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When mechanical stimulation was applied to free swimming Paramecium, forward swimming velocity transiently increased due to activation of the posterior mechanosensory channels. The behavior response, known as "escape response," requires membrane hyperpolarization and the activation of K-channel type adenylate cyclases. Our hypothesis is that this escape response also involves activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. HCN channels are activated by hyperpolarization and are modulated by cyclic nucleotides such as cAMP and cGMP. They play a critical role in many excitable cells in higher animals. If HCN channels act in Paramecium, this should help to enhance and prolong hyperpolarization, thereby increasing the swimming speed of Paramecium. This study used RNAi to examine the role of the HCN channel 1 in the escape responses by generating hcn1-gene knockdown cells (hcn1-KD). These cells showed reduced mechanically-stimulated escape responses and a lack of cGMP-dependent increases in swimming speed. Electrophysiological experiments demonstrated reduced hyperpolarization upon injection of large negative currents in hcn1-KD cells. This is consistent with a decrease in HCN1 channel activity and changes in the escape response. These findings suggest that HCN1 channels are K + channels that regulate the escape response of Paramecium by amplifying the hyperpolarizations elicited by posterior mechanical stimulation., (© 2024 International Society of Protistologists.)

Anomalous origin of the left coronary artery from the pulmonary artery is rare but causes myocardial ischemia and sudden death. A few patients with this anomaly can survive to adulthood without sufficient collateral coronary flow or surgical intervention. We present here a case of acute inferior myocardial infarction, which may occur due to thrombotic occlusion of the right coronary artery, in a 63-year-old woman with anomalous origin of the left coronary artery from the pulmonary artery, providing specific coronary angiographic findings. < Learning objective : In this manuscript, we present a rare case of coronary heart disease. The coronary angiography and the multidetector computed tomographic coronary angiography provided specific findings for the diagnosis.>.

The purpose of this study was to examine the effects of nipradilol on the cardiac function and mRNA expression in Wistar rats with a myocardial infarction (MI) that was created by ligation of the anterior descending coronary. Ten mg x kg(-1) x day(-1) of nipradilol were administrated to the rats in random order, and hemodynamic and Doppler-echocardiographic findings and myocardial mRNA expression were analyzed at 4 weeks after MI. Although left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) were increased in the MI rats, nipradilol significantly reduced the degree of the increase in both parameters. MI also significantly increased the weight of the left and right ventricles, and increased the left ventricular end-diastolic dimension (LVDd), effects that were attenuated by nipradilol. The MI rats showed decreased fractional shortening as systolic dysfunction and decreased E wave deceleration rate as diastolic dysfunction, and nipradilol significantly prevented these. Nipradilol significantly suppressed the increase in the non-infarcted myocardial mRNA expression of atrial natriuretic peptide, brain natriuretic peptide and collagen I and III. In conclusions, nipradilol prevents the cardiac remodeling that is accompanied by systolic and diastolic dysfunction, and inhibits abnormal myocardial gene expression after MI.

The purpose of this study was to examine the effect of diltiazem on cardiac dysfunction and the change in cardiac gene expression after myocardial infarction in rats. On the first day after myocardial infarction, rats were randomly assigned to a diltiazem treatment (Dil, n = 7) or an untreated group (MI, n = 8). We then performed Doppler echocardiographic examinations on the rats and measured their hemodynamics at 4 weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Diltiazem decreased the mean aortic pressure and heart rate. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 18 +/- 2 mmHg and 5 +/- 1 mmHg (P < 0.01). Diltiazem reduced LVEDP to 14 +/- 1 mmHg (P < 0.05), but it did not change CVP. The weight of the right ventricle in MI was significantly larger than in the control rats (control, n = 7, 0.46 +/- 0.02 g/kg vs. MI, 0.81 +/- 0.06 g/kg; P < 0.01). The left ventricular end-diastolic dimension (LVDd) in MI increased to 8.8 +/- 0.3 mm (P < 0.01, control, 6.1 +/- 0.3 mm). Diltiazem prevented an increase in the weight of the right ventricle (0.69 +/- 0.03 g/kg, P < 0.05) and LVDd (7.7 +/- 0.2 mm, P < 0.05 to MI). The rats within MI showed systolic dysfunction, defined by a decreased ejection fraction (control, 67 +/- 2% vs. MI, 36 +/- 3%, P < 0.01), and diastolic dysfunction, defined by the E-wave deceleration rate (control, 13.4 +/- 1.6 m/s2 vs. MI, 30.4 +/- 3.4 m/s2; P < 0.01). Diltiazem significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, ANP, and collagen type I and III mRNAs in the noninfarcted left ventricle and right ventricle were significantly suppressed by treatment with diltiazem. alpha-Skeletal actin increased in MI, and alpha-skeletal actin was more increased with Dil. In conclusion, diltiazem prevents cardiac dysfunction and morphological change due to left ventricular remodeling after experimental myocardial infarction.

Atherosclerotic disease of the aortic arch is thought to be a potential source of cerebral emboli, but this disease in the branch of the aortic arch has not been extensively explored. This study assessed atherosclerotic lesions in the thoracic aorta and the branches of the aortic arch using transesophageal echocardiography in patients with cerebral infarction, and simultaneously searched for potential cardiac sources for emboli. Thrombi were detected in the left atrial appendage in nine of 54 patients with cerebral infarction and these patients were excluded. The remaining 45 patients with cerebral infarction (31 males and 14 females aged 68.5 +/- 7.4 years) and 35 normal subjects (21 males and 14 females aged 69.2 +/- 9.5 years) were evaluated. The thickness of the wall was measured in the branches of the aortic arch (brachiocephalic trunk, left common carotid artery and left subclavian artery) as well as the thoracic aorta (ascending aorta, aortic arch and descending aorta). Atherosclerotic lesions were defined as increased echogenicity of the intima (intimal thickening), calcification, protruded plaque, ulceration or plaque with cystic lesion. The thicknesses of the wall in the aortic arch (3.84 +/- 1.25 vs 2.71 +/- 1.33 mm, p < 0.01), left common carotid artery (2.67 +/- 1.10 vs 2.16 +/- 0.91 mm, p < 0.05) and the left subclavian artery (2.52 +/- 0.67 vs 2.15 +/- 0.88 mm, p < 0.05) were significantly greater in patients than in the normal subjects. The incidence of plaque or ulceration was significantly increased in patients with cerebral infarction compared with the normal subjects in the aortic arch (76% vs 43%, p < 0.05) and left common carotid artery (44% vs 17%, p < 0.05). Transesophageal echocardiography can detect possible sources of emboli in the branches of the aortic arch as well as the thoracic arch in patients with cerebral infarction.