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On February 23, 2018, PubMed Central Canada (PMC Canada) will be taken offline permanently. No author manuscripts will be deleted, and the approximately 2,900 manuscripts authored by Canadian Institutes of Health Research (CIHR)-funded researchers currently in the archive will be copied to the National Research Council’s (NRC) Digital Repository over the coming months. These manuscripts along with all other content will also remain publicly searchable on PubMed Central (US) and Europe PubMed Central, meaning such manuscripts will continue to be compliant with the Tri-Agency Open Access Policy on Publications.

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1.  Search for lepton flavour violation in the eμ continuum with the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s} = 7~\mbox{TeV}$\end{document}pp collisions at the LHC 
Aad, G. | Abbott, B. | Abdallah, J. | Abdelalim, A. A. | Abdesselam, A. | Abdinov, O. | Abi, B. | Abolins, M. | Abramowicz, H. | Abreu, H. | Acerbi, E. | Acharya, B. S. | Adams, D. L. | Addy, T. N. | Adelman, J. | Adomeit, S. | Adragna, P. | Adye, T. | Aefsky, S. | Aguilar-Saavedra, J. A. | Aharrouche, M. | Ahlen, S. P. | Ahles, F. | Ahmad, A. | Ahsan, M. | Aielli, G. | Akdogan, T. | Åkesson, T. P. A. | Akimoto, G. | Akimov, A. V. | Akiyama, A. | Aktas, A. | Alam, M. S. | Alam, M. A. | Albrand, S. | Aleksa, M. | Aleksandrov, I. N. | Aleppo, M. | Alessandria, F. | Alexa, C. | Alexander, G. | Alexandre, G. | Alexopoulos, T. | Alhroob, M. | Aliev, M. | Alimonti, G. | Alison, J. | Aliyev, M. | Allport, P. P. | Allwood-Spiers, S. E. | Almond, J. | Aloisio, A. | Alon, R. | Alonso, A. | Alviggi, M. G. | Amako, K. | Amelung, C. | Ammosov, V. V. | Amorim, A. | Amorós, G. | Amram, N. | Anastopoulos, C. | Andeen, T. | Anders, C. F. | Anderson, K. J. | Andreazza, A. | Andrei, V. | Anduaga, X. 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M. | Falciano, S. | Falou, A. C. | Fang, Y. | Fanti, M. | Farbin, A. | Farilla, A. | Farley, J. | Farooque, T. | Farrington, S. M. | Farthouat, P. | Fasching, D. | Fassnacht, P. | Fassouliotis, D. | Fatholahzadeh, B. | Favareto, A. | Fayard, L. | Fazio, S. | Febbraro, R. | Federic, P. | Fedin, O. L. | Fedorko, I. | Fedorko, W. | Fehling-Kaschek, M. | Feligioni, L. | Fellmann, D. | Felzmann, C. U. | Feng, C. | Feng, E. J. | Fenyuk, A. B. | Ferencei, J. | Fernandes, B. | Fernando, W. | Ferrag, S. | Ferrando, J. | Ferrara, V. | Ferrari, A. | Ferrari, P. | Ferrari, R. | Ferrer, A. | Ferrer, M. L. | Ferrere, D. | Ferretti, C. | Ferretto Parodi, A. | Fiascaris, M. | Fiedler, F. | Filipčič, A. | Filippas, A. | Filthaut, F. | Fincke-Keeler, M. | Fiolhais, M. C. N. | Fiorini, L. | Firan, A. | Fischer, G. | Fischer, P. | Fisher, M. J. | Fisher, S. M. | Flammer, J. | Flechl, M. | Fleck, I. | Fleckner, J. | Fleischmann, P. | Fleischmann, S. | Flick, T. | Flores