Validation and reliability of a Japanese version of the Shoulder Pain and Disability Index: A cross-sectional study

BackgroundThe Shoulder Pain and Disability Index (SPADI) is a simple disease specific questionnaire that is used to evaluate the impact of shoulder disorders. The purpose of this study was to translate the SPADI into Japanese (SPADI-Jp) and evaluate its reliability and validity in Japanese patients with shoulder disorders.MethodsCross-cultural adaptation of the SPADI was performed according to international guidelines. A total of 100 patients with shoulder disorders participated in this study. Each participant was asked to finish the SPADI-Jp, Disability of Arm, Shoulder and Hand (DASH), and the Short-Form 36 (SF-36) at the initial visit. Thirty-four patients repeated the SPADI-Jp to assess the test–retest reliability. The test–retest reliability was quantified using the interclass correlation coefficient (ICC), while Cronbach's alpha was calculated to assess the internal consistency. The construct validity was assessed using Spearman's rank correlation coefficients.ResultsInternal consistency in the SPADI-Jp was very high (0.969), as measured by the Cronbach's alpha. The ICC of the SPADI-Jp was 0.930. There was a strong, positive correlation between the DASH and the SPADI-Jp (r = 0.837, p < 0.001). The SPADI-Jp was significantly correlated with most of the SF-36 subscales. The correlations of the SPADI-Jp with physical subscales of the SF-36 were stronger than those with the other subscales.ConclusionsWe demonstrated that the SPADI-Jp is a reliable and valid self-assessment tool. Because cross-cultural adaptation, validation, and reliability of the disease-specific questionnaire for shoulder pain and disability have not been evaluated in Japan, the SPADI-Jp can be useful for evaluating such patients in the Japanese population.     

Survival and sinus rhythm maintenance after modified Cox/maze procedure and mitral valve operation in patients with chronic atrial fibrillation

OBJECTIVE: Sinus rhythm gained after the Cox/maze procedure concomitant with mitral valve operation has demonstrated long-term attrition during the follow-up, no information exists on whether the type of mitral valve operation--(repair vs. replacement)--affects this sinus rhythm maintenance rate. We retrospectively studied patients undergoing concomitant mitral valve operation and Cox/maze procedure to answer this question. METHODS: Between April 1993 and August 1995, 87 consecutive patients--35 men and 52 women (mean age: 59.3 years)--with chronic atrial fibrillation and mitral valve disease underwent the modified Cox/maze procedure and concomitant mitral valve operation, with 56 having mitral valve repair (repair group) and 31 mitral valve replacement (replacement group). Patients were followed up and changes in rhythm studied retrospectively. RESULTS: Follow-up for a mean 51.3 +/- 11.6 months was completed in 82 of 83 long-term survivors (99%). Repair group surgery survival was 98.1 +/- 1.9% at 1 year and 94.2 +/- 3.2% at 5 based on the Kaplan-Meier method. Replacement group surgery survival was 85.7 +/- 5.9% at 1 year and 82.9 +/- 6.4% at 5. Probability in sinus rhythm maintenance for the repair group at 1 year was 88.6 +/- 5.4% and at 5 years was 67.6 +/- 9.1%. Probability in sinus rhythm maintenance for the replacement group at 1 year was 95.7 +/- 4.3% and at 5 years was 65.0 +/- 11.1%. CONCLUSIONS: Medium-term results after the Cox/maze III procedure concomitant with mitral valve operation are good. The attrition of sinus rhythm maintenance appears similar by the completion of 5-year follow-up.     

Photoreceptor status after resolved macular edema in branch retinal vein occlusion treated with tissue plasminogen activator

PURPOSE: To evaluate the integrity of photoreceptors in macular edema (ME) associated with branch retinal vein occlusion after intravitreal tissue plasminogen activator. DESIGN: Retrospective, interventional case series. METHODS: Nineteen eyes with ME by branch retinal vein occlusion were treated with intravitreal tissue plasminogen activator injection. We assessed visual acuity (VA) and the presence or absence in the fovea of a third high reflectance band (HRB) by optical coherence tomography at the final visit. RESULTS: No differences were found in age, preoperative VA, and foveal thickness between the groups with or without the third HRB. After treatment, the mean VA improved significantly (P < .05) in both groups. At the final visit, the mean VA in the group without HRB was significantly poorer than the group with HRB (P = .0042); foveal thickness did not differ between the groups. CONCLUSIONS: The integrity of the third HRB in the fovea is associated with VA after the resolution of ME.     

