103 research outputs found

    Antioxidant Activity and Lipid-Lowering Effect of Essential Oils Extracted from Ocimum sanctum L. Leaves in Rats Fed with a High Cholesterol Diet

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    It has been reported that Ocimum sanctum L. (OS) leaves decrease serum lipid profile in normal and diabetic animals. No experimental evidences support the anti-hyperlipidemic and antioxidative actions against hypercholesterolemia. Moreover the identity of the specific chemical ingredients in OS leaves responsible for these pharmacological effects are unknown. Since OS leaves are rich in essential oil (EO). Therefore the present study was conducted to investigate the anti-hyperlipidemic and antioxidative activities of EO extracted from OS leaves in rats fed with high cholesterol (HC) diet. EO was extracted by the hydrodistillation method and the chemical constituents were then identified by Gas Chromatography-Mass Spectrometry. The experiment was performed in Male Wistar rats fed with 2.5 g%(w/w) of cholesterol diet for seven weeks. During the last 3 weeks, rats were daily fed with EO. The results showed that phenyl propanoid compounds including eugenol and methyl eugenol were the major constituents of EO. EO suppressed the high serum lipid profile and atherogenic index as well as serum lactate dehydrogenase and creatine kinase MB subunit without significant effect on high serum levels of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in rats fed with HC diet. In addition, EO was found to decrease the high levels of thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPx) and superoxide dismutase (SOD) without impacting catalase (CAT) in the cardiac tissue while in the liver, it decreased high level of TBARS without significantly effecting GPx, SOD and CAT. Histopathological results confirmed that EO preserved the myocardial tissue. It can be concluded that EO extracted from OS leaves has lipid-lowering and antioxidative effects that protect the heart against hypercholesterolemia. Eugenol that is contained in EO likely contribute to these pharmacological effects

    Improvement of Glucose Metabolism in Patients with Impaired Glucose Tolerance or Diabetes by Long-Term Administration of a Palatinose-Based Liquid Formula as a Part of Breakfast

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    A palatinose-based liquid formula (palatinose-formula), suppresses postprandial plasma glucose and insulin levels in healthy men. The objective of this study was to investigate the effects of long-term palatinose-formula ingestion on glucose metabolism in patients with impaired glucose tolerance (IGT) or type 2 diabetes. Two patients with IGT and 7 patients with type 2 diabetes participated in the palatinose-formula and dextrin-based liquid formula (dextrin-formula) loading test and long-term palatinose-formula administration study. After a 3-month control period, palatinose-formula (1046 kJ) was ingested daily by patients as a part of breakfast for 5 months. In the loading test, palatinose-formula suppressed postprandial plasma glucose and insulin levels and areas under the curve compared with those after dextrin-formula ingestion. In the long-term study, glycated hemoglobin levels (after 3 months and 5 months of treatment) and serum 8-hydroxydeoxyguanosine levels (after 5 months of treatment) were markedly decreased comparing with those at baseline. Intake of 1046 kJ palatinose-formula as a part of breakfast over a long-term period may be effective for improvement of glucose metabolism in patients with IGT or type 2 diabetes

