Repetitive afterglow in zirconia by pulsed near-infrared irradiation toward biological temperature sensing.

Photoluminescence provides information about the surrounding environment. In this study, aiming to develop a non-invasive deep body-temperature sensing method, we investigated photoluminescence properties of afterglow zirconia (ZrO2) by pulsed near-infrared (NIR) light irradiation based on the biological temperature. Pulsed light irradiation produced optically stimulated luminescence, followed by afterglow, with the property of repeating 100 times or more. Furthermore, the basic principle of temperature measurement was demonstrated through afterglow decay curve measurements. The use of harmless ZrO2 as a sensing probe and NIR light, which is relatively permeable to living tissues, is expected to realize temperature measurements in the brain and may also facilitate optogenetic treatment.

Dysphagia worsens short-term outcomes in patients with acute exacerbation of heart failure.

Dysphagia, defined as a dysfunction in any stage or process of eating, is common in patients with acute exacerbation of heart failure (HF). In some diseases, dysphagia worsens in-hospital mortality, length of hospital stay, and discharge disposition. However, it remains unclear whether dysphagia is associated with poor short-term outcomes in HF patients. The objective of the present study was to determine whether dysphagia affects short-term outcomes in patients with acute exacerbation of HF. A total of 327 patients hospitalized with acute exacerbation of HF were eligible for the study. Patients were divided into a dysphagia group (DG) or a non-dysphagia group (NDG) based on results of the functional oral intake scale (FOIS), which evaluates a patient's ability of eating and swallowing. FOIS is a 7-point scale, with a level of ≤ 5 indicating dysphagia. Following the withdrawal of 16 patients, short-term outcomes such as in-hospital mortality, length of hospital stay, and discharge disposition, of 311 patients were analyzed. All indexes of short-term outcomes were significantly worse in the DG than in the NDG. After propensity score matching, which was performed to adjust for baseline characteristics such as age, sex, height, weight, body mass index, medical history, complications, HF severity, ejection fraction, and biochemical data excluding nutritional status, all short-term outcomes remained significantly worse in the DG than in the NDG. Multivariate analysis showed that FOIS was an independent predictor of in-hospital survival, length of hospital stay, and discharge to home. The present study suggested that dysphagia affected short-term outcomes in patients with acute exacerbation of HF. Therefore, early detection and intervention of dysphagia in HF patients are important.

Temperature dependence of afterglow in zirconia and its optically-stimulated luminescence by bone-through irradiation for biological temperature probe.

Development of minimally invasive and site-selective biological temperature sensing is quite important in medical field. This study presents a novel temperature sensing technique based on afterglow and optically-stimulated luminescence (OSL). The dependence of afterglow photoluminescent intensity on the environmental temperature of zirconia (ZrO2) phosphor is examined to validate its use as a sensing probe. In addition, assuming the measurement in deep-part of human body, we have applied the information gathered from our validation to observe OSL from the ZrO2 by irradiation with near-infrared laser through a bone sample. This study demonstrates an alternative medical application of phosphor, and introduces an elemental-technology for the temperature sensing.

Dysphagia Hinders Hospitalized Patients with Heart Failure from Being Discharged to Home.

Dysphagia, defined as a dysfunction in any stage or process of eating, is common among heart failure (HF) patients. In some diseases state, dysphagia hinders patients from being discharged to home. However, it remains unclear whether dysphagia affects discharge disposition of HF patients. This study aimed to identify the impact of dysphagia on discharge disposition of HF patients. A total of 323 patients, hospitalized with acute exacerbation of HF, were eligible for the study (excluding patients who lived at nursing care facilities before admission). Following the withdrawal of 37 patients, a total of 286 patients were analyzed. Dysphagia was determined using the functional oral intake scale (FOIS), which evaluates a patient's ability to swallow. The FOIS is a 7-point scale, with a level of ≤ 5 indicating dysphagia. Of the 286 patients analyzed, 231 (80.8%) were discharged to home, and 55 were discharged to nursing care facilities or rehabilitation hospitals (non-home). FOIS level was significantly lower, and dysphagia incidence was significantly higher among patients discharged to non-home than among those discharged to home. Multivariate analysis showed that FOIS level was an independent predictor of discharge disposition. Additionally, after propensity score matching, which was performed to adjust for baseline characteristics, FOIS level remained significantly lower in patients discharged to non-home than in those discharged to home. In conclusion, dysphagia hinders patients hospitalized with HF from being discharged to home. We conclude that evaluating dysphagia and its severity on admission is useful for predicting discharge disposition in patients hospitalized with HF.

