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Accumulating evidence suggests insulin and insulin signaling may be involved in the pathophysiology of Alzheimer disease (AD). The relationship between insulin-mediated glucoregulation and brain structure has not been assessed in individuals with AD.Nondemented (Clinical Dementia Rating [CDR] 0, n = 31) and early stage AD (CDR 0.5 and 1, n = 31) participants aged 65 years and older had brain MRI to determine whole brain and hippocampal volume and 3-hour IV glucose tolerance tests to determine glucose and insulin area under the curve (AUC). Linear regression models were used to assess the relationship of insulin and glucose with brain volume, cognition, and dementia severity.In early AD, insulin and glucose AUCs were related to whole brain (insulin beta = 0.66, p0.001; glucose beta = 0.45, p0.01) and hippocampal volume (insulin beta = 0.42, p0.05; glucose beta = 0.46, p0.05). These relationships were independent of age, sex, body mass index, body fat, cardiorespiratory fitness, physical activity, cholesterol, and triglycerides. Insulin AUC, but not glucose, was associated with cognitive performance in early AD (beta = 0.40, p = 0.04). Insulin AUC was associated with dementia severity (Pearson r = -0.40, p = 0.03). Glucose and insulin were not related to brain volume or cognitive performance in nondemented individuals.Increased peripheral insulin is associated with reduced Alzheimer disease (AD)-related brain atrophy, cognitive dysfunction, and dementia severity, suggesting that insulin signaling may play a role in the pathophysiology of AD.

Greenstick fractures suffered during growth have a high risk for refracture and posttraumatic deformity, particularly at the forearm diaphysis. The use of a preemptive completion of the fracture by manipulation of the concave cortex is controversial and data supporting this approach are few.Aim of this study was to determine the factors which predispose to refracture and deformities, and to define therapeutic strategies.We prospectively gathered clinical and radiographic data over a period of one year on greenstick fractures of the middle third of the forearm in children as part of a multi-centre study. Endpoint was a follow-up visit at one year. Radiographic deformity, state of consolidation at resumption of physical activities and refracture rate were analysed statistically (ANOVA, Student's t-test and Pearson's chi-square test) with regard to patient age, gender, fracture type, therapy and time in plaster.We collected the data of 103 patients (63 boys, 40 girls), average age 6.6 years (1.3-14.5 years), the vast majority of whom had a combined greenstick fracture of the radius and ulna. 6.7% of the patients sustained a refracture within 49 days (29-76) after plaster removal. They were significantly older (p=0.017) with a significantly higher incidence of manual completion of the fracture with radiographic signs of partial consolidation (p=0.025). Residual deformities were significantly smaller after completion of the fracture compared to reduction without completion (p=0.019) or plaster fixation alone (p0.005).Completion of a greenstick fracture does not prevent refracture. Nevertheless, it diminishes the extent of secondary deformities in cases where the primary angulation exceeds the remodelling capacity. Prevention of refracture should include a routine radiographic follow-up 4-6 weeks after injury with continuation of plaster fixation in cases of partial consolidation.

Von Mai 1996 bis Marz 2001 wurden 204 Kinder mit 261 Hamangiomen behandelt und nach Regression nachkontrolliert. Sie wurden operativ, mit Laser und adjuvant mit Interferon therapiert. Die Indikation fur die einzelne Therapieform wird dargestellt. Der Neodym-Yag-Laser (1064nm) wurde in percutaner, interstitieller und direkter Technik angewandt. 131 Patienten wurden einmal gelasert,63 Patienten 2-5 mal. 5 Patienten hatten eine zusatzliche Therapie mit Interferon bzw. Corticosteroid. Bei 180 Kindern konnte das Wachstum durch die Lasertherapie zuverlassig gestoppt werden. 10 Patienten wurden primar, 14 sekundar operativ korrigiert. Die fruhe Lasertherapie kann die Ausbreitung in der Regel verhindern, die adjuvante Interferontherapie scheint bei speziellen aggressiv wachsenden Formen hilfreich, die Volumenreduktion vor der Operation sinnvoll.

