357 research outputs found
PORK QUALITY ASSESSMENT THROUGH IMAGE SEGMENTATION AND SUPPORT VECTOR MACHINE IMPLEMENTATION
Pork is the most consumed meat in the Philippines, and efficient quality control is essential for ensuring the safety of its consumers. Current manual procedures of meat inspection are time-consuming and laboratory-intensive considering the large amount of supply to be examined. This research aims to construct a rapid objective system of pork quality assessment with respect to meat freshness through Support Vector Machine (SVM) implementation, and to ultimately have an accuracy rate of Ăąâ°Â„ 90%. 35 meat samples were collected, and their images were acquired. 30 of these were randomly designated as part of the training dataset while the rest were designated as part of the testing dataset. Of the 30 training samples, 6 were randomly chosen for the creation of a microbial profile. In all of the acquired image samples, image segmentation was performed and the RGB, HSV, Lab, and statistical texture features were extracted. These were inputted in 15 different SVM configurations. SVM classification yielded an accuracy rate of 93.33 %. Results from the microbial profile revealed considerable microbial activity at the 5th and 6th intervals (10th and 12th hour) with 2 and 3 colonies formed, respectively. With the ability of the SVM to distinguish between samples with respect to the hour interval and with the supplementation of the microbial profile, an objective artificial intelligence mechanism for freshness detection was successfully created.Keywords: Meat quality, Image segmentation, Support vector machine, Artificial intelligenc
Parenting and toddler selfâregulation in lowâincome families: What does sleep have to do with it?
Toddlerhood is a sensitive period in the development of selfâregulation, a set of adaptive skills that are fundamental to mental health and partly shaped by parenting. Healthy sleep is known to be critical for selfâregulation; yet, the degree to which child sleep alters interactive childâparent processes remains understudied. This study examines associations between observed parenting and toddler selfâregulation, with toddler sleep as a moderator of this association. Toddlers in lowâincome families (N = 171) and their mothers were videotaped during free play and a selfâregulation challenge task; videos were coded for mothersâ behavior and affect (free play) and toddlersâ selfâregulation (challenge task). Mothers reported their childâs nighttime sleep duration via questionnaire. Results revealed significant Sleep Ă Maternal Negative Affect and Sleep Ă Maternal Negative Control interactions. Children who did not experience negative parenting had good selfâregulation regardless of their nighttime sleep duration. For children who did experience negative parenting, selfâregulation was intact among those who obtained more nighttime sleep, but significantly poorer among children who were getting less nighttime sleep. Thus, among children who were reported to obtain less nighttime sleep, there were more robust associations between negative parenting and poorer selfâregulation than among toddlers who were reported to obtain more sleep.RESUMENLos primeros años de la niñez son un perĂodo sensible en el desarrollo de la autoâregulaciĂłn, un grupo de habilidades adaptables que son fundamentales para la salud mental y a las que en parte les da forma la crianza. Es sabido que el dormir bien es esencial para la autoâregulaciĂłn y, aun asĂ, el nivel al que el sueño del niño altera los procesos interactivos entre progenitor y niño permanece poco estudiado. Este estudio examina las asociaciones entre la crianza observada y la autoâregulaciĂłn del niño pequeño, tomando como moderador de tal asociaciĂłn el proceso de dormir del niño pequeño. Se grabĂł en video a niños pequeños de familias de bajos ingresos (N=171) y sus madres durante una sesiĂłn de juego libre y una tarea de autoâregulaciĂłn que suponĂa un reto; los videos fueron codificados en cuanto al comportamiento y afecto de las madres (juego libre) y la autoâregulaciĂłn de los niños pequeños (tarea que suponĂa reto). Las madres reportaron acerca del sueño nocturno de sus niños por medio de un cuestionario. Los resultados revelaron interacciones significativas en cuanto al dormir y el negativo afecto materno, asĂ como el dormir y el negativo control materno. Los niños que no experimentaron una crianza negativa tenĂan una buena autoâregulaciĂłn independientemente de la duraciĂłn de su sueño nocturno. En el caso de los niños que