Microtopography of titanium suppresses osteoblastic differentiation but enhances chondroblastic differentiation of rat femoral periosteum-derived cells

Despite the clinical fact that endosseous titanium implants directly contacts periosteum, the behavior and response of the periosteum-derived cells to surface topography of titanium have rarely been studied. This study examines the effect of titanium surface microtopography on osteoblastic and possibly-modulated chondroblastic phenotypes of femoral periosteum-derived cells. Rat femoral periosteum-derived cells were cultured on either relatively smooth, machined titanium surface or acid-etched, micro-roughened titanium surface. The osteoblastic gene expressions, including collagen I, osteopontin and osteocalcin, were downregulated on the acid-etched surface, compared with the machined surface. Alkaline phosphatase and mineralization activities on the acid-etched surface were approximately 20% of those on the machined surface. Instead, chondroblastic specific genes, including collagen II and IX, and sox 9, were exclusively expressed or highly upregulated on the acid-etched surface. Alcian blue stain revealed an extensive deposition of glycosaminoglycan on the acid-etched surface. The cultured matrix on the acid-etched surface lacked the submicron globular structures that were extensively seen on the machined surface, and contained a remarkably increased percentage of sulfur relative to calcium compared with the culture on the machined surface. These results indicated that titanium microroughness suppresses the osteoblastic phenotype and induces or at least considerably enhances the chondroblastic phenotype of the periosteal cells, suggesting the unique role of titanium surface topography in regulating the periosteal cell differentiation. The suppressive effect of titanium microroughness on the periosteal cells toward the osteoblastic linage was contrasted to the known promotive effect on the bone marrow-derived osteoblasts.     

An initial analysis of preoperative serum CA 125 levels in patients with early stage ovarian carcinoma

Preoperative serum CA 125 levels were determined for 36 patients with Stage I and II ovarian carcinoma. Levels ranged from 9 to 1962 U/ml with a mean of 216 U/ml. In Stage I patients, CA 125 levels averaged 133 U/ml and in Stage II patients 382 U/ml. Nine of 24 Stage I (38%) and 9 of 12 Stage II patients (75%) had CA 125 levels in excess of 65 U/ml in a population somewhat overrepresented in mucinous tumors. Patients with non-mucinous neoplasms had CA 125 elevations more often--in 75% of the cases--than those with mucinous tumors. A larger study will be required to more precisely estimate the fraction of early stage patients with elevated preoperative serum CA 125 levels; however, this investigation demonstrates an assay sensitivity minimally adequate to initiate a pilot evaluation of serum CA 125 levels in a population at risk for ovarian carcinoma.     

Recurrent low output syndrome after the weaning from mechanical circulatory support for postcardiotomy cardiogenic shock

We reviewed the cases of recurrent low output syndrome (LOS) after the weaning from mechanical circulatory support for postcardiotomy cardiogenic shock. Twelve patients were divide into 2 groups according to whether low output syndrome recurred or not, consisting of a recurrent low output syndrome (+) group [re-LOS (+) group, n = 6] and a recurrent low output syndrome (-) group [re-LOS (-) group, n = 6]. Between 2 groups, there was no statistical difference in preoperative left ventricular ejection fraction (LVEF), aortic closs-clamping time and cardiac index at the weaning from mechanical circulatory support. Only the LVEF at the weaning in the re-LOS (+) group was significantly less than that in the re-LOS (-) group (0.39 +/- 0.08 vs 0.62 +/- 0.19, p < 0.05). All patients in the re-LOS (-) group survived to discharge, while in the re-LOS (+) group, although 3 patients were re-supported by intra-aortic balloon pumping, 4 of 6 patients died of multiple organ failure and 2 survivors were in New York Heart Association class III. The results suggest that the key to survive to discharge after the weaning from mechanical circulatory support is whether the cardiac contraction could recover or not.     

The proliferative response of p53 knock-out mouse-derived vascular smooth muscle cell line, P53LMAC01, to PDGF, when compared with human aortic smooth muscle cells

To develop an in vitro experimental model of vascular smooth muscle cell hyperplasia, a major feature in chronic cardiac rejection, we studied a novel vascular smooth muscle cell line, P53LMAC01 (AC01), which was established from aortic smooth muscles of p53 knock-out mice, to determine its response to a platelet-derived growth factor (PDGF) and to Cyclosporin A (CsA). The responses were compared with those of human aortic smooth muscle cells (AOSMC). The AC01 exhibited a distinct proliferative response to PDGF similar to that of AOSMC under serum-free conditions. 10 ng/ml of PDGF-BB increased by a factor of 4.5 and PDGF-AB doubled the thymidine uptake, but PDGF-AA caused only a slight increase. The proliferation was markedly inhibited by 10(-6) M of CsA but less affected by 10(-7) M. These results indicate that the AC01 cell line could provide a convenient experimental system for investigating chronic rejection in vitro and that the system might work as a screening model of agents for treating transplant-related arteriosclerosis.     

Prognostic value of nonlinear heart rate dynamics in hemodialysis patients with coronary artery disease

BACKGROUND: Although altered nonlinear heart rate dynamics predicts death in patients with coronary artery disease (CAD), its prognostic value in chronic hemodialysis patients with CAD is unknown. METHODS: We analyzed 24-hour electrocardiogram for nonlinear heart rate dynamics and heart rate variability in a retrospective cohort of 81 chronic hemodialysis patients with CAD. RESULTS: During a follow-up period of 31 +/- 20 months, 19 cardiac and 8 noncardiac deaths were observed. Cox hazards model, including diabetes, left ventricular ejection fraction, and the number of diseased coronary arteries, revealed that abnormal alpha2 (defined as both increase and decrease in alpha2 because of its J curve relationship with cardiac mortality), decreased approximate entropy and decreased heart rate variability (triangular index and ultra-low frequency power) were significant and independent predictors of cardiac death. No significant and independent predictive power for noncardiac death was observed in either the heart rate dynamics or the heart rate variability measures. The predictive power of alpha2 and approximate entropy was independent of that of triangular index and ultra-low frequency power. Combinations of two categories of measures improved the predictive accuracy; overall accuracy of approximate entropy + ultra-low frequency power for cardiac death was 87%. CONCLUSION: Altered nonlinear heart rate dynamics are independent predictors of cardiac death in chronic hemodialysis patients with CAD and their combinations with decreased heart rate variability provide clinically useful markers for risk stratification.