980 resultados para Ahteenmäki-Pelkonen, Leena


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The paradoxically low infant mortality rates for Mexican Americans in Texas have been attributed to inaccuracies in vital registration and idiosyncracies in Mexican migration in rural areas along the U.S.-Mexico border. This study examined infant (IMR), neonatal (NMR), and postneonatal (PNMR) mortality rates of Mexican Americans in an urban, non-border setting, using linked birth and death records of the 1974-75 single live birth cohort (N = 68,584) in Harris County, Texas, which includes the city of Houston and is reported to have nearly complete birth and death registration. The use of parental nativity with the traditional Spanish surname criterion made it possible to distinguish infants of Mexican-born immigrants from those of Blacks, Anglos, other Hispanics, and later-generation, more Anglicized Mexican Americans. Mortality rates were analyzed by ethnicity, parental nativity, and cause of death, with respect to birth weight, birth order, maternal age, legitimacy status, and time of first prenatal care.^ While overall IMRs showed Spanish surname rates slightly higher than Anglo rates, infants of Mexican-born immigrants had much lower NMRs than did Anglos, even for moderately low birth weight infants. However, among infants under 1500 grams, presumably unable to be discharged home in the neonatal period, Mexican Americans had the highest NMR. The inconsistency suggested unreported deaths for Mexican American low birth weight infants after hospital discharge. The PNMR of infants of Mexican immigrants was also lower than for Anglos, and the usual mortality differentials were reversed: high-risk categories of high birth order, high maternal age, and late/no prenatal care had the lowest PNMRs. Since these groups' characteristics are congruent with those of low-income migrants, the data suggested the possibility of migration losses. Cause of death analysis suggested that prematurity and birth injuries are greater problems than heretofore recognized among Mexican Americans, and that home births and "shoebox burials" may be unrecorded even in an urban setting.^ Caution is advised in the interpretation of infant mortality rates for a Spanish surname population of Mexican origin, even in an urban, non-border area with reportedly excellent birth and death registration. ^

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We hypothesized that feeding pregnant rats with a high-fat diet would increase both circulating 17β-estradiol (E2) levels in the dams and the risk of developing carcinogen-induced mammary tumors among their female offspring. Pregnant rats were fed isocaloric diets containing 12% or 16% (low fat) or 43% or 46% (high fat) of calories from corn oil, which primarily contains the n − 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The plasma concentrations of E2 were significantly higher in pregnant females fed a high n − 6 PUFA diet. The female offspring of these rats were fed with a laboratory chow from birth onward, and when exposed to 7,12-dimethylbenz(a)anthracene had a significantly higher mammary tumor incidence (60% vs. 30%) and shorter latency for tumor appearance (11.4 ± 0.5 weeks vs. 14.2 ± 0.6 weeks) than the offspring of the low-fat mothers. The high-fat offspring also had puberty onset at a younger age, and their mammary glands contained significantly higher numbers of the epithelial structures that are the targets for malignant transformation. Comparable changes in puberty onset, mammary gland morphology, and tumor incidence were observed in the offspring of rats treated daily with 20 ng of E2 during pregnancy. These data, if extrapolated to humans, may explain the link among diet, early puberty onset, mammary parenchymal patterns, and breast cancer risk, and indicate that an in utero exposure to a diet high in n − 6 PUFA and/or estrogenic stimuli may be critical for affecting breast cancer risk.

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Acknowledgements We would like to thank Cochrane Work Trials Search Co-ordinators Leena Isotalo and Kaisa Neuvonen for developing the search strategy and Managing Editor Jani Ruotsalainen and Co-ordinating Editor Jos Verbeek for editing the text and providing helpful comments. We would also like to thank Richard Othieno for his contributions to the protocol.

