Objective To identify differentially expression of microRNAs associated with expression of estrogen receptor α(ERα)and progesterone receptor(PR)between type Ⅰ and type Ⅱ endometrial adenocarcinoma.Methods Two kinds of endometrial adenocarcinoma cell lines,Ishikawa and KLE,was transplanted into node mice and biopsied to identify the expression of ERα,PR and p53,and test their response to estrogen and progesterone.Cultured the two cell lines under the estrogen-free and progesteronefree circumstance,total RNA was isolated to identify the differentially expressed microRNAs by microarray for prediction the microRNAs which target ESR1 and PGR by software miRANDA and TargetScan,and then was validated by real-time PCR in two cell lines cultured both in vivo and in vitro and ten specimens from patients.Results Ishikawa cell line was confirmed from type Ⅰ endometrial adenocarcinoma.KLE cell line was confirmed from typeⅡendometrial adenocarcinoma.One hundred and twenty-six differentially expressed microRNAs between the two cell lines were identified by mieroRNA microarray,among of which may target ESR1 inchded hsa-miR-100,99a,and may tgrget PGR included hsa-miR-378,768-3p-The differential expression of hsa-miR-100,99a,378,768-3p identified by microarray between Ishikawa and KLE in vivo and in vitro was equal to that by real-time PCR,while Hsa-miR-100 was significantly down expressed in type Ⅰ group specimens compared to type Ⅱ group(P＜0.01).Conclusion Hsa-miR-100 is significantly down-expressed in type Ⅰ endometrial adenocarcinoma compared to type Ⅱ,which may be a great potential to target ESR1.

Interferon response is the first line of host defense against virus infection. Recent years have witnessed tremendous progress in understanding of fish innate response to virus infection, especially in fish interferon antiviral response. A line of fish genes involved in interferon antiviral response have been identified and functional studies further reveal that fish possess an IFN antiviral system similar to mammals. However, fish virus-induced interferon genes contain introns similar to mammalian type III interferon genes although they encode proteins similar to type I interferons, which makes it hard to understand the evolution of vertebrate interferon genes directly resulting in a debate on nomenclature of fish interferon genes. Actually, fish display some unique mechanisms underlying interferon antiviral response. This review documents the recent progress on fish interferon response and its molecular mechanism.
Animals ; Fish Diseases ; immunology ; virology ; Fish Proteins ; genetics ; metabolism ; Fishes ; immunology ; virology ; Gene Expression Regulation ; Interferons ; genetics ; immunology ; STAT1 Transcription Factor ; metabolism ; Virus Diseases ; immunology ; veterinary

Even though mutations in LMNA have been reported in patients with typical dilated cardiomyopathy (DCM) and atrioventricular block (AVB) previously, the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval. Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2, where the LMNA gene was located. Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA, which resulted in an E82K mutation. The E82K mutation co-segregated with all affected individuals in the family, and was not present in 200 normal controls. Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades. Ejection fractions were documented in 5 patients with DCM, but 4 showed a normal value of [Symbol: see text]50%. Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients. This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM. The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.

Even though mutations in LMNA have been reported in patients with typical dilated cardio-myopathy(DCM)and atrioventricular block(AVB)previously,the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval.Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2,where the LMNA gene was located.Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA,which resulted in an E82K mutation.The E82K mutation co-segregated with all affected individuals in the family,and was not present in 200 normal controls.Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades.Ejection fractions were documented in 5 patients with DCM,but 4 showed a normal value of ≥50%.Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients.This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM.The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.