Mitochondrial Cardiomyopathy with a Unique 99mTc-MIBI/123I-BMIPP Mismatch Pattern.

A 42-year-old man was referred to our hospital due to chest pain, diabetes mellitus, and sensorineural hearing loss. Transthoracic echocardiography revealed diffuse left ventricular hypokinesis. He was diagnosed with mitochondrial disease and a c.A3243G mutation was identified in his mitochondrial DNA. This case of mitochondrial cardiomyopathy demonstrated a low uptake of 123I-BMIPP, while the uptake of 99mTc-MIBI was preserved. In contrast, previous reports have noted the increased uptake of123I-BMIPP and the decreased uptake of 99mTc-MIBI. This is the first study to show this unique 99mTc-MIBI/123I-BMIPP mismatch pattern. We also discuss the relationships among the cardiac scintigraphy, cardiac magnetic resonance imaging, and histopathology findings.

Cognitive Dysfunction and Malnutrition Are Independent Predictor of Dysphagia in Patients with Acute Exacerbation of Congestive Heart Failure.

Early detection and intervention for dysphagia is important in patients with congestive heart failure (CHF). However, previous studies have focused on how many patients with dysphagia develop CHF. Studies focusing on the comorbidity of dysphagia in patients with CHF are rare. Additionally, risk factors for dysphagia in patients with CHF are unclear. Thus, the aim of this study was to clarify risk factors for dysphagia in patients with acute exacerbation of CHF. A total of 105 patients, who were admitted with acute exacerbation of CHF, were enrolled. Clinical interviews, blood chemistry analysis, electrocardiography, echocardiography, Mini-Mental State Examination (MMSE), exercise tolerance tests, phonatory function tests, and evaluation of activities of daily living (ADL) and nutrition were conducted on admission. After attending physicians permitted the drinking of water, swallowing screening tests were performed. Patients were divided into a dysphagia group (DG) or a non-dysphagia group (non-DG) based on Functional Oral Intake Scale level. Among the 105 patients, 38 had dysphagia. A greater number of patients had history of aspiration pneumonia and dementia, and there was a higher age, N-terminal pro-B-type natriuretic peptide level in the DG compared with the non-DG. MMSE scores, exercise tolerance, phonatory function, status of ADL, nutrition, albumin, and transthyretin were lower in the DG compared with the non-DG. In multivariate analysis, after adjusting for age and sex, MMSE, BI score, and transthyretin was independently associated with dysphagia. Comorbidity of dysphagia was 36.1% in patients with acute exacerbation of CHF, and cognitive dysfunction and malnutrition may be an independent predictor of dysphagia.

Hypertension promotes phosphorylation of focal adhesion kinase and proline-rich tyrosine kinase 2 in rats: implication for the pathogenesis of hypertensive vascular disease.

