MicroRNA-455 suppresses the oncogenic function of HDAC2 in human colorectal cancer.

Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3'UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (P<0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (P<0.01). Moreover, miR-455 decreased the expression of HDAC2 (P<0.01). miR-455 remarkably decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after transfection while inducing cell apoptosis (P<0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.

Pattern and Predictors of Hospital Readmission During the First Year After Lung Transplantation.

Hospital readmission after lung transplantation negatively affects quality of life and resource utilization. A secondary analysis of data collected prospectively was conducted to identify the pattern of (incidence, count, cumulative duration), reasons for and predictors of readmission for 201 lung transplant recipients (LTRs) assessed at 2, 6, and 12 mo after discharge. The majority of LTRs (83.6%) were readmitted, and 64.2% had multiple readmissions. The median cumulative readmission duration was 19 days. The main reasons for readmission were other than infection or rejection (55.5%), infection only (25.4%), rejection only (9.9%), and infection and rejection (0.7%). LTRs who required reintubation (odds ratio [OR] 1.92; p = 0.008) or were discharged to care facilities (OR 2.78; p = 0.008) were at higher risk for readmission, with a 95.7% cumulative incidence of readmission at 12 mo. Thirty-day readmission (40.8%) was not significantly predicted by baseline characteristics. Predictors of higher readmission count were lower capacity to engage in self-care (incidence rate ratio [IRR] 0.99; p = 0.03) and discharge to care facilities (IRR 1.45; p = 0.01). Predictors of longer cumulative readmission duration were older age (arithmetic mean ratio [AMR] 1.02; p = 0.009), return to the intensive care unit (AMR 2.00; p = 0.01) and lower capacity to engage in self-care (AMR 0.99; p = 0.03). Identifying LTRs at risk may assist in optimizing predischarge care, discharge planning and long-term follow-up.

A Randomized Controlled Trial of a Mobile Health Intervention to Promote Self-Management After Lung Transplantation.

Lung transplant recipients are encouraged to perform self-management behaviors, including (i) monitoring health indicators, (ii) adhering to their regimen, and (iii) reporting abnormal health indicators to the transplant coordinator, yet performance is suboptimal. When hospital discharge was imminent, this two-group trial randomized 201 recipients to use either the mobile health (mHealth) intervention (n = 99) or usual care (n = 102), to compare efficacy for promoting self-management behaviors (primary outcomes) and self-care agency, rehospitalization, and mortality (secondary outcomes) at home during the first year after transplantation. The mHealth intervention group performed self-monitoring (odds ratio [OR] 5.11, 95% confidence interval [CI] 2.95-8.87, p < 0.001), adhered to medical regimen (OR 1.64, 95% CI 1.01-2.66, p = 0.046), and reported abnormal health indicators (OR 8.9, 95% CI 3.60-21.99, p < 0.001) more frequently than the usual care group. However, the two groups did not differ in rehospitalization (OR 0.78, 95% CI 0.36-1.66, p = 0.51) or mortality (hazard ratio 1.71, 0.68-4.28, p = 0.25). The positive impact of the mHealth intervention on self-management behaviors suggests that the intervention holds promise and warrants further testing.

Comparative analysis of bilirubin in correlation to albumin between nephrotic syndrome patients and postoperative gastroparesis syndrome patients.

This study aimed to disclose the potential causality of low bilirubin in patients with nephrotic syndrome (NS). Correlation analysis was carried out on total bilirubin (TBIL) to serum albumin (ALB), urine protein (Upr), and urinary microalbumin/creatinine (Umalb/cr) for three groups in a case-control study. P < 0.001 was observed for TBIL, ALB, Umalb/cr, and Upr between the NS and chronic nephritis (CN) groups, and P values of 0.0001, 1.000, 0.0001, and 0.0001 were observed for TBIL, ALB, Umalb/cr, and Upr, respectively, between the postoperative gastroparesis (PGS) and CN groups. The values of r and P in correlation to TBIL were 0.549 and 0.000 for ALB, -0.405 and 0.000 for Umalb/cr, and -0.448 and 0.000 for Upr in the NS group; -0.007 and 0.959 for ALB, 0.213 and 0.091 for Umalb/cr, and -0.082 and 0.519 for Upr in the PGS group; and 0.509 and 0.000 for ALB, -0.431 and 0.000 for Umalb/cr, and -0.362 and 0.002 for Upr in the CN group. A probable causality is implied between the low level of blood bilirubin and its loss in urine in NS patients. This conclusion may provide a theoretical basis for the feasibility of therapies against oxidative stress in NS patients.

Identification of RNA editing sites in cotton (Gossypium hirsutum) chloroplasts and editing events that affect secondary and three-dimensional protein structures.

RNA editing can alter individual nucleotides in primary transcripts, which can cause the amino acids encoded by edited RNA to deviate from the ones predicted from the DNA template. We investigated RNA editing sites of protein-coding genes from the chloroplast genome of cotton. Fifty-four editing sites were identified in 27 transcripts, which is the highest editing frequency found until now in angiosperms. All these editing sites were C-to-U conversion, biased toward ndh genes and U_A context. Examining published editotypes in various angiosperms, we found that RNA editing mostly converts amino acid from hydrophilic to hydrophobic and restores evolutionary conserved amino acids. Using bioinformatics to analyze the effect of editing events on protein secondary and three-dimensional structures, we found that 21 editing sites can affect protein secondary structures and seven editing sites can alter three-dimensional protein structures. These results imply that 24 editing sites in cotton chloroplast transcripts may play an important role in their protein structures and functions.

Differential expression of alpha 1 and beta subunits of voltage dependent Ca2+ channel at the neuromuscular junction of normal and P/Q Ca2+ channel knockout mouse.

Voltage-dependent calcium channels (VDCC) have a key role in neuronal function transforming the voltage signals into intracellular calcium signals. They are composed of the pore-forming alpha(1) and the regulatory alpha(2)delta, gamma and beta subunits. Molecular and functional studies have revealed which alpha(1) subunit gene product is the molecular constituent of each class of native calcium channel (L, N, P/Q, R and T type). Electrophysiological and immunocytochemical studies have suggested that at adult mouse motor nerve terminal (MNT) only P/Q type channels, formed by alpha(1A) subunit, mediate evoked transmitter release. The generation of alpha(1A)-null mutant mice offers an opportunity to study the expression and localization of calcium channels at a synapse with complete loss of P/Q calcium channel. We have investigated the expression and localization of VDCCs alpha(1) and beta subunits at the wild type (WT) and knockout (KO) mouse neuromuscular junction (NMJ) using fluorescence immunocytochemistry. The alpha(1A) subunit was observed only at WT NMJ and was absent at denervated muscles and at KO NMJ. The subunits alpha(1B), alpha(1D) and alpha(1E) were also present at WT NMJ and they were over- expressed at KO NMJ suggesting a compensatory expression due to the lack of the alpha(1A). On the other hand, the beta(1b), beta(2a) and beta(4) were present at the same levels in both genotypes. The presence of other types of VDCC at WT NMJ indicate that they may play other roles in the signaling process which have not been elucidated and also shows that other types of VDCC are able to substitute the alpha(1A) subunit, P/Q channel under certain pathological conditions.