Castillo, L. R. | Flowerdew, M. J. | Föhlisch, F. | Fonseca Martin, T. | Fopma, J. | Formica, A. | Forti, A. | Fortin, D. | Fournier, D. | Fowler, A. J. | Fowler, K. | Fox, H. | Francavilla, P. | Franchino, S. | Francis, D. | Frank, T. | Franklin, M. | Franz, S. | Fraternali, M. | Fratina, S. | Freestone, J. | French, S. T. | Froeschl, R. | Froidevaux, D. | Frost, J. A. | Fukunaga, C. | Fullana Torregrosa, E. | Fuster, J. | Gabaldon, C. | Gabizon, O. | Gadfort, T. | Gadomski, S. | Gagliardi, G. | Gagnon, P. | Galea, C. | Gallas, E. J. | Gallas, M. V. | Gallo, V. | Gallop, B. J. | Gallus, P. | Galyaev, E. | Gan, K. K. | Gao, Y. S. | Gaponenko, A. | Garberson, F. | Garcia-Sciveres, M. | García, C. | García Navarro, J. E. | Gardner, R. W. | Garelli, N. | Garitaonandia, H. | Garonne, V. | Garvey, J. | Gatti, C. | Gaudio, G. | Gaumer, O. | Gaur, B. | Gauthier, L. | Gauzzi, P. | Gavrilenko, I. L. | Gay, C. | Gaycken, G. | Gazis, E. N. | Ge, P. | Gee, C. N. P. | Geerts, D. A. A. | Geich-Gimbel, Ch. | Gellerstedt, K. | Gemme, C. | Gemmell, A. | Genest, M. H. | Gentile, S. | George, M. | George, S. | Gerlach, P. | Gershon, A. | Geweniger, C. | Ghazlane, H. | Ghodbane, N. | Giacobbe, B. | Giagu, S. | Giakoumopoulou, V. | Giangiobbe, V. | Gianotti, F. | Gibbard, B. | Gibson, A. | Gibson, S. M. | Gieraltowski, G. F. | Gilchriese, M. | Gillberg, D. | Gillman, A. R. | Gingrich, D. M. | Ginzburg, J. | Giokaris, N. | Giordani, M. P. | Giordano, R. | Giorgi, F. M. | Giovannini, P. | Giraud, P. F. | Giugni, D. | Giusti, P. | Gjelsten, B. K. | Gladilin, L. K. | Glasman, C. | Glatzer, J. | Glazov, A. | Glitza, K. W. | Glonti, G. L. | Godfrey, J. | Godlewski, J. | Goebel, M. | Göpfert, T. | Goeringer, C. | Gössling, C. | Göttfert, T. | Goldfarb, S. | Goldin, D. | Golling, T. | Golovnia, S. N. | Gomes, A. | Gomez Fajardo, L. S. | Gonçalo, R. | Goncalves Pinto Firmino Da Costa, J. | Gonella, L. | Gonzalez, S. | González de la Hoz, S. | Gonzalez Silva, M. L. | Gonzalez-Sevilla, S. | Goodson, J. J. | Goossens, L. | Gorbounov, P. A. | Gordon, H. A. | Gorelov, I. | Gorfine, G. | Gorini, B. | Gorini, E. | Gorišek, A. | Gornicki, E. | Gorokhov, S. A. | Gosdzik, B. | Gosselink, M. | Gostkin, M. I. | Gouanère, M. | Gough Eschrich, I. | Gouighri, M. | Goujdami, D. | Goulette, M. P. | Goussiou, A. G. | Goy, C. | Grabowska-Bold, I. | Grabski, V. | Grafström, P. | Grah, C. | Grahn, K-J. | Grancagnolo, F. | Grancagnolo, S. | Grassi, V. | Gratchev, V. | Grau, N. | Gray, H. M. | Gray, J. A. | Graziani, E. | Grebenyuk, O. G. | Green, B. | Greenfield, D. | Greenshaw, T. | Greenwood, Z. D. | Gregor, I. M. | Grenier, P. | Griesmayer, E. | Griffiths, J.
