Anxiety,Depression, and Resilience of Healthcare Workers in Japan During the Coronavirus Disease 2019 Outbreak

Objective Coronavirus disease 2019 (COVID-19) is spreading around the world. The aim of this study was to assess the degree of anxiety, depression, resilience, and other psychiatric symptoms among healthcare workers in Japan during the COVID-19 pandemic. Methods This survey involved medical healthcare workers at the Japanese Red Cross Medical Center (Tokyo, Japan) between April 22 and May 15, 2020. The degree of symptoms of anxiety, depression, and resilience was assessed using the Japanese versions of the 7-item Generalized Anxiety Disorder Scale (GAD-7), Center for Epidemiologic Studies Depression Scale (CES-D), and 10-item Connor-Davidson Resilience Scale. Furthermore, we added original questionnaires comprising three factors: (i) anxiety and fear of infection and death; (ii) isolation and unreasonable treatment; and (iii) motivation and escape behavior at work. Results In total, 848 healthcare workers participated in this survey: 104 doctors, 461 nurses, 184 other co-medical staff, and 99 office workers. Among all participants, 85 (10.0%) developed moderate-to-severe anxiety disorder, and 237 (27.9%) developed depression. Problems with anxiety and fear of infection and death, isolation and unreasonable treatment, and motivation and escape from work were higher in the depression group than in the non-depression group (total CES-D score ≥ 16 points). Being a nurse and high total GAD-7 scores were risk factors of depression. Older workers and those with higher resilience were less likely to develop depression than others. Conclusion During the COVID-19 epidemic, many healthcare workers suffered from psychiatric symptoms. Psychological support and interventions for protecting the mental health of them are needed.     

Epicardium is required for sarcomeric maturation and cardiomyocyte growth in the ventricular compact layer mediated by transforming growth factor β and fibroblast growth factor before the onset of coronary circulation

The epicardium, which is derived from the proepicardial organ (PE) as the third epithelial layer of the developing heart, is crucial for ventricular morphogenesis. An epicardial deficiency leads to a thin compact layer for the developing ventricle; however, the mechanisms leading to the impaired development of the compact layer are not well understood. Using chick embryonic hearts, we produced epicardium‐deficient hearts by surgical ablation or blockade of the migration of PE and examined the mechanisms underlying a thin compact myocardium. Sarcomeric maturation (distance between Z‐lines) and cardiomyocyte growth (size) were affected in the thin compact myocardium of epicardium‐deficient ventricles, in which the amounts of phospho‐smad2 and phospho‐ERK as well as expression of transforming growth factor (TGF)β2 and fibroblast growth factor (FGF)2 were reduced. TGFβ and FGF were required for the maturation of sarcomeres and growth of cardiomyocytes in cultured ventricles. In ovo co‐transfection of dominant negative (dN)‐Alk5 (dN‐TGFβ receptor I) and dN‐FGF receptor 1 to ventricles caused a thin compact myocardium. Our results suggest that immature sarcomeres and small cardiomyocytes are the causative architectures of an epicardium‐deficient thin compact layer and also that epicardium‐dependent signaling mediated by TGFβ and FGF plays a role in the development of the ventricular compact layer before the onset of coronary circulation.     

Prediction of no-reflow phenomenon after successful percutaneous coronary intervention in patients with acute myocardial infarction: intravascular ultrasound findings.

Plaque characterization by intravascular ultrasound (IVUS) before percutaneous coronary intervention (PCI) was evaluated in 81 consecutive patients with acute myocardial infarction (AMI) to establish if IVUS can predict the occurrence of the 'no-reflow' phenomenon. Angiographic no-reflow was defined as TIMI flow grade 1 or 2 without any mechanical obstruction in the epicardial artery. Patients were divided into 2 groups according to the post-PCI angiograms: normal flow (group R, n=60) and no-reflow (group NR, n=21). Although the incidence of either soft or noncalcified plaque was not statistically different between the groups, positive vessel remodeling was more frequent in group NR than in group R (57.1% vs 31.6%, p<0.05). Lipid core was also more frequently found in group NR than in group R (61.9% vs 25.0%, p<0.01). Positively remodeled vessels with lipid-rich plaques as characterized by IVUS before PCI predicted the occurrence of angiographic no reflow with a sensitivity of 43% and a specificity of 60%.     

