Purpose:The conventional volumetric approaches of measuring cardiac function are loaddependent, and are not able to discriminate functional changes in the infarct, transition and remote myocardium. We examined phase-dependent regional mechanical changes in the infarct, transition and remote regions after acute myocardial infarction (MI) in a preclinical mouse model using cardiovascular magnetic resonance imaging (CMR). Methods:We induced acute MI in six mice with left anterior descending coronary artery ligation. We then examined cardiac (infarct, transition and remote-zone) morphology and function utilizing 9.4 T high field CMR before and 2 weeks after the induction of acute MI. Myocardial scar tissue was evaluated by using CMR with late gadolinium enhancement (LGE). After determining global function through volumetric analysis, regional wall motion was evaluated by measuring wall thickening and radial velocities. Strain rate imaging was performed to assess circumferential contraction and relaxation at the myocardium, endocardium, and epicardium.Results: There was abnormal LGE in the anterior walls after acute MI suggesting a successful MI procedure. The transition zone consisted of a mixed signal intensity, while the remote zone contained viable myocardium. As expected, the infarct zone had demonstrated severely decreased myocardial velocities and strain rates, suggesting reduced contraction and relaxation function. Compared to pre-infarct baseline, systolic and diastolic velocities (v S and v D ) were significantly reduced at the transition zone (v S : −1.86±0.16 cm/s vs −0.68±0.13 cm/s, P < 0.001. v D : 1.86±0.17 cm/s vs 0.53±0.06 cm/s, P < 0.001) and remote zone (v S : −1.86±0.16 cm/s vs −0.65±0.12 cm/s, P < 0.001. v D : 1.86±0.16 cm/s vs 0.51±0.04 cm/s, P < 0.001). Myocardial peak systolic and diastolic strain rates (SR S and SR D ) were significantly lower in the transition zone

Angiogenesis plays a key role in the initiation of growth and metastatic process in cancers. The angiogenic switch may be one of the earliest events in conferring a metastatic potential to the tumor. Further evolution in this multi-step cascade is controlled by the positive and negative regulators of angiogenesis. Recent advances in molecular biology have given a better insight into the mechanisms governing head neck cancer with promising data elaborating the role of angiogenesis. Metastasis to neck nodes is a very important determinant of prognosis, and is more frequently encountered than distant metastasis in head and neck cancers. Systematic PUBMED search of English-language literature of studies involving humans between 1990 and 2008 using the Mesh terms 'pathologic neovascularization', 'head and neck neoplasms', 'lymphatic metastasis' was performed. Quality assessment of selected studies included clinical pertinence, publication in peer reviewed journals, adequate number of enrolled patients. The present article reviews the utility value of various angiogenic parameters and markers that have been utilized to predict regional metastasis including micro vessel density, positive and negative regulators of angiogenesis, and genetic markers for angiogenesis. Although there seems promising preclinical and clinical evidence paving way for novel diagnostic and therapeutic interventions, the implicit role of angiogenesis in metastatic head and neck cancers needs further substantiation.

FTO is superior to PTO for the treatment of amblyopia. The greatest amount of improvement in visual acuity was seen in simple myopes and the least in simple hyperopes. Compliance is critical for successful treatment of amblyopia.

Background: Myocardial Gal3 (galectin-3) expression is associated with cardiac inflammation and fibrosis. Increased Gal3 portends susceptibility to heart failure and death. There are no data reporting the causative role of Gal3 to mediate cardiac fibro-inflammatory response and heart failure. Methods: We developed a cardioselective Gal3 gain-of-function mouse ( Gal3+/+ ) using α-myosin heavy chain promotor. We confirmed Gal3-transgene expression with real-time polymerase chain reaction and quantified cardiac/circulating Gal3 with Western blot and immunoassays. We used echocardiogram and cardiac magnetic resonance imaging to measure cardiac volumes, function, and myocardial velocities. Ex vivo, we studied myocardial inflammation/fibrosis and downstream TGF (transforming growth factor) β1-mRNA expression. We examined the effects of acute myocardial ischemia in presence of excess Gal3 by inducing acute myocardial infarction in mice. Two subsets of mice including mice treated with N-acetyl-seryl-aspartyl-lysyl-proline (a Gal3-inhibitor) and mice with genetic Gal3 loss-of-function ( Gal3 −/−) were studied for comparative analysis of Gal3 function. Results: Gal3+/+ mice had increased cardiac/circulating Gal3. Gal3+/+ mice showed excess pericardial fat pad, dilated ventricles and cardiac dysfunction, which was partly normalized by N-acetyl-seryl-aspartyl-lysyl-proline. Cardiac magnetic resonance imaging showed reduced myocardial contractile velocities in Gal3+/+ . The majority of Gal3+/+ mice did not survive acute myocardial infarction, and the survivors had profound cardiac dysfunction. Myocardial histology of Gal3+/+ mice showed macrophage/mast-cell infiltration, fibrosis and higher TGFβ1-mRNA expression, which were mitigated by both Gal3 gene deletion and N-acetyl-seryl-aspartyl-lysyl-proline administration. Conclusions: Our study shows that cardioselective Gal3 overexpression leads to multiple cardiac phenotypic defects including ventricular dilation and cardiac dysfunction. Pharmacological Gal3 inhibition conferred protective effects with reduction of inflammation and fibrosis. Our study highlights the importance of translational studies to counteract Gal3 function and prevent cardiac dysfunction.

Cardiac amyloidosis (CA) is a common and potentially fatal infiltrative cardiomyopathy. Contrast-enhanced cardiac MRI (CMR) is used as a diagnostic tool. However, utility of CMR for the comprehensive analysis of biventricular strains and strain rates is not reported as extensively as echocardiography. In addition, RV strain analysis using CMR has not been described previously. Objectives: We sought to study the global and regional indices of biventricular strain and strain rates in endomyocardial biopsy (EMB)-proven, genotyped cases of CA. Methods: A database of 80 EMBs was curated from 2012 to 2019 based on histology. A total of 19 EMBs positive for CA were subjected to further tissue-characterization with histology, and compared with four normal biopsy specimens. Samples were genotyped for ATTR- or AL-subtypes. Five patients, with both echocardiography and contrast-enhanced CMR performed 72-h apart, were subjected to comprehensive analysis of biventricular strain and strain-rates. Results: Histology confirmed that the selected samples were indeed positive for cardiac amyloid. Echocardiography showed reduced global and regional left-ventricular (LV) longitudinal strain indices. CMR with tissue-characterization of LV showed global reductions in circumferential, radial and longitudinal strains and strain-rates, following a general trend with the echocardiographic findings. The basal right-ventricular (RV) segments had reduced circumferential strains with no changes in longitudinal strain. Conclusions: In addition to providing a clinical diagnosis of CA based on contrast clearance-dynamics, CMR can be a potent tool for accurate functional assessment of global and regional changes in strain and strain-rates involving both LV and RV. Further studies are warranted to validate and curate the strain imaging capacity of CMR in CA.