This paper presents a search for the t-channel exchange of an R-parity violating scalar top quark (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\tilde{t}$\end{document}) in the e±μ∓ continuum using 2.1 fb−1 of data collected by the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s}=7~\mbox{TeV}$\end{document}pp collisions at the Large Hadron Collider. Data are found to be consistent with the expectation from the Standard Model backgrounds. Limits on R-parity-violating couplings at 95 % C.L. are calculated as a function of the scalar top mass (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}$\end{document}). The upper limits on the production cross section for pp→eμX, through the t-channel exchange of a scalar top quark, ranges from 170 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=95~\mbox{GeV}$\end{document} to 30 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=1000~\mbox{GeV}$\end{document}.
doi:10.1140/epjc/s10052-012-2040-z
PMCID: PMC4370899  PMID: 25814838
2.  Targeted Antimicrobial Treatment to Re-establish a Healthy Microbial Flora for Long-term Protection 
Advances in Dental Research  2012;24(2):94-97.
Streptococcus mutans has been implicated as the major acid-producing (cariogenic) bacterium. Dietary sugars and other factors may cause an imbalance of oral microflora that enables S. mutans to become dominant in the multi-species biofilms on the tooth surface, which could lead to dental caries. The application of broad-spectrum antimicrobials often results in re-colonization and re-dominance of S. mutans within oral flora, while in contrast, therapies capable of selective elimination of S. mutans from oral microbial communities may help to re-establish the normal flora and provide long-term protection. C16G2, a novel synthetic antimicrobial peptide with specificity for S. mutans, was found to have robust killing efficacy and selectivity for S. mutans in vitro. A subsequent pilot human study found that a single application of C16G2 in the oral cavity (formulated in a mouthrinse vehicle) was associated with a reduction in plaque and salivary S. mutans, lactic acid production, and enamel demineralization during the entire 4-day testing period. C16G2 is now being developed as a new anticaries drug.
doi:10.1177/0022034512453725
PMCID: PMC3420366  PMID: 22899688
microbial ecology; microbiology; microbial genetics; caries; dental biofilm; microbiota
3.  Biochemistry of epidermal stem cells☆ 
Biochimica et biophysica acta  2012;1830(2):2427-2434.
Background
The epidermis is an important protective barrier that is essential for maintenance of life. Maintaining this barrier requires continuous cell proliferation and differentiation. Moreover, these processes must be balanced to produce a normal epidermis. The stem cells of the epidermis reside in specific locations in the basal epidermis, hair follicle and sebaceous glands and these cells are responsible for replenishment of this tissue.
Scope of review
A great deal of effort has gone into identifying protein epitopes that mark stem cells, in identifying stem cell niche locations, and in understanding how stem cell populations are related. We discuss these studies as they apply to understanding normal epidermal homeostasis and skin cancer.
Major conclusions
An assortment of stem cell markers have been identified that permit assignment of stem cells to specific regions of the epidermis, and progress has been made in understanding the role of these cells in normal epidermal homeostasis and in conditions of tissue stress. A key finding is the multiple stem cell populations exist in epidermis that give rise to different structures, and that multiple stem cell types may contribute to repair in damaged epidermis.
General significance
Understanding epidermal stem cell biology is likely to lead to important therapies for treating skin diseases and cancer, and will also contribute to our understanding of stem cells in other systems. This article is part of a Special Issue entitled Biochemistry of Stem Cells.
doi:10.1016/j.bbagen.2012.07.002
PMCID: PMC4038073  PMID: 22820019
Stem cell Hair follicle; Interfollicular stem cell; Epidermis; Keratinocyte
4.  On the Biomechanical Role of Glycosaminoglycans in the Aortic Heart Valve Leaflet 
Acta biomaterialia  2012;9(1):4653-4660.
