någon större inverkan på medarbetarskapet. Enligt resultatet verkar inte organisationens storlek heller påverka det upplevda medarbetarskapet beroende på om man har arbetsledning eller inte. Däremot verkar arbetsledning påverka medarbetarskap

Atmospheric Deposition of Inorganic Elements and Organic Compounds at the Inlets of the Venice Lagoon

The Venice Lagoon is subjected to long-range transport of contaminants via aerosol from the near Po Valley. Moreover, it is an area with significant local anthropogenic emissions due to the industrial area of Porto Marghera, the urban centres, and the glass factories and with emissions by ships traffic within the Lagoon. Furthermore, since 2005, the Lagoon has also been affected by the construction of the MOSE (Modulo Sperimentale Elettromeccanico—Electromechanical Experimental Module) mobile dams, as a barrier against the high tide. This work presents and discusses the results from chemical analyses of bulk depositions, carried out in different sites of the Venice Lagoon. Fluxes of pollutants were also statistically analysed on PCA with the aim of investigating the spatial variability of depositions and their correlation with precipitations. Fluxes of inorganic pollutants depend differently on precipitations, while organic compounds show a more seasonal trend. The statistical analysis showed that the site in the northern Lagoon has lower and almost homogeneous fluxes of pollutants, while the other sites registered more variable concentrations. The study also provided important information about the annual trend of pollutants and their evolution over a period of about five years, from 2005 to 2010

Association of Polymorphisms of the CHI3L1 Gene with Asthma and Atopy: A Populations-Based Study of 6514 Danish Adults

YKL-40 is a chitinase-like glycoprotein encoded by the chitinase 3-like 1 gene, CHI3L1, localized at chromosome 1q32.1. Increased levels of serum YKL-40 have been reported to be a biomarker for asthma and a reduced lung function. Interestingly, the C-allele of the -131 C-->G (rs4950928) polymorphism of CHI3L1 has been shown to associate with bronchial hyperresponsiveness and reduced lung function suggesting that variations in CHI3L1 may influence risk of asthma. The objective of the present study was to investigate the association of common variation in the CHI3L1 locus with asthma, atopy and lung function in a large population-based sample of adults.Eleven single nucleotide polymorphisms (SNPs) of CHI3L1 including rs4950928 were genotyped in 6514 individuals. Asthma was defined as self-reported history of physician-diagnosed asthma. Total IgE and specific IgE to inhalant allergens were measured on serum samples. Lung function was measured by spirometry. Homozygosity of the rs4950928 G allele as compared to homozygosity of the C allele was associated with self-reported physician diagnosed asthma (OR 1.5 (95% CI, 1.00-2.26)) and with prevalence of atopic asthma (OR 1.93 (95% CI, 1.21-3.07)) after adjustment for age, sex, smoking status, socio-economic class and BMI. Carriers of rs883125 G allele had a significantly lower prevalence of atopy (OR 0.82 (CI, 0.72; 0.94)) as compared to homozygosity of the C allele. None of the SNPs examined were significantly associated with FEV1. However, two SNPs (rs10399931 and rs4950930) appeared to be significantly associated with FEV(1)/FVC-ratio. Subgroup analyses of never-smokers did not consistently influence the associations in an either positively og negatively way.In contrast to previous studies, the rs4950928 G allele, and not the C allele, was found to be associated with asthma. A few other SNPs of the CHI3L1 was found to be significantly associated with atopy and FEV1/FVC ratio, respectively. Thus, more studies seem warranted to establish the role of CHI3L1 gene in asthma and atopy

The Type 2 Diabetes Associated Minor Allele of rs2237895 KCNQ1 Associates with Reduced Insulin Release Following an Oral Glucose Load