Indocyanine green and trypan blue: intracellular uptake and extracellular binding by human retinal pigment epithelial cells

PURPOSE: To examine the intracellular uptake and extracellular binding of indocyanine green (ICG) and trypan blue (TB) by human retinal pigment epithelium (RPE) cells in vitro at clinically relevant concentrations. METHODS: Human RPE cells (ARPE19 cells) were exposed to 0.01%, 0.05%, and 0.25% ICG or 0.06%, 0.15%, and 0.25% TB for 15 seconds, 30 seconds, and 5 minutes, and the dye concentrations taken up by the cells were evaluated by spectrophotometric analysis. RESULTS: ICG was significantly taken up by ARPE19 cells after exposure to 0.05% for 5 minutes, 0.01% for 30 seconds, and 0.25% ICG for 15 seconds, whereas TB was not taken up by RPE cells under the conditions in this study. CONCLUSION: ICG is bound and taken up by RPE cells at concentrations lower than clinically used, and TB is not. Understanding the effects of dyes on ocular tissues leads to more effective and safer dye-assisted vitrectomy protocols, although the experimental setting is different from the clinical situation.     

Visual field defects after macular hole surgery with indocyanine green-assisted internal limiting membrane peeling

PURPOSE: To report visual field defects after macular hole surgery with indocyanine green (ICG)-assisted internal limiting membrane (ILM) peeling. DESIGN: Interventional consecutive case series. METHODS: A retrospective review of 140 eyes with macular hole after vitrectomy with ILM peeling. The group with 0.25% of ICG for ILM peeling consisted of 96 eyes. The group without ICG consisted of 44 eyes. RESULTS: Nasal visual field defects occurred in 11 eyes, temporal visual field defects in seven eyes, and concentric visual field defects in one eye. In the group with ICG, nasal visual field defects were far higher in the left eye than in the right eye. CONCLUSIONS: We speculate that the postoperative nasal visual field defects were caused by the enhanced toxicity of ICG resulting from the exposure to illumination.     

Infarct Size Limitation by Bradykinin Receptor Activation Is Mediated by the Mitochondrial But Not by the Sarcolemmal KATP Channel

Earlier studies have shown that activation of bradykinin B₂ receptor triggers protein kinase C (PKC)-mediated cardioprotective mechanism in ischemic preconditioning (PC). In the present study, we examined whether the effector in this B₂-receptor triggered pathway of PC is the ATP sensitive potassium (K_ATP) channel in the mitochondria (mito-K_ATP channel) or K_ATP channel in the sarcolemma (sarc-K_ATP channel). Isolated rabbit hearts were perfused with modified Krebs-Henseleit buffer in a Langendorff mode, and regional myocardial ischemia was induced by occluding a left coronary artery for 30 min and then reperfusing for 2 hours. Infarct size was determined by triphenyltetrazolium chloride staining and expressed as a percentage of area at risk (% IS/AR). Infusion of bradykinin (500 nmol/L) for 15 min prior to ischemia significantly reduced % IS/AR from 37.4 ± 2.9 (SE) of the untreated controls to 12.0 ± 3.3%. This protective effect of bradykinin was completely abolished by coinfusion of 5-hydroxydecanoate (5-HD, 50 mol/L), a selective mito-K_ATP channel blocker (% IS/AR = 44.2 ± 6.4). In contrast, a high dose of HMR1098 (20 mol/L), which is a newly developed sarc-K_ATP channel selective blocker with IC₅₀ of 0.6 mol/L, failed to modify the infarct size limitation by preischemic infusion of bradykinin (% IS/AR = 11.7 ± 3.4). Neither 5-HD nor HMR1098 alone modified infarct size (% IS/AR = 37.8 ± 3.8 and 35.1 ± 6.2, respectively). These results suggest that opening of the mito-K_ATP channel but not the sarc-K_ATP channel is involved in infarct size limitation by a mechanism triggered by bradykinin B₂ receptor activation.     