experimentaron una crianza negativa, la autoâregulaciĂłn quedĂł intacta en aquellos que lograban mĂĄs tiempo nocturno de dormir, pero fue significativamente mĂĄs pobre en los niños que tenĂan menos tiempo de sueño nocturno. Por tanto, en el caso de los niños indicados en el reporte con menos tiempo de dormir nocturno, se dieron asociaciones mĂĄs robustas entre la crianza negativa y una mĂĄs pobre autoâregulaciĂłn que entre los niños pequeños indicados en el reporte con mĂĄs tiempo de dormir.RĂSUMĂLa petite enfance est une pĂ©riode sensible dans le dĂ©veloppement de lâautoârĂ©gulation, un ensemble de compĂ©tences qui sont fondamentales pour la santĂ© mentale et en partie formĂ©es par le parentage. Lâon sait quâun sommeil sain est critique pour lâautoârĂ©gulation et pourtant la mesure dans laquelle le sommeil de lâenfant altĂšre les processus interactifs enfantâparent demeure peu Ă©tudiĂ©e. Cette Ă©tude examine les liens entre le parentage observĂ© et lâautoârĂ©gulation du petit enfant, le sommeil de lâenfant ayant un effet modĂ©rateur dans ce lien. Des jeunes enfants de familles issues de milieux dĂ©favorisĂ©s (N=171) et leurs mĂšres ont Ă©tĂ© filmĂ©s durant un jeu libre et un exercice de dĂ©fi dâautoârĂ©gulation. Les vidĂ©os ont Ă©tĂ© codĂ©es pour le comportement des mĂšres et lâaffect (jeu libre) et lâautoârĂ©gulation des jeunes enfants (exercice de dĂ©fi). Les mĂšres ont fait Ă©tat de la durĂ©e de sommeil nocturne de leur enfant au moyen dâun questionnaire. Les rĂ©sultats ont rĂ©vĂ©lĂ© que : sommeil significatif x lâaffect nĂ©gatif maternel et le sommeil x nĂ©gatif maternel contrĂŽle les interactions. Les enfants qui nâavaient pas fait lâexpĂ©rience dâun parentage nĂ©gatif avaient une bonne autoârĂ©gulation quelle quâait Ă©tĂ© la durĂ©e du sommeil nocturne. Pour les enfants ayant fait lâexpĂ©rience dâune parentage nĂ©gatif, lâautoârĂ©gulation Ă©tait intacte chez ceux ayant plus dormi, mais bien moindre chez les enfants qui avaient moins dormi. Donc, chez les enfants ayant moins de sommeil nocturne les liens bien plus robustes ont Ă©tĂ© dĂ©couverts entre le parentage nĂ©gatif et une moindre autoârĂ©gulation que chez les petits enfants dormant plus durant la nuit.ZUSAMMENFASSUNGDas Kleinkindalter ist ein sensibler Zeitraum fĂŒr die Entwicklung der Selbstregulation â einer Reihe von AnpassungsfĂ€higkeiten, die fĂŒr die psychische Gesundheit grundlegend sind und teilweise durch Erziehung geprĂ€gt werden. Gesunder Schlaf ist bekanntlich entscheidend fĂŒr die Selbstregulation, aber das AusmaĂ, in dem der Kinderschlaf interaktive Prozesse zwischen Kind und Eltern verĂ€ndert, ist bisher nur unzureichend erforscht wurden. Diese Studie untersucht ZusammenhĂ€nge zwischen beobachtetem Erziehungsverhalten und der Selbstregulation von Kleinkindern, wobei der Schlaf der Kleinkinder als Moderator dieser Assoziation fungiert. Kleinkinder aus einkommensschwachen Familien (N=171) und ihre MĂŒtter wurden wĂ€hrend des freien Spiels und einer herausfordernden Aufgabe zur Selbstregulation gefilmt; die Videos wurden fĂŒr das Verhalten und die Affekte der MĂŒtter (freies Spiel) und die Selbstregulation der Kleinkinder (herausfordernde Aufgabe) kodiert. Die MĂŒtter berichteten per Fragebogen ĂŒber die nĂ€chtliche Schlafdauer ihres Kindes. Die Ergebnisse zeigten signifikante Interaktionen fĂŒr Schlaf und mĂŒtterlichen negativen Affekt sowie fĂŒr Schlaf und mĂŒtterliche negative Kontrollinteraktionen. Kinder, die keine negative Erziehung erlebten, hatten eine gute Selbstregulation, unabhĂ€ngig von ihrer nĂ€chtlichen Schlafdauer. Bei Kindern, die eine negative Erziehung erfuhren, war die Selbstregulation bei denen, die mehr Nachtschlaf erhielten, intakt und bei Kindern, die weniger Nachtschlaf erhielten, jedoch deutlich schlechter. So gab es bei Kindern, von denen berichtet wurde, dass sie weniger Nachtschlaf erhielten, robustere Assoziationen zwischen negativer Erziehung und schlechterer Selbstregulation als bei Kleinkindern, von denen berichtet wurde, dass sie mehr Schlaf erhielten.æéČäœćć
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.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/150525/1/imhj21783.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/150525/2/imhj21783_am.pd
Upregulated sirtuin 1 by miRNA-34a is required for smooth muscle cell differentiation from pluripotent stem cells
