Changes in acceleration and deceleration factors associated with active gait speed adjustment.

[Purpose] The ability to actively adjust walking speed is fundamental and the factors enabling it should be assessed. The present study aimed to demonstrate how active gait speed is kinematically adjusted. [Participants and Methods] Walking acceleration and deceleration were evaluated in 16 healthy adults using three-axis accelerometers and surface electromyographs. The root mean square (RMS) of each axis in the center-of-gravity acceleration was calculated as an index of gait stability. Electron myograph data were obtained from images captured of the right lower muscles, and the integral value of total muscle activity per gait cycle was calculated. [Results] The RMS of each axis increased during acceleration and decreased during deceleration. The integral values of total activity of the gastrocnemius, biceps femoris, and tibialis anterior muscles increased in acceleration. In contrast, the values increased in the biceps femoris but decreased in other muscles during deceleration. [Conclusion] These results suggest that the specific kinematic mechanisms of each factor regulate the acceleration and deceleration of walking. In addition, these mechanisms and factors indicate how exercise therapy may be used in rehabilitation to improve the ability to adjust walking speed in daily life.

Evaluating the immediate effect of the speed alteration task on walking stability using the Timed Up and Go test.

[Purpose] This study aimed to investigate how the speed alteration task, which gradually increases or conversely decreases walking speed, affected walking stability. [Participants and Methods] Thirteen healthy young adults performed two walking tasks as follows: the speed alteration task, in which the walking speed was gradually increased or decreased, and the speed constant task, in which the walking speed was maintained at a comfortable level. Before and after each task, the Timed Up and Go test was performed to analyze time, walking speed, and trajectory. The overall score of the Timed Up and Go test, as well as the scores of the three major segments (i.e., forward, turning around, and return), and nine subsegments, were calculated and analyzed. [Results] During the speed alteration task, parameters including time and walking speed of the Timed Up and Go test were significantly improved. Also, the same parameters increased significantly in the forward and return segments. These increases were also observed in the first subsegment of the forward segment and the second subsegment of the return segment. [Conclusion] The speed alteration task improved walking stability, so it could be used in gait training to improve walking stability.

A macroscopic anatomical study of the appropriate palpation zone of the gluteus medius muscle.

[Purpose] Few previous studies have delimitated the palpation zone of the gluteus medius muscle with a focus on its fiber bundles. The purpose of this study was to clarify the morphological characteristics of the gluteus medius muscle using an anatomical approach, and to define its proper palpation zone. [Participants and Methods] In this study, we evaluated thirteen halves of the pelvic region in seven formalin-fixed cadavers. We identified the borders between the iliotibial band and gluteus medius muscle, and between the gluteus medius and gluteus maximus muscles, on the iliac crest. Furthermore, we quantified the border points of the gluteus medius' fiber bundles and observed its anatomical and morphological characteristics. [Results] We identified two fiber bundles in the gluteus medius muscle, an anterior and a posterior fiber bundle, and detected that a portion of the posterior fibers was located subcutaneously. [Conclusion] We propose that the region where the posterior fibers of the gluteus medius muscle are located subcutaneously is an appropriate zone for the palpation of this muscle.

Pulmonary embolism caused by intimal sarcoma of the pulmonary artery.

We herein report the case of a 39-year-old woman with a pulmonary embolism caused by intimal sarcoma of the pulmonary artery. She presented with shortness of breath and leg edema. Computed tomography showed a low density area that extended from the main pulmonary artery to the bilateral pulmonary arteries. We diagnosed her to have a pulmonary thromboembolism. The thrombosis did not decrease after the administration of anti-coagulant therapy, and she underwent resection of the thrombotic tissue. Histopathologically, the surgical specimen was not found to be thrombotic tissue but rather an intimal sarcoma of the pulmonary artery. After undergoing surgery, she received radiation therapy and chemotherapy; however, she died 31 months after being diagnosed.

Altered metabolism of low-density lipoprotein and very-low-density lipoprotein remnant in autosomal recessive hypercholesterolemia: results from stable isotope kinetic study in vivo.

BACKGROUND: Autosomal recessive hypercholesterolemia (ARH) exhibits different responsiveness to statins compared with that in homozygous familial hypercholesterolemia (FH). However, few data exist regarding lipoprotein metabolism of ARH. Therefore, we aimed to clarify lipoprotein metabolism, especially the remnant lipoprotein fractions of ARH before and after statin therapy. METHODS AND RESULTS: We performed a lipoprotein kinetic study in an ARH patient and 7 normal control subjects, using stable isotope methodology (10 mg/kg of [(2)H(3)]-leucine). These studies were performed at baseline and after the 20 mg daily dose of atorvastatin. Tracer/tracee ratio of apolipoprotein B (apoB) was determined by gas chromatography/mass spectrometry and fractional catabolic rates (FCR) were determined by multicompartmental modeling, including remnant lipoprotein fractions. FCR of low-density lipoprotein (LDL) apoB of ARH was significantly lower than those of control subjects (0.109 versus 0.450±0.122 1/day). In contrast, the direct removal of very-low-density lipoprotein remnant was significantly greater in ARH than those in control subjects (47.5 versus 2±2%). Interestingly, FCR of LDL apoB in ARH dramatically increased to 0.464 1/day, accompanying reduction of LDL cholesterol levels from 8.63 to 4.22 mmol/L after treatment with atorvastatin of 20 mg/d for 3 months. CONCLUSIONS: These results demonstrate that ARH exhibits decreased LDL clearance associated with decreased FCR of LDL apoB and increased clearance for very-low-density lipoprotein remnant. We suggest that increased clearance of remnant lipoprotein fractions could contribute to the great responsiveness to statins, providing new insights into the lipoprotein metabolism of ARH and the novel pharmacological target for LDLRAP1.

