Time filter

Source Type

Cincinnati, OH, United States

Brumm S.,Cincinnati Veteran Affairs Medical Center | Theisen K.,Xavier University | Falciglia M.,Cincinnati Veteran Affairs Medical Center | Falciglia M.,University of Cincinnati
Diabetes Educator | Year: 2016

Purpose: The purpose of the study was to evaluate a diabetes transition care program in a population of veterans with diabetes by calculating 30-day readmission rates and assessing glycemic control. Methods: Hospitalized patients with poorly controlled diabetes were identified to participate in the diabetes transition care program. The program included follow-up through a postdischarge telephone call by the diabetes educator, with an opportunity for a face-to-face clinic visit. A retrospective before-and-after study design was used. Analysis included calculating the readmission rate and the pre- and postintervention A1C rates to evaluate the intervention. Results: Of the 40 participants, 100% completed the intervention. All 40 participants received a postdischarge telephone call as follow-up, with 20% presenting for a face-to-face visit. The 30-day readmission rate for the cohort was 10%, in comparison to 14.3% for patients who did not receive the intervention but were otherwise comparable. For those who had repeat A1C measurements conducted 2 to 8 months after time of enrollment in the program (n = 33), average A1C declined −2.2%, from 11.3% (100 mmol/mol) to 9.1% (76 mmol/mol). Conclusions: Diabetes-specific transition of care for those with complex psychiatric, medical, and social needs was feasible, with good outcomes in hospital readmission rates and glycemic control, when executed by an adult nurse practitioner who was the inpatient diabetes educator. © 2016, © 2016 The Author(s). Source

Lee M.-T.,Cincinnati | Ouyang B.,Cincinnati | Ho S.-M.,Cincinnati | Ho S.-M.,Center for Environmental Genetics | And 6 more authors.
Molecular and Cellular Endocrinology | Year: 2013

Estrogen receptor β (ERβ) and its isoforms have different putative functions and expression patterns in prostate cancer. Current studies on 5'-most exons, 0K and 0N, show that their respective promoters are actively involved in transcription. These data, however, do not explain why ERβ isoforms are differentially expressed in normal and cancerous tissues, since 0K and 0N transcripts are detectable in clinical specimens. Various combinations of 5' untranslated exons, termed exon 0Xs, associate with promoter 0K only and exon 0Xs accommodate upstream open reading frames (uORFs) reducing protein expression. Moreover, ERβ1, 2, and 5 are transcriptionally linked to promoter 0K; exon 0Xs are spliced only into ERβ2 and ERβ5 transcripts, suggesting that their expressions are regulated post-transcriptionally by exon 0Xs. This study reveals that expression of ERβ1 is regulated primarily at the transcriptional level, whereas that of ERβ2 and ERβ5 is controlled by the interplay between transcriptional and post-transcriptional regulation. © 2013 Elsevier Ireland Ltd. Source

Leung Y.-K.,University of Cincinnati | Chan Q.K.-Y.,Chinese University of Hong Kong | Ng C.-F.,Chinese University of Hong Kong | Ma F.M.-T.,Chinese University of Hong Kong | And 6 more authors.
PLoS ONE | Year: 2014