    Metabolic syndrome and rehabilitation results in patients after stroke

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    WSTĘP. Celem pracy były: — ocena częstości występowania zespołu metabolicznego u pacjentów po udarze mózgu rehabilitowanych na oddziale; — ocena wpływu rehabilitacji na stan funkcjonalny pacjentów po 3-tygodniowym okresie rehabilitacji; — ocena wpływu 3-tygodniowej rehabilitacji na stan funkcjonalny pacjentów po udarze mózgu z lub bez zespołu metabolicznego. MATERIAŁ I METODY. W analizie uwzględniono 68 pacjentów (31 kobiet i 37 mężczyzn) po udarze mózgu w przedziale wiekowym 43-80 lat (śr. wieku 57,71 roku). U chorych analizowano występowanie poszczególnych składowych zespołu metabolicznego. Zespół metaboliczny stwierdzono u 27 chorych. Oceniano sprawność funkcjonalną z wykorzystaniem wskaźnika Barthel, stopień niedowładu według skali Brunnström przy przyjęciu na oddział oraz po 3-tygodniowym okresie rehabilitacji. WYNIKI. W badanej grupie po 3-tygodniowym okresie rehabilitacji na oddziale stwierdzono zmniejszenie stopnia niedowładu ocenianego w skali Brunnström w kończynie górnej średnio o 0,4 punktu, w ręce o 0,33 punktu, w kończynie dolnej o 0,34 punktu. Stwierdzono również poprawę sprawności funkcjonalnej ocenianej według skali Brunnström średnio o 0,3 punktu, wskaźnikiem Barthel średnio o 3 punkty. Nie stwierdzono istotnych różnic między efektami rehabilitacji u pacjentów z zespołem metabolicznym i pacjentów, u których nie stwierdzono zespołu metabolicznego. WNIOSKI. 1. Krótkotrwała rehabilitacja szpitalna wpływa na zmniejszenie stopnia niedowładu oraz poprawę stanu funkcjonalnego i zdolności do samoobsługi chorych po udarze mózgu. 2. Występowanie zespołu metabolicznego nie jest przeciwwskazaniem do rehabilitacji. 3. Występowanie zespołu metabolicznego u chorych po udarze mózgu nie różnicuje wyników rehabilitacji.INTRODUCTION. The aim of this study was: — evaluation of metabolic syndrome incidence in patients after brain stroke rehabilitation in ward; — evaluation of rehabilitation effect on functional state of patients after three-weeks’ rehabilitation period; — evaluation of tree weeks’ rehabilitation effects on functional state of patients after brain stroke with medical syndrome and without this syndrome. MATERIAL AND METHODS. the analysed included 68 patients (31 women and 37 men) after brain stroke aged 43-80 (age mean 57.71 yrs). Occurrence of particular metabolic syndrome components was analysed in patients. Ability with the use of Barthel index, paresis grade by Brunnström scale admitting to word also after three-weeks’ rehabilitation period were evaluated. RESULTS. After three weeks‘ rehabilitation period in word, decrease in paresis grade evaluated by Brunnström scale in upper extremity on average by 0.40 pts in hand by 0.33 pts, in lower extremity by 0.34 pts was found in studied group. Improvement functional ability estimated by Brunnström functional scale on average by 0.30 pts, by Barthel index on average by 3 pts was also found. Substantial differences were not found between rehabilitation effects in patients with metabolic syndrome (27 people) and patients in whom metabolic syndrome was not found. CONCLUSIONS. 1. Short-term hospital influences decrease in paresis grade also improvement of functional state and patients’ self-service ability after brain stroke. 2. Occurrence of metabolic syndrome is not concentration against rehabilitation. 3. Occurrence of metabolic syndrome in patients after brain stroke does not differentiate rehabilitation results

    Being stressed and active!? An analysis of different aspects of the relationship between physical activity, individual perceived stress, and individual health

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    Die sportwissenschaftliche Forschung zeigt deutlich, dass Sport und körperliche Aktivität positive Effekte für die Gesundheit haben, im Gegensatz dazu aber erlebter Stress negative Folgen hat. Es stellt sich die Frage, welche Rollen und Effekte Sport im Stress-Gesundheit Kontext spielen kann. In drei Studien wurde der Moderatoreffekt von Sport auf den Zusammenhang zwischen Stress und Beschwerden sowie der Effekt von erlebtem Stress auf die Sportaktivität selbst untersucht

    Graduate School degrees conferred, 1892-1942

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    Acetyl-Coa Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

