scholarly journals Effects of stimulus incongruity on children’s curiosity as measured by looking time and expression change

1971 ◽  
Vol 25 (4) ◽  
pp. 232-234 ◽  
Author(s):  
Margaret R. Connolly ◽  
Lauren Harris
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Li Yu ◽  
Miao Liu ◽  
Zhenxin Wang ◽  
Te Liu ◽  
Suying Liu ◽  
...  

Abstract Background Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder with various manifestations and complex etiology. Follicular fluid (FF) serves as the complex microenvironment for follicular development. However, the correlation between the concentration of steroid in FF and the pathogenesis of PCOS is still unclear. Methods Twenty steroid levels in FF from ten patients with PCOS and ten women with male-factor infertility undergoing in vitro fertilization were tested by liquid chromatography-tandem mass spectrometry (LC-MS/MS) in order to explore their possibly correlation with PCOS. Meanwhile, the mRNA levels of core enzymes in steroid synthesis pathway from exosomes of FF were also detected by qPCR. Results The estriol (p < 0.01), estradiol (p < 0.05) and prenenolone (p < 0.01) levels in FF of PCOS group were significantly increased, compared to the normal group, and the progesterone levels (p < 0.05) were decreased in PCOS group. Increased mRNA levels of CYP11A, CYP19A and HSD17B2 of exosomes were accompanied by the hormonal changes in FF. Correlation analysis showed that mRNA levels of CYP11A and HSD17B2 were negatively correlated with percent of top-quality embryos and rate of embryos develop to blastocyst. Conclusion Our results suggest that increased levels of estrogen and pregnenolone in follicular fluid may affect follicle development in PCOS patients, and the mechanism is partially related to HSD17B1, CYP19A1 and CYP11A1 expression change in FF exosomes.


2021 ◽  
Author(s):  
Xiaopeng Xu ◽  
Bingqing Wang ◽  
Zhuoyuan Jiang ◽  
Qi Chen ◽  
Ke Mao ◽  
...  

Abstract Craniofacial microsomia (CFM, OMIM%164 210) is one of the most common congenital facial abnormalities worldwide, but it’s genetic risk factors and environmental threats are poorly investigated, as well as their interaction, making the diagnosis and prenatal screening of CFM impossible. We perform a comprehensive association study on the largest CFM cohort of 6074 samples. We identify 15 significant (P &lt; 5 × 10−8) associated genomic loci (including eight previously reported) and decipher 107 candidates based on multi-omics data. Gene Ontology term enrichment found that these candidates are mainly enriched in neural crest cell (NCC) development and hypoxic environment. Single-cell RNA-seq data of mouse embryo demonstrate that nine of them show dramatic expression change during early cranial NCC development whose dysplasia is involved in pathogeny of CFM. Furthermore, we construct a well-performed CFM risk-predicting model based on polygenic risk score (PRS) method and estimate seven environmental risk factors that interacting with PRS. Single-nucleotide polymorphism-based PRS is significantly associated with CFM [P = 7.22 × 10−58, odds ratio = 3.15, 95% confidence interval (CI) 2.74–3.63], and the top fifth percentile has a 6.8-fold CFM risk comparing with the 10th percentile. Father’s smoking increases CFM risk as evidenced by interaction parameter of −0.324 (95% CI −0.578 to −0.070, P = 0.011) with PRS. In conclusion, the newly identified risk loci will significantly improve our understandings of genetics contribution to CFM. The risk prediction model is promising for CFM prediction, and father’s smoking is a key environmental risk factor for CFM through interacting with genetic factors.


Gene ◽  
2012 ◽  
Vol 504 (2) ◽  
pp. 318
Author(s):  
Gyu-Hwi Nam ◽  
Kung Ahn ◽  
Jin-Han Bae ◽  
Byung-Wook Cho ◽  
Kyung-Do Park ◽  
...  

2009 ◽  
Vol 39 (1) ◽  
pp. 61-71 ◽  
Author(s):  
John Zagorski ◽  
Maria Obraztsova ◽  
Michael A. Gellar ◽  
Jeffrey A. Kline ◽  
John A. Watts