While the role of collagen and elastin fibrous components in heart valve valvular biomechanics has been extensively investigated [see Sacks et al. 2009 J. Biomech. 42, 1804-24], the biomechanical role of the glycosaminoglycan (GAG) gelatinous-like material phase remains unclear. In the present study, we investigated the biomechanical role of GAGs in porcine aortic valve (AV) leaflets under tension utilizing enzymatic removal. Tissue specimens were removed from the belly region of porcine AVs and subsequently treated with either an enzyme solution for GAG removal, or a control (buffer with no enzyme) solution. A dual stress level test methodology was used to determine the effects at low and high (physiological) stress levels). In addition, planar biaxial tests were conducted both on-axis (i.e. aligned to the circumferential and radial axes) and at 45° off-axis to induce maximum shear, to explore the effects of augmented fiber rotations on the fiber-fiber interactions. Changes in hysteresis were used as the primary metric of GAG functional assessment. A simulation of the low force experimental setup was also conducted to clarify the internal stress system and provide viscoelastic model parameters fo this loading range. Results indicated that under planar tension the removal of GAGs had no measureable affect extensional mechanical properties (either on- or 45° off-axis) including peak stretch, hysteresis, or creep. Interestingly, in the low force range, hysteresis was markedly reduced from 35.96 ± 2.65% in control group to 25.00 ± 1.64% (p < 0.001) as a result of GAG removal. Collectively, these results suggest that GAGs do not play a direct role in modulating the time-dependent tensile properties of valvular tissues. Rather, they appear to be strongly connected with fiber-fiber and fiber-matrix interactions at low forces levels. Thus, we speculate that GAGs may be important in providing a damping mechanism to reduce leaflet flutter when the leaflet is not under high tensile stress.
doi:10.1016/j.actbio.2012.09.031
PMCID: PMC3508081  PMID: 23036945
Glycosaminoglycan; Heart valve; Mechanical properties; Mechanical test
5.  Pupil size varies with word listening and response selection difficulty in older adults with hearing loss 
Psychophysiology  2012;50(1):23-34.
Listening to speech in noise can be exhausting, especially for older adults with impaired hearing. Pupil dilation is thought to track the difficulty associated with listening to speech at various intelligibility levels for young and middle-aged adults. This study examined changes in the pupil response with acoustic and lexical manipulations of difficulty in older adults with hearing loss. Participants identified words at two signal-to-noise ratios (SNRs) among options that could include a similar-sounding lexical competitor. Growth Curve Analyses revealed that the pupil response was affected by an SNR-by-lexical competition interaction, such that it was larger and more delayed and sustained in the harder SNR condition, particularly in the presence of lexical competition. Pupillometry detected these effects for correct trials and across reaction times, suggesting it provides additional evidence of task difficulty than behavioral measures alone.
doi:10.1111/j.1469-8986.2012.01477.x
PMCID: PMC3527636  PMID: 23157603
6.  Auditory Cortex Signs of Age-Related Hearing Loss 
Age-related hearing loss, or presbyacusis, is a major public health problem that causes communication difficulties and is associated with diminished quality of life. Limited satisfaction with hearing aids, particularly in noisy listening conditions, suggests that central nervous system declines occur with presbyacusis and may limit the efficacy of interventions focused solely on improving audibility. This study of 49 older adults (M = 69.58, SD = 8.22 years; 29 female) was designed to examine the extent to which low and/or high frequency hearing loss was related to auditory cortex morphology. Low and high frequency hearing constructs were obtained from a factor analysis of audiograms from these older adults and 1,704 audiograms from an independent sample of older adults. Significant region of interest and voxel-wise gray matter volume associations were observed for the high frequency hearing construct. These effects occurred most robustly in a primary auditory cortex region (Te1.0) where there was also elevated cerebrospinal fluid with high frequency hearing loss, suggesting that auditory cortex atrophies with high frequency hearing loss. These results indicate that Te1.0 is particularly affected by high frequency hearing loss and may be a target for evaluating the efficacy of interventions for hearing loss.
