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Vs Group (v + group)
Selected AbstractsLong-Term Effect of Incadronate Disodium (YM-175) on Fracture Healing of Femoral Shaft in Growing RatsJOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2001Chaoyang Li Abstract The aim of this study was to investigate the long-term effect of incadronate on fracture healing of the femoral shaft in rats. Female Sprague-Dawley 8-week-old rats were injected subcutaneously (sc) with either vehicle (V group) or two doses of incadronate (10 ,g/kg and 100 ,g/kg) three times a week for 2 weeks. Right femoral diaphysis was then fractured and fixed with intramedullary stainless wire. Just after fracture, incadronate treatment was stopped in pretreatment groups (P groups: P-10 and P-100) or continued in continuous treatment groups (C groups: C-10 and C-100). All rats were killed at 25 weeks or 49 weeks after surgery. Fractured femur was evaluated radiologically and mechanically and then stained in Villanueva bone stain and embedded in methyl methacrylate. Undecalcified cross-sections from the fracture area were evaluated microradiologically and histomorphometrically. Radiographic observation showed that the fracture line disappeared in all groups. Cross-sectional area in the C-100 group was the biggest among all groups and in the C-10 group was larger than that in the V group at 25 weeks. Histological and histomorphometric observations showed that the process of fracture healing was delayed under continuous treatment with incadronate as evidenced by the delay of both lamellar cortical shell formation and resolution of original cortex in C groups. Percent linear labeling perimeter, mineral apposition rate (MAR), and bone formation rate (BFR) in C groups significantly decreased compared with the other groups, indicating that the callus remodeling was suppressed under continuous treatment, especially with a high dose. Mechanical study showed that the stiffness and ultimate load of the fractured femur in the C 100 group were the highest among all groups at both 25 weeks and 49 weeks. In conclusion, this study showed that long-term continuous treatment with incadronate delayed the process of fracture healing of femur in rats, especially under high dose but it did not impair the recovery of mechanical integrity of the fracture. [source] Left Ventricular Lead Proximity to an Akinetic Segment and Impact on Outcome of Cardiac Resynchronization TherapyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2006DANIEL ARZOLA-CASTANER M.D. Background: Previous studies report that the optimal pacing site for cardiac resynchronization therapy (CRT) is along the left ventricular (LV) lateral and postero-lateral (PL) wall. However, little is known regarding whether pacing over an akinetic site impacts the contractile response and long-term outcome from CRT. Methods and Results: A total of 38 patients with ischemic cardiomyopathy were studied for their acute hemodynamic and 12-month clinical response to CRT. The intraindividual percentage change in dP/dt (%,dP/dt), over baseline, was derived from the mitral regurgitation (MR) Doppler profile with CRT on versus off. Two-dimensional echocardiography was used for myocardial segmentation and determinination of akinetic sites. LV lead implant site was determined using angiographic and radiographic data and categorized as being "on" (group 1) or "off" (group 2) an akinetic site. Long-term response was measured as a combined endpoint of hospitalization for heart failure and/or all cause mortality at 12 months. Time to primary endpoint was estimated by the Kaplan-Meier method. Clinical characteristics and acute hemodynamic response was similar in both (group 1 [n = 14]; %,dP/dt 48.8 ± 67.4% vs group 2 [n = 24]; %,dP/dt 32.2 ± 40.1%, P = 0.92). No difference in long-term outcome was observed (P = 0.59). In contrast, lead placement in PL or mid-lateral (ML) positions was associated with a better acute hemodynamic response when compared to antero-lateral (AL) positions (PL, %,dP/dt 45.7 ± 50.7% and ML, %,dP/dt 45.1 ± 58.8% vs AL, %,dP/dt 2.9 ± 30.9%, respectively, P = 0.014). Conclusion: LV lead proximity to an akinetic segment does not impact acute hemodynamic or 12-month clinical response to CRT. [source] An evaluation of transient elastography in the discrimination of HBeAg-negative disease from inactive hepatitis B carriersJOURNAL OF VIRAL HEPATITIS, Issue 11 2009S. Maimone Summary., Liver biopsy is frequently required in HBeAg-negative disease to determine the stage of fibrosis. It can be difficult to distinguish cohorts with undetectable HBeAg who may have varying degrees of fibrosis due to different stages of disease. We have assessed the utility of transient elastography (TE) to evaluate differences in HBeAg-negative patients. A total of 220 HBsAg-positive individuals were studied: 125 (group 1) had an inactive HBsAg carrier state and 95 (group 2) were HBeAg-negative, anti-HBe-positive patients with persistently or intermittent elevation of alanine aminotransferase (ALT) and/or HBV DNA >105 copies/mL. Mean stiffness was 4.83 ± 1.2 kPa in group 1 vs 8.53 ± 6 kPa in group 2 (P < 0.001); statistically significant differences were also found between AST/ULN ALT/ULN ratios, HBV DNA in group 1 vs group 2, respectively (P < 0.001). In the multivariate analysis, the only variable independently associated with the stage of fibrosis was the stiffness. This study shows that mean hepatic stiffness by elastography is significantly lower in patients with inactive hepatitis B compared to those with HBeAg-negative disease. The procedure is a useful adjunct to diagnosis to confirm a clinical pattern of disease, and for more selective use of liver biopsy before considering antiviral therapy. [source] Ascites after liver transplantation,A mysteryLIVER TRANSPLANTATION, Issue 5 2004Charmaine A. Stewart Ascites after liver transplantation, although uncommon, presents a serious clinical dilemma. The hemodynamic changes that support the development of ascites before liver transplantation are resolved after transplant; therefore, persistent ascites (PA) after liver transplantation is unexpected and poorly characterized. The aim of this study was to define the clinical factors associated with PA after liver transplantation. This was a retrospective case,control analysis of patients who underwent liver transplantation at the University of Pennsylvania. PA occurring for more than 3 months after liver transplantation was confirmed by imaging studies. PA was correlated with multiple recipient and donor variables, including etiology of liver disease, preoperative ascites, prior portosystemic shunt (PS), donor age, and cold ischemic (CI) time. There were 2 groups: group 1, cases with PA transplanted from November 1990 to July 2001, and group 2, consecutive, control subjects who underwent liver transplantation between September 1999 and December 2001. Both groups were followed to censoring, May 2002, or death. Twenty-five from group 1 had ascites after liver transplantation after a median follow-up of 2.6 years. In group 1 vs group 2 (n = 106), there was a male predominance 80% vs 61% (P = .10) with similar age 52 years; chronic hepatitis C virus (HCV) was diagnosed in 88% vs 44% (P < .0001); preoperative ascites and ascites refractory to treatment were more prevalent in group 1 (P = .0004 and P =.02, respectively), and CI was higher in group 1, (8.5 hours vs 6.3 hours, P = .002). Eight of the 25 (group 1) had portal hypertension with median portosystemic gradient 16.5 mm Hg (range, 16,24). PS was performed in 7 of 25 cases, which resulted in partial resolution of ascites. The development of PA after liver transplantation is multifactorial; HCV, refractory ascites before liver transplantation, and prolonged CI contribute to PA after liver transplantation. (Liver Transpl 2004;10:654,660.) [source] | ||||||||||