© 2015 Macmillan Publishers Limited. All rights reserved. microRNA-34a (miR-34a) and sirtuin 1 (SirT1) have been extensively studied in tumour biology and longevityaging, but little is known about their functional roles in smooth muscle cell (SMC) differentiation from pluripotent stem cells. Using well-established SMC differentiation models, we have demonstrated that miR-34a has an important role in SMC differentiation from murine and human embryonic stem cells. Surprisingly, deacetylase sirtuin 1 (SirT1), one of the top predicted targets, was positively regulated by miR-34a during SMC differentiation. Mechanistically, we demonstrated that miR-34a promoted differentiating stem cells' arrest at G0G1 phase and observed a significantly decreased incorporation of miR-34a and SirT1 RNA into Ago2-RISC complex upon SMC differentiation. Importantly, we have identified SirT1 as a transcriptional activator in the regulation of SMC gene programme. Finally, our data showed that SirT1 modulated the enrichment of H3K9 tri-methylation around the SMC gene-promoter regions. Taken together, our data reveal a specific regulatory pathway that miR-34a positively regulates its target gene SirT1 in a cellular context-dependent and sequence-specific manner and suggest a functional role for this pathway in SMC differentiation from stem cells in vitro and in vivo
Prediction of 7-year psychopathology from mother-infant joint attention behaviours: a nested caseâcontrol study
<br>Background: To investigate whether later diagnosis of psychiatric disorder can be predicted from analysis of mother-infant joint attention (JA) behaviours in social-communicative interaction at 12 months.</br>
<br>Method:
Using data from a large contemporary birth cohort, we examined 159 videos of a mother-infant interaction for joint attention behaviour when children were aged one year, sampled from within the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Fifty-three of the videos involved infants who were later considered to have a psychiatric disorder at seven years and 106 were same aged controls. Psychopathologies included in the case group were disruptive behaviour disorders, oppositional-conduct disorder, attention-deficit/hyperactivity disorder, pervasive development disorder, anxiety and depressive disorders. Psychiatric diagnoses were obtained using the Development and Wellbeing Assessment when the children were seven years old.</br> <br>Results: None of the three JA behaviours (shared look rate, shared attention rate and shared attention intensity) showed a significant association with the primary outcome of caseâcontrol status. Only shared look rate predicted any of the exploratory sub-diagnosis outcomes and was found to be positively associated with later oppositional-conduct disorders (OR [95% CI]: 1.5 [1.0, 2.3]; pâ=â0.041).</br><br>Conclusions: JA behaviours did not, in general, predict later psychopathology. However, shared look was positively associated with later oppositional-conduct disorders. This suggests that some features of JA may be early markers of later psychopathology. Further investigation will be required to determine whether any JA behaviours can be used to screen for families in need of intervention.</br>
MicroRNAs in pulmonary arterial remodeling
Pulmonary arterial remodeling is a presently irreversible pathologic hallmark of pulmonary arterial hypertension (PAH). This complex disease involves pathogenic dysregulation of all cell types within the small pulmonary arteries contributing to vascular remodeling leading to intimal lesions, resulting in elevated pulmonary vascular resistance and right heart dysfunction. Mutations within the bone morphogenetic protein receptor 2 gene, leading to dysregulated proliferation of pulmonary artery smooth muscle cells, have been identified as being responsible for heritable PAH. Indeed, the disease is characterized by excessive cellular proliferation and resistance to apoptosis of smooth muscle and endothelial cells. Significant gene dysregulation at the transcriptional and signaling level has been identified. MicroRNAs are small non-coding RNA molecules that negatively regulate gene expression and have the ability to target numerous genes, therefore potentially controlling a host of gene regulatory and signaling pathways. The major role of miRNAs in pulmonary arterial remodeling is still relatively unknown although research data is emerging apace. Modulation of miRNAs represents a possible therapeutic target for altering the remodeling phenotype in the pulmonary vasculature. This review will focus on the role of miRNAs in regulating smooth muscle and endothelial cell phenotypes and their influence on pulmonary remodeling in the setting of PAH
MiR-107 and MiR-185 Can Induce Cell Cycle Arrest in Human Non Small Cell Lung Cancer Cell Lines
