205 research outputs found

    Scattering of therapeutic radiation in the presence of craniofacial bone reconstruction materials

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    PurposeRadiation scattering from bone reconstruction materials can cause problems from prolonged healing to osteoradionecrosis. Glass fiber reinforced composite (FRC) has been introduced for bone reconstruction in craniofacial surgery but the effects during radiotherapy have not been previously studied. The purpose of this study was to compare the attenuation and back scatter caused by different reconstruction materials during radiotherapy, especially FRC with bioactive glass (BG) and titanium.MethodsThe effect of five different bone reconstruction materials on the surrounding tissue during radiotherapy was measured. The materials tested were titanium, glass FRC with and without BG, polyether ether ketone (PEEK) and bone. The samples were irradiated with 6 MV and 10 MV photon beams. Measurements of backscattering and dose changes behind the sample were made with radiochromic film and diamond detector dosimetry.ResultsAn 18% dose enhancement was measured with a radiochromic film on the entrance side of irradiation for titanium with 6 MV energy while PEEK and FRC caused an enhancement of 10% and 4%, respectively. FRC‐BG did not cause any measurable enhancement. The change in dose immediately behind the sample was also greatest with titanium (15% reduction) compared with the other materials (0–1% enhancement). The trend is similar with diamond detector measurements, titanium caused a dose enhancement of up to 4% with a 1 mm sample and a reduction of 8.5% with 6 MV energy whereas FRC, FRC‐BG, PEEK or bone only caused a maximum dose reduction of 2.2%.ConclusionsGlass fiber reinforced composite causes less interaction with radiation than titanium during radiotherapy and could provide a better healing environment after bone reconstruction.</p

    Abdominal adipose tissue and liver fat imaging in very low birth weight adults born preterm : birth cohort with sibling-controls

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    Preterm birth at very low birth weight (VLBW, < 1500 g) is associated with an accumulation of cardiovascular and metabolic risk factors from childhood at least to middle age. Small-scale studies suggest that this could partly be explained by increased visceral or ectopic fat. We performed magnetic resonance imaging on 78 adults born preterm at VLBW in Finland between 1978 and 1990 and 72 term same-sex siblings as controls, with a mean age of 29 years. We collected T1-weighted images from the abdomen, and magnetic resonance spectra from the liver, subcutaneous abdominal adipose tissue, and tibia. The adipose tissue volumes of VLBW adults did not differ from their term siblings when adjusting for age, sex, and maternal and perinatal factors. The mean differences were as follows: subcutaneous - 0.48% (95% CI - 14.8%, 16.3%), visceral 7.96% (95% CI - 10.4%, 30.1%), and total abdominal fat quantity 1.05% (95% CI - 13.7%, 18.4%). Hepatic triglyceride content was also similar. VLBW individuals displayed less unsaturation in subcutaneous adipose tissue (- 4.74%, 95% CI - 9.2%, - 0.1%) but not in tibial bone marrow (1.68%, 95% CI - 1.86%, 5.35%). VLBW adults displayed similar adipose tissue volumes and hepatic triglyceride content as their term siblings. Previously reported differences could thus partly be due to genetic or environmental characteristics shared between siblings. The VLBW group displayed less unsaturation in subcutaneous abdominal adipose tissue, suggesting differences in its metabolic activity and energy storage.Peer reviewe

    Combining probability distributions of sea level variations and wave run-up to evaluate coastal flooding risks

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    Tools for estimating probabilities of flooding hazards caused by the simultaneous effect of sea level and waves are needed for the secure planning of densely populated coastal areas that are strongly vulnerable to climate change. In this paper we present a method for combining location-specific probability distributions of three different components: (1) long-term mean sea level change, (2) short-term sea level variations and (3) wind-generated waves. We apply the method at two locations in the Helsinki archipelago to obtain total water level estimates representing the joint effect of the still water level and the wave run-up for the present, 2050 and 2100. The variability of the wave conditions between the study sites leads to a difference in the safe building levels of up to 1&thinsp;m. The rising mean sea level in the Gulf of Finland and the uncertainty related to the associated scenarios contribute notably to the total water levels for the year 2100. A test with theoretical wave run-up distributions illustrates the effect of the relative magnitude of the sea level variations and wave conditions on the total water level. We also discuss our method's applicability to other coastal regions.</p

    Deletions at 14q in malignant mesothelioma detected by microsatellite marker analysis

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    Previous molecular cytogenetic studies by comparative genomic hybridization (CGH) on primary tumours of human malignant mesothelioma have revealed that loss of genetic material at chromosome 14q is one of the most frequently occurring aberrations. Here we further verify the frequency and pattern of deletions at 14q in mesothelioma. A high-resolution deletion mapping analysis of 23 microsatellite markers was performed on 18 primary mesothelioma tumours. Eight of these had previously been analysed by CGH. Loss of heterozygosity or allelic imbalance with at least one marker was detected in ten of 18 tumours (56%). Partial deletions of varying lengths were more common than loss of all informative markers, which occurred in only one tumour. The highest number of tumours with deletions at a specific marker was detected at 14q11.1–q12 with markers D14S283 (five tumours), D14S972 (seven tumours) and D14S64 (five tumours) and at 14q23–q24 with markers D14S258 (five tumours), D14S77 (five tumours) and D14S284 (six tumours). We conclude from these data that genomic deletions at 14q are more common than previously reported in mesothelioma. Furthermore, confirmation of previous CGH results was obtained in all tumours but one. This tumour showed deletions by allelotyping, but did not show any DNA copy number change at 14q by CGH. Although the number of tumours allelotyped was small and the deletion pattern was complex, 14q11.1–q12 and 14q23–q24 were found to be the most involved regions in deletions. These regions provide a good basis for further molecular analyses and may highlight chromosomal locations of tumour suppressor genes that could be important in the tumorigenesis of malignant mesothelioma. © 1999 Cancer Research Campaig