Fulvestrant (ICI-182,780) has recently been shown to effectively suppress prostate cancer cell growth in vitro and in vivo. But it is unclear whether microRNAs play a role in regulating oncogene expression in fulvestrant-treated prostate cancer. Here, this study reports hsa-miR-765 as the first fulvestrant-driven, ERβ-regulated miRNA exhibiting significant tumor suppressor activities like fulvestrant, against prostate cancer cell growth via blockage of cell-cycle progression at the G2/M transition, and cell migration and invasion possibly via reduction of filopodia/intense stress-fiber formation. Fulvestrant was shown to upregulate hsa-miR-765 expression through recruitment of ERβ to the 5′-regulatory-region of hsa-miR-765. HMGA1, an oncogenic protein in prostate cancer, was identified as a downstream target of hsa-miR-765 and fulvestrant in cell-based experiments and a clinical study. Both the antiestrogen and the hsa-miR-765 mimic suppressed HMGA1 protein expression. In a neo-adjuvant study, levels of hsa-miR-765 were increased and HMGA1 expression was almost completely lost in prostate cancer specimens from patients treated with a single dose (250 mg) of fulvestrant 28 days before prostatectomy. These findings reveal a novel fulvestrant signaling cascade involving ERβ-mediated transcriptional upregulation of hsa-miR-765 that suppresses HMGA1 protein expression as part of the mechanism underlying the tumor suppressor action of fulvestrant in prostate cancer. © 2014 Leung et al. Source

Lam H.-M.,University of Cincinnati | Suresh Babu C.V.,University of Cincinnati | Wang J.,University of Cincinnati | Yuan Y.,University of Cincinnati | And 4 more authors.
Molecular and Cellular Endocrinology | Year: 2012

Multiple phosphorylation sites on the human estrogen receptor (hER)α were identified and shown to influence mammary carcinogenesis. In contrast, functional phosphorylation sites of hERβ have yet to be experimentally identified and validated. Here, using mass spectrometry, we uncovered three serines (S75, S87, and S105) in the N-terminus of hERβ as targets of ERK1/2 and p38 kinases. We raised a specific antibody against phosphorylated S105 (pS105) and demonstrated that this site was endogenously phosphorylated in MDA-MB-231 and BT-474 cells. A phospho-mimetic mutant generated from hERβ1 was found to exhibit higher transactivation activity than hERβ1. Ectopic expression of this mutant inhibited cell migration and invasion, but did not affect cell growth and cell-cycle progression in these cell models. In breast cancer specimens, pS105-hERβ immunoreactivity was detected with a higher prevalence and intensity than that of hERβ1. These results underscore the functional importance of the first experimentally identified hERβ-phosphorylation site in breast cancer. © 2012 Elsevier Ireland Ltd. Source

Tang W.-Y.,University of Cincinnati | Levin L.,University of Cincinnati | Talaska G.,University of Cincinnati | Cheung Y.Y.,University of Cincinnati | And 6 more authors.
Environmental Health Perspectives | Year: 2012

Background: Maternal factors are implicated in the onset of childhood asthma. Differentiation of naïve CD4+ T lymphocytes into pro-allergic T-helper 2 cells induces interleukin (IL)4 expression and inhibits interferon (IFN)γ expression accompanied by concordant methylation changes in the promoters of these genes. However, it has yet to be established whether maternal exposure to polycyclic aromatic hydrocarbons (PAHs) can alter these gene promoters epigenetically during fetal development. Objectives: In this study we sought to elucidate the relationship between maternal PAH exposure and promoter methylation status of IFNγ and IL4. Methods: We assessed the effects of benzo[a]pyrene (BaP), a representative airborne PAH, on the methylation status of the IFNγ and IL4 promoters in Jurkat cells and two lung adenocarcinoma cell lines, and on gene expression. In addition, we evaluated methylation status of the IFNγ promoter in cord white blood cells from 53 participants in the Columbia Center for Children's Environmental Health cohort. Maternal PAH exposure was estimated by personal air monitoring during pregnancy. Results: In vitro exposure of the cell models to low, noncytotoxic doses (0.1 and 1 nM) of BaP elicited increased promoter hypermethylation and reduced expression of IFNγ, but not IL4. IFNγ promoter methylation in cord white blood cells was associated with maternal PAH exposure in the cohort study subsample. Conclusion: Consistent with the results for the cell lines, maternal exposure to PAHs was associated with hypermethylation of IFNγ in cord blood DNA from cohort children. These findings support a potential role of epigenetics in fetal reprogramming by PAH-induced environmental diseases. Source

Discover hidden collaborations