ABSTRACT
Eldercare programs such as health consultations and physiotherapy that improve the well-being and extend the life expectancy of people in rural or sparsely populated areas is a socially important though costly problem. We ran a pilot project to test the effectiveness potential of telerehabilitation using markerless motion capture technology integrated in a fast and low-latency IMT-2020 (5G) mobile network. Accelerating technological innovations and the surge in advances of telehealth will greatly impact conventional home visit or outpatient rehabilitation services, working in concert with or even supplanting them, given the potential lower cost and better utilization of time.
Subject(s)
Telemedicine , Telerehabilitation , Ambulatory Care , Humans , Physical Therapy Modalities , Pilot ProjectsABSTRACT
Mechanical stress by pressure overload due to hypertension or valvular heart disease such as aortic valve stenosis induces cardiac hypertrophy. It has been well established that the mechanical stretch of cardiac myocytes in vitro induces hypertrophic responses such as the expression of immediate early response genes including c-fos. However, it remains uncertain whether the mechanical forces due to pure atmospheric pressure can induce similar responses in cardiac myocytes. We thus cultured rat neonatal cardiac myocytes in an atmospheric pressure chamber apparatus and determined the effects of pure pressure stress on c-fos gene expression. Pressures greater than 80 mmHg enhanced c-fos mRNA after 30 minutes. These results suggest that pure atmospheric pressure overload can also induce early hypertrophic responses in cardiac myocytes.
Subject(s)
Cardiomegaly/genetics , Gene Expression Regulation, Developmental , Myocytes, Cardiac/metabolism , Proto-Oncogene Proteins c-fos/genetics , RNA, Messenger/genetics , Animals , Animals, Newborn , Cardiomegaly/metabolism , Cardiomegaly/pathology , Cells, Cultured , Disease Models, Animal , Myocytes, Cardiac/pathology , Proto-Oncogene Proteins c-fos/biosynthesis , RNA, Messenger/biosynthesis , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
BACKGROUND: There are few biological markers, which strictly show the severity of congestive heart failure (CHF). METHODS AND RESULTS: Lymphocyte G-protein coupled receptor kinase (GRK) mRNA expression was measured by quantitative reverse transcription-polymerase chain reaction in 15 CHF patients: 5 patients classified as New York Heart Association class-II treated with angiotensin converting enzyme inhibitor (ACEI) (IIA), 5 patients in class-II without ACEI (IIC), and 5 patients in class-III treated with ACEI (IIIA). GRK mRNA level in IIIA was significantly higher than those in IIA (p<0.05). GRK mRNA level in IIA were significantly lower than those in IIC (p<0.05). CONCLUSIONS: The expression level of lymphocyte GRK might show the severity of CHF, and ACEI treatment could reduce the level of GRK in CHF patients.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/pharmacology , G-Protein-Coupled Receptor Kinase 1/genetics , Gene Expression Regulation, Enzymologic/drug effects , Heart Failure/enzymology , Heart Failure/genetics , Adult , Aged , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Biomarkers/blood , Female , G-Protein-Coupled Receptor Kinase 1/analysis , G-Protein-Coupled Receptor Kinase 1/metabolism , Heart Failure/drug therapy , Humans , Lymphocytes/chemistry , Lymphocytes/enzymology , Male , Middle Aged , RNA, Messenger/analysis , RNA, Messenger/genetics , Receptors, Adrenergic, beta/drug effects , Receptors, Adrenergic, beta/physiology , Reverse Transcriptase Polymerase Chain Reaction , Severity of Illness IndexABSTRACT
Immature vascular smooth muscle cells (VSMCs) proliferate responding to extrinsic mitogens and accumulate in neointima after arterial injuries. Cell proliferation is positively regulated by cyclin/cyclin-dependent kinase (CDK) complex and negatively controlled by CDK inhibitors; CKIs such as p27(kip1) and p57(kip2). In this study, embryonic rat thoracic aorta VSMCs; A10 were G0/G1 arrested by serum starvation, re-stimulated with serum, and harvested every four hours. Both CKIs co-expressed in quiescent VSMCs and rapidly diminished by stimulation. Protein level of p27(kip1) was regulated by both transcription and post-transcription, but that of p57(kip2) was mainly by post-transcription. Supplemental overexpression of p57(kip2) inhibited the activations of G1 cyclin/CDKs and subsequent hyperphosphorylations of all three retinoblastoma pocket proteins as well as G1/S transition of cell cycle. Our findings suggest that the downregulations of not only p27(kip1), but also p57(kip2) responding to mitogenic stimulation, play key roles in the cell cycle progression of VSMCs.
