Eighteen-lead electrocardiography (18-ECG) includes, in addition to those in standard 12-lead ECG (12-ECG), six additional chest leads: V7–V9 and V3RV5R. Leads V7–V9 require the patient to be in a lateral decubitus position for the electrodes to be attached to the back. Synthesized 18-ECG (syn18-ECG) is a method that only records 12-ECG and uses computational logic to record the posterior wall (V7–V9) and right-sided (V3R–V5R) leads. We review the clinical utility of syn18-ECG in conditions including acute coronary syndromes, arrhythmias, acute pulmonary embolism, and Duchenne muscular dystrophy. The syn18-ECG waveform correlates well with the actual 18-ECG waveform, indicating that syn18-ECG is an excellent substitute for 18-ECG, excluding negative T waves. ST elevation in leads V7–V9 has the effect of reducing missed acute coronary syndromes in the posterior wall. In cases of arrhythmia, syn18-ECG can accurately estimate the target site of radiofrequency catheter ablation using a simple algorithm. The use of additional leads in Duchenne muscular dystrophy is expected to provide new insights. To facilitate gaining more knowledge regarding diseases that have not yet been investigated, it is imperative that the cost of syn18-ECG is reduced in the future.

The tumor suppressor gene Reversion-inducing cysteine-rich protein with Kazal motifs (Reck) encodes a membrane-anchored protease regulator expressed in multiple tissues in mouse embryos and is essential for embryonic development. In postnatal mice, however, physiological roles for the RECK protein remain unclear. We found in this study that Reck is abundantly expressed in growth hormone (GH)-producing cells (somatotrophs) in the anterior pituitary gland (AP). We also found that two types of viable Reck mutant mice, one with reduced RECK expression (Hypo mice) and the other with induced Reck deficiency from 10 days after birth (iKO mice treated with tamoxifen), exhibit common phenotypes including decreases in body size and plasma levels of insulin-like growth factor-1 (IGF1). To gain insights into the function of RECK in the AP, we characterized several somatotroph-associated molecules in the AP of these mice. Immunoreactivity of GH was greatly reduced in tamoxifen-treated iKO mice; in these mice, two membrane receptors involved in the stimulation of GH secretion [growth hormone secretagogue receptor (GHSR) and growth hormone releasing hormone receptor (GHRHR)] were decreased, however, their mRNAs were increased. Decrease in GHSR immunoreactivity and concomitant increase in its mRNA were also found in the other mutant line, Hypo. Furthermore, reduced immunoreactivity of growth hormone receptor (GHR) and concomitant increase in its mRNA was also found in the liver of Hypo mice. These results raise the possibility that RECK supports proper functioning of the GH/IGF1 axis in mice, thereby affecting their growth and metabolism.

Background/Objectives: Duchenne muscular dystrophy (DMD) is an X-linked inherited muscle disease. Patients with DMD demonstrate improved prognosis with angiotensin-converting enzyme inhibitors and beta-blockers at the time of cardiac dysfunction. However, most deaths due to DMD are due to cardiac dysfunction. Fragmented QRS (fQRS) is an abnormal finding that forms a notch in the QRS wave on electrocardiography (ECG) and is associated with fibrosis and scarring of the myocardium. Methods: Patients with DMD were examined for the number of leads of fQRS, their sites of appearance, changes in cardiac dysfunction, and age using the chest leads of a synthesized 18-ECG. A retrospective analysis of 184 patients under 20 years of age with DMD and known genetic mutations was performed; they were divided into three age groups: 3–10, 11–15, and 16–20 years. The chest leads of the ECG were defined as follows: V1-3, anterior leads; V4-6, lateral leads; V7-9, posterior leads; and V3R-V5R, right-sided chest leads. Cardiac dysfunction was defined as a left ventricular (LV) ejection fraction <53% on the same day, and echocardiography was performed. LV dilation was defined as dilation beyond the normal range, considering the body surface area. Results: In 167 of 184 patients (91%), fQRS was present in one or more chest leads. The number of fQRS leads in the anterior and lateral walls was significantly higher in 16–20-year-olds than in 3–10-year-olds. The total number of chest leads with fQRS was 4.9 ± 3.1 in the cardiac dysfunction group and 3.5 ± 2.5 in the preserved group. The cardiac dysfunction group had a significantly greater number of fQRS leads than did the preserved group (p = 0.003). The group with LV dilation had a significantly greater number of fQRS leads than did the non-dilation group (p = 0.009). Conclusions: The fQRS site is associated with age, cardiac dysfunction, and LV dilation. Multivariate regression analysis revealed that the number of anterior leads of the fQRS correlated with age and that of lateral leads of the fQRS with cardiac dysfunction and LV dilation. The number of fQRS leads on the lateral wall marks cardiac dysfunction and LV dilation.

Super-resolution microscopy achieves a few nanometers resolution, but protein quantification and colocalization is limited by its labeling density. Here we present a method to map molecular complexes using the multiplexed data of IRIS super- resolution imaging. We developed antiserum-derived Fab IRIS probes for high- density labeling of endogenous targets, and image analysis, Protein Cluster coloring (PC-coloring), which employs pixel-based principal component analysis and clustering. PC-coloring was first used to map regions of distinct ratios of targets on the image. The molecular complex formation was then evaluated by correlation between all combinations of two proteins in each PC-colored region. We elucidate receptor recruitment and the complex formation in a clathrin-coated structure (CCS) which is pre-assembled prior to endocytosis. Upon EGF stimulation, EGFR-, EGFR-Grb2-complex- and Grb2-dominant regions lined up from the CCS rim. Along the interior of Grb2-dominant regions, Eps15, FCHo1/2 and intersectin-1 formed a complex with Grb2. The interior of Eps15-FCHo1/2 complexes was lined with Eps15-intersectin-1 complexes. The results reveal a laminar complex formation of EGFR, Grb2 and CCS components at the recruitment sites.