Management of Bone Defects in Orthopedic Trauma.

Treatment of traumatic bone defects is dictated by a multitude of clinical factors including the defect size, patient comorbidities, soft tissue condition, and the possibility of infection present in the defect. With a variety of treatment strategies described, it is critical to choose the approach that will maximize outcomes in addressing this difficult problem. When addressing small-scale defects, bone grafting is the primary treatment.

Regulation of regional norepinephrine spillover in heart failure: the effect of angiotensin II and beta-adrenergic agonists in the forearm circulation.

Background: Prejunctional receptors for angiotensin II (A-II) and norepinephrine (NE) have been reported to facilitate NE release. If operative in patients with congestive heart failure (CHF), such receptors could participate in positive feedback cycles amplifying sympathoactivation.

Methods And Results: A-II and isoproterenol (ISO) would increase regional NE spillover via facilitation of presynaptic release of NE in the forearm circulation of patients with chronic stable CHF.

Cardiac troponin I and creatine kinase-MB mass to rule out myocardial injury in hospitalized patients with renal insufficiency.

Serum cardiac troponin I measurement is preferred to creatine kinase-MB mass for the diagnosis of acute myocardial infarction in patients with renal insufficiency. Unexplained increases in cardiac troponin I in this population requires further evaluation and close follow-up.

Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle.

Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT.