Bioconversion of D-galacturonate to keto-deoxy-L-galactonate (3-deoxy-L-threo-hex-2-ulosonate) using filamentous fungi

<p>Abstract</p> <p>Background</p> <p>The D-galacturonic acid derived from plant pectin can be converted into a variety of other chemicals which have potential use as chelators, clarifiers, preservatives and plastic precursors. Among these is the deoxy-keto acid derived from L-galactonic acid, keto-deoxy-L-galactonic acid or 3-deoxy-L-<it>threo</it>-hex-2-ulosonic acid. The keto-deoxy sugars have been found to be useful precursors for producing further derivatives. Keto-deoxy-L-galactonate is a natural intermediate in the fungal D-galacturonate metabolic pathway, and thus keto-deoxy-L-galactonate can be produced in a simple biological conversion.</p> <p>Results</p> <p>Keto-deoxy-L-galactonate (3-deoxy-L-<it>threo</it>-hex-2-ulosonate) accumulated in the culture supernatant when <it>Trichoderma reesei </it>Δ<it>lga1 </it>and <it>Aspergillus niger </it>Δ<it>gaaC </it>were grown in the presence of D-galacturonate. Keto-deoxy-L-galactonate accumulated even if no metabolisable carbon source was present in the culture supernatant, but was enhanced when D-xylose was provided as a carbon and energy source. Up to 10.5 g keto-deoxy-L-galactonate l^-1was produced from 20 g D-galacturonate l^-1and <it>A. niger </it>Δ<it>gaaC </it>produced 15.0 g keto-deoxy-L-galactonate l^-1from 20 g polygalacturonate l^-1, at yields of 0.4 to 1.0 g keto-deoxy-L-galactonate [g D-galacturonate consumed]^-1. Keto-deoxy-L-galactonate accumulated to concentrations of 12 to 16 g l^-1intracellularly in both producing organisms. This intracellular concentration was sustained throughout production in <it>A. niger </it>Δ<it>gaaC</it>, but decreased in <it>T. reesei</it>.</p> <p>Conclusions</p> <p>Bioconversion of D-galacturonate to keto-deoxy-L-galactonate was achieved with both <it>A. niger </it>Δ<it>gaaC </it>and <it>T. reesei </it>Δ<it>lga1</it>, although production (titre, volumetric and specific rates) was better with <it>A. niger </it>than <it>T. reesei</it>. <it>A. niger </it>was also able to produce keto-deoxy-L-galactonate directly from pectin or polygalacturonate demonstrating the feasibility of simultaneous hydrolysis and bioconversion. Although keto-deoxy-L-galactonate accumulated intracellularly, concentrations above ~12 g l^-1were exported to the culture supernatant. Lysis may have contributed to the release of keto-deoxy-L-galactonate from <it>T. reesei </it>mycelia.</p

Peripherally Administered Y-2-Receptor Antagonist BIIE0246 Prevents Diet-Induced Obesity in Mice With Excess Neuropeptide Y, but Enhances Obesity in Control Mice

Neuropeptide Y (NPY) plays an important role in the regulation of energy homeostasis in the level of central and sympathetic nervous systems (SNSs). Genetic silencing of peripheral Y-2-receptors have anti-obesity effects, but it is not known whether pharmacological blocking of peripheral Y-2-receptors would similarly benefit energy homeostasis. The effects of a peripherally administered Y-2-receptor antagonist were studied in healthy and energy-rich conditions with or without excess NPY. Genetically obese mice overexpressing NPY in brain noradrenergic nerves and SNS (OE-NPYD beta H) represented the situation of elevated NPY levels, while wildtype (WT) mice represented the normal NPY levels. Specific Y-2-receptor antagonist, BIIE0246, was administered (1.3 mg/kg/day, i.p.) for 2 or 4.5 weeks to OE-NPYD beta H and WT mice feeding on chow or Western diet. Treatment with Y-2-receptor antagonist increased body weight gain in both genotypes on chow diet and caused metabolic disturbances (e.g., hyperinsulinemia and hypercholesterolemia), especially in WT mice. During energy surplus (i.e., on Western diet), blocking of Y-2-receptors induced obesity in WT mice, whereas OE-NPYD beta H mice showed reduced fat mass gain, hepatic glycogen and serum cholesterol levels relative to body adiposity. Thus, it can be concluded that with normal NPY levels, peripheral Y-2-receptor antagonist has no potential for treating obesity, but oppositely may even induce metabolic disorders. However, when energy-rich diet is combined with elevated NPY levels, e.g., stress combined with an unhealthy diet, Y-2-receptor antagonism has beneficial effects on metabolic status

