Correction to: Osteogenic prospective of deriving human dental stem cells in collagen matrix boost.

The original version of this article unfortunately contained a mistake. The country was incorrect in the authors affiliations. It should read as "ROC". The corrected affiliations are given below.

Osteogenic prospective of deriving human dental stem cells in collagen matrix boost.

Stem cells derived from oral tissue represent a highly attractive alternative source for clinical bone regeneration because they can be collected by non-invasive or minimally invasive procedures. Herein, we describe the human dental stem cells (DSCs) deriving from buccal fat pads (BFP), dental pulp (DP) of impacted teeth, and periodontal ligaments (PDL) to obtain BFPSCs, DPSCs, and PDLSCs, respectively. Cells were purified with selected medium and expanded through passages in stem cell culture medium. Purified cells were characterized for stemness by their growth rate, immunostaining, and multilineage differentiation ability. They showed plastic adherence, expression of stemness-specific markers, and multilineage differentiation potential. Immunocytochemistry analysis confirmed that DPSCs had more osteogenic potential than BFSCs and PDLSCs. Calcium-rich deposits, evaluated by von Kossa and Alizarin red staining, showed greater mineralization when DPSCs were cultured on collagen type I matrix than without collagen. Furthermore, DPSC-seeded collagen type I matrix maintained consistent osteogenesis and boosted mineral formation by 1-2 weeks over that in DPSCs cultured without collagen. Radiographic analysis of DPSC-seeded collagen type I matrix transplanted into rat cranial defects showed significant bone regeneration after 8 weeks. These results suggested that the redundant oral tissue can be used as a source of adult multipotent stem cells for clinical bone regeneration. Triple overlay images with biomarkers (red), nuclei (blue) and bright field morphology of DPSCs. The specifically osteo-differentiation shown by osteocalcin (left) expression and lack of sox9 (right) expressed in the images below which were cultured with collagen matrix, contrast with no collagen matrix group above.

A population-based cohort study of symptomatic gallstone disease in diabetic patients.

AIM: To investigate the prevalence of gallstone disease (GSD) and to evaluate the risk of symptomatic GSD among diabetic patients. METHODS: The study was conducted by analyzing the National Health Research Institutes (NHRI) dataset of ambulatory care patients, inpatient claims, and the updated registry of beneficiaries from 2000 to 2008. A total of 615,532 diabetic patients without a prior history of hospital treatment or ambulatory care visits for symptomatic GSD were identified in the year 2000. Age- and gender-matched control individuals free from both GSD and diabetes from 1997 to 1999 were randomly selected from the NHIR database (n = 614,871). The incidence densities of symptomatic GSD were estimated according to the subjects' diabetic status. The distributions of age, gender, occupation, income, and residential area urbanization were compared between diabetic patients and control subjects using Cox proportion hazards models. Differences between the rates of selected comorbidities were also assessed in the two groups. RESULTS: Overall, 60,734 diabetic patients and 48,116 control patients developed symptomatic GSD and underwent operations, resulting in cumulative operation rates of 9.87% and 7.83%, respectively. The age and gender distributions of both groups were similar, with a mean age of 60 years and a predominance of females. The diabetic group had a significantly higher prevalence of all comorbidities of interest. A higher incidence of symptomatic GSD was observed in females than in males in both groups. In the control group, females under the age of 64 had a significantly higher incidence of GSD than the corresponding males, but this difference was reduced with increasing age. The cumulative incidences of operations for symptomatic GSD in the diabetic and control groups were 13.06 and 9.52 cases per 1000 person-years, respectively. Diabetic men exhibited a higher incidence of operations for symptomatic GSD than did their counterparts in the control group (12.35 vs 8.75 cases per 1000 person-years). CONCLUSION: The association of diabetes with increased symptomatic GSD may provide insight to the treatment or management of diabetes in clinical settings.

Novel biomarkers predict liver fibrosis in hepatitis C patients: alpha 2 macroglobulin, vitamin D binding protein and apolipoprotein AI.

BACKGROUND: The gold standard of assessing liver fibrosis is liver biopsy, which is invasive and not without risk. Therefore, searching for noninvasive serologic biomarkers for liver fibrosis is an importantly clinical issue. METHODS: A total of 16 healthy volunteers and 45 patients with chronic hepatitis C virus (HCV) were enrolled (F0: n = 16, F1: n = 7, F2: n = 17, F3: n = 8 and F4: n = 13, according to the METAVIR classification). Three serum samples of each fibrotic stage were analyzed by two-dimension difference gel electrophoresis (2D-DIGE). The differential proteins were identified by the cooperation of MALDI-TOF/TOF and MASCOT; then western blotting and Bio-Plex Suspension Array were used to quantify the protein levels. RESULTS: Three prominent candidate biomarkers were identified: alpha 2 macroglobulin (A2M) is up regulated; vitamin D binding protein (VDBP) and apolipoprotein AI (ApoAI) are down regulated. The serum concentration of A2M was significantly different among normal, mild (F1/F2) and advanced fibrosis (F3/F4) (p < 0.01). The protein levels of VDBP and ApoAI were significantly higher in normal/mild fibrosis, when compared to those in advanced fibrosis (both p < 0.01). CONCLUSIONS: This study not only reveals three putative biomarkers of liver fibrosis (A2M, VDBP and ApoAI) but also proves the differential expressions of those markers in different stages of fibrosis. We expect that combination of these novel biomarkers could be applied clinically to predict the stage of liver fibrosis without the need of liver biopsy.