Species richness correlations between taxa calculated from species-area relationships

Predicting the species richness of certain taxa from the richness of others could be of great value in biodiversity conservation. If we know how the species richness of groups of organisms correlate to each other under different circumstances, inventories of only a few well-known taxa could be enough to establish the biodiversity values of different areas. In this master thesis I have examined the richness correlations between taxa from species-area relationships extracted from the literature to evaluate the possibilities of this approach. Calculations of the pairwise correlation between the residuals of the species-area relationships of different taxa found in the literature resulted in 503 correlation coefficients. Of the 79 taxa covered, the most frequently examined groups (several taxa included) were plants > butterflies > true bugs > birds > mammals. Only 157 of the 503 correlations were significant. An average effect size of 0.373 (95 % CL = 0.059) indicates positive but usually weak correlations between taxa in the very heterogeneous dataset. The dataset was divided into a number of categories (according to spatial scale, taxonomic distance, trophic position, biotope and climatic region) to investigate some hypotheses, for example (1) that richness of closely related taxa are likely to be more correlated than distantly related taxa, and (2) that correlations between plants and animals are higher than correlations among plants or among animal groups. Between families – within order comparisons had significantly higher correlation than comparisons in all other taxonomical classes except between kingdoms. These results were in agreement with my hypotheses concerning taxonomic distance and trophic position. No universal indicator taxon has been found to predict the species richness of other taxa. With more careful studies in certain biotopes and at appropriate spatial scale perhaps good indicator groups can be discovered. These are unlikely to be universal and it is probable that indicator taxa are only useful at regional scales.Förutsägelser av artrikedom hos vissa organismgrupper från diversiteten hos andra grupper skulle vara till stor hjälp i naturvårdsarbetet. Om man vet hur artrikedomen hos organismgrupper korrelerar med varandra under olika betingelser, kan man genom att bara inventera ett fåtal taxa bedöma ett områdes biodiversitetsvärden. I mitt examensarbete har jag undersökt diversitets-korrelationerna mellan taxa från art-areakurvor hämtade i litteraturen för att kunna utvärdera möjligheterna av denna infallsvinkel som hjälp i naturvårdsarbetet. Genom att räkna ut den parvisa korrelationen mellan residualerna från art-areakurvorna hos olika taxa i litteraturen fick jag 503 korrelationskoefficienter. Av de 79 inbegripna taxa var de vanligaste undersökta grupperna (flera taxa inkluderade) växter > fjärilar > skinnbaggar > fåglar > däggdjur. Endast 157 av 503 korrelationer var signifikanta. En medeleffektstorlek på 0,373 (95 % konfidensintervall = 0,314 - 0,432) indikerar positiva men svaga korrelationer mellan taxa i det väldigt heterogena datamaterialet. Materialet delades upp i ett antal kategorier (enligt rumslig skala, taxonomisk distans, trofisk position, biotop och klimatisk region) för att undersöka några hypoteser, till exempel (1) att diversitetskorrelationer mellan nära besläktade taxa är högre än mellan avlägset besläktade taxa, och (2) att korrelationer mellan växter och djur är högre än mellan växter eller mellan djurgrupper. Korrelationer för jämförelser mellan familjer – inom ordning var signifikant högre än för jämförelser i alla andra taxonomiska klasser utom för jämförelser mellan riken. Dessa resultat överensstämde med mina hypoteser om taxonomisk distans och trofisk position. Någon universell indikatorgrupp som förutsäger artdiversiteten hos andra grupper har inte hittats. Kanske kan lämpliga indikatorgrupper upptäckas med mer grundliga studier i särskilda biotoper och på passande rumslig skala. Dessa kommer sannolikt inte att vara universella och det är troligt att indikatortaxa bara är användbara på regional skala

Laryngeal aktivitet vid reglering av röststyrka: En jämförelse mellan personer med och utan sångträningserfarenhet

Inledning: I denna uppsats undersöktes glottala och fonationsaerodynamiska värden vid olika röststyrkenivåer, med syfte att öka kunskapen om vad som händer på laryngeal nivå när vi höjer och sänker röststyrkan. En grupp sångare jämfördes med personer som inte fått röstträning för att ta reda på om det finns skillnader mellan grupperna i relation till de glottala parametrarna hastighetskvot och öppetkvot samt de fonationsaerodynamiska parameterarna subglottalt tryck, luftflöde genom glottis och lufttrycksmotstånd i glottis. Metod: De metoder som användes var laryngoskopisk höghastighetsfilmning/digital kymografi och Phonatory Aerodynamic System. Resultat: Med ökad intensitet ökade luftflöde genom glottis, glottalt motstånd och subglottalt tryck. Öppetkvot minskade med ökad intensitet. Hastighetskvot visade inget signifikant samband med intensitet. Undersökning av varje grupp för sig visade att sambandet luftflödeintensitet endast gällde sångare och öppetkvot-intensitet gällde endast personer utan sångträning. Sambandet subglottalt tryck-intensitet var starkare för personer utan sångerfarenhet. Gruppen sångare hade signifikant mindre glottalt motstånd. Jämförelser av fonationsaerodynamiska och glottala värden visade att vid svag röststyrkenivå var glottalt motstånd och subglottalt tryck större hos personer med större öppetkvot. Vid stark röststyrka var flödet större och det glottala motståndet mindre hos personer med större hastighetskvot. Diskussion: Reglering av röststyrka kan ske på olika sätt, och det kan påverkas av sångträningserfarenhet. Resultaten tyder på att sångare använder luftflöde för att höja och sänka röststyrkan, medan ej sångtränade personer reglerar röststyrka med hjälp av stämvecksaktivitet (öppetkvot). Det skulle kunna bero på att sångare har högre krav på konsekvens i stämvecksrörelser oavsett röststyrkenivå