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Polyamines are required for optimal growth and function of cells. Regulation of their cellular homeostasis is therefore tightly controlled. The key regulatory enzyme for polyamine catabolism is the spermidine/spermine N1-acetyltransferase (SSAT). Depletion of cellular polyamines has been associated with inhibition of growth and programmed cell death. To investigate the physiological function SSAT, we generated a transgenic rat line overexpressing the SSAT gene under the control of the inducible mouse metallothionein I promoter. Administration of zinc resulted in a marked induction of pancreatic SSAT, overaccumulation of putrescine, and appearance of N1-acetylspermidine with extensive depletion of spermidine and spermine in transgenic animals. The activation of pancreatic polyamine catabolism resulted in acute pancreatitis. In nontransgenic animals, an equal dose of zinc did not affect pancreatic polyamine pools, nor did it induce pancreatitis. Acetylated polyamines, products of the SSAT-catalyzed reaction, are metabolized further by the polyamine oxidase (PAO) generating hydrogen peroxide, which might cause or contribute to the pancreatic inflammatory process. Administration of specific PAO inhibitor, MDL72527 [N1,N2-bis(2,3-butadienyl)-1,4-butanediamine], however, did not affect the histological score of the pancreatitis. Induction of SSAT by the polyamine analogue N1,N11-diethylnorspermine reduced pancreatic polyamines levels only moderately and without signs of organ inflammation. In contrast, the combination of N1,N11-diethylnorspermine with MDL72527 dramatically activated SSAT, causing profound depletion of pancreatic polyamines and acute pancreatitis. These results demonstrate that acute induction of SSAT leads to pancreatic inflammation, suggesting that sufficient pools of higher polyamine levels are essential to maintain pancreatic integrity. This inflammatory process is independent of the production of hydrogen peroxide by PAO.

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Lysyl hydroxylase (EC 1.14.11.4), a homodimer, catalyzes the formation of hydroxylysine in collagens. Recently, an isoenzyme termed lysyl hydroxylase 2 has been cloned from human sources [M. Valtavaara, H. Papponen, A.-M. Pirttilä, K. Hiltunen, H. Helander and R. Myllylä (1997) J. Biol. Chem. 272, 6831–6834]. We report here on the cloning of a third human lysyl hydroxylase isoenzyme, termed lysyl hydroxylase 3. The cDNA clones encode a 738 amino acid polypeptide, including a signal peptide of 24 residues. The overall amino acid sequence identity between the processed human lysyl hydroxylase 3 and 1 polypeptides is 59%, and that between the processed lysyl hydroxylase 3 and 2 polypeptides is 57%, whereas the identity to the processed Caenorhabditis elegans polypeptide is only 45%. All four recently identified critical residues at the catalytic site, two histidines, one aspartate, and one arginine, are conserved in all these polypeptides. The mRNA for lysyl hydroxylase 3 was found to be expressed in a variety of tissues, but distinct differences appear to exist in the expression patterns of the three isoenzyme mRNAs. Recombinant lysyl hydroxylase 3 expressed in insect cells by means of a baculovirus vector was found to be more soluble than lysyl hydroxylase 1 expressed in the same cell type. No differences in catalytic properties were found between the recombinant lysyl hydroxylase 3 and 1 isoenzymes. Deficiency in lysyl hydroxylase 1 activity is known to cause the type VI variant of the Ehlers–Danlos syndrome, and it is therefore possible that deficiency in lysyl hydroxylase 3 activity may lead to some other variant of this syndrome or to some other heritable connective tissue disorder.

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Erythropoietin (EPO) promotes neuronal survival after hypoxia and other metabolic insults by largely unknown mechanisms. Apoptosis and necrosis have been proposed as mechanisms of cellular demise, and either could be the target of actions of EPO. This study evaluates whether antiapoptotic mechanisms can account for the neuroprotective actions of EPO. Systemic administration of EPO (5,000 units/kg of body weight, i.p.) after middle-cerebral artery occlusion in rats dramatically reduces the volume of infarction 24 h later, in concert with an almost complete reduction in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling of neurons within the ischemic penumbra. In both pure and mixed neuronal cultures, EPO (0.1–10 units/ml) also inhibits apoptosis induced by serum deprivation or kainic acid exposure. Protection requires pretreatment, consistent with the induction of a gene expression program, and is sustained for 3 days without the continued presence of EPO. EPO (0.3 units/ml) also protects hippocampal neurons against hypoxia-induced neuronal death through activation of extracellular signal-regulated kinases and protein kinase Akt-1/protein kinase B. The action of EPO is not limited to directly promoting cell survival, as EPO is trophic but not mitogenic in cultured neuronal cells. These data suggest that inhibition of neuronal apoptosis underlies short latency protective effects of EPO after cerebral ischemia and other brain injuries. The neurotrophic actions suggest there may be longer-latency effects as well. Evaluation of EPO, a compound established as clinically safe, as neuroprotective therapy in acute brain injury is further supported.

