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There is no consensus about the ideal method for diagnosis in patients who have already undergone endoscopic ultrasound fine needle aspiration (EUS-FNA), and the inconclusive material is often obtained. The aim was to evaluate the diagnostic yield of the second EUS-FNA of pancreatic lesions.', 'A retrospective analysis of prospectively collected data of patients with EUS-FNA of pancreatic lesions is performed. All patients who underwent more than one EUS-FNA for the evaluation of suspected pancreatic cancer over a 7-year period were included in the analysis.', 'A total of 296 EUS-FNAs of the pancreas were performed in 257 patients. The diagnostic yield with the first EUS-FNA was 78.6% (202/257). Thirty-nine (13.3%) FNAs were repeated in 34 patients; 17 (50%) patients were women. The mean ± standard deviation (SD) age was 58.8 ± 16.1 years. The location of the lesions in the pancreatic gland, from which the second biopsies were taken, was head of the pancreas, n = 28 (82.4%), body of the pancreas, n = 3 (8.8%), and tail, n = 3 (8.8%). The mean ± SD of the size of the lesion was 36.3 ± 14.6 mm. The second EUS-FNA was more likely to be positive for diagnosis in patients with an "atypical" histological result in the first EUS-FNA (odds ratio [OR]: 4.04; 95% confidence interval [CI]: 0.9-18.3), in contrast to patients with a first EUS-FNA reported as "normal" (OR: 0.21; 95% CI: 0.06-0.71). Overall, the diagnostic yield of the second EUS-FNA was 58.8% (20/34) with an increase to 86.3% overall (222/257).
Is repeat endoscopic ultrasound fine needle aspiration after a first negative procedure useful in pancreatic lesions?

The relationship of bipolar disorder (BD) and altered thyroid function is increasingly recognized. Recently, a behavioral phenotype of co-occurring deviance on the Anxious/Depressed (A/D), Attention Problems (AP), and Aggressive Behavior (AB) syndrome scales has been identified as the Child Behavior Checklist Dysregulation Profile (CBCL-DP), which itself has been linked to BD. This study tested for differences in thyroid function within a sample of n=114 psychiatric children and adolescents with and without the CBCL-DP.', 'A CBCL-DP score was generated based on the composite of the crucial CBCL syndrome scales (A/D, AP, AB). Participants with a CBCL-DP score >or=2.5 SDs above average constituted the CBCL-DP subgroup (n=53). Those with CBCL-DP scores of 1 SD or less above average percentile were regarded as controls (n=61). Groups were compared regarding serum levels of TSH, fT3 and fT4.', 'In participants showing the CBCL-DP, basal serum TSH was elevated compared to controls. More CBCL-DP subjects than controls showed subclinical hypothyroidism. No differences were observed for serum fT3 and fT4 levels.
Is severe affective and behavioral dysregulation in youth associated with increased serum TSH?

In vivo differentiation of cardiac myocytes is associated with downregulation of the glucose transporter isoform GLUT1 and upregulation of the isoform GLUT4. Adult rat cardiomyocytes in primary culture undergo spontaneous dedifferentiation, followed by spreading and partial redifferentiation, which can be influenced by growth factors. We used this model to study the signaling mechanisms modifying the expression of GLUT4 in cardiac myocytes.', 'Adult rat cardiomyocytes in primary culture exhibited spontaneous upregulation of GLUT1 and downregulation of GLUT4, suggesting resumption of a fetal program of GLUT gene expression. Treatment with IGF-1 and, to a minor extent, FGF-2 resulted in restored expression of GLUT4 protein and mRNA. Activation of p38 MAPK mediated the increased expression of GLUT4 in response to IGF-1. Transient transfection experiments in neonatal cardiac myocytes confirmed that p38 MAPK could activate the glut4 promoter. Electrophoretic mobility shift assay in adult rat cardiomyocytes and transient transfection experiments in neonatal cardiac myocytes indicated that MEF2 was the main transcription factor transducing the effect of p38 MAPK activation on the glut4 promoter.

Is regulation of glucose transporter expression in cardiac myocytes : p38 MAPK a strong inducer of GLUT4?