BACKGROUND: MicroRNAs (miRNAs) are short single stranded noncoding RNAs that suppress gene expression through either translational repression or degradation of target mRNAs. The annealing between messenger RNAs and 5' seed region of miRNAs is believed to be essential for the specific suppression of target gene expression. One miRNA can have several hundred different targets in a cell. Rapidly accumulating evidence suggests that many miRNAs are involved in cell cycle regulation and consequentially play critical roles in carcinogenesis. METHODOLOGY/PRINCIPAL FINDINGS: Introduction of synthetic miR-107 or miR-185 suppressed growth of the human non-small cell lung cancer cell lines. Flow cytometry analysis revealed these miRNAs induce a G1 cell cycle arrest in H1299 cells and the suppression of cell cycle progression is stronger than that by Let-7 miRNA. By the gene expression analyses with oligonucleotide microarrays, we find hundreds of genes are affected by transfection of these miRNAs. Using miRNA-target prediction analyses and the array data, we listed up a set of likely targets of miR-107 and miR-185 for G1 cell cycle arrest and validate a subset of them using real-time RT-PCR and immunoblotting for CDK6. CONCLUSIONS/SIGNIFICANCE: We identified new cell cycle regulating miRNAs, miR-107 and miR-185, localized in frequently altered chromosomal regions in human lung cancers. Especially for miR-107, a large number of down-regulated genes are annotated with the gene ontology term 'cell cycle'. Our results suggest that these miRNAs may contribute to regulate cell cycle in human malignant tumors
miR-34a Repression in Proneural Malignant Gliomas Upregulates Expression of Its Target PDGFRA and Promotes Tumorigenesis
Glioblastoma (GBM) and other malignant gliomas are aggressive primary neoplasms of the brain that exhibit notable refractivity to standard treatment regimens. Recent large-scale molecular profiling has revealed distinct disease subclasses within malignant gliomas whose defining genomic features highlight dysregulated molecular networks as potential targets for therapeutic development. The âproneuralâ designation represents the largest and most heterogeneous of these subclasses, and includes both a large fraction of GBMs along with most of their lower-grade astrocytic and oligodendroglial counterparts. The pathogenesis of proneural gliomas has been repeatedly associated with dysregulated PDGF signaling. Nevertheless, genomic amplification or activating mutations involving the PDGF receptor (PDGFRA) characterize only a subset of proneural GBMs, while the mechanisms driving dysregulated PDGF signaling and downstream oncogenic networks in remaining tumors are unclear. MicroRNAs (miRNAs) are a class of small, noncoding RNAs that regulate gene expression by binding loosely complimentary sequences in target mRNAs. The role of miRNA biology in numerous cancer variants is well established. In an analysis of miRNA involvement in the phenotypic expression and regulation of oncogenic PDGF signaling, we found that miR-34a is downregulated by PDGF pathway activation in vitro. Similarly, analysis of data from the Cancer Genome Atlas (TCGA) revealed that miR-34a expression is significantly lower in proneural gliomas compared to other tumor subtypes. Using primary GBM cells maintained under neurosphere conditions, we then demonstrated that miR-34a specifically affects growth of proneural glioma cells in vitro and in vivo. Further bioinformatic analysis identified PDGFRA as a direct target of miR-34a and this interaction was experimentally validated. Finally, we found that PDGF-driven miR-34a repression is unlikely to operate solely through a p53-dependent mechanism. Taken together, our data support the existence of reciprocal negative feedback regulation involving miR-34 and PDGFRA expression in proneural gliomas and, as such, identify a subtype specific therapeutic potential for miR-34a
The Co-Regulation of Emotions Between Mothers and their Children with Autism
Thirty-four toddlers with autism and their mothers participated in an early intervention targeting joint engagement. Across the 24 intervention sessions, any significant distress episode in the child was coded for emotion regulation outcomes including child negativity, child emotion self-regulation, and mother emotion co-regulation. Results revealed that emotion regulation strategies by both mother and child were employed during distress episodes. An effect of intervention was found such that children decreased their expression of negativity across the intervention and mothers increased their emotional and motivational scaffolding. The results of this study indicate a positive effect of an intervention targeting joint engagement on emotion co-regulation outcomes