Myocardial bridging increases the risk of coronary spasm

BACKGROUND: Myocardial bridging (MB) has been associated with cardiac events. Whether coronary spasm is one factor contributing to those events is unknown. HYPOTHESIS: This study investigated whether the likelihood of coronary spasm is increased in patients with MB. METHODS: A spasm-provocation test was performed by infusing acetylcholine into the left coronary artery in 114 Japanese patients with chest pain. The test result was defined as positive when the diameter of the coronary artery was reduced by > or = 50% and ST-segment changes were documented. Myocardial bridging was defined as a > 15% reduction in coronary arterial diameter during systole after intracoronary injection of nitroglycerin. RESULTS: Myocardial bridging was identified in 41 patients (36%) and was located in the mid-segment of the left anterior descending coronary artery (LAD) in all patients. Patients with MB experienced coronary spasm more frequently than patients without MB (MB+: 73%; MB-: 40%, p = 0.0006). Furthermore, among patients with a positive spasm-provocation test, coronary spasm occurred more frequently in the mid-segment of the LAD in patients with MB than in those without MB (MB+: 73%; MB-: 45%, p = 0.0259). Multivariate regression analysis demonstrated that MB was a predictor of coronary spasm (odds ratio: 3.478, p = 0.0088). CONCLUSIONS: These results suggest that MB increases the risk of coronary spasm and that coronary spasm may be the proximate etiology of cardiac events associated with MB.     

Carbon fibre reinforced cellulose-based polymers: intensifying interfacial adhesion between the fibre and the matrix

Interfacial interactions governing the interfacial adhesion between cellulose propionate and carbon fibre surface are placed under scrutiny to pave the way towards the development of green cellulose-based carbon fibre reinforced polymers. A range of molecular entities are deposited on the surface by initially grafting aromatic structures with appropriate functions via diazonium species followed by further derivatization of these entities. Cellulose propionate was also bound covalently to the surface via a tosylated derivative invoking its facile nucleophilic displacement reaction with surface-grafted amino functions. Significant increase in interfacial shear strength was obtained for the cellulose propionate-grafted carbon fibre composite as well as for the 4-(aminomethyl)benzene-functionalized sample, in the latter case possible hydrogen bonding took place with the cellulose propionate matrix. Furthermore, the positive effect of a highly lipophilic and yet compact –CF₃ substituent was also noted. In order to let the grafted structure efficiently penetrate into the matrix, steric factors, lipophilicity and potential secondary interactions should be considered. It needs to be pointed out that we provide the first synthetic strategy to covalently bind cellulose derivatives to a largely graphitic surface and as such, it has relevance to carbonaceous materials being applied in cellulose-based innovative materials in the future.

Interfacial adhesion of a cellulose propionate/carbon fibre composite is tailored providing a synthetic strategy to bind cellulose derivatives to graphitic surfaces.     

Left ventricular oxygen utilization efficiency is impaired in chronic streptozotocin-diabetic sheep

OBJECTIVE: Energy metabolism is altered in the diabetic heart. However, direct in vivo evidence that diabetes impairs energetics at the chamber level is lacking. Therefore, we investigated the effect of diabetes on left ventricular (LV) energetics in a chronic ovine model. METHODS: Diabetes was induced in Merino-cross sheep with streptozotocin. Experiments were performed in five animals following 12 months untreated diabetes and six animals served as controls. Open-chest anesthetized sheep were instrumented to determine the LV pressure-volume relationship, oxygen consumption and free fatty acid uptake. RESULTS: Diabetes impaired LV contractility (1.5+/-0.5 vs. 2.3+/-0.5 mmHg/ml, P<0.01). Stroke work was preserved but stroke work efficiency (stroke work/pressure-volume area) deteriorated (52+/-4 vs. 58+/-3%, P<0.01). Plasma free fatty acid levels increased (1885+/-1078 vs. 354+/-203 mmol/l, P<0.01) as did LV free fatty acid uptake (312+/-278 vs. 90+/-47 micromol/beat per 100 g LV, P=0.04). Contractile efficiency decreased (31.9+/-1.4 vs. 50.0+/-8.7%, P<0.01) while unloaded oxygen consumption did not change significantly. Therefore, LV oxygen utilization efficiency (stroke work/LV oxygen consumption) was compromised in the diabetic heart (14.9+/-2.8 vs. 24.3+/-4.0%, P<0.001). CONCLUSION: This is the first study to demonstrate that diabetes alters ventricular energetics in vivo. LV oxygen utilization efficiency is impaired as a consequence of decreased contractile efficiency and stroke work efficiency. Impaired efficiency of oxygen utilization may explain in part the increased sensitivity of the diabetic heart to ischemia and the accelerated deterioration of ventricular function in diabetic patients.