doi:10.1007/s10162-012-0332-5
PMCID: PMC3441956  PMID: 22618352
presbyacusis; age-related hearing loss; auditory cortex
7.  Randomized Pharmacodynamic and Pharmacogenetic Trial of Dronabinol Effects on Colon Transit in Irritable Bowel Syndrome-Diarrhea 
Background
Genetic variation in endocannabinoid metabolism is associated with colonic transit in irritable bowel syndrome (IBS) with diarrhea (IBS-D). The nonselective cannabinoid (CB) receptor agonist, dronabinol (DRO), reduced fasting colonic motility in nonconstipated IBS. FAAH and CNR1 variants influenced DRO’s effects on colonic motility. Our aims were: 1) To compare dose-related effects of DRO to placebo (PLA) on gut transit in IBS-D; and 2) To examine influence of genetic variations in CB mechanisms on DRO’s transit effects.
Methods
36 IBS-D volunteers were randomized (double-blind, concealed allocation) to twice daily PLA (n=13), DRO 2.5mg (n=10), or DRO 5mg (n=13) for two days. We assessed gastric, small bowel, and colonic transit by validated radioscintigraphy and genotyped the single nucleotide polymorphisms CNR1 rs806378 and FAAH rs324420. Data analysis utilized a dominant genetic model.
Key Results
Overall treatment effects of DRO on gastric, small bowel, or colonic transit were not detected. CNR1 rs806378 CT/TT was associated with a modest delay in colonic transit at 24h compared to CC (p=0.13 for differential treatment effects on post- minus pre-treatment changes in colonic transit by genotype). No significant interaction of treatment with FAAH rs324420 was detected.
Conclusions/Inferences
Overall, DRO 2.5mg or 5mg twice daily for two days had no effect on gut transit in IBS-D. There appears to be a treatment-by-genotype effect whereby DRO preferentially delays colonic transit in those with the CNR1 rs806378 CT/TT genotypes. Further study of CB pharmacogenetics may help identify a subset of IBS-D patients most likely to benefit from CB agonist therapy.
doi:10.1111/j.1365-2982.2011.01874.x
PMCID: PMC3775711  PMID: 22288893
cannabinoid; anandamide; FAAH; motility; nonselective; receptor; gastric; small bowel
8.  The Natural History of Dental Caries Lesions 
Journal of Dental Research  2012;91(9):841-846.
Dental caries is a ubiquitous disease affecting all age groups and segments of the population. It is known that not all caries lesions progress to cavitation, but little is known regarding the progression pattern of caries lesions. This study’s purpose was to evaluate the natural history of dental caries using a standardized, visually based system, the International Caries Detection and Assessment System (ICDAS). The study population consisted of 565 consenting children, who were enrolled and examined at baseline and at regular intervals over 48 months with ICDAS and yearly bitewing radiographs. Of these, 338 children completed all examinations. Not all lesions cavitated at the same rate, differing by surface type and baseline ICDAS severity score and activity status. With increasing severity, the percentage of lesions progressing to cavitation increased: 19%, 32%, 68%, and 66% for ICDAS scores 1, 2, 3, and 4, respectively. Lesions on occlusal surfaces were more likely to cavitate, followed by buccal pits, lingual grooves, proximal surfaces, and buccal and lingual surfaces. Cavitation was more likely on molars, followed by pre-molars and anterior teeth. Predictors of cavitation included age, gender, surfaces and tooth types, and ICDAS severity/activity at baseline. In conclusion, characterization of lesion severity with ICDAS can be a strong predictor of lesion progression to cavitation.
doi:10.1177/0022034512455030
PMCID: PMC3420396  PMID: 22821238
longitudinal study; dental caries; ICDAS; activity; lesion progression; Hispanic
9.  Word Intelligibility and Age Predict Visual Cortex Activity during Word Listening 
Cerebral Cortex (New York, NY)  2012;22(6):1360-1371.