An enhanced device for transluminal retrieval of vascular stents without surgical procedures: experimental studies.

BACKGROUND: Although efforts have been focused on developing endovascular procedures by which intravascular devices such as stents could be effectively deployed, few data exist regarding devices for the nonsurgical retrieval of deployed stents. Therefore, we designed to enable retrieval of deployed stents without a surgical procedure. METHODS: The device consisted of four components: ultra-low profile forceps with 2.0 mm in diameter, conducting shaft with 1.8 mm in diameter, control handle by which the forceps is opened or closed, and a covering sheath. This device was designed to advance into the vessel lumen along a 0.014-inch guidewire by over the wire fashion. RESULTS: The forceps could firmly catch nonexpanded as well as expanded tubular-type stents with open cells in an in vitro model that was 4.0 mm in diameter. Then, we used this device in porcine renal arteries with 2.5-5.0 mm in diameter. At first, a fragmented 0.014-inch guidewire could be safely removed without vessel damage that was confirmed by intravascular ultrasound. This device could successfully remove four of five inappropriately and 11 of 14 appropriately deployed stents. Under these conditions, intravascular ultrasound demonstrated minor vessel wall dissection in two-third of cases. CONCLUSIONS: These results demonstrate that the present device can be used for transluminal removal of foreign bodies such as nonexpanded as well as expanded stents in acute phase. Further miniaturization may enable using this type of device in the renal as well as coronary arteries.

Impact of severe earthquake on the occurrence of acute coronary syndrome and stroke in a rural area of Japan.

BACKGROUND: Although acute coronary syndrome (ACS) and stroke are known to increase after earthquake, few data exist regarding the effect of earthquake on these cardiovascular events in rural areas. METHODS AND RESULTS: The Noto Peninsula earthquake with a magnitude of 6.9 occurred at 9:45 a.m. on 25 March 2007. The first case of ACS occurred approximately 15 min later, whereas cerebral hemorrhage (CH) occurred 72 h after the onset of earthquake. During the 35 days after earthquake, among 49 patients who were attended by local ambulance, 5 patients with ACS (10.2%) and 8 with CH (16.3%) were documented and 4 died. The total number of both ACS and CH cases was greater than the averages for the same period of the past 3 years in this area (2.0 vs 5 and 2.3 vs 8, P<0.01). Interestingly, the most cases of ACS had occurred within 7 days after earthquake and for CH not until 35 days later. CONCLUSIONS: Even in rural areas a severe earthquake results in increased incidence of ACS and CH, which can occur at different times after the event, although the effects of other environmental factors should be further investigated.

A novel method for determining functional LDL receptor activity in familial hypercholesterolemia: application of the CD3/CD28 assay in lymphocytes.

BACKGROUND: The objective of this study was to develop a new and simple method for measuring low-density lipoprotein receptor (LDLR) activity using peripheral lymphocytes enabling us to clinically diagnose familial hypercholesterolemia (FH) and ascertain the involved mutations (such as K790X mutation), that might not be clearly detected in the conventional method. METHODS: Our method comprised the following 2 features: first, we used anti-CD3/CD28 beads to stimulate T-lymphocytes to obtain a uniform fraction of lymphocytes and maximum up-regulation of LDLR. Second, we excluded the possibility of overestimation of lymphocyte signals bound only to its surface, by adding heparin to the cultured lymphocytes used for the LDLR assay. RESULTS: Based on the genetic mutation, the FH subjects were divided into 2 groups, K790X, (n=20) and P664L, (n=5), and their LDLR activities was measured by this method, which was found to be 55.3+/-8.9% and 63.9+/-13.8%, respectively, of that of the control group (n=15). In comparison, the LDLR activity was 86.1+/-11.6% (K790X) and 73.3+/-6.3% (P664L) of that of the control group when measured by the conventional method, indicating that impairment of LDLR function in FH K790X subjects was much more clearly differentiated with our method than with the conventional method (paired t-test, p<0.0001). The levels of LDLR expression also showed similar tendencies, that is, 89.4+/-13.2% (K790X) and 76.9+/-17.4% (P664L) of that of the control group when measured by the conventional method, and 78.1+/-9.7% (K790X) and 70.3+/-26.5% (P664L) when measured by our new method. In addition, we confirmed that there was little influence of statin treatment on LDLR activity among the study subjects when our method was used. CONCLUSION: These results demonstrate that our new method is applicable for measuring LDLR activity, even in subjects with an internally defective allele, and that T-lymphocytes of the FH K790X mutation possess characteristics of that allele.