    Plasma melatonin is reduced in Huntington's disease

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    This study was undertaken to determine whether the production of melatonin, a hormone regulating sleep in relation to the light/dark cycle, is altered in Huntington's disease. We analyzed the circadian rhythm of melatonin in a 24-hour study of cohorts of control, premanifest, and stage II/III Huntington's disease subjects. The mean and acrophase melatonin concentrations were significantly reduced in stage II/III Huntington's disease subjects compared with controls. We also observed a nonsignificant trend toward reduced mean and acrophase melatonin in premanifest Huntington's disease subjects. Onset of melatonin rise was significantly more temporally spread in both premanifest and stage II/III Huntington's disease subjects compared with controls. A nonsignificant trend also was seen for reduced pulsatile secretion of melatonin. Melatonin concentrations are reduced in Huntington's disease. Altered melatonin patterns may provide an explanation for disrupted sleep and circadian behavior in Huntington's disease, and represent a biomarker for disease state. Melatonin therapy may help the sleep disorders seen in Huntington's disease

    The specificity and the development of social-emotional competence in a multi-ethnic-classroom

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    <p>Abstract</p> <p>Background</p> <p>Ethnic diversity in schools increases due to globalization. Thus, the children's social-emotional competence development must be considered in the context of a multi-ethnic classroom.</p> <p>Methods</p> <p>In this study, the social-emotional competence of 65 Asian-American and Latin-American children was observed at the beginning and the end of their kindergarten year.</p> <p>Results</p> <p>Initially, significant differences existed among these ethnic groups in respect to moral reasoning. Furthermore, the male children showed more dysregulated aggression but the female children implemented more moral reasoning than their male counterparts. These ethnic specificities did not disappear over the course of the year. In addition, a significant change in avoidance strategies as well as expressed emotions in the narrative took place over the course of one year.</p> <p>Conclusion</p> <p>Ethnic specificity in social-emotional competence does exist independent of gender at the beginning as well as at the end of the kindergarten year in a multi-ethnic kindergarten classroom.</p

    IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome

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    Expansion of the polyglutamine repeat within the protein Huntingtin (Htt) causes Huntington's disease, a neurodegenerative disease associated with aging and the accumulation of mutant Htt in diseased neurons. Understanding the mechanisms that influence Htt cellular degradation may target treatments designed to activate mutant Htt clearance pathways. We find that Htt is phosphorylated by the inflammatory kinase IKK, enhancing its normal clearance by the proteasome and lysosome. Phosphorylation of Htt regulates additional post-translational modifications, including Htt ubiquitination, SUMOylation, and acetylation, and increases Htt nuclear localization, cleavage, and clearance mediated by lysosomal-associated membrane protein 2A and Hsc70. We propose that IKK activates mutant Htt clearance until an age-related loss of proteasome/lysosome function promotes accumulation of toxic post-translationally modified mutant Htt. Thus, IKK activation may modulate mutant Htt neurotoxicity depending on the cell's ability to degrade the modified species

    Increased Prothrombin, Apolipoprotein A-IV, and Haptoglobin in the Cerebrospinal Fluid of Patients with Huntington's Disease

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    Huntington's disease (HD) is a progressive neurodegenerative disease caused by an unstable CAG trinucleotide repeat expansion. The need for biomarkers of onset and progression in HD is imperative, since currently reliable outcome measures are lacking. We used two-dimensional electrophoresis and mass spectrometry to analyze the proteome profiles in cerebrospinal fluid (CSF) of 6 pairs of HD patients and controls. Prothrombin, apolipoprotein A-IV (Apo A-IV) and haptoglobin were elevated in CSF of the HD patients in comparison with the controls. We used western blot as a semi-quantified measurement for prothrombin and Apo A-IV, as well as enzyme linked immunosorbent assay (ELISA) for measurement of haptoglobin, in 9 HD patients and 9 controls. The albumin quotient (Qalb), a marker of blood-brain barrier (BBB) function, was not different between the HD patients and the controls. The ratios of CSF prothrombin/albumin (prothrombin/Alb) and Apo A-IV/albumin (Apo A-IV/Alb), and haptoglobin level were significantly elevated in HD. The ratio of CSF prothrombin/Alb significantly correlated with the disease severity assessed by Unified Huntington's Disease Rating Scale (UHDRS). The results implicate that increased CSF prothrombin, Apo A-IV, and haptoglobin may be involved in pathogenesis of HD and may serve as potential biomarkers for HD

    Evaluation of a Previously Suggested Plasma Biomarker Panel to Identify Alzheimer's Disease

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    There is an urgent need for biomarkers in plasma to identify Alzheimer's disease (AD). It has previously been shown that a signature of 18 plasma proteins can identify AD during pre-dementia and dementia stages (Ray et al, Nature Medicine, 2007). We quantified the same 18 proteins in plasma from 174 controls, 142 patients with AD, and 88 patients with other dementias. Only three of these proteins (EGF, PDG-BB and MIP-1δ) differed significantly in plasma between controls and AD. The 18 proteins could classify patients with AD from controls with low diagnostic precision (area under the ROC curve was 63%). Moreover, they could not distinguish AD from other dementias. In conclusion, independent validation of results is important in explorative biomarker studies
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