Atherosclerosis is initiated by adhesion and infiltration of inflammatory leukocytes into the intima, where non-receptor protein tyrosine kinases, such as focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (PYK2), play important roles as intracellular messengers of mechanical and biochemical signals. In the present study, we examined whether FAK and PYK2 are up-regulated by elevated blood pressure or circulating humoral factors in hypertension. We used a rat model of abdominal aortic banding that allows separate evaluation of elevated blood pressure (upper body) and circulating humoral factors (lower body). We obtained the proximal and distal aortas of the banding site, 6 hours, 3 days, and 1 and 4 weeks after the banding procedure, for evaluation of phosphorylation of FAK and PYK2 by Western blotting. Arterial pressure was significantly elevated only in the upper body throughout the experimental period. The expression of FAK and the FAK phosphorylation were significantly increased at 1 and 4 weeks only in the proximal aorta. This was also the case for the expression of total PYK2 and the PYK2 phosphorylation. In contrast, there was no significant change in FAK or PYK2 phosphorylation in the distal aorta, whereas plasma levels of angiotensin II were systemically elevated. In sham-operated rats, no change in FAK or PYK2 phoshorylation was noted in the proximal and distal aortas. These results indicate that phosphorylation of FAK and PYK2 is upregulated by elevated blood pressure but not by humoral factors in the rat aorta, demonstrating novel aspects of atherogenesis in hypertension.

[Two cases of patients with Parkinson's disease developing valvular heart disease while taking cabergoline].

We experienced 2 patients of valvular heart disease in Parkinson's patients taking cabergoline. Patient 1 was a 79-year-old woman who began taking 4 mg cabergoline daily after being diagnosed with Parkinson's disease (PD) in June 2003. She presented with dyspnea in November 2005. The patient had cardiomegaly, pulmonary congestion, and pleural effusion, and an echocardiogram showed valvular heart disease in the form of aortic regurgitation (AR) (grade I), tricuspid regurgitation (TR) (grade I), and mitral regurgitation (MR) (grade III). Cabergoline was thought to have caused these phenomena, so it was replaced with pramipexole, and after administration of diuretics and angiotensin-converting enzyme inhibitors (ACEIs) the patient's symptoms gradually disappeared. MR, AR and TR also disappeared 3 months later. Patient 2 was a 74-year-old woman who presented with sluggish movement in April 2001 and subsequently developed Parkinson's. While being administered 700 mg levodopa (Menesit) and 4 mg cabergoline, the patient presented with shortness of breath in April 2005. An echocardiogram showed valvular heart disease in the form of MR (grade I) and TR (grade I). Heart function improved with the administration of diuretics. However, heart function again worsened in November 2005, and the patient presented with edema of the lungs and lower limbs. An echocardiogram in January 2006 showed worsening MR (grade III) and TR (grade II), and the patient also had pulmonary hypertension. ACEIs were administered along with diuretics and cabergoline was replaced with pramipexole, but the patient also developed malignant syndrome and disseminated intravascular coagulation (DIC) and later died. Patient 2 is the first case in Japan of death due to heart failure caused by the side effects of cabergoline. Caution is usually needed when treating a Parkinson's patient for valvular heart disease due to a dopamine agonist, and periodic checks for heart murmurs and echocardiography are crucial. When signs of heart failure develop during treatment with an ergot preparation of dopamine agonist, it is essential to immediately either stop the administration of the ergot preparation or change to a non-ergot preparation of dopamine agonist.

Enhanced pulsatile pressure accelerates vascular smooth muscle migration: implications for atherogenesis of hypertension.

