One-year outcomes of an osteoporosis liaison services program initiated within a healthcare system.

Due to the huge gap in the care of patients with osteoporosis and fragility fractures, we aimed to explore the effectiveness of the osteoporosis liaison service (OLS) in osteoporosis care. We found that OLS can improve osteoporosis care, including increasing medication compliance, increasing calcium/vitamin D/protein intake, and reducing fall rate. INTRODUCTION: A significant gap exists in the care of patients with osteoporosis and fragility fractures. This study aimed to evaluate 1-year outcomes of an osteoporosis liaison service (OLS) program that includes two independent components: medication management services (MMS) to improve medication adherence and fracture liaison services (FLS) for secondary prevention. METHODS: Patients with new hip fracture or untreated vertebral fractures enrolled in the FLS program (n = 600), and those with osteoporosis medication management issues but not necessarily fragility fractures enrolled in the MMS program (n = 499) were included. To evaluate outcomes, care coordinators assessed baseline items adapted from the 13 Best Practices Framework (BPF) standards of the International Osteoporosis Foundation, with telephone follow-up every 4 months for 1 year. RESULTS: Mean age of this cohort was 76.2 ± 10.3 years, 78.8% were female. After 1-year participation in the program, all patients had received bone mineral density tests, and medication adherence for the entire cohort at 12 months was 91.9 ± 19.6%, with significant improvement in fall rates (23.4% reduction), exercise rates (16.8% increase), calcium intake (26.5% increase), vitamin D intake (26.4% increase), and adequate protein intake (17.3% increase) (all p < 0.05). After 1-year OLS program, the overall rates of mortality, incident fracture, and falls were 6.6%, 4.0%, and 24.3%, respectively. CONCLUSIONS: The OLS program is associated with improved osteoporosis care, including increased medication adherence, calcium/vitamin D and protein intake, and reduced fall rate.

Influence of the DCC gene on proliferation and carcinoembryonic antigen expression in the human colorectal cancer cell line SW1116.

This study investigated the effects of stable transfection of the exogenous wild-type DCC gene on growth of the human colorectal carcinoma cell line SW1116 in vitro. The DCC gene was amplified from normal human colon tissue by reverse transcription-polymerase chain reaction and used to construct a recombinant expression plasmid, pcDNA3.1(+)-DCC. DCC-negative SW1116 cells were transfected with pcDNA3.1(+)-DCC. Cell viability was tested by the methyl thiazolyl tetrazolium (MTT) assay. Immunofluorescence staining was used to determine the effects of pcDNA3.1(+)-DCC on carcinoembryonic antigen (CEA) expression in transfected cells. The number of cells in the population transfected with pcDNA3.1(+)-DCC was lower than in that transfected with the control pcDNA3.1(+) plasmid or in normal cells (t1 = 3.645, P1 < 0.05, t2 = 3.132, P2 < 0.05) at 3-6 days after transfection, and the proliferation rate of pcDNA3.1(+)-DCC transfected cells was also lower (t1 = 2.134, P2 < 0.05; t2 = 2.736, P2 < 0.05). The total viability of pcDNA3.1(+)-DCC transfected cells was lower than that of normal cells (t1 = 3.053, P1 < 0.05) at 2-6 days after transfection, and of control-transfected cells (t2 = 2.816, P2 < 0.05) after 2, 4, 5, and 6 days. The population of pcDNA3.1(+)-DCC transfected colored of green fluorescent cells and their fluorescent intensities were lower than those of control-transfected and normal cells. Therefore, the transfected DCC gene can suppress cell proliferation and lead to downregulation of CEA expression in SW1116 cells, which might weaken its infiltration and metastasis abilities.

A novel nomogram associated with regulatory T cells infiltration by weighted gene co-expression network analysis for predicting survival in patients with colon cancer.

OBJECTIVE: Traditional diagnostic strategies are unable to accurately discriminate between patients with poor and satisfied prognosis in colon cancer. Therefore, it is urgently recommended to identify new biomarkers in favor of better selection of patients at higher risk of recurrence or poor outcomes, with the aim of early intervention or avoiding overtreatment. MATERIALS AND METHODS: The weighted gene correlation network analysis (WGCNA), together with the proportion of tumor infiltrating immune cells, were employed to screen the key module related to immune infiltration. Using these genes among the key module, a predictive signature was generated via LASSO and multi-Cox regression method. Moreover, a novel nomogram was further developed by combining important clinical parameters and the predictive signature. RESULTS: Genes among the green module, indicating the highest correlation with regulatory T cells (Tregs), were incorporated into the establishment of predictive model. Then, a Tregs-related risk signature (TRRS) consisting of four genes (NRG1, TEX11, OVOL3 and FCRL2) was established, which performed well in predicting the mortality risk of colon cancer in both internal and external validation groups (p=0.004 for TCGA training set, p=0.016 for TCGA testing set and p=0.03 for GSE39582 dataset). Combining TNM stage and age, we developed a nomogram for 1-, 3-, 5-year OS, presenting a more reliable predictive performance in survival based on the receiver operating characteristic (ROC) curves and calibration curves (3-year AUC: 0.83 and 0.74 in the TCGA and GEO database, respectively). CONCLUSIONS: We constructed a four-gene signature for predicting the prognosis of patients with colon cancer, and further developed the nomogram together with TNM stage and age to improve the predictive efficacy.

[Agreement evaluation of the severity of oral epithelial dysplasia in oral leukoplakia].

Objective: To evaluate the inter-observer agreement of the severity of oral epithelial dysplasia in oral leukoplakia, providing a theoretical basis for the development of a more objective grading system. Methods: This study included 60 digital pathological slides of oral leukoplakia from Oral Medicine Department of West China Hospital of Stomatology, Sichuan University, and 239 tissue microarray images of oral leukoplakia from State Key Laboratory of Oral Diseases, Sichuan University, to evaluate the agreement of grading. Besides, 1 000 patches were generated from the 60 digital pathological slides and were divided into 500 small-sized patches (224 pixel×224 pixel) and 500 large-sized patches (1 024 pixel×1 024 pixel), to evaluate the agreement of feature detection. Gradings and feature detections were completed by three pathological experts from the oral pathology departments of two Grade 3, Class A stomatological hospitals in China. Kappa coefficient was used to quantify the inter-observer agreement among pathologists. Results: Minimal agreement was found in the grading of oral epithelial dysplasia among pathologists (Kappa=0.30 in the pathological slide group, Kappa=0.30 in the tissue microarray group). None agreement was found in feature detection within the small-sized patches group (median Kappa=0.14 for architectural features, median Kappa=0.18 for cytological features), and minimal agreement was found in feature detection within the large-sized patches group (median Kappa=0.25 for architectural features, median Kappa=0.25 for cytological features). Conclusions: Generally, the agreement of grading and feature detection of oral epithelial dysplasia in oral leukoplakia is poor. Development of a more objective grading system of oral epithelial dysplasia based on artificial intelligence may be helpful to improve the agreement.