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    Acetyl-CoA is a metabolite at the crossroads of central metabolism and the substrate of histone acetyltransferases regulating gene expression. In many tissues fasting or lifespan extending calorie restriction (CR) decreases glucose-derived metabolic flux through ATP-citrate lyase (ACLY) to reduce cytoplasmic acetyl-CoA levels to decrease activity of the p300 histone acetyltransferase (HAT) stimulating pro-longevity autophagy. Because of this, compounds that decrease cytoplasmic acetyl-CoA have been described as CR mimetics. But few authors have highlighted the potential longevity promoting roles of nuclear acetyl-CoA. For example, increasing nuclear acetyl-CoA levels increases histone acetylation and administration of class I histone deacetylase (HDAC) inhibitors increases longevity through increased histone acetylation. Therefore, increased nuclear acetyl-CoA likely plays an important role in promoting longevity. Although cytoplasmic acetyl-CoA synthetase 2 (ACSS2) promotes aging by decreasing autophagy in some peripheral tissues, increased glial AMPK activity or neuronal differentiation can stimulate ACSS2 nuclear translocation and chromatin association. ACSS2 nuclear translocation can result in increased activity of CREB binding protein (CBP), p300/CBP-associated factor (PCAF), and other HATs to increase histone acetylation on the promoter of neuroprotective genes including transcription factor EB (TFEB) target genes resulting in increased lysosomal biogenesis and autophagy. Much of what is known regarding acetyl-CoA metabolism and aging has come from pioneering studies with yeast, fruit flies, and nematodes. These studies have identified evolutionary conserved roles for histone acetylation in promoting longevity. Future studies should focus on the role of nuclear acetyl-CoA and histone acetylation in the control of hypothalamic inflammation, an important driver of organismal aging

    TCDD:n vaikutus joidenkin syömistä säätelevien geenien ilmentymiseen hypotalamuksessa ja lähetti-RNA:n mittaaminen RT-qPCR-menetelmää käyttäen