Fine Mapping of Gene Regions Regulating Neurodegeneration

Loss of nerve cells and axons is a common feature of common complex neurodegenerative disorders, such as Alzheimer’s and Parkinson’s diseases. However, also Multiple Sclerosis (MS), primarily an autoimmune disorder, has a prominent neurodegenerative component. In complex disorders, many components affecting disease development and disease progression in combination make up the overall risk. In general, we divide these factors into inherited genetic factors and environmental factors. In addition, there are sometimes complex gene-environment interactions that make it difficult to identify individual risk components. In this thesis, I have focused on a translational approach to find genetic determinants of nerve cell survival in a simplified experimental model of nerve injury-induced neurodegeneration. The aim has been to find novel genes/pathways whose relevance subsequently can be tested in human disease. Through various genetic mapping approaches I demonstrate a strong inverse correlation between neuronal survival and expression and protein levels of an enzyme involved in detoxification of certain oxidation by-products. This enzyme, Glutathione S-Transferase alpha 4 (Gsta4), is highly efficient in catalysing the reduction of the neurotoxic aldehyde 4- hydroxynonenal (HNE), which is generated during lipid peroxidation and has previously been implicated in the pathogenesis of various neurodegenerative disorders. The relevance of this mechanism was also tested in a model of traumatic brain injury, where Gsta4 levels inversely correlate with degree of neuronal loss as well. In addition, rats with higher Gsta4 levels have a more favourable outcome after injection of HNE directly into the cortex. Taken together, these two studies provide strong support for the notion that the identified pathway is highly important for ability to cope with oxidative stress and in turn of relevance for nerve cell survival in different types of acute injury. Finally, a possible role for Gsta4 is tested in experimental autoimmune encephalomyelitis (EAE), a model of MS. No discernible clinical effect was observed between congenic rats with higher Gsta4 expression and the parental strain. However, lower Gsta4 expression was associated with a stronger autoantibody response. Protein modifications by HNE have in other inflammatory models been documented to induce a stronger antibody response, which is consistent with the obtained results. Intrathecal antibody production is an important diagnostic marker in MS, and hypothetically the HNE pathway can play a role for disease course through both neurotoxicity and amplification of the immune response. This was tested in a large case control cohort of MS, where suggested associations both to clinical and immune phenotypes were found. In summary, the results presented encourage further studies on the Gsta4-HNE pathway both in conditions of acute nerve injury and autoimmune neuroinflammation

Сборник тестов по медицинской биологии и общей генетике (с пояснениями) для проверки уровня знаний студентов I курса по специальности "лечебное дело"

БИОЛОГИЯ МЕДИЦИНСКАЯБИОЛОГИЯГЕНЕТИКАСборник составлен по основным разделам курса (сущность жизни, молекулярно-генетический, клеточный, онтогенетический, популяционно-видовой и биосферно-биогеоценотический) для проверки усвоения знаний при проведении итоговых занятий

Green tea powder and Lactobacillus plantarum affect gut microbiota, lipid metabolism and inflammation in high-fat fed C57BL/6J mice

BACKGROUND: Type 2 diabetes is associated with obesity, ectopic lipid accumulation and low-grade inflammation. A dysfunctional gut microbiota has been suggested to participate in the pathogenesis of the disease. Green tea is rich in polyphenols and has previously been shown to exert beneficial metabolic effects. Lactobacillus plantarum has the ability to metabolize phenolic acids. The health promoting effect of whole green tea powder as a prebiotic compound has not been thoroughly investigated previously. METHODS: C57BL/6J mice were fed a high-fat diet with or without a supplement of 4% green tea powder (GT), and offered drinking water supplemented with Lactobacillus plantarum DSM 15313 (Lp) or the combination of both (Lp + GT) for 22 weeks. Parameters related to obesity, glucose tolerance, lipid metabolism, hepatic steatosis and inflammation were examined. Small intestinal tissue and caecal content were collected for bacterial analysis. RESULTS: Mice in the Lp + GT group had significantly more Lactobacillus and higher diversity of bacteria in the intestine compared to both mice in the control and the GT group. Green tea strongly reduced the body fat content and hepatic triacylglycerol and cholesterol accumulation. The reduction was negatively correlated to the amount of Akkermansia and/or the total amount of bacteria in the small intestine. Markers of inflammation were reduced in the Lp + GT group compared to control. PLS analysis of correlations between the microbiota and the metabolic variables of the individual mice showed that relatively few components of the microbiota had high impact on the correlation model. CONCLUSIONS: Green tea powder in combination with a single strain of Lactobacillus plantarum was able to promote growth of Lactobacillus in the intestine and to attenuate high fat diet-induced inflammation. In addition, a component of the microbiota, Akkermansia, correlated negatively with several metabolic parameters known to be risk factors for the development of type 2 diabetes

