Diffuse nonatherosclerotic coronary aneurysms: an unusual cause of sudden death in a young male and a literature review

Coronary artery aneurysms are uncommon, usually associated with atherosclerosis and rarely involve all 3 main coronary arteries. Sudden death from documented thrombosis within large coronary aneurysms has been rarely reported. The authors report a case of a previously healthy 36-year-old male who presented with myocardial infarction complicated by sudden cardiac death. The patient was successfully resuscitated, and coronary angiography revealed diffuse, severe aneurysmal disease without evidence of atherosclerosis. A thrombus was visualized in a large aneurysm of the proximal left anterior descending artery, and there was total occlusion of a second diagonal branch, presumably due to thrombus embolization. The patient had no history of Kawasaki disease, and evaluation revealed no inflammatory or autoimmune condition. Optimal treatment and prognosis for patients with nonatherosclerotic coronary aneurysms remains unclear. Our patient was treated medically with chronic warfarin and low-dose aspirin therapy and recovered without complication.     

Decreased mtDNA, oxidative stress, cardiomyopathy, and death from transgenic cardiac targeted human mutant polymerase gamma

POLG is the human gene that encodes the catalytic subunit of DNA polymerase gamma (Pol gamma), the replicase for human mitochondrial DNA (mtDNA). A POLG Y955C point mutation causes human chronic progressive external ophthalmoplegia (CPEO), a mitochondrial disease with eye muscle weakness and mtDNA defects. Y955C POLG was targeted transgenically (TG) to the murine heart. Survival was determined in four TG (+/-) lines and wild-type (WT) littermates (-/-). Left ventricle (LV) performance (echocardiography and MRI), heart rate (electrocardiography), mtDNA abundance (real time PCR), oxidation of mtDNA (8-OHdG), histopathology and electron microscopy defined the phenotype. Cardiac targeted Y955C POLG yielded a molecular signature of CPEO in the heart with cardiomyopathy (CM), mitochondrial oxidative stress, and premature death. Increased LV cavity size and LV mass, bradycardia, decreased mtDNA, increased 8-OHdG, and cardiac histopathological and mitochondrial EM defects supported and defined the phenotype. This study underscores the pathogenetic role of human mutant POLG and its gene product in mtDNA depletion, mitochondrial oxidative stress, and CM as it relates to the genetic defect in CPEO. The transgenic model pathophysiologically links human mutant Pol gamma, mtDNA depletion, and mitochondrial oxidative stress to the mtDNA replication apparatus and to CM.     

Evaluation of the optic nerve head vessel density in the patients with asymmetric pseudoexfoliative glaucoma: an OCT angiography study

Graefe's Archive for Clinical and Experimental Ophthalmology - To evaluate vascular microcirculation changes of the optic nerve head (ONH) in the patients with asymmetric pseudoexfoliative...     

Drosophila RISC Component VIG and Its Homolog Vig2 Impact Heterochromatin Formation

Heterochromatin formation plays an important role in gene regulation and the maintenance of genome integrity. Here we present results from a study of the D. melanogaster gene vig, encoding an RNAi complex component and its homolog vig2 (CG11844) that support their involvement in heterochromatin formation and/or maintenance. Protein null mutations vig^EP812 and vig2^PL470 act as modifiers of Position Effect Variegation (PEV). VIG and Vig2 are present in polytene chromosomes and partially overlap with HP1. Quantitative immunoblots show depletion of HP1 and HP2 (large isoform) in isolated nuclei from the vig^EP812 mutant. The vig2^PL470 mutant strain demonstrates a decreased level of H3K9me2. Pull-down experiments using antibodies specific to HP1 recovered both VIG and Vig2. The association between HP1 and both VIG and Vig2 proteins depends on an RNA component. The above data and the developmental profiles of the two genes suggest that Vig2 may be involved in heterochromatin targeting and establishment early in development, while VIG may have a role in stabilizing HP1/HP2 chromatin binding during later stages.     

Increased proliferation is associated with CNS invasion in meningiomas

Journal of Neuro-Oncology - Meningiomas are the most common benign intracranial neoplasms. CNS invasion in meningiomas has been integrated into the 2016 WHO classification of CNS tumors as a...     

Thresholds for damage to the human retina by white light

The power of white light that is needed to produce ophthalmoscopically visible retinal burns was determined in six human subjects. For a 3° diameter retinal image and 1 sec exposure, the minimum energy that caused a visible lesion was 3·2 cal/cm² in brown-eyed subjects and approximately twice this value in blue-eyed subjects. The energy that was required to produce a lesion increased as exposure duration was increased, presumably because of heat loss to adjacent tissues.     

Both type I and II insulin-like growth factor receptor binding increase during lactogenesis in bovine mammary tissue

Bovine GH is a potent stimulant of lactation, and the insulin-like growth factors I and II (IGF-I and -II) are believed to mediate GH's growth-promoting actions. Since all of IGF's known actions are mediated through its receptor subtypes, we analyzed the distribution of IGF receptor subtypes in lactating and nonlactating bovine mammary tissue. Analysis of competition curves showed that IGF-I had greater potency than IGF-II in competing with [125I]IGF-I for binding to membranes prepared from both lactating and nonlactating animals. An insulin concentration of 4 micrograms/ml displaced less than 40% of the [125I]IGF-I bound to membranes prepared from both lactating and nonlactating animals, indicating that a high percentage of [125I]IGF-I was bound to the type II receptor. Lactation was associated with an increase in the total amount of [125I]IGF-I bound, and this change was due to an increase in binding to both receptor subtypes. Specifically, membranes prepared from lactating animals had a 3-fold increase in binding competed for by insulin and a 2-fold increase in binding not competed for by insulin. Affinity cross-linking of [125I]IGF-I to membranes prepared from both lactating and nonlactating animals, followed by polyacrylamide gel electrophoresis (PAGE) and autoradiography, showed that 260K and 135K bands were present. Competition experiments indicated that unlabeled IGF-I effectively competed for binding to the 260K band, whereas insulin did not. Binding to the 135K band could be inhibited by both IGF-I and insulin. The intensity of the labeled bands showed that type II receptors were relatively more abundant than type I receptors in membranes from both lactating and nonlactating animals. Membranes prepared from lactating animals showed both 135K and 127K species of the type I receptor, whereas nonlactating animals showed only the 135K band. We conclude that type I and II receptors are present in bovine mammary tissue, and type II predominate. Lactation is associated with increases in the concentration of both receptor subtypes, especially type I receptors. Lactation may be associated with structural changes in the type I receptor. These changes in receptor distribution could play a role in modulating the physiological effects of the IGFs on mammary tissue.