Phospholipid composition of erythrocyte membrane under conditions of postmyocardial infarction cardiosclerosis

Changes in phospholipid composition of the erythrocyte membranes have been studied in experimental postmyocardial infarction cardiosclerosis. Erythrocyte membranes from animals with cardiosclerosis formed after experimental occlusions of coronary arteries were characterized by significant decrease of a minor phospholipid, phosphatydylinositol (by more than 40%) and the increase of the major phospholipid, phosphatydylethanolamine (by 20%). There was high content of lipid peroxidation products, malondialdehyde and conjugated dienes and the decrease in the activity of antioxidant enzymes, catalase and superoxide dismutase in blood serum of these animals. We have concluded the formation of postmyocardial infarction cardiosclerosis is accompanied by the increase of free radical reactions. This causes changes in phospholipid composition of cell membranes and the decrease of compensatory capacities of the enzymatic antioxidant system. These changes form a metabolic background, which can influence cardiac remodeling properties.     

Apelin-13 increases myocardial progenitor cells and improves repair postmyocardial infarction

Apelin is an endogenous ligand for the angiotensin-like 1 receptor (APJ) and has beneficial effects against myocardial ischemia-reperfusion injury. Little is known about the role of apelin in the homing of vascular progenitor cells (PCs) and cardiac functional recovery postmyocardial infarction (post-MI). The present study investigated whether apelin affects PC homing to the infarcted myocardium, thereby mediating repair and functional recovery post-MI. Mice were infarcted by coronary artery ligation, and apelin-13 (1 mg·kg(-1)·day(-1)) was injected for 3 days before MI and for 14 days post-MI. Homing of vascular PCs [CD133(+)/c-Kit(+)/Sca1(+), CD133(+)/stromal cell-derived factor (SDF)-1α(+), and CD133(+)/CXC chemokine receptor (CXCR)-4(+)] into the ischemic area was examined. Myocardial Akt, endothelial nitric oxide synthase (eNOS), VEGF, jagged1, notch3, SDF-1α, and CXCR-4 expression were assessed at 24 h and 14 days post-MI. Functional analyses were performed on day 14 post-MI. Mice that received apelin-13 treatment demonstrated upregulation of SDF-1α/CXCR-4 expression and dramatically increased the number of CD133(+)/c-Kit(+)/Sca1(+), CD133(+)/SDF-1α(+), and c-Kit(+)/CXCR-4(+) cells in infarcted hearts. Apelin-13 also significantly increased Akt and eNOS phosphorylation and upregulated VEGF, jagged1, and notch3 expression in ischemic hearts. This was accompanied by a significant reduction of myocardial apoptosis. Furthermore, treatment with apelin-13 promoted myocardial angiogenesis and attenuated cardiac fibrosis and hypertrophy together with a significant improvement of cardiac function at 14 days post-MI. Apelin-13 increases angiogenesis and improves cardiac repair post-MI by a mechanism involving the upregulation of SDF-1α/CXCR-4 and homing of vascular PCs.     

A case of Kartagener's syndrome: Importance of early diagnosis and treatment

Kartagener''s syndrome is a very rare congenital malformation comprising of a classic triad of sinusitis, situs inversus and bronchiectasis. Primary ciliary dyskinesia is a genetic disorder with manifestations present from early life and this distinguishes it from acquired mucociliary disorders. Approximately one half of patients with primary ciliary dyskinesia have situs inversus and, thus are having Kartagener syndrome. We present a case of 12 year old boy with sinusitis, situs inversus and bronchiectasis. The correct diagnosis of this rare congenital autosomal recessive disorder in early life is important in the overall prognosis of the syndrome, as many of the complications can be prevented if timely management is instituted, as was done in this in this case.     

A rare midbrain infarction presenting with plus-minus lid syndrome with ataxia: a case report

From antiquity to present day, the act of recording and publishing our observations with patients remains essential to the art of medicine and the care of patients. Neurology is rich with case reports over the centuries. They contribute to our understanding and knowledge of disease entities, and are a cornerstone of our professional development as physicians and the care of our patients. This editorial seeks to enthuse and invigorate house staff and practicing physicians everywhere to continue the long and time-honored tradition of neurology case reporting.     

A case of hypereosinophilic syndrome

A report is presented on a case of hypereosinophilic syndrome (HES) characterized by an increase of leukocytes to 70.0 X 10(9) per litre and a percentage of eosinophils up to 87 per cent in the differential hemogram. As a peculiarity hitherto not described increased values were observed in 4 immunoglobulin fractions, IgA, IgG, IgM and with an extreme content of IgE of more than 40.000 IU/ml.