BACKGROUND: Polymorphisms in the potassium channel, voltage-gated, KQT-like subfamily, member 1 (KCNQ1) have recently been reported to associate with type 2 diabetes. The primary aim of the present study was to investigate the putative impact of these KCNQ1 polymorphisms (rs2283228, rs2237892, rs2237895, and rs2237897) on estimates of glucose stimulated insulin release. METHODOLOGY/PRINCIPAL FINDINGS: Genotypes were examined for associations with serum insulin levels following an oral glucose tolerance test (OGTT) in a population-based sample of 6,039 middle-aged and treatment-naïve individuals. Insulin release indices estimated from the OGTT and the interplay between insulin sensitivity and insulin release were investigated using linear regression and Hotelling T2 analyses. Applying an additive genetic model the minor C-allele of rs2237895 was associated with reduced serum insulin levels 30 min (mean+/-SD: (CC) 277+/-160 vs. (AC) 280+/-164 vs. (AA) 299+/-200 pmol/l, p = 0.008) after an oral glucose load, insulinogenic index (29.6+/-17.4 vs. 30.2+/-18.7vs. 32.2+/-22.1, p = 0.007), incremental area under the insulin curve (20,477+/-12,491 vs. 20,503+/-12,386 vs. 21,810+/-14,685, p = 0.02) among the 4,568 individuals who were glucose tolerant. Adjustment for the degree of insulin sensitivity had no effect on the measures of reduced insulin release. The rs2237895 genotype had a similar impact in the total sample of treatment-naïve individuals. No association with measures of insulin release were identified for the less common diabetes risk alleles of rs2237892, rs2237897, or rs2283228. CONCLUSION: The minor C-allele of rs2237895 of KCNQ1, which has a prevalence of about 42% among Caucasians was associated with reduced measures of insulin release following an oral glucose load suggesting that the increased risk of type 2 diabetes, previously reported for this variant, likely is mediated through an impaired beta cell function

G-allele of Intronic rs10830963 in MTNR1B Confers Increased Risk of Impaired Fasting Glycemia and Type 2 Diabetes Through an Impaired Glucose-Stimulated Insulin Release: Studies Involving 19,605 Europeans

OBJECTIVE Genome-wide association studies have identified several variants within the MTNR1B locus that are associated with fasting plasma glucose (FPG) and type 2 diabetes. We refined the association signal by direct genotyping and examined for associations of the variant displaying the most independent effect on FPG with isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), type 2 diabetes, and measures of insulin release and peripheral and hepatic insulin sensitivity. RESEARCH DESIGN AND METHODS We examined European-descent participants in the Inter99 study (n = 5,553), in a sample of young healthy Danes (n = 372), in Danish twins (n = 77 elderly and n = 97 young), in additional Danish type 2 diabetic patients (n = 1,626) and control subjects (n = 505), in the Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study (n = 4,656), in the North Finland Birth Cohort 86 (n = 5,258), and in the Haguenau study (n = 1,461). RESULTS The MTNR1B intronic variant, rs10830963, carried most of the effect on FPG and showed the strongest association with FPG (combined P = 5.3 × 10−31) and type 2 diabetes. The rs10830963 G-allele increased the risk of i-IFG (odds ratio [OR] 1.64, P = 5.5 × 10−11) but not i-IGT. The G-allele was associated with a decreased insulin release after oral and intravenous glucose challenges (P < 0.01) but not after injection of tolbutamide. In elderly twins, the G-allele associated with hepatic insulin resistance (P = 0.017). CONCLUSIONS The G-allele of MTNR1B rs10830963 increases risk of type 2 diabetes through a state of i-IFG and not through i-IGT. The same allele associates with estimates of β-cell dysfunction and hepatic insulin resistance

Variation in CHI3LI in Relation to Type 2 Diabetes and Related Quantitative Traits