Subject(s)
Cell Cycle/physiology , Cyclin-Dependent Kinase Inhibitor p57/metabolism , Down-Regulation , Muscle, Smooth, Vascular/cytology , Muscle, Smooth, Vascular/metabolism , Animals , Cells, Cultured , Cyclin G , Cyclin G1 , Cyclin-Dependent Kinase Inhibitor p57/genetics , Cyclins/metabolism , Gene Expression Regulation, Enzymologic , Protein Binding , RNA, Messenger/genetics , Rats , SerumABSTRACT
BACKGROUND: Enhanced expression of G protein-coupled receptor kinase (GRK) has been reported in failing hearts and in the present study the stability of enhanced GRK mRNA expression, and the correlation between the expression level of GRK mRNA in peripheral lymphocytes and in the heart were both evaluated. METHODS AND RESULTS: Isoproterenol was injected into rats for 2 weeks, and then GRK5 mRNA was assessed by quantitative reverse transcriptase-palymerase chain reaction. An enhanced expression of cardiac GRK5 mRNA was observed even after 4 weeks of recovery. The isoproterenol-induced increased expression of GRK2 and GRK5 mRNA was equally observed in the heart and lymphocytes, and there was a close correlation between the heart and lymphocytes in the level of expression of each GRK mRNA. CONCLUSIONS: The GRK mRNA level is maintained at a high level for a long period without continuous beta-adrenergic receptor stimulation. The level in circulating lymphocytes could be used as a surrogate marker to estimate the level of cardiac GRK expression and, presumably, the beta-adrenergic receptor function of cardiomyocytes.
Subject(s)
Adrenergic beta-Agonists/administration & dosage , Cyclic AMP-Dependent Protein Kinases/biosynthesis , Gene Expression Regulation/drug effects , Isoproterenol/administration & dosage , Lymphocytes/metabolism , Myocardium/metabolism , Protein Serine-Threonine Kinases/biosynthesis , Animals , Cyclic AMP-Dependent Protein Kinases/genetics , G-Protein-Coupled Receptor Kinase 5 , Male , Myocytes, Cardiac/metabolism , Protein Serine-Threonine Kinases/genetics , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Rats , Receptors, Adrenergic, beta/metabolism , beta-Adrenergic Receptor KinasesABSTRACT
BACKGROUND: Animal models are indispensable in order to investigate the mechanism of various diseases and to explore the counter measures for those disease states. Although there are several animal models of ischemic heart diseases, surgical interventions required to create myocardial ischemia sometimes give rise to a problem in the yield of model. This study describes a new technique for inducing myocardial ischemia in rats. METHODS AND RESULTS: A 0.014-inch guidewire was introduced via the carotid artery and selectively advanced into the coronary arteries under fluoroscopy. Transmural myocardial ischemia was confirmed by ST-segment elevation and by the appearance of left ventricular wall motion abnormalities on the echocardiogram. Reversibility of the wire-induced myocardial ischemia was demonstrated by complete resolution of both ST-segment elevation and wall motion abnormalities after removing the wire. CONCLUSION: Wire-induced myocardial ischemia was reproducible and is less invasive than conventional ischemic models in rats. This method is a powerful and useful tool for the investigation of ischemic heart disease in small animals.