MicroRNA-34a Modulates c-Myc Transcriptional Complexes to Suppress Malignancy in Human Prostate Cancer Cells
MicroRNA-34a (miR-34a), a potent mediator of tumor suppressor p53, has been reported to function as a tumor suppressor and miR-34a was found to be downregulated in prostate cancer tissues. We studied the functional effects of miR-34a on c-Myc transcriptional complexes in PC-3 prostate cancer cells. Transfection of miR-34a into PC-3 cells strongly inhibited in vitro cell proliferation, cell invasion and promoted apoptosis. Transfection of miR-34a into PC-3 cells also significantly inhibited in vivo xenograft tumor growth in nude mice. miR-34a downregulated expression of c-Myc oncogene by targeting its 3âČ UTR as shown by luciferase reporter assays. miR-34a was found to repress RhoA, a regulator of cell migration and invasion, by suppressing c-MycâSkp2âMiz1 transcriptional complex that activates RhoA. Overexpression of c-Myc reversed miR-34a suppression of RhoA expression, suggesting that miR-34a inhibits invasion by suppressing RhoA through c-Myc. miR-34a was also found to repress c-Myc-pTEFB transcription elongation complex, indicating one of the mechanisms by which miR-34a has profound effects on cellular function. This is the first report to document that miR-34a suppresses assembly and function of the c-MycâSkp2âMiz1 complex that activates RhoA and the c-Myc-pTEFB complex that elongates transcription of various genes, suggesting a novel role of miR-34a in the regulation of transcription by c-Myc complex
MicroRNA-34a is a potent tumor suppressor molecule in vivo in neuroblastoma
<p>ABSTRACT</p> <p>Background</p> <p>Neuroblastoma is a paediatric cancer which originates from precursor cells of the sympathetic nervous system and accounts for 15% of childhood cancer mortalities. With regards to the role of miRNAs in neuroblastoma, miR-34a, mapping to a chromosome 1p36 region that is commonly deleted, has been found to act as a tumor suppressor through targeting of numerous genes associated with cell proliferation and apoptosis.</p> <p>Methods</p> <p>A synthetic miR-34a (or negative control) precursor molecule was transfected into NB1691<sup>luc </sup>and SK-N-AS<sup>luc </sup>neuroblastoma cells. Quantitative PCR was used to verify increased miR-34a levels in NB1691<sup>luc </sup>and SK-N-AS<sup>luc </sup>cell lines prior to <it>in vitro </it>and <it>in vivo </it>analysis. <it>In vitro </it>analysis of the effects of miR-34a over expression on cell growth, cell cycle and phosphoprotein activation in signal transduction pathways was performed. Neuroblastoma cells over expressing miR-34a were injected retroperitoneally into immunocompromised CB17-SCID mice and tumor burden was assessed over a 21 day period by measuring bioluminescence (photons/sec/cm<sup>2</sup>).</p> <p>Results</p> <p>Over expression of miR-34a in both NB1691<sup>luc </sup>and SK-N-AS<sup>luc </sup>neuroblastoma cell lines led to a significant decrease in cell number relative to premiR-negative control treated cells over a 72 hour period. Flow cytometry results indicated that miR-34a induced cell cycle arrest and subsequent apoptosis activation. Phosphoprotein analysis highlighted key elements involved in signal transduction, whose activation was dysregulated as a result of miR-34a introduction into cells. As a potential mechanism of miR-34a action on phosphoprotein levels, we demonstrate that miR-34a over-expression results in a significant reduction of <it>MAP3K9 </it>mRNA and protein levels. Although <it>MAP3K9 </it>is a predicted target of miR-34a, direct targeting could not be validated with luciferase reporter assays. Despite this fact, any functional effects of reduced MAP3K9 expression as a result of miR-34a would be expected to be similar regardless of the mechanism involved. Most notably, <it>in vivo </it>studies showed that tumor growth was significantly repressed after exogenous miR-34a administration in retroperitoneal neuroblastoma tumors.</p> <p>Conclusion</p> <p>We demonstrate for the first time that miR-34a significantly reduces tumor growth in an <it>in vivo </it>orthotopic murine model of neuroblastoma and identified novel effects that miR-34a has on phospho-activation of key proteins involved with apoptosis.</p
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