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Calcified amorphous tumor of the heart in an adult female: a case report

<p>Abstract</p> <p>Introduction</p> <p>Cardiac calcified amorphous tumor is a rare, non-neoplastic intra-cavity cardiac mass composed of calcium deposits in a background of amorphous degenerating fibrinous material. Only a few cases of this rare lesion have been reported in the available literature. Clinico-pathological differentiation of this lesion from calcified atrial myxoma, calcified thrombi or other cardiac neoplasms is extremely difficult; hence pathologic examination is the mainstay of diagnosis. To the best of our knowledge this entity has not been reported in the Indian literature.</p> <p>Case presentation</p> <p>A 40-year-old woman of Indian origin presented with progressive dyspnea, fatigue and cough. She was diagnosed as having a calcified right atrial mass. The mass was excised. Histologic examination revealed the mass to be composed of amorphous eosinophilic fibrin with dense calcification. No myxomatous tissue was seen and a final diagnosis of calcified amorphous tumor of the heart was rendered.</p> <p>Conclusions</p> <p>Calcified amorphous tumor is a rare cardiac lesion with an excellent outcome following complete surgical removal. Since clinico-radiologic differentiation from other cardiac masses is not possible in most cases, histopathological examination is the only modality for diagnosis. Hence, histopathologists should be aware of this rare entity in the differential diagnoses of cardiac mass.</p

Redox imbalance in peripheral blood of type 1 myotonic dystrophy patients

Objectives: The aim of our study was to determine if redox imbalance caused by the activities of antioxidant enzymes existed in erythrocytes of type 1 myotonic dystrophy ( DM1) patients. Methods: The activities of erythrocyte superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were measured in 30 DM1 patients and 15 healthy controls ( HCs). The obtained values were correlated with the Muscular Impairment Rating Scale ( MIRS) score and creatine kinase ( CK). Results: Superoxide dismutase and catalase activities were lower in DM1 patients compared to HCs. A positive correlation was found between disease duration and MIRS score as well as with glutathione reductase activity. In DM1 patients, there were positive correlations between catalase, glutathione peroxidase, and glutathione reductase activities. After sub-dividing DM1 patients according to CK levels, superoxide dismutase activity was still statistically different from HCs. However, catalase activity was significantly lower only in DM1 patients with increased CK. Discussion: Undesirable alterations in antioxidant enzyme activities during DM1 disease progression may result in conditions favoring oxidative stress and changes in metabolism which together could contribute to muscle wasting

Dobutamine stress echocardiography for assessing the role of dynamic intraventricular obstruction in left ventricular ballooning syndrome

<p>Abstract</p> <p>Background</p> <p>Dynamic intraventricular obstruction has been observed in patients with left ventricular ballooning syndrome (LVBS) and has been hypothesized as a possible mechanism of the syndrome. The aim of this study was to assess the prevalence and significance of dynamic intraventricular obstruction in patients with LVBS.</p> <p>Methods and Results</p> <p>Dobutamine stress echocardiography was carried out in 22 patients with LVBS (82% apical), all women, aged 68 ± 9 years. At baseline 1 patient had a > 30 mmHg LV gradient; during stress a LV gradient > 30 mm Hg developed in 6/21 patients (28%) and was caused by systolic anterior motion of the mitral valve in the 3 patients with severe gradient (mean 116 ± 29 mmHg), who developed mitral regurgitation and impaired apical wall motion and by obstruction at mid-ventricular level in the other 3 with a moderate gradient (mean 46 ± 16 mmHg). Compared with patients without obstruction those with obstruction had a greater mean septal thickness (11.6 ± .6 vs 9.8. ± 3, p < .01), a higher prevalence of septal hypertrophy (71% vs 7%, p < .005) and a higher peak wall motion score index (1.62 ± .4 vs 1.08 ± .4, p < .01).</p> <p>Conclusion</p> <p>Spontaneous or dobutamine-induced dynamic LV obstruction is documented in 32% of patients with LVBS, is correlated with the presence of septal hypertrophy and may play a role in the development of LVBS in this subset of patients. In those without septal hypertrophy a dynamic obstruction is rarely induced with dobutamine and is unlikely to be a major pathogenetic factor of the syndrome.</p

The unstructured C-terminus of the τ subunit of Escherichia coli DNA polymerase III holoenzyme is the site of interaction with the α subunit