Röntgenhoitajan osaaminen magneettitutkimuksissa

Opinnäytetyön tavoitteena oli tuottaa tietoa röntgenhoitajan magneettitutkimusosaamisesta. Opinnäytetyön tarkoituksena oli kartoittaa systemaattisella kirjallisuuskatsauksella kansainvälistä tietoa röntgenhoitajan magneettitutkimusosaamisesta. Opinnäytetyön tehtävät olivat seuraavat: Mitä röntgenhoitajan magneettitutkimusosaaminen on? Miten röntgenhoitajan magneettitutkimusosaaminen on hankittu? Opinnäytetyö toteutettiin systemaattisena kirjallisuuskatsauksena. Aineiston sisällönanalyysi tehtiin röntgenhoitajan magneettitutkimusosaamisen osalta teoriaohjaavasti ja magneettitutkimusosaamisen hankkimisen osalta aineistolähtöisesti. Röntgenhoitajan osaaminen jakautuu kuvantamistutkimuksen toteuttamisen osaamiseen, turvallisuusosaamisen ja työelämäosaamiseen. Tulosten perusteella röntgenhoitajan magneettitutkimuksen toteuttamisen osaaminen sisältää potilaan kohtaamiseen liittyvää osaamista, kuvantamisosaamista ja tulkintaosaamista. Turvallisuusosaaminen koostuu tutkimusteknisestä turvallisuusosaamisesta ja potilastyön turvallisuusosaamisesta. Työelämäosaamiseen kuuluu ammatillisessa viitekehyksessä toimiminen ja toiminnallisessa viitekehyksessä toimiminen. Röntgenhoitajan osaamisen hankkiminen jakautuu työpaikalla tapahtuvaan sisäiseen koulutukseen ja valmistumisen jälkeen suoritettaviin erikoistumisopintoihin. Opinnäytetyön tulosten perusteella röntgenhoitajan magneettitutkimusosaamisen osa-alueiden sisältö on kansainvälisesti samansuuntaista verrattuna suomalaisen tutkimuksen tuloksiin. Selkeä ero on röntgenhoitajan tulkintaosaamisen sisällössä. Kansainvälisesti lisäkoulutuksen saanut röntgenhoitaja voi tulkita magneettitutkimuksia. Jatkotutkimusaiheena esitetään tutkimusta röntgenhoitajien tulkintaosaamisesta ja magneettitutkimusosaamisen hankkimisesta Suomessa.The objective of this study was to produce information about the competence of a radiographer in magnetic resonance imaging (MRI). The purpose of this study was to gather international information by a systematic review of the literature. The objective of the study was broken into two questions, what is the competence of a radiographer in MRI and how was this competence acquired? The answer to the former question was acquired by theory-based analysis of the sources used in the systematic review and the answer to the latter was based only on the sources themselves. The competence of a radiographer in MRI divides into three sub-competences which are imaging competence, safety competence and work environment competence. The findings of this study suggest that the imaging competence consists of interacting with the patient, imaging of the patient and reporting of the resulting images. The safety competence; furthermore, consists of technical and patient safety. Finally, the work environment competence consists of working both professionally and functionally. The findings show that radiographers acquire their competence through workplace learning and by participating in postgraduate programmes. The findings of this study show that there are only slight differences in the competence of a radiographer in MRI internationally compared to Finland. However, the most significant difference is in the imaging competence as in some countries a trained radiographer can report the MRI examination, unlike in Finland. Further studies are required to determine if radiographers in Finland could report the MRI examination and to what extent

Live LAB environments offer opportunities for RDI activities in ecosystems

Universities of applied science engage in applied research, development and innovation activities. These activities serve teaching, promote working life, regional development and renew the economic structure of the region, as well as provide opportunities for continuous learning. (Universities of Applied Sciences Act, Finlex. In practice, research carried out in universities of applied science is often applied research that primarily produces practical applications – for example, it creates new methods and means of solving problems or looks for applications for the results of basic research (Statistics Finland). Universities of Applied Science reach their helping hand to public and private organizations in their area. Organizations are facing complex challenges and need to constantly innovate to remain competitive. Organizations often have limited access to research and development, so they have adopted different forms of collaboration and open platforms to innovate new things. (Greve et al., 2021.

Peripherally Administered Y2-Receptor Antagonist BIIE0246 Prevents Diet-Induced Obesity in Mice With Excess Neuropeptide Y, but Enhances Obesity in Control Mice