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Eight otherwise healthy diabetic volunteers took a daily antioxidant supplement consisting of vitamin E (200 IU), vitamin C (250 mg) and α-lipoic acid (90 mg) for a period of 6 weeks. Diabetic dapsone hydroxylamine-mediated methaemoglobin formation and resistance to erythrocytic thiol depletion was compared with age and sex-matched non-diabetic subjects. At time zero, methaemoglobin formation in the non-diabetic subjects was greater at all four time points compared with that of the diabetic subjects. Resistance to glutathione depletion was initially greater in non-diabetic compared with diabetic samples. Half-way through the study (3 weeks), there were no differences between the two groups in methaemoglobin formation and thiol depletion in the diabetic samples was now lower than the non-diabetic samples at 10 and 20 min. At 6 weeks, diabetic erythrocytic thiol levels remained greater than those of non-diabetics. HbA1c values were significantly reduced in the diabetic subjects at 6 weeks compared with time zero values. At 10 weeks, 4 weeks after the end of supplementation, the diabetic HbA1c values significantly increased to the point where they were not significantly different from the time zero values. Total antioxidant status measurement (TAS) indicated that diabetic plasma antioxidant capacity was significantly improved during antioxidant supplementation. Conversion of α-lipoic acid to dihydrolipoic acid (DHLA) in vivo led to potent interference in a standard fructosamine assay kit, negating its use in this study. This report suggests that triple antioxidant therapy in diabetic volunteers attenuates the in vitro experimental oxidative stress of methaemoglobin formation and reduces haemoglobin glycation in vivo. © 2003 Elsevier Science B.V. All rights reserved.

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Tellurite glasses are photonic materials of special interest to the branch of optoelectronic and communication, due to its important optical properties such as high refractive index, broad IR transmittance, low phonon energy etc. Tellurite glasses are solutions to the search of potential candidates for nonlinear optical devices. Low phonon energy makes it an efficient host for dopant ions like rare earths, allowing a better environment for radiative transitions. The dopant ions maintain majority of their individual properties in the glass matrix. Tellurites are less toxic than chalcogenides, more chemically and thermally stable which makes them a highly suitable fiber material for nonlinear applications in the midinfrared and they are of increased research interest in applications like laser, amplifier, sensor etc. Low melting point and glass transition temperature helps tellurite glass preparation easier than other glass families.In order to probe into the versatility of tellurite glasses in optoelectronic industry; we have synthesized and undertaken various optical studies on tellurite glasses. We have proved that the highly nonlinear tellurite glasses are suitable candidates in optical limiting, with comparatively lower optical limiting threshold. Tuning the optical properties of glasses is an important factor in the optoelectronic research. We have found that thermal poling is an efficient mechanism in tuning the optical properties of these materials. Another important nonlinear phenomenon found in zinc tellurite glasses is their ability to switch from reverse saturable absorption to saturable absorption in the presence of lanthanide ions. The proposed thesis to be submitted will have seven chapters.

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Objective: Real-time functional magnetic resonance imaging (rt-fMRI) neurofeedback (NF) uses feedback of the patient’s own brain activity to self-regulate brain networks which in turn could lead to a change in behaviour and clinical symptoms. The objective was to determine the effect of neurofeedback and motor training and motor training (MOT) alone on motor and non-motor functions in Parkinson’s disease (PD) in a 10-week small Phase I randomised controlled trial. Methods: 30 patients with PD (Hoehn & Yahr I-III) and no significant comorbidity took part in the trial with random allocation to two groups. Group 1 (NF: 15 patients) received rt-fMRI-NF with motor training. Group 2 (MOT: 15 patients) received motor training alone. The primary outcome measure was the Movement Disorder Society – Unified Parkinson’s Disease Rating Scale-Motor scale (MDS-UPDRS-MS), administered pre- and post-intervention ‘off-medication’. The secondary outcome measures were the ‘on-medication’ MDS-UPDRS, the Parkinson’s disease Questionnaire-39, and quantitative motor assessments after 4 and 10 weeks. Results: Patients in the NF group were able to upregulate activity in the supplementary motor area by using motor imagery. They improved by an average of 4.5 points on the MDS-UPDRS-MS in the ‘off-medication’ state (95% confidence interval: -2.5 to -6.6), whereas the MOT group improved only by 1.9 points (95% confidence interval +3.2 to -6.8). However, the improvement did not differ significantly between the groups. No adverse events were reported in either group. Interpretation: This Phase I study suggests that NF combined with motor training is safe and improves motor symptoms immediately after treatment, but larger trials are needed to explore its superiority over active control conditions. Clinical Trial website : Unique Identifier: NCT01867827 URL: https://clinicaltrials.gov/ct2/show/NCT01867827?term=NCT01867827&rank=1