AIMS: Clinical studies have suggested that pulsatile pressure is an independent risk factor for atherosclerosis. However, it is unknown whether enhanced pulsatile pressure per se directly accelerates vascular smooth muscle cell (VSMC) migration, an important process of atherosclerosis. METHODS AND RESULTS: Using our original Pressure-loading system with a Boyden chamber, we examined the direct effects of variable pressures and pulse rates on migration of rat aortic VSMCs in vitro. High pulse pressure (180/90 mmHg, pulsatile vs. 180 mmHg, static), high mean pressure (180/90 vs. 90/0 mmHg, with the same pulse pressure), wide pulse pressure (190/110 vs. 170/130 mmHg, with the same mean pressure), and high pulse rate (120 vs. 40 per min) significantly accelerated the VSMC migration (1.35, 2.38, 1.38 and 1.27-fold, respectively). The increase in intracellular calcium levels measured by fura-2/AM fluorescence was proportional to the magnitude of pressure loaded. The pressure-promoted VSMC migration was significantly inhibited by a phospholipase-C inhibitor U-73122 or a calmodulin inhibitor W-7. Inositol 1,4,5-trisphosphate receptor blockers 2-aminoethoxydiphenyl borate or xestospongin-C significantly inhibited the VSMC migration, whereas a ryanodine receptor blocker ryanodine had no effects. Furthermore, a calcium channel blocker (CCB), azelnidipine, and an angiotensin type-1 receptor blocker, olmesartan, also significantly inhibited the VSMC migration. CONCLUSION: These results provide direct evidence for the pro-atherogenic effects of enhanced pulsatile pressure and also suggest that the anti-atherogenic actions of CCBs and angiotensin type-1 receptor blockers are mediated in part by their direct inhibitory effects on VSMC migration in addition to their anti-hypertensive effects.

Increased static pressure promotes migration of vascular smooth muscle cells: involvement of the Rho-kinase pathway.

Vascular smooth muscle cell (VSMC) migration plays a pivotal role in the pathogenesis of arteriosclerosis, under influences of various mechanical factors. Thus, we examined whether static pressure promotes VSMC migration and if so, whether Rho-kinase is involved. Rat VSMCs were cultured on chambers coated on fibronectin, vitronectin, laminin, or type IV collagen, under pressure-free conditions and at 90 and 180 mm Hg. In monolayer-wounding assay, VSMC migration was significantly increased after 72 hours at 180 mm Hg on both fibronectin (11.3 +/- 3.4-fold vs. pressure-free conditions) and vitronectin (10.6 +/- 0.7-fold; both P < 0.05). In Boyden chamber assay, the VSMC migration was again significantly increased at 180 mm Hg on both fibronectin (4.0 +/- 0.5-fold) and vitronectin (5.0 +/- 0.8-fold; both P < 0.05). Neutralizing antibodies against beta1-, beta3- and beta5-integrins, all of which play an important role in cell migration, significantly inhibited the pressure-promoted VSMC migration. Static pressure also significantly increased Rho-kinase activity in VSMC, as evaluated by the extent of phosphorylation of its downstream substrate, ezrin-radixin-moesin. Fasudil, a selective Rho-kinase inhibitor, significantly suppressed the pressure-promoted VSMC migration with reduced Rho-kinase activity. These results indicate that increased static pressure promotes VSMC migration through the integrin/Rho-kinase signaling, suggesting the therapeutic importance of this mechanism for the treatment of hypertensive vascular diseases.

Efficacy of acute inhalation of nitric oxide in patients with primary pulmonary hypertension using chronic use of continuous epoprostenol infusion.

BACKGROUND: There have only been a few reports published on combination therapy for patients with primary pulmonary hypertension (PPH). METHODS AND RESULTS: Fifteen patients with PPH (4 men and 11 women, 34.5+/-12.1 years old) had received chronic administration of epoprostenol and the additive effects of inhaled nitric oxide (NO) and the hemodynamic changes were evaluated. In addition, the difference in the effect of acute NO loading before and after the epoprostenol therapy was compared in 6 of these patients. Under chronic use of epoprostenol, mean pulmonary arterial pressure, mean right atrial pressure and pulmonary vascular resistance were decreased with acute inhalation of NO. However, cardiac output, mean aortic pressure and systemic vascular resistance were unchanged. As a result, the pulmonary to systemic vascular resistance ratio was reduced. Moreover, after chronic use of epoprostenol, the change (delta) in cardiac output with NO inhalation was increased and the NO-induced decrease in pulmonary vascular resistance was augmented compared to those before the induction. CONCLUSION: Nitric oxide inhalation further improved the hemodynamics when combined with chronic use of epoprostenol in PPH patients. These results suggest the possibility that combination therapies can be used in the treatment for PPH patients.