Neuropeptide Y (NPY) plays an important role in the regulation of energy homeostasis in the level of central and sympathetic nervous systems (SNSs). Genetic silencing of peripheral Y2-receptors have anti-obesity effects, but it is not known whether pharmacological blocking of peripheral Y2-receptors would similarly benefit energy homeostasis. The effects of a peripherally administered Y2-receptor antagonist were studied in healthy and energy-rich conditions with or without excess NPY. Genetically obese mice overexpressing NPY in brain noradrenergic nerves and SNS (OE-NPYDβH) represented the situation of elevated NPY levels, while wildtype (WT) mice represented the normal NPY levels. Specific Y2-receptor antagonist, BIIE0246, was administered (1.3 mg/kg/day, i.p.) for 2 or 4.5 weeks to OE-NPYDβH and WT mice feeding on chow or Western diet. Treatment with Y2-receptor antagonist increased body weight gain in both genotypes on chow diet and caused metabolic disturbances (e.g., hyperinsulinemia and hypercholesterolemia), especially in WT mice. During energy surplus (i.e., on Western diet), blocking of Y2-receptors induced obesity in WT mice, whereas OE-NPYDβH mice showed reduced fat mass gain, hepatic glycogen and serum cholesterol levels relative to body adiposity. Thus, it can be concluded that with normal NPY levels, peripheral Y2-receptor antagonist has no potential for treating obesity, but oppositely may even induce metabolic disorders. However, when energy-rich diet is combined with elevated NPY levels, e.g., stress combined with an unhealthy diet, Y2-receptor antagonism has beneficial effects on metabolic status

Data_Sheet_1.docx

<p>Neuropeptide Y (NPY) plays an important role in the regulation of energy homeostasis in the level of central and sympathetic nervous systems (SNSs). Genetic silencing of peripheral Y₂-receptors have anti-obesity effects, but it is not known whether pharmacological blocking of peripheral Y₂-receptors would similarly benefit energy homeostasis. The effects of a peripherally administered Y₂-receptor antagonist were studied in healthy and energy-rich conditions with or without excess NPY. Genetically obese mice overexpressing NPY in brain noradrenergic nerves and SNS (OE-NPY^DβH) represented the situation of elevated NPY levels, while wildtype (WT) mice represented the normal NPY levels. Specific Y₂-receptor antagonist, BIIE0246, was administered (1.3 mg/kg/day, i.p.) for 2 or 4.5 weeks to OE-NPY^DβH and WT mice feeding on chow or Western diet. Treatment with Y₂-receptor antagonist increased body weight gain in both genotypes on chow diet and caused metabolic disturbances (e.g., hyperinsulinemia and hypercholesterolemia), especially in WT mice. During energy surplus (i.e., on Western diet), blocking of Y₂-receptors induced obesity in WT mice, whereas OE-NPY^DβH mice showed reduced fat mass gain, hepatic glycogen and serum cholesterol levels relative to body adiposity. Thus, it can be concluded that with normal NPY levels, peripheral Y₂-receptor antagonist has no potential for treating obesity, but oppositely may even induce metabolic disorders. However, when energy-rich diet is combined with elevated NPY levels, e.g., stress combined with an unhealthy diet, Y₂-receptor antagonism has beneficial effects on metabolic status.</p

Longitudinal Metabolome-Wide Signals Prior to the Appearance of a First Islet Autoantibody in Children Participating in the TEDDY Study

Children at increased genetic risk for type 1 diabetes (T1D) after environmental exposures may develop pancreatic islet autoantibodies (IA) at a very young age. Metabolic profile changes over time may imply responses to exposures and signal development of the first IA. Our present research in The Environmental Determinants of Diabetes in the Young (TEDDY) study aimed to identify metabolome-wide signals preceding the first IA against GAD (GADA-first) or against insulin (IAA-first). We profiled metabolomes by mass spectrometry from children's plasma at 3-month intervals after birth until appearance of the first IA. A trajectory analysis discovered each first IA preceded by reduced amino acid proline and branched-chain amino acids (BCAAs), respectively. With independent time point analysis following birth, we discovered dehydroascorbic acid (DHAA) contributing to the risk of each first IA, and γ-aminobutyric acid (GABAs) associated with the first autoantibody against insulin (IAA-first). Methionine and alanine, compounds produced in BCAA metabolism and fatty acids, also preceded IA at different time points. Unsaturated triglycerides and phosphatidylethanolamines decreased in abundance before appearance of either autoantibody. Our findings suggest that IAA-first and GADA-first are heralded by different patterns of DHAA, GABA, multiple amino acids, and fatty acids, which may be important to primary prevention of T1D

Early probiotic supplementation and the risk of celiac disease in children at genetic risk

Abstract Probiotics are linked to positive regulatory effects on the immune system. The aim of the study was to examine the association between the exposure of probiotics via dietary supplements or via infant formula by the age of 1 year and the development of celiac disease autoimmunity (CDA) and celiac disease among a cohort of 6520 genetically susceptible children. Use of probiotics during the first year of life was reported by 1460 children. Time-to-event analysis was used to examine the associations. Overall exposure of probiotics during the first year of life was not associated with either CDA (n = 1212) (HR 1.15; 95%CI 0.99, 1.35; p = 0.07) or celiac disease (n = 455) (HR 1.11; 95%CI 0.86, 1.43; p = 0.43) when adjusting for known risk factors. Intake of probiotic dietary supplements, however, was associated with a slightly increased risk of CDA (HR 1.18; 95%CI 1.00, 1.40; p = 0.043) compared to children who did not get probiotics. It was concluded that the overall exposure of probiotics during the first year of life was not associated with CDA or celiac disease in children at genetic risk