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Tutkimukseni käsittelee dialogipartikkeleita joo ja niin pikaviestikeskusteluissa. Otan huomioon myös partikkeliketjut, jotka sisältävät dialogipartikkelin joo tai niin. Aineistona tutkimuksessa käytän kahta Whatsapp-pikaviestiohjelmalla käytyä keskusteluketjua. Keskustelut on käyty reaaliaikaisesti älypuhelimella. Tavoitteenani on selvittää, minkälaisia tehtäviä dialogipartikkelit joo ja niin saavat pikaviestikeskusteluissa ja eroavatko niiden tehtävät puhutuissa keskusteluissa käytettyjen dialogipartikkelien tehtävistä. Vertaan tuloksiani Marja-Leena Sorjosen tekemiin tutkimuksiin dialogipartikkeleista. Tarkastelen dialogipartikkeleita keskustelunanalyyttisin metodein. Huomioin dialogipartikkelia edeltävän vuoron ja sen, miten keskustelu etenee partikkelin sisältävän vuoron jälkeen. Otan myös huomioon laajemman sekvenssin ja toiminnan, johon partikkelin sisältävä ja sitä edeltävä vuoro kuuluvat. Lisäksi tarkastelen sitä, miten pikaviestikeskusteluissa prosodian puuttuminen ja vierusparien jakautuneisuus vaikuttavat dialogipartikkelien joo ja niin käyttöön. Dialogipartikkelit saavat keskusteluissa pääosin samoja tehtäviä kuin puhutuissa keskusteluissa. Suurimman poikkeuksen muodostaa jatkajina toimivien dialogipartikkelien ryhmä. Pikaviestikeskusteluissa jatkajina toimivat dialogipartikkelit eivät koskaan vastaa jaoteltuun tietoon ja kehottavat erittäin harvoin keskustelukumppaniaan jatkamaan. Keskustelukumppania saatetaan pyytää jatkamaan kysyvällä dialogipartikkelilla joo tai niin, jos keskustelija ei koe saaneen tarpeeksi tietoa toiselta keskustelijalta. Tällöin partikkelin lopussa on kysymysmerkki. Prosodian puuttumista pikaviestikeskusteluista keskustelijat kompensoivat venyttämällä dialogipartikkelien kirjoitusasua, esimerkiksi muotoon jooo tai niii. Dialogipartikkelien sävyyn vaikutetaan myös välimerkeillä, kuten huutomerkillä tai kysymysmerkillä. Dialogipartikkelin sisältämä sävy ja se, sisältääkö partikkeli esimerkiksi erimielisyyttä, on kuitenkin aina tulkittava suhteessa dialogipartikkelin esiintymiskontekstiin. Vierusparien jakautuneisuus pikaviestikeskusteluissa ei vaikuta dialogipartikkelien käyttöön. Tutkimukseni laajentaa dialogipartikkelien tutkimusta, sillä tutkimukseni aineisto koostuu puhuttujen keskustelujen sijaan kirjoitetuista pikaviestikeskusteluita. Pikaviestikeskustelut muistuttavat paljon puhuttuja keskusteluja, ja siksi niihin keskittyvä tutkimus tarjoaa mielenkiintoisen näkökulman puhutun ja kirjoitetun kielen rajankäyntiin. Tutkimukseni paneutuu tähän rajankäyntiin tietyn kieliopillisen kategorian, dialogipartikkelien,