ABSTRACT
Objective MicroRNAs are differentially expressed in colorectal cancer tumor tissues and adjacent normal tissues, which play an important role in the development of colorectal cancer. This study aims to investigate the expression of microRNA-7-5p in colorectal cancer patients and its influence on the proliferation and apoptosis of colon cancer cell CaCo2. Methods The high-throughput microarray was used to screen differentially expressed microRNAs, and real-time quantitative PCR (RT-PCR) was used to detect the expression of microRNA-7-5p in 10 cases of colorectal cancer patients and corresponding adjacent normal tissues. Western blot was performed to detect the expression of intestinal trefoil factor (TFF3) in different tissues and CaCo2 cells after transfection with microRNA-7-5p. The expression of TFF3 in different tissues and CaCo2 cells transfected with microRNA-7-5p was detected. TUNEL combined with flow cytometry was used to detect the apoptosis of CaCo2 cells after transfection. The CCK-8 assay was used to detect the proliferation of CaCo2 cells after transfection. Results The relative expression of MicroRNA-7-5p in colorectal cancer tissue was 0.409 ± 0.095, which was significantly lower than that of normal tissue adjacent to cancer (1.000 ± 0.014), and the difference was statistically significant (P <0.01). The relative expression of TFF3 in colorectal cancer tissues was significantly higher than that in normal adjacent tissues (P <0.01). The relative expression of TFF3 in CaCo2 cells decreased in the overexpressed microRNA-7-5p of the control group (0.729 ± 0.041). The proliferation ability (0.930 ± 0.007) was significantly lower in the blank control group (0.990 ± 0.005) (P <0.01), and it could increase the proportion of early apoptotic cells (50.700 ± 0.989) and late apoptotic cells (40.525 ± 0.515). Conclusion MicroRNA-7-5p is lowly expressed in colorectal cancer and is associated with the occurrence and development of colorectal cancer. Up-regulated microRNA-7-5p inhibits the proliferation of colon cancer cell CaCo2 and promotes its apoptosis.
ABSTRACT
<p><b>OBJECTIVE</b>To compare the differences between full-term and VLBW premature infants at term equivalent for the whole and sub-regional corpus callosum areas in order to provide reference for monitoring the extrauterine development of corpus callosum in VLBW premature infants.</p><p><b>METHODS</b>Brain MR image data of 24 term infants with a gestational age of 39 weeks were collected within 24 hours after birth. Brain MR image of 30 VLBW neonates at 39 weeks' gestational age equivalent were successfully obtained. Routine T1WI, T2WI and DWI were applied. T1-weighted images on the mid-sagittal slice were selected, analyzed and measured. Forty-nine eligible MR images of them were chosen, 21 cases from the full-term infant group and 28 cases from the premature infant group. Corpus callosum and brain MR images were then sketched by two radiographic doctors. All data were analyzed by the Image Processing Function of MATLAB R2010a, and the whole corpus callosum and six sub-regions were obtained.</p><p><b>RESULTS</b>The whole corpus callosum, anterior mid-body, posterior mid-body, isthmus and splenium area in the premature infant group were smaller than those in the full-term infant group (P<0.05), but the differences of Genu and rostral body area between the two groups was not statistically significant (P>0.05).</p><p><b>CONCLUSIONS</b>The areas of the whole corpus callosum, anterior mid-body, posterior mid-body, isthmus and splenium in VLBW preterm infants at term are reduced, suggesting that the posterior end of the corpus callosum is probably most vulnerable to insults following pathogenic factors.</p>
Subject(s)
Humans , Infant, Newborn , Corpus Callosum , Infant, Premature , Infant, Very Low Birth Weight , Magnetic Resonance ImagingABSTRACT
We discuss what document types account for the calculation of the journal impact factor (JIF) as published in the Journal Citation Reports (JCR). Based on a brief review of articles discussing how to predict JIFs and taking data differences between the Web of Science (WoS) and the JCR into account, we make our own predictions. Using data by cited-reference searching for Thomson Scientific's WoS, we predict 2007 impact factors (IFs) for several journals, such as Nature, Science, Learned Publishing and some Library and Information Sciences journals. Based on our colleagues' experiences we expect our predictions to be lower bounds for the official journal impact factors. We explain why it is useful to derive one's own journal impact factor.