Methylglyoxal Induces Inflammation,Metabolic Modulation and Oxidative Stress in Myoblast Cells

Uremic sarcopenia is a serious clinical problem associated with physical disability and increased morbidity and mortality. Methylglyoxal (MG) is a highly reactive, dicarbonyl uremic toxin that accumulates in the circulatory system in patients with chronic kidney disease (CKD) and is related to the pathology of uremic sarcopenia. The pathophysiology of uremic sarcopenia is multifactorial; however, the details remain unknown. We investigated the mechanisms of MG-induced muscle atrophy using mouse myoblast C2C12 cells, focusing on intracellular metabolism and mitochondrial injury. We found that one of the causative pathological mechanisms of uremic sarcopenia is metabolic flow change to fatty acid synthesis with MG-induced ATP shortage in myoblasts. Evaluation of cell viability revealed that MG showed toxic effects only in myoblast cells, but not in myotube cells. Expression of mRNA or protein analysis revealed that MG induces muscle atrophy, inflammation, fibrosis, and oxidative stress in myoblast cells. Target metabolomics revealed that MG induces metabolic alterations, such as a reduction in tricarboxylic acid cycle metabolites. In addition, MG induces mitochondrial morphological abnormalities in myoblasts. These changes resulted in the reduction of ATP derived from the mitochondria of myoblast cells. Our results indicate that MG is a pathogenic factor in sarcopenia in CKD.     

Hemodynamic shear stress and its role in atherosclerosis

Atherosclerosis, the leading cause of death in the developed world and nearly the leading cause in the developing world, is associated with systemic risk factors including hypertension, smoking, hyperlipidemia, and diabetes mellitus, among others. Nonetheless, atherosclerosis remains a geometrically focal disease, preferentially affecting the outer edges of vessel bifurcations. In these predisposed areas, hemodynamic shear stress, the frictional force acting on the endothelial cell surface as a result of blood flow, is weaker than in protected regions. Studies have identified hemodynamic shear stress as an important determinant of endothelial function and phenotype. Arterial-level shear stress (>15 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile, while low shear stress (<4 dyne/cm2), which is prevalent at atherosclerosis-prone sites, stimulates an atherogenic phenotype. The functional regulation of the endothelium by local hemodynamic shear stress provides a model for understanding the focal propensity of atherosclerosis in the setting of systemic factors and may help guide future therapeutic strategies.     

Optical coherence tomographic findings of the anterior segment after nonpenetrating deep sclerectomy

PURPOSE: To evaluate the efficacy of optical coherence tomography for the analysis of anterior segment after glaucoma surgery. DESIGN: Interventional case report. METHODS: In a 79-year-old man with primary open-angle glaucoma, optical coherence tomography was performed on the left eye after nonpenetrating deep sclerectomy. RESULTS: Optical coherence tomography showed thinning of the conjunctiva over the filtering bleb, presence of a space under the scleral flap that is considered as a lake, and presence of fibrous tissue in the bleb. CONCLUSION: This case indicates that optical coherence tomography, a noninvasive, noncontact optical imaging modality, may be useful for analysis of the anterior segment after glaucoma surgery.     

Anesthesia for a severe ankylosing spondylitis patient whose posture had been restricted to only sitting for over 20 years

A 42-year-old woman with an Arnold-Chiari abnormality was scheduled for cervical spine surgery. She had severe ankylosing spondylitis, and all her joints from ankles to occipitocervical joint were fixed except hip joints, which had been replaced with artificial joints 20 years before. She could bend her upper body only in a range from -20 to 70 degree from the sitting position. Her posture had been restricted to only sitting for over 20 years, and she complained vertigo when positioned in supine position. The trachea was intubated with an aid of bronchofiberscopy under sedation in sitting position, and then anesthesia was induced with propofol and fentanyl. When she was turned to prone position, nasal bleeding was noticed and the surgery was performed in a modified sitting position. The intra- and post-operative course was uneventful. The present case indicates that long-term restriction only to sitting position modulates circulatory control in response to changing postures, and that preoperative evaluation for appropriate posture for surgery is mandatory.     

Chronic demyelinating neuropathy and intra-axonal polyglucosan bodies

Summary In this study we evaluated the relationship between polyglucosan bodies and peripheral nerve lesions. The biopsied sural nerve from a patient with late-onset chronic sensori-motor neuropathy showed many intra-axonal polyglucosan bodies and segmental demyelination/remyelination. The formation of Schwann cell hyperplasia around the demyelinated axons was found at the sites of polyglucosan bodies. These findings suggest that demyelinating neuropathy is a part of the spectrum of the diseases characterized by the accumulation of polyglucosan bodies within cellular compartments.