The distractibility that older adults experience when listening to speech in challenging conditions has been attributed in part to reduced inhibition of irrelevant information within and across sensory systems. Whereas neuroimaging studies have shown that younger adults readily suppress visual cortex activation when listening to auditory stimuli, it is unclear the extent to which declining inhibition in older adults results in reduced suppression or compensatory engagement of other sensory cortices. The current functional magnetic resonance imaging study examined the effects of age and stimulus intelligibility in a word listening task. Across all participants, auditory cortex was engaged when listening to words. However, increasing age and declining word intelligibility had independent and spatially similar effects: both were associated with increasing engagement of visual cortex. Visual cortex activation was not explained by age-related differences in vascular reactivity but rather auditory and visual cortices were functionally connected across word listening conditions. The nature of this correlation changed with age: younger adults deactivated visual cortex when activating auditory cortex, middle-aged adults showed no relation, and older adults synchronously activated both cortices. These results suggest that age and stimulus integrity are additive modulators of crossmodal suppression and activation.
doi:10.1093/cercor/bhr211
PMCID: PMC3357178  PMID: 21862447
aging; crossmodal; fMRI; speech perception; vascular reactivity
10.  Human Evoked Cortical Activity to Silent Gaps in Noise: Effects of Age, Attention, and Cortical Processing Speed 
Ear and Hearing  2012;33(3):330-339.
Objectives
The goal of this study was to examine the degree to which age-related differences in early or automatic levels of auditory processing and attention-related processes explain age-related differences in auditory temporal processing. We hypothesized that age-related differences in attention and cognition compound age-related differences at automatic levels of processing, contributing to the robust age effects observed during challenging listening tasks.
Design
We examined age-related and individual differences in cortical event-related potential (ERP) amplitudes and latencies, processing speed, and gap detection from twenty-five younger and twenty-five older adults with normal hearing. ERPs were elicited by brief silent periods (gaps) in an otherwise continuous broadband noise and were measured under two listening conditions, passive and active. During passive listening, participants ignored the stimulus and read quietly. During active listening, participants button pressed each time they detected a gap. Gap detection (percent detected) was calculated for each gap duration during active listening (3, 6, 9, 12 and 15 ms). Processing speed was assessed using the Purdue Pegboard test and the Connections Test. Repeated measures ANOVAs assessed effects of age on gap detection, processing speed, and ERP amplitudes and latencies. An “attention modulation” construct was created using linear regression to examine the effects of attention while controlling for age-related differences in auditory processing. Pearson correlation analyses assessed the extent to which attention modulation, ERPs, and processing speed predicted behavioral gap detection. Results: Older adults had significantly poorer gap detection and slower processing speed than younger adults. Even after adjusting for poorer gap detection, the neurophysiological response to gap onset was atypical in older adults with reduced P2 amplitudes and virtually absent N2 responses. Moreover, individual differences in attention modulation of P2 response latencies and N2 amplitudes predicted gap detection and processing speed in older adults. That is, older adults with P2 latencies that decreased and N2 amplitudes that increased with active listening had faster processing speed and better gap detection than those older adults whose P2 latencies increased and N2 amplitudes decreased with attention
Conclusions
Results from the current study are broadly consistent with previous findings that older adults exhibit significantly poorer gap detection than younger adults in challenging tasks. Even after adjusting for poorer gap detection, older and younger adults showed robust differences in their electrophysiological responses to sound offset. Furthermore, the degree to which attention modulated the ERP was associated with individual variation in measures of processing speed and gap detection. Taken together, these results suggests an age-related deficit in early or automatic levels of auditory temporal processing and that some older adults may be less able to compensate for declines in processing by attending to the stimulus. These results extend our previous findings and support the hypothesis that age-related differences in cognitive or attention-related processing, including processing speed, contribute to an age-related decrease in gap detection.
doi:10.1097/AUD.0b013e31823fb585
PMCID: PMC3340542  PMID: 22374321
11.  Early accumulation of intracellular fibrillar oligomers and late congophilic amyloid angiopathy in mice expressing the Osaka intra-Aβ APP mutation 
Translational Psychiatry  2012;2(11):e183-.
