Temple University

About: Temple University is a education organization based out in Philadelphia, Pennsylvania, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32154 authors who have published 64375 publications receiving 2219828 citations.

How the prosodic cues in motherese might assist language learning.

Abstract: The function of motherese has become a pivotal issue in the language-learning literature. The current research takes the approach of asking whether the prosodic characteristics that are distinctive to motherese could play a special role in facilitating the acquisition of syntax. Hirsh-Pasek, Kemler Nelson, Jusczyk, Cassidy, Druss & Kennedy (1987) showed that infants aged 0;7-0;10 are sensitive to prosodic cues that would help them segment the speech stream into perceptual units that correspond to clauses. The present study shows that infants' sensitivity to segment-marking cues in ongoing speech holds for motherese but not for adult-directed speech. The finding is that, for motherese only, infants orient longer to speech that has been interrupted at clausal boundaries than to matched speech that has been interrupted at within-clause locations. This selective preference indicates that the prosodic qualities of motherese provide infants with cues to units of speech that correspond to grammatical units of language-a potentially fundamental contribution of motherese to the learning of syntax.

Fusobacterium in colonic flora and molecular features of colorectal carcinoma

Abstract: Fusobacterium species are part of the gut microbiome in humans. Recent studies have identified overrepresentation of Fusobacterium in colorectal cancer tissues, but it is not yet clear whether this is pathogenic or simply an epiphenomenon. In this study, we evaluated the relationship between Fusobacterium status and molecular features in colorectal cancers through quantitative real-time PCR in 149 colorectal cancer tissues, 89 adjacent normal appearing mucosae and 72 colonic mucosae from cancer-free individuals. Results were correlated with CpG island methylator phenotype (CIMP) status, microsatellite instability (MSI), and mutations in BRAF , KRAS , TP53 , CHD7 , and CHD8 . Whole-exome capture sequencing data were also available in 11 cases. Fusobacterium was detectable in 111 of 149 (74%) colorectal cancer tissues and heavily enriched in 9% (14/149) of the cases. As expected, Fusobacterium was also detected in normal appearing mucosae from both cancer and cancer-free individuals, but the amount of bacteria was much lower compared with colorectal cancer tissues (a mean of 250-fold lower for Pan-fusobacterium ). We found the Fusobacterium -high colorectal cancer group (FB-high) to be associated with CIMP positivity ( P = 0.001), TP53 wild-type ( P = 0.015), hMLH1 methylation positivity ( P = 0.0028), MSI ( P = 0.018), and CHD7 / 8 mutation positivity ( P = 0.002). Among the 11 cases where whole-exome sequencing data were available, two that were FB-high cases also had the highest number of somatic mutations (a mean of 736 per case in FB-high vs. 225 per case in all others). Taken together, our findings show that Fusobacterium enrichment is associated with specific molecular subsets of colorectal cancers, offering support for a pathogenic role in colorectal cancer for this gut microbiome component. Cancer Res; 74(5); 1311–8. ©2014 AACR .

Increased expression of leptin and the leptin receptor as a marker of breast cancer progression: possible role of obesity-related stimuli

Abstract: Purpose: Recent in vitro studies suggested that the autocrine leptin loop might contribute to breast cancer development by enhancing cell growth and survival. To evaluate whether the leptin system could become a target in breast cancer therapy, we examined the expression of leptin and its receptor (ObR) in primary and metastatic breast cancer and noncancer mammary epithelium. We also studied whether the expression of leptin/ObR in breast cancer can be induced by obesity-related stimuli, such as elevated levels of insulin, insulin-like growth factor-I (IGF-I), estradiol, or hypoxic conditions. Experimental Design: The expression of leptin and ObR was examined by immunohistochemistry in 148 primary breast cancers and 66 breast cancer metastases as well as in 90 benign mammary lesions. The effects of insulin, IGF-I, estradiol, and hypoxia on leptin and ObR mRNA expression were assessed by reverse transcription-PCR in MCF-7 and MDA-MB-231 breast cancer cell lines. Results: Leptin and ObR were significantly overexpressed in primary and metastatic breast cancer relative to noncancer tissues. In primary tumors, leptin positively correlated with ObR, and both biomarkers were most abundant in G3 tumors. The expression of leptin mRNA was enhanced by insulin and hypoxia in MCF-7 and MDA-MB-231 cells, whereas IGF-I and estradiol stimulated leptin mRNA only in MCF-7 cells. ObR mRNA was induced by insulin, IGF-I, and estradiol in MCF-7 cells and by insulin and hypoxia in MDA-MB-231 cells. Conclusions: Leptin and ObR are overexpressed in breast cancer, possibly due to hypoxia and/or overexposure of cells to insulin, IGF-I, and/or estradiol.