Moderate to severe pulmonary embolism (PE) can cause pulmonary arterial hypertension and right ventricular (RV) heart damage. Previous studies from our laboratory indicate that the basal outflow tract of the RV is injured and has acute inflammation followed by tissue remodeling while the apex appears normal. The present studies examine transcription responses to chronic PE in RV apex and outflow tracts using DNA microarrays to identify transcription responses by region. Changes predominated in the RV outflow tract (8,575 genes showed ≥1.5-fold expression change). Gene ontology and KEGG analyses indicated a significant decrease in genes involved in cellular respiration and energy metabolism and increases in inflammatory cell adhesion molecules and extracellular matrix proteins. Signal pathways for wound healing such as fibroblast growth factor, collagen synthesis, and CCN proteins (named for the first three members of the family: cysteine-rich protein 61, connective tissue growth factor, and nephroblastoma overexpressed gene) were strongly upregulated. In comparison, few genes (422) showed significant change in the RV apex tissue. Apex-selective genes included two genes affecting metabolism and a stretch-sensitive transcription factor (ankyrin repeat domain 1). We conclude that the RV outflow tract is subject to strong proinflammatory and profibrotic remodeling transcriptional responses in chronic PE. Severe loss of genes involved in cellular respiration is consistent with previous histology indicating a shift in cell types present within the outflow tract tissue away from highly energy-dependant cardiomyocytes to less metabolically active cells during remodeling. The apex region of the RV had few compensating adaptations.


2009 ◽  
Vol 103 (5) ◽  
pp. 629-642 ◽  
Author(s):  
Catherine-Ines Kolditz ◽  
Elisabeth Plagnes-Juan ◽  
Edwige Quillet ◽  
Florence Lefèvre ◽  
Françoise Médale

Energy intake and genetic background are major determinants of muscle fat content in most animals, including man. We combined genetic selection and dietary energy supply to study the metabolic pathways involved in genetic and nutritional control of fat deposition in the muscle of rainbow trout (Oncorhynchus mykiss). Two experimental lines of rainbow trout, selected for lean (L) or fat (F) muscle, were fed with diets containing either 10 or 23 % lipids from the first feeding, up to 6 months. At the end of the trial, trout exhibited very different values of muscle fat content (from 4·2 to 10·1 % wet weight). Using microarrays made from a rainbow trout multi-tissue cDNA library, we analysed the molecular changes occurring in the muscle of the two lines when fed the low-energy or high-energy diet. The results from microarray analysis revealed that eleven metabolism-related genes were differentially expressed according to the diet while selection resulted in expression change for twenty-six genes. The most striking observation was the increased level of transcripts encoding the VLDL receptor and fatty acid translocase/CD36 following both the high-fat diet and upward selection for muscle fat content, suggesting that these two genes are relevant molecular markers of fat deposition in the white muscle of rainbow trout.


2016 ◽  
Vol 07 (02) ◽  
pp. 352-423
Author(s):  
ByungHoon B. Kim ◽  
Kaiesa L. Peets ◽  
Jamekia S. Grant ◽  
Joshua S. Hicks ◽  
Dominique C. Zellous ◽  
...  

2018 ◽  
Author(s):  
Cerys S Manning ◽  
Veronica Biga ◽  
James Boyd ◽  
Jochen Kursawe ◽  
Bodvar Ymisson ◽  
...  

AbstractDuring embryogenesis cells make fate decisions within complex tissue environments. The levels and dynamics of transcription factor expression regulate these decisions. Here we use single cell live imaging of an endogenous HES5 reporter and absolute protein quantification to gain a dynamic view of neurogenesis in the embryonic mammalian spinal cord. We report that dividing neural progenitors show both aperiodic and periodic HES5 protein fluctuations. Mathematical modelling suggests that in progenitor cells the HES5 oscillator operates close to its bifurcation boundary where stochastic conversions between dynamics are possible. HES5 expression becomes more frequently periodic as cells transition to differentiation which, coupled with an overall decline in HES5 expression, creates a transient period of oscillations with higher fold expression change. This increases the decoding capacity of HES5 oscillations and correlates with interneuron versus motor neuron cell fate. Thus, HES5 undergoes complex changes in gene expression dynamics as cells differentiate.


2020 ◽  
Author(s):  
Alison L.M. Caldwell ◽  
Jolene K. Diedrich ◽  
Maxim N. Shokhirev ◽  
Nicola J. Allen

AbstractAstrocytes negatively impact neuronal development in many neurodevelopmental disorders (NDs), however how they do this, and if mechanisms are shared across disorders, is not known. We developed an in vitro system to ask how astrocyte protein secretion and gene expression change in three genetic NDs. We identified disorder specific changes, and changes common to all disorders. ND astrocytes increase release of Igfbp2, a secreted inhibitor of IGF. IGF rescues neuronal deficits in many NDs, and we found blocking Igfbp2 partially rescues inhibitory effects of Rett Syndrome astrocytes, suggesting increased astrocyte Igfbp2 contributes to decreased IGF signaling in NDs. We identified increased BMP signaling in ND astrocytes is upstream of protein secretion changes, including Igfbp2, and blocking BMP signaling in Fragile X Syndrome astrocytes reverses inhibitory effects on neurite outgrowth. We provide a resource of astrocyte secreted proteins in health and NDs, and identify novel targets for intervention in diverse NDs.


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