CHI3LI encoding the inflammatory glycoprotein YKL-40 is located on chromosome 1q32.1. YKL-40 is involved in inflammatory processes and patients with Type 2 Diabetes (T2D) have elevated circulating YKL-40 levels which correlate with their level of insulin resistance. Interestingly, it has been reported that rs10399931 (-329 G/A) of CHI3LI contributes to the inter-individual plasma YKL-40 levels in patients with sarcoidosis, and that rs4950928 (-131 C/G) is a susceptibility polymorphism for asthma and a decline in lung function. We hypothesized that single nucleotide polymorphisms (SNPs) or haplotypes thereof the CHI3LI locus might influence risk of T2D. The aim of the present study was to investigate the putative association between SNPs and haplotype blocks of CHI3LI and T2D and T2D related quantitative traits.Eleven SNPs of CHI3LI were genotyped in 6514 individuals from the Inter99 cohort and 2924 individuals from the outpatient clinic at Steno Diabetes Center. In cas-control studies a total of 2345 T2D patients and 5302 individuals with a normal glucose tolerance test were examined. We found no association between rs10399931 (OR, 0.98 (CI, 0.88-1.10), p = 0.76), rs4950928 (0.98 (0.87-1.10), p = 0.68) or any of the other SNPs with T2D. Similarly, we found no significant association between any of the 11 tgSNPs and T2D related quantitative traits, all p>0.14. None of the identified haplotype blocks of CHI3LI showed any association with T2D, all p>0.16.None of the examined SNPs or haplotype blocks of CHI3LI showed any association with T2D or T2D related quantitative traits. Estimates of insulin resistance and dysregulated glucose homeostasis in T2D do not seem to be accounted for by the examined variations of CHI3LI

Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease

Exploring Positional and Functional Candidate Genes for Type 2 Diabetes

Type 2 diabetes (T2D) is a complex, metabolic disorder characterized by hyperglycaemia because of defects in insulin secretion and sensitivity. The rapid increase in T2D is likely to reflect the influence of both genetic and environmental factors in disease development. However, the genetic aetiology of T2D remains largely unknown. Thus, the aim of this thesis was to study the role of genetic variation in positional and functional candidate genes for T2D. In the first study, we studied association between polymorphisms in the FXN gene and T2D. We excluded that polymorphisms in FXN have a role in T2D susceptibility. The ?common variation common disease? hypothesis suggests that common polymorphisms increase susceptibility to common disorders. Thus, it is reasonable to hypothesize that variants in genes causing rare monogenic forms of diabetes also harbours polymorphisms that increase susceptibility for the more common late onset T2D. Mutations in the HNF-1a gene cause Maturity Onset Diabetes of the Young (MODY) type 3, and this is the most frequent form of monogenic diabetes. We studied polymorphisms in this gene and observed that the I27L and A98V polymorphisms were associated with decreased insulin secretion and a modest increase in risk of future T2D, especially in overweight individuals. In a subsequent study polymorphisms in the HNF-4a, GCK and HNF-1b genes (causing MODY 1, 2 and 5 respectively) were studied. An HNF-4a P2 promoter variant was associated with elevated rates of hepatic glucose production during hyperinsulinaemic euglycaemic clamp and increased future risk of T2D. A polymorphism in the GCK promoter was associated with increased fasting plasma glucose levels that maintained unchanged during follow-up, but had no effect on risk of future T2D. Genetic variation in the HNF-1b gene did not confer increased risk of future T2D. Glucose stimulated insulin secretion is dependent on electrical activity in the beta-cells, hence ion-channels in the beta-cells are potential candidate genes for T2D. We also showed that polymorphisms in the CACNA1E gene, which encodes for the CaV2.3 pore forming subunit were associated with reduced second phase insulin secretion and increased risk of future T2D. In conclusion, these results suggest that: 1) common variation in MODY genes confer an increased risk of future T2D, particularly in individuals with increased insulin demands; 2) variation in the CACNA1E gene is associated with T2D and contribute to regulation of second phase insulin secretion