The acute respiratory distress syndrome (ARDS) frequently results in a fibroproliferative response that precludes effective alveolar repair. Transforming growth factor-alpha (TGF-alpha), a potent epithelial and mesenchymal cell mitogen, may modulate the response to lung injury. In this study, we determined whether bronchoalveolar lavage fluid (BALF) concentrations of TGF-alpha are increased during the first 2 wk after the onset of ARDS and, if so, whether increased TGF-alpha levels in lavage fluid are associated with increased levels of procollagen peptide III (PCP III), a biological marker of fibroproliferation, and with increased fatality rates. We enrolled 74 consecutive patients with ARDS prospectively identified on admission to the intensive care unit of a tertiary care hospital, and 11 patients with chronic interstitial lung disease. Thirteen healthy volunteers served as control subjects. TGF-alpha concentrations were measured in BALF recovered on Days 3, 7, and 14 after the onset of ARDS (total of 130 lavage samples). TGF-alpha was detected in the lavage fluid of 90% of patients with ARDS (67 of 74), and in 100% of patients with idiopathic pulmonary fibrosis (IPF) (10 of 10), but in none of 13 normal volunteers. At each day tested, the median lavage TGF-alpha level of patients with ARDS was significantly higher than that of normals. The overall fatality rate was 45% (33 of 74 patients). In a univariate analysis, the median TGF-alpha levels in nonsurvivors were 1.5-fold higher at Day 7 (p = 0.06) and 1.8-fold higher at Day 14 (p = 0.048). The fatality rate was 4 times higher (CI 1.6, 17.5) for patients with both increased lavage TGF-alpha and PCP III concentrations at Day 7 than for patients with low TGF-alpha and PCP III values, indicating a synergistic relationship between TGF-alpha and PCP III. We conclude that increased levels of TGF-alpha in BALF are common in patients with ARDS and that lavage TGF-alpha is associated with a marker of the fibroproliferative response in sustained ARDS.

Lung transplantation has recently offered hope for prolonged survival in patients with cystic fibrosis. Patients with cystic fibrosis have a 7% prevalence of associated liver disease and portal hypertension. These patients have been previously excluded from consideration for lung transplantation. The natural history of cystic fibrosis-associated liver disease suggests a benign and protracted course in most cases. At the University of Washington, 14 of 53 patients (26%) have undergone lung transplantation for cystic fibrosis-related respiratory failure. We report the outcome of double lung transplantation in four of these 14 patients who also had cystic fibrosis-associated liver disease and portal hypertension, all of whom were symptom free from their liver disease. All four patients are alive and well without complications 4 to 31 months after transplantation. We conclude that the presence of cystic fibrosis-associated liver disease with portal hypertension, in the setting of good synthetic function (albumin3.0 gm/L and normal prothrombin time), normal serum bilirubin, minimal varices, without ascites or encephalopathy, should not be an absolute contraindication to lung transplantation. We recommend that other transplantation centers also include this patient population in consideration for lung transplantation.

A 70-year-old woman developed ventricular fibrillation subsequent to initiation of phentermine therapy. She was hospitalised and experienced recurrent ventricular fibrillation. During cardiac catheterisation, she was found to have a right coronary artery vasospasm, which resolved with intravenous nitroglycerin. Her phentermine was discontinued and the patient remained symptom free at last follow-up.

1,3-Butanediol is an ethanol dimer that induces systemic ketosis. It has previously been shown to increase hypoxic survival time and reduce neurologic deficit in several experimental preparations. The aim of this study was to determine if the mechanism of 1,3-butanediol-induced cerebral protection was elevation of blood ketone levels, blood glucagon levels, or both. Blood beta-hydroxybutyrate levels, glucagon levels, or both produced by a previously reported protective dose of 1,3-butanediol (47 mmol/kg) were simulated by direct i.v. infusion of the ketone beta-hydroxybutyrate and glucagon separately and in combination, and the effect on hypoxic survival time in instrumented Levine rats (unilateral carotid ligation and hypoxic exposure) was determined. To test if the mechanism was a direct or osmotic effect of the alcohol, an equimolar dose of ethanol (47 mmol/kg) was administered and the effect on hypoxic survival time was compared with that produced by 1,3-butanediol. As in previous studies, 1,3-butanediol significantly increased hypoxic survival time (241% of control, Scheffe p less than 0.05). Various doses of beta-hydroxybutyrate and glucagon were infused to approximate the blood levels of beta-hydroxybutyrate and glucagon produced by a protective dose of 1,3-butanediol. Although beta-hydroxybutyrate or glucagon infusions produced blood levels of these substances that were comparable with those produced by administering butanediol, they failed to prolong hypoxic survival time as long as 1,3-butanediol. No correlation was detected between hypoxic survival time and blood levels of beta-hydroxybutyrate, glucagon, insulin, or glucose. An equimolar dose of ethanol did not significantly increase hypoxic survival time.(ABSTRACT TRUNCATED AT 250 WORDS)