Effects of comprehensive nursing with cognitive behavioral therapy in orthodontic osteodilated arch treatment.

Background: This work explored the effects of cognitive behavior therapy (CBT)-based comprehensive nursing intervention (CNI) mode in arch expansion to treat patients with orthodontic osteodilated arch (OOA).

Aim: To explore the application effect of CBT-based CNI model in orthodontic expansion arch treatment.

Methods: Using convenient sampling method, 81 patients with OOA were selected and rolled into a control group (Ctrl group, 40 cases) and an observation group (Obs group, 41 cases).

MYCN amplification plus 1p36 loss of heterozygosity predicts ultra high risk in bone marrow metastatic neuroblastoma.

Background: This study aimed to better understand the prognostic effect of multiple genetic markers and identify more subpopulations at ultra high risk of poor outcome in bone marrow (BM) metastatic neuroblastoma (NB).

Methods: We screened the MYCN, 1p36 and 11q23 loss of heterozygosity (LOH) statuses of 154 patients by interphase fluorescence in situ hybridization of BM cells. The clinical characteristics of patients with the three markers and their associations with prognosis were analysed.

Downregulating CREBBP inhibits proliferation and cell cycle progression and induces daunorubicin resistance in leukemia cells.

Low expression levels of CREB‑binding protein (CREBBP) have been demonstrated to be associated with high minimal residual disease at the end of induction therapy and adverse long‑term outcomes in pediatric patients with acute lymphoblastic leukemia (ALL). However, the effect of low CREBBP expression on the prognosis of ALL has not yet been investigated. In the present study, CREBBP was downregulated and overexpressed in ALL cell lines (Jurkat and Reh).

Chromosome band 11q23 deletion predicts poor prognosis in bone marrow metastatic neuroblastoma patients without MYCN amplification.

Background: Interphase fluorescence in situ hybridization (FISH) of bone marrow cells has been confirmed to be a direct and valid method to assess the v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) amplification in patients with bone marrow metastatic neuroblastoma. MYCN amplification alone, however, is insufficient for pretreatment risk stratification. Chromosome band 11q23 deletion has recently been included in the risk stratification of neuroblastoma.

[Post-transcriptional regulation of chicken PPARγ transcript variant 3 by upstream open reading frame].

Peroxisome proliferator-activated receptor gamma (PPARγ) is a critical regulator of adipogenesis. Our previous study showed that unlike human and mouse PPARγ transcripts, several chicken PPARγ transcript variants contain upstream open reading frames (uORFs) in their 5'untranslated region (5'TR). To decipher the role of uORFs in post-transcriptional regulation of chicken PPARγ gene, we constructed wild-type (psiCHECK2-cPPARγ3-5'UTR-WT) and a uORF mutant (the upstream ATG (uATG) was mutated to stop codon TGA) 5'UTR reporters (psiCHECK2-cPPARγ3- 5'UTR-Mut) of chicken PPARγ transcript variant 3 (cPPARγ3).

The prognostic potential of coilin in association with p27 expression in pediatric acute lymphoblastic leukemia for disease relapse.

Background: Cajal body (CB) is a nucleic organelle where small nuclear ribonucleoproteins undergo modification, maturation, splicing and/or assembly. Coilin is the marker structural protein of CBs. The expression level and cellular localization of coilin is sensitive to chemotherapeutic reagents, such as cisplatin.

Genetic and epigenetic regulation of PPARγ during adipogenesis.

Peroxisome proliferator-activated receptor gamma (PPARγ) is the master regulator of adipogenesis and adipose tissue development. It also plays crucial roles in many other biological processes, including lipid and glucose metabolism and energy homeostasis. Recently, evidence has been accumulating that the PPARγ gene is not only genetically regulated, but also epigenetically regulated by DNA methylation, histone modification, non-coding RNA and chromosome remodeling.

amplification predicts poor prognosis based on interphase fluorescence in situ hybridization analysis of bone marrow cells in bone marrow metastases of neuroblastoma.

Background: gene amplification is related to risk stratification. Therefore it is important to identify accurately the level of the gene as early as possible in neuroblastoma (NB); however, for patients with bone marrow (BM) metastasis who need chemotherapy before surgery, timely detection of the gene is not possible due to the unavailability of primary tumors.

Methods: gene status was evaluated in 81 BM metastases of NB by interphase fluorescence in situ hybridization (FISH) analysis of BM cells.

Functional analysis of the upstream regulatory region of chicken miR-17-92 cluster.

miR-17-92 cluster plays important roles in cell proliferation, differentiation, apoptosis, animal development and tumorigenesis. The transcriptional regulation of miR-17-92 cluster has been extensively studied in mammals, but not in birds. To date, avian miR-17-92 cluster genomic structure has not been fully determined.

MicroRNA-24 modulates aflatoxin B1-related hepatocellular carcinoma prognosis and tumorigenesis.

MicroRNA-24 (miR-24) may be involved in neoplastic process; however, the role of this microRNA in the hepatocellular carcinoma (HCC) related to aflatoxin B1 (AFB1) has not been well elaborated. Here, we tested miR-24 expression in 207 pathology-diagnosed HCC cases from high AFB1 exposure areas and HCC cells. We found that miR-24 was upregulated in HCC tumor tissues relative to adjacent noncancerous tissue samples, and that the high expression of miR-24 was significantly correlated with larger tumor size, higher microvessel density, and tumor dedifferentiation.

HDAC inhibitor sodium butyrate augments the MEF2C enhancement of Nampt expression under hypoxia.

Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD). Although elevated level of Nampt expression has been observed in various cancers, the involvement of Nampt promoter regulation was not well understood. We have identified a cluster of MEF2 recognition sites upstream of the functional hypoxia response elements (HREs) within the human Nampt promoter, and demonstrated that the two MEF2 sites at -1272 and -1200 were functional to upregulate the promoter activity by luciferase reporter assays.

HIF1 regulates WSB-1 expression to promote hypoxia-induced chemoresistance in hepatocellular carcinoma cells.

WSB-1 is involved in DNA damage response by targeting homeodomain-interacting protein kinase 2 (HIPK2) for ubiquitination and degradation. Here, we report that hypoxia significantly up-regulates the expression of WSB-1 in human hepatocellular carcinoma (HCC) cells. We also provide evidence that WSB-1 is a target of hypoxia-inducible factor 1 (HIF-1).

[Recent advance in DNA epigenetic modifications-the sixth base in the genome].

Recently, 5-hydroxymethyl cytosine (5-hmC) has been discovered as a naturally existed component of normal mammalian genomic DNAs, and it is generally accepted as the sixth base in the genome. This review will introduce the recent advances in the researches on 5-hmC of its formation, tissue-specific distribution, the roles in cell differentiation and gene expression regulation, and the connections as a epigenetic marker with diseases, such as various cancers. We also summarized the current development of the methodologies to detect methylated or hydroxymetholated cytosines of cells at the genomic levels.