N-1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism

Obesity is a major health problem, and although caloric restriction and exercise are successful strategies to lose adipose tissue in obese individuals, a simultaneous decrease in skeletal muscle mass, negatively effects metabolism and muscle function. To deeper understand molecular events occurring in muscle during weight-loss, we measured the expressional change in human skeletal muscle following a combination of severe caloric restriction and exercise over 4 days in 15 Swedish men. Key metabolic genes were regulated after the intervention, indicating a shift from carbohydrate to fat metabolism. Nicotinamide N-methyltransferase (NNMT) was the most consistently upregulated gene following the energy-deficit exercise. Circulating levels of N-1-methylnicotinamide (MNA), the product of NNMT activity, were doubled after the intervention. The fasting-fed state was an important determinant of plasma MNA levels, peaking at similar to 18 h of fasting and being lowest similar to 3 h after a meal. In culture, MNA was secreted by isolated human myotubes and stimulated lipolysis directly, with no effect on glucagon or insulin secretion. We propose that MNA is a novel myokine that enhances the utilization of energy stores in response to low muscle energy availability. Future research should focus on applying MNA as a biomarker to identify individuals with metabolic disturbances at an early stage.Peer reviewe

The first case of Brucella canis in Sweden: background, case report and recommendations from a northern European perspective

Infection with Brucella canis has been diagnosed in Sweden for the first time. It was diagnosed in a three-year-old breeding bitch with reproductive disturbances. Fifteen in-contact dogs were tested repeatedly and all of them were negative for B. canis. The source of infection could not be defined. The present article describes the case and the measures undertaken and gives a short review over B. canis. Recommendations on how to avoid the infection in non-endemic countries are given

NK-like homeodomain proteins activate NOTCH3-signaling in leukemic T-cells

<p>Abstract</p> <p>Background</p> <p>Homeodomain proteins control fundamental cellular processes in development and in cancer if deregulated. Three members of the NK-like subfamily of homeobox genes (NKLs), TLX1, TLX3 and NKX2-5, are implicated in T-cell acute lymphoblastic leukemia (T-ALL). They are activated by particular chromosomal aberrations. However, their precise function in leukemogenesis is still unclear. Here we screened further NKLs in 24 T-ALL cell lines and identified the common expression of MSX2. The subsequent aim of this study was to analyze the role of MSX2 in T-cell differentiation which may be disturbed by oncogenic NKLs.</p> <p>Methods</p> <p>Specific gene activity was examined by quantitative real-time PCR, and globally by expression profiling. Proteins were analyzed by western blot, immuno-cytology and immuno-precipitation. For overexpression studies cell lines were transduced by lentiviruses.</p> <p>Results</p> <p>Quantification of MSX2 mRNA in primary hematopoietic cells demonstrated higher levels in CD34+ stem cells as compared to peripheral blood cells and mature CD3+ T-cells. Furthermore, analysis of MSX2 expression levels in T-cell lines after treatment with core thymic factors confirmed their involvement in regulation. These results indicated that MSX2 represents an hematopoietic NKL family member which is downregulated during T-cell development and may functionally substituted by oncogenic NKLs. For functional analysis JURKAT cells were lentivirally transduced, overexpressing either MSX2 or oncogenic TLX1 and NKX2-5, respectively. These cells displayed transcriptional activation of NOTCH3-signaling, including NOTCH3 and HEY1 as analyzed by gene expression profiling and quantitative RT-PCR, and consistently attenuated sensitivity to gamma-secretase inhibitor as analyzed by MTT-assays. Furthermore, in addition to MSX2, both TLX1 and NKX2-5 proteins interacted with NOTCH-pathway repressors, SPEN/MINT/SHARP and TLE1/GRG1, representing a potential mechanism for (de)regulation. Finally, elevated expression of NOTCH3 and HEY1 was detected in primary TLX1/3 positive T-ALL cells corresponding to the cell line data.</p> <p>Conclusion</p> <p>Identification and analysis of MSX2 in hematopoietic cells implicates a modulatory role via NOTCH3-signaling in early T-cell differentiation. Our data suggest that reduction of NOTCH3-signaling by physiological downregulation of MSX2 expression during T-cell development is abrogated by ectopic expression of oncogenic NKLs, substituting MSX2 function.</p