Det energiproducerande huset

We are heading towards a huge switch of how energy is produced with fossil fuels being replaced by renewable energy sources. It is not difficult to replace the energy you use in the house and there is no need for futuristic technology. There are already many established products on the market such as high efficiency vacuum solar collectors, heat pumps & small wind power stations that can supply the energy being used in a house. The company Sol & Energiteknik SE AB in Huskvarna has many different products which can reduce the need for an outside energy distributor. An average house in Sweden uses 15 000 kWh for heating, 5000 kWh for tap water and 5000 kWh for electricity. These figures are based on each household using 14 000 kWh for heating, 5000 kWh for tap water and 8100 kWh for electricity. A wood furnace delivers the heat and the electricity is bought from the electricity company Fortum. Before you decide to change how you heat your house or the way you get your electricity, you need to calibrate the dimension of your system. You should make your house more energy efficient and buy products that run on less electricity than your old ones. By replacing the way of heating the tap water with 5 modules of Intelli-Heat vacuum pipes with the total area of 11,4 m2 which are orientated in a south direction with an angle of 90 degrees, you get 6200 kWh hot tap water from March to November. The demand for heating is covered with the heat pump - NIBE Fighter 1135; 6 kW. From 3600 kWh of electricity and a COP of 3 you get 11 000 kWh of hot water. All the heat is stored in a 2000 litres accumulator tank which should store the heat for three days depending on the outdoor temperature. The electricity in the house is produced by a wind power station from Hannevind AB. An 11 kW plant can produce 20 000 kWh electricity when the wind speed is 6 m/s. At locations where the wind speed is lower than 6 m/s, the plant of course will produce less electricity. In Jönköping, where the average wind speed is 4,2 m/s, a plant like this will produce 6900 kWh/year. To compensate the lower energy production in the summer, when the wind speed is lower, you can rig up 10 m2 of photovoltaic panels. They produce about 1000 kWh electricity per year and are simply connected to the grid through a wall socket. The grid will be used as a backup, which means, when you got shortage of electricity you buy it from the electricity company which owns the grid. When there is too much electricity you send it out on the grid so others can use the electricity. The cost of a system like this will range from 200 000 to 460 000 Swedish crowns depending on where in Sweden you live. You have to adapt your system to where you live, if you for example live on a very windy location you may focus on the wind power station and maybe give up the heat pump. An annual cost of 33 000 Swedish crowns plus the cost of the electricity you have to buy from the electricity company, is quite expensive but you should keep in mind that the energy is as good as free when everything is paid after 15-20 years. In locations where the wind speed is insufficient (below 4 m/s) you can choose to join a wind power cooperative. Then you can buy the electricity from the wind power – co operative to get a much better price than from an ordinary electricity company. One kWh electricity from Svensk vindkraftkooperativ costs 0,606 Swedish crowns unlike one kWh from for example Fortum where it costs 1,07 Swedish crowns

Local delivery of minocycline-loaded PLGA nanoparticles from gelatin-coated neural implants attenuates acute brain tissue responses in mice

Background: Neural interfaces often elicit inflammatory responses and neuronal loss in the surrounding tissue which adversely affect the function and longevity of the implanted device. Minocycline, an anti-inflammatory pharmaceutics with neuroprotective properties, may be used for reducing the acute brain tissue responses after implantation. However, conventional administration routes require high doses which can cause adverse systemic side effects. Therefore, the aim of this study was to develop and evaluate a new drug-delivery-system for local and sustained administration of minocycline in the brain. Methods: Stainless steel needles insulated with Parylene-C were dip-coated with non-crosslinked gelatin and minocycline-loaded PLGA nanoparticles (MC-NPs) were incorporated into the gelatin-coatings by an absorption method and subsequently trapped by drying the gelatin. Parylene-C insulated needles coated only with gelatin were used as controls. The expression of markers for activated microglia (CD68), all microglia (CX3CR1-GFP), reactive astrocytes (GFAP), neurons (NeuN) and all cell nuclei (DAPI) surrounding the implantation sites were quantified at 3 and 7 days after implantation in mice. Results: MC-NPs were successfully incorporated into gelatin-coatings of neural implants by an absorption method suitable for thermosensitive drug-loads. Immunohistochemical analysis of the in vivo brain tissue responses, showed that MC-NPs significantly attenuate the activation of microglial cells without effecting the overall population of microglial cells around the implantation sites. A delayed but significant reduction of the astrocytic response was also found in comparison to control implants. No effect on neurons or total cell count was found which may suggest that the MC-NPs are non-toxic to the central nervous system. Conclusions: A novel drug-nanoparticle-delivery-system was developed for neural interfaces and thermosensitive drug-loads. The local delivery of MC-NPs was shown to attenuate the acute brain tissue responses nearby an implant and therefore may be useful for improving biocompatibility of implanted neuro-electronic interfaces. The developed drug-delivery-system may potentially also be used for other pharmaceutics to provide highly localized and therefore more specific effects as compared to systemic administration