Apolipoprotein B gene mutations and fatty liver in Japanese hypobetalipoproteinemia.

BACKGROUND: Familial hypobetalipoproteinemia (FHBL) is a hereditary disorder characterized by decreased plasma concentrations of low-density lipoprotein cholesterol. The best-characterized causes of FHBL are apolipoprotein B (apoB) gene mutations, which produce truncated apoB proteins. Fatty liver is thought to be frequent in FHBL, owing to impaired secretion of very-low-density lipoprotein from the liver. Homozygotes for FHBL present with extremely low concentrations of plasma lipids, and may suffer from deficiencies of fat-soluble vitamins. The objectives of this study were to identify apoB-defective FHBL subjects and investigate fatty liver in Japanese population. METHODS: We screened 14 hypocholesterolemic subjects for apoB gene mutations by PCR-SSCP and performed liver ultrasonography in a Japanese population. RESULTS: We identified an apoB-82 homozygote in one subject and an apoB-13.7 heterozygote in another subject. Four of 6 individuals with FHBL presented with fatty liver in those 2 FHBL families. Liver biopsy of the apoB-13.7 heterozygote, which had obesity and insulin resistance, showed severe fatty liver. The apoB-82 homozygote was asymptomatic with fat-soluble vitamin concentrations being normal, possibly due to spared secretion of apoB-48 from the intestine and increased plasma concentrations of high-density lipoprotein cholesterol. CONCLUSION: ApoB gene mutations might not be rare and that fatty liver might be frequent in Japanese FHBL.

Marked aortic valve stenosis progression after receiving long-term aggressive cholesterol-lowering therapy using low-density lipoprotein apheresis in a patient with familial hypercholesterolemia.

In 1982, a 49-year-old Japanese woman had been referred to our hospital for further investigation of her hypercholesterolemia. She was diagnosed as heterozygous familial hypercholesterolemia, because of Achilles tendon xanthoma and a family history of primary hypercholesterolemia. Three years later, she had chest pain on effort and angina pectoris was diagnosed by coronary angiography. At that time, she underwent coronary artery bypass grafting surgery with 2 saphenous vein grafts (SVG). Because more aggressive cholesterol-lowering therapy was needed for secondary prevention of coronary artery disease (CAD), weekly low-density lipoprotein (LDL) apheresis was started postoperatively, combined with drug therapy. Since 1986, her serum total cholesterol levels before and after LDL apheresis remained approximately 200 mg/dl and 90 mg/dl, respectively. Although her coronary sclerosis, including the SVG, did not progress appreciably for a period of 20 years, stenotic changes of the aortic valve developed rapidly at age 70, leading to aortic valve replacement surgery in 2005 at age 72. These findings suggest that careful attention to the progression of aortic valve stenosis is needed for extreme hypercholesterolemic patients even under optimal cholesterol-lowering therapy for the secondary prevention of CAD.

High frequency of a retinoid X receptor gamma gene variant in familial combined hyperlipidemia that associates with atherogenic dyslipidemia.

OBJECTIVE: The genetic background of familial combined hyperlipidemia (FCHL) has not been fully clarified. Because several nuclear receptors play pivotal roles in lipid metabolism, we tested the hypothesis that genetic variants of nuclear receptors contribute to FCHL. METHODS AND RESULTS: We screened all the coding regions of the PPARalpha, PPARgamma2, PPARdelta, FXR, LXRalpha, and RXRgamma genes in 180 hyperlipidemic patients including 60 FCHL probands. Clinical characteristics of the identified variants were evaluated in other 175 patients suspected of coronary disease. We identified PPARalpha Asp140Asn and Gly395Glu, PPARgamma2 Pro12Ala, RXRgamma Gly14Ser, and FXR -1g->t variants. Only RXRgamma Ser14 was more frequent in FCHL (15%, P<0.05) than in other primary hyperlipidemia (4%) and in controls (5%). Among patients suspected of coronary disease, we identified 9 RXRgamma Ser14 carriers, who showed increased triglycerides (1.62+/-0.82 versus 1.91+/-0.42 [mean+/-SD] mmol/L, P<0.05), decreased HDL-cholesterol (1.32+/-0.41 versus 1.04+/-0.26, P<0.05), and decreased post-heparin plasma lipoprotein lipase protein levels (222+/-85 versus 149+/-38 ng/mL, P<0.01). In vitro, RXRgamma Ser14 showed significantly stronger repression of the lipoprotein lipase promoter than RXRgamma Gly14. CONCLUSION: These findings suggest that RXRgamma contributes to the genetic background of FCHL.