The τ subunit of Escherichia coli DNA polymerase III holoenzyme interacts with the α subunit through its C-terminal Domain V, τC16. We show that the extreme C-terminal region of τC16 constitutes the site of interaction with α. The τC16 domain, but not a derivative of it with a C-terminal deletion of seven residues (τC16Δ7), forms an isolable complex with α. Surface plasmon resonance measurements were used to determine the dissociation constant (KD) of the α−τC16 complex to be ∼260 pM. Competition with immobilized τC16 by τC16 derivatives for binding to α gave values of KD of 7 μM for the α−τC16Δ7 complex. Low-level expression of the genes encoding τC16 and τC16▵7, but not τC16Δ11, is lethal to E. coli. Suppression of this lethal phenotype enabled selection of mutations in the 3′ end of the τC16 gene, that led to defects in α binding. The data suggest that the unstructured C-terminus of τ becomes folded into a helix–loop–helix in its complex with α. An N-terminally extended construct, τC24, was found to bind DNA in a salt-sensitive manner while no binding was observed for τC16, suggesting that the processivity switch of the replisome functionally involves Domain IV of τ

Mutations and SNPs of human cardiac sodium channel alpha subunit gene (SCN5A) in Japanese patients with Brugada syndrome

Background: Brugada syndrome is an inherited arrhythmogenic disease characterized by right bundle branch block pattern and ST segment elevation, leading to the change of V1 to V3 on electrocardiogram, and an increased risk of sudden cardiac death resulting from ventricular fibrillation. The sodium channel alpha 5 subunit (SCN5A) gene encodes a cardiac voltage-dependent sodium channel, and SCN5A mutations have been reported in Brugada syndrome. However, single nucleotide polymorphisms (SNPs) and gene mutations have not been well investigated in Japanese patients with Brugada syndrome. Methods and Results: The SCN5A gene was examined in 58 patients by using PCR and the ABI 3130xl sequencer, revealing 17 SNP patterns and 13 mutations. Of the 13 mutations, 8 were missense mutations (with amino acid change), 4 were silent mutations (without amino acid change), and one case was a mutation within the splicing junction. Six of the eight missense mutations were novel mutations. Interestingly, we detected an R1664H mutation, which was identified originally in long QT syndrome. Conclusion: We found 13 mutations of the SCN5A gene in 58 patients with Brugada syndrome. The disease may be attributable to some of the mutations and SNPs

Loss of Akt activity increases circulating soluble endoglin release in preeclampsia:identification of inter-dependency between Akt-1 and heme oxygenase-1

Aims - Endothelial dysfunction is a hallmark of preeclampsia. Desensitization of the phosphoinositide 3-kinase (PI3K)/Akt pathway underlies endothelial dysfunction and haeme oxygenase-1 (HO-1) is decreased in preeclampsia. To identify therapeutic targets, we sought to assess whether these two regulators act to suppress soluble endoglin (sEng), an antagonist of transforming growth factor-ß (TGF-ß) signalling, which is known to be elevated in preeclampsia. Methods and results - Vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor (FGF-2), angiopoietin-1 (Ang-1), and insulin, which all activate the PI3K/Akt pathway, inhibited the release of sEng from endothelial cells. Inhibition of the PI3K/Akt pathway, by overexpression of phosphatase and tensin homolog (PTEN) or a dominant-negative isoform of Akt (Aktdn) induced sEng release from endothelial cells and prevented the inhibitory effect of VEGF-A. Conversely, overexpression of a constitutively active Akt (Aktmyr) inhibited PTEN and cytokine-induced sEng release. Systemic delivery of Aktmyr to mice significantly reduced circulating sEng, whereas Aktdn promoted sEng release. Phosphorylation of Akt was reduced in preeclamptic placenta and this correlated with the elevated level of circulating sEng. Knock-down of Akt using siRNA prevented HO-1-mediated inhibition of sEng release and reduced HO-1 expression. Furthermore, HO-1 null mice have reduced phosphorylated Akt in their organs and overexpression of Aktmyr failed to suppress the elevated levels of sEng detected in HO-1 null mice, indicating that HO-1 is required for the Akt-mediated inhibition of sEng. Conclusion - The loss of PI3K/Akt and/or HO-1 activity promotes sEng release and positive manipulation of these pathways offers a strategy to circumvent endothelial dysfunction