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    Dioxins are pervasive environmental contaminants, to which people are generally exposed through foods of animal origin. Children, before and after birth, are especially susceptible to their toxicity, while the risks to adults seem quite small at current exposure levels. The dioxins bind to a specialised intracellular AH receptor, directly influencing the expression of a substantial number of genes and resulting to variable toxicity depending on the affected species and the strain, as well as the gender and age of the individual. This is exemplified in the dramatic variability of the acute toxicity of the most potent dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD]) within one species: H/W rats tolerate over 1000-fold larger doses than the L E strain. On the other hand, one of the few unifying features of acute TCDD intoxication in many laboratory species is a dramatic feed intake reduction and weight loss, termed the wasting syndrome. In this research, the pathophysiological challenge of wasting was tackled in two studies by measuring the effect of one dose of TCDD on hypothalamic mRNA levels of AHR-related proteins and feeding regulatory factors in the resistant H/W and sensitive L E rats. In the latter two experiments the perviously-employed quantitative reverse transcription PCR (RT-qPCR) methodology was refined: A set of stable reference genes for RT-qPCR was first sought, and then the identified reference genes were employed in a study comparing the robustness of various RT and qPCR enzymes and mapping the RT-qPCR variation sources. The small constitutive and TCDD-induced differences in the hypothalamic mRNA expression of some AHR signalling cascade molecules between L E and H/W rat are most likely not causally related to the wasting syndrome. However, a functional AHR signalling cascade appears to be present in the hypothalamus. The lack of any drastic changes in hypothalamic neuropeptide or receptor mRNA following TCDD treatment speak against a severe cytotoxic effect on, or permanent hyperexcitation of the cells. Notably, the employed hypothalamic block sampling might miss expression changes confined to a localised point and omits the various extra-hypothalamic systems in eating regulation. The future studies should thus be targeted to individual nuclei, but to also have a wider scope of eating regulation both inside and outside CNS. The number of genes displaying an acceptable steadiness of expression in the face of lethal TCDD toxicity is small and besides this the RT stability has a strong influence on the usability of the potential reference genes. Furthermore, RT variance markedly exceeds qPCR variance, stressing the importance of replication at the RT level. Finally, linear hierarchical models and Bayesian inference offer an efficient way to build a coherent statistical model of the whole RT-qPCR experiment maximising the use of the data.Dioksiinit ovat kaikkialle maapallolle levinneitä ympäristömyrkkyjä, joille suomalaiset altistuvat lähinnä eräiden Itämeren kalojen välityksellä. Sikiönkehitys ja lapsuus ovat erityisen alttiita dioksiinien myrkkyvaikutuksille, mutta aikuisille niiden aiheuttama vaara nykyisillä altistustasoilla lienee melko pieni. Elimistössä dioksiinit sitoutuvat solunsisäisen AH-reseptoriin, joka aktivoituessaan muuttaa satojen geenien ilmentymistä. Nämä ilmentymismuutokset, ja lopulta haitalliset vaikutukset elimistössä, näyttävät kuitenkin riippuvan eläinlajista, -kannasta iästä ja kudoksesta jossa aktivaatio tapahtuu. Dioksiinien myrkyllisyyden mekanismit ovatkin huonosti ymmärrettyjä. Esimerkki myrkyllisyyden vaihtelevuudesta on kahden rottakanan herkkyysero myrkyllisimmälle 2,3,7,8-tetraklooridibentso-p-dioksiinille eli TCDD:lle: H/W-kannan rotat kestävät yli 1000 kertaa suurempia myrkkyannoksia kuin L E-kanta. Dioksiinien yksi harvoista monilla koe-eläimillä samanlaista, mutta herkkyyseroiltaan yhtä suurista, vaikutuksista on jo yhden myrkyllisen annoksen aiheuttama voimakas ruokahalun ja painon lasku, niin sanottu näivettymisoireyhtymä. Tutkimuksessani pyrin selvittämään näivettymisoireyhtymän mekanismeja altistamalla H/W- ja L E-rottia yhdelle annokselle TCDD:tä ja mittaamalla geenien ilmentymisen muutoksia hypotalamuksessa kvantitatiivista käänteiskopiointi-PCR (RT-qPCR) -menetelmää käyttäen. Mitatut lähetti-RNA:t tuottavat AH-reseptorin signalointiin liittyviä proteiineja ja syömisen säätelyyn liittyviä neuropeptidejä tai reseptoreita. Väitöskirjan toisessa osassa parannettiin herkän RT-qPCR-menetelmän luottavuutta etsimällä sen tarvitsemia kontrolligeenejä ja kartoittamalla käänteiskopiointi (RT)- ja PCR-reaktioiden virhelähteitä. Hypotalamuksen AH-reseptorin signalointireitti toimii, mutta lähetti-RNA:n perustasot tai niiden vähäiset muutokset TCDD:n annostelun jälkeen eivät näytä selittävän H/W ja L E-kantojen herkkyyseroja. Neuropeptideissä todettiin vain pieniä muutoksia, joten TCDD ei aiheuttane hypotalamuksen syömistä säätelevän järjestelmän solujen merkittäviä toiminnan muutoksia. Mittaukset tehtiin kokonaisista kudospaloista ja tämä voi estää tumaketason vaikutusten havaitsemisen, eikä myöskään huomioi tärkeitä hypotalamuksen ulkopuolisia syömistä ja energiatasapainoa sääteleviä järjestelmiä. TCDD:n aiheuttamiin myrkkyvaikutuksiin reagoimattomia kontrolligeenejä löytyi neljä ja näistä kahden lähetti-RNA:n käänteiskopiointi toimi luotettavasti. RT-qPCR-menetelmän analysointiin käytetty lineaarinen hierarkkinen malli ja beyesiläinen päättely toimivat hyvin RT- ja PCR-reaktioiden virhelähteiden erottelussa. Tämän tutkimuksen tulokset auttavat suuntaamaan tulevia näivettymisoireyhtymätutkimuksia ja parantamaan RT-qPCR-menetelmän luotettavuutta

    Faculty Publications & Presentations, 2008-2009

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