Pathogenic amyloid-β peptide precursor (APP) mutations clustered around position 693 of APP—position 22 of the Aβ sequence—are commonly associated with congophilic amyloid angiopathy (CAA) and intracerebral hemorrhages. In contrast, the Osaka (E693Δ) intra-Aβ APP mutation shows a recessive pattern of inheritance that leads to AD-like dementia despite low brain amyloid on in vivo positron emission tomography imaging. Here, we investigated the effects of the Osaka APP mutation on Aβ accumulation and deposition in vivo using a newly generated APP transgenic mouse model (E22ΔAβ) expressing the Osaka mutation together with the Swedish (K670N/M671L) double mutation. E22ΔAβ mice exhibited reduced α-processing of APP and early accumulation of intraneuronal fibrillar Aβ oligomers associated with cognitive deficits. In line with our in vitro findings that recombinant E22Δ-mutated Aβ peptides form amyloid fibrils, aged E22ΔAβ mice showed extracellular CAA deposits in leptomeningeal cerebellar and cortical vessels. In vitro results from thioflavin T aggregation assays with recombinant Aβ peptides revealed a yet unknown antiamyloidogenic property of the E693Δ mutation in the heterozygous state and an inhibitory effect of E22Δ Aβ42 on E22Δ Aβ40 fibrillogenesis. Moreover, E22Δ Aβ42 showed a unique aggregation kinetics lacking exponential fibril growth and poor seeding effects on wild-type Aβ aggregation. These results provide a possible explanation for the recessive trait of inheritance of the Osaka APP mutation and the apparent lack of amyloid deposition in E693Δ mutation carriers.
doi:10.1038/tp.2012.109
PMCID: PMC3565767  PMID: 23149447
Alzheimer's disease; APP; congophilic amyloid angiopathy; intraneuronal Aβ; Osaka mutation
12.  Down-Regulation of HtrA1 Activates the Epithelial-Mesenchymal Transition and ATM DNA Damage Response Pathways 
PLoS ONE  2012;7(6):e39446.
Expression of the serine protease HtrA1 is decreased or abrogated in a variety of human primary cancers, and higher levels of HtrA1 expression are directly related to better response to chemotherapeutics. However, the precise mechanisms leading to HtrA1 down regulation during malignant transformation are unclear. To investigate HtrA1 gene regulation in breast cancer, we characterized expression in primary breast tissues and seven human breast epithelial cell lines, including two non-tumorigenic cell lines. In human breast tissues, HtrA1 expression was prominent in normal ductal glands. In DCIS and in invasive cancers, HtrA1 expression was greatly reduced or lost entirely. HtrA1 staining was also reduced in all of the human breast cancer cell lines, compared with the normal tissue and non-tumorigenic cell line controls. Loss of HtrA1 gene expression was attributable primarily to epigenetic silencing mechanisms, with different mechanisms operative in the various cell lines. To mechanistically examine the functional consequences of HtrA1 loss, we stably reduced and/or overexpressed HtrA1 in the non-tumorigenic MCF10A cell line. Reduction of HtrA1 levels resulted in the epithelial-to-mesenchymal transition with acquisition of mesenchymal phenotypic characteristics, including increased growth rate, migration, and invasion, as well as expression of mesenchymal biomarkers. A concomitant decrease in expression of epithelial biomarkers and all microRNA 200 family members was also observed. Moreover, reduction of HtrA1 expression resulted in activation of the ATM and DNA damage response, whereas overexpression of HtrA1 prevented this activation. Collectively, these results suggest that HtrA1 may function as a tumor suppressor by controlling the epithelial-to-mesenchymal transition, and may function in chemotherapeutic responsiveness by mediating DNA damage response pathways.
doi:10.1371/journal.pone.0039446
PMCID: PMC3383700  PMID: 22761798

Results 1-12 (12)