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61.

Purpose

Deep tissue hypoxia has been hypothesized in the pathogenesis of complex regional pain syndrome type 1 (CRPS 1) for some patients. The purpose of this study was to determine if near-infrared spectroscopy (NIRS) could detect differences in deep tissue oxygen saturation (StO2) and microcirculatory function in the hands of patients with CRPS 1.

Methods

Tissue oxygen saturation was evaluated at baseline and during an ischemia reperfusion challenge using vascular occlusion testing (VOT) in affected vs unaffected hands of patients with unilateral upper limb CRPS 1. A non-randomized experimental study design was used with baseline StO2 as the primary outcome measure. Secondary outcome measures were occlusion and reperfusion slopes from VOT. Values were compared with the unaffected, contralateral hand and with the dominant and non-dominant hands of sex and age-matched volunteers. Correlations between values derived from NIRS and measures of pain and function from the Brief Pain Inventory (BPI) and the Disability of the Arm, Shoulder and Hand (DASH) questionnaires were explored.

Results

Independent of handedness, the baseline StO2 of the affected hands of ten CRPS 1 patients was significantly lower than that of their unaffected hands (?5.8%; 95% confidence interval [CI] ?10.6 to ?1.0; P = 0.02). The baseline StO2 of affected CRPS 1 hands was also significantly lower than the non-dominant hands of ten volunteers (?7.3%; 95% CI ?12.4 to ?2.3; P = 0.007). Differences in VOT occlusion and reperfusion slopes did not reveal changes that could be uniquely attributed to CRPS 1. No significant correlations were detected between values derived from VOT and values for pain and function obtained from BPI and DASH questionnaires for patients with CRPS 1.

Conclusions

Hands of patients affected by CRPS 1 of the upper limb showed significantly lower StO2 compared with their unaffected contralateral hand as well as the hands of control subjects. This trial was registered at: ClinicalTrials.gov: NCT01586377.  相似文献   
62.
We report an unusual case of myocardial mycotic aneurysm of the left ventricle resulting from a healed myocardial abscess caused by an aortic regurgitant jet lesion. The diagnosis was made during intraoperative transesophageal echocardiography and confirmed by surgical inspection. The echocardiographic features are described.  相似文献   
63.
The lateral mobility of proteins within cell membranes is usually thought to be dependent on their size and modulated by local heterogeneities of the membrane. Experiments using single-particle tracking on reconstituted membranes demonstrate that protein diffusion is significantly influenced by the interplay of membrane curvature, membrane tension, and protein shape. We find that the curvature-coupled voltage-gated potassium channel (KvAP) undergoes a significant increase in protein mobility under tension, whereas the mobility of the curvature-neutral water channel aquaporin 0 (AQP0) is insensitive to it. Such observations are well explained in terms of an effective friction coefficient of the protein induced by the local membrane deformation.Brownian motion plays an essential role in biological processes. Since the pioneering experiments of Perrin (1), the observation of diffusing objects has emerged as a mean to extract the rheological properties of the surrounding medium or the probe particle size. The theoretical investigation of diffusion of proteins within membranes has been studied widely going back to P. G. Saffman and M. Delbrück (SD). They investigated the hydrodynamic drag acting on a membrane inclusion when the membrane is described as a 2D fluid sheet of viscosity embedded within a less viscous fluid of viscosity η (2). In this theory, the diffusion coefficient D0 in the limit of a large viscosity contrast between the membrane and bulk fluid is given by:The length is the length scale over which flow is generated within the bilayer by the inclusion, kBT is the thermal energy, and γ is Euler’s constant. This model predicts a logarithmic dependence of D0 on the protein radius ap, which has been confirmed for some in vitro experiments on membranes containing transmembrane proteins (see ref. 3 and references therein). In contrast, the experiments of Gambin et al. (4) showed significant deviations from the SD theory.A possible origin for the discrepancy observed by Gambin et al. (4) is the significant local membrane deformation due to the interaction between the inclusion and the lipid bilayer (5). Naji et al. suggested in ref. 6 that inclusions experience additional dissipation, either due to internal flows within the membrane or to additional fluid flows produced by the deformed membrane. This work triggered a number of theoretical studies investigating the coupling of inclusion proteins with the membrane that had been pioneered by the Seifert’s group (see ref. 7 and references therein). Such studies have systematically gone beyond the SD model by including additional effects (812). So far, a thorough verification of these ideas has not been attempted. To investigate the effect of the protein–lipid coupling on the protein mobility, we study its dependence on membrane tension, because this parameter affects the local membrane deformation.In this work, we compare the mobility of two transmembrane proteins with the same lateral size, aquaporin 0 (AQP0) and a voltage-gated potassium channel (KvAP), reconstituted in giant unilamellar vesicles (GUVs). Whereas AQP0 does not deform locally the bilayer, KvAP locally bends the membrane (13). Using single-particle tracking (SPT), we demonstrate that the curvature-coupled protein KvAP undergoes a significant increase in mobility under tension, whereas the mobility of the curvature-neutral water channel AQP0 is insensitive to it. This difference, which goes beyond the SD model, is explained by an approach that includes the interplay between membrane deformation and friction with the surrounding medium and within the bilayer. This is compelling evidence that the Brownian motion of a shaping-membrane protein is not simply dependent on the inclusion size but also related to the lateral extension of the deformed membrane patch, which depends on tension.  相似文献   
64.
Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease characterized by deficient α‐L‐iduronidase activity, leading to the accumulation of poorly degraded glycosaminoglycans (GAGs). Children with MPS I exhibit high incidence of spine disease, including accelerated disc degeneration and vertebral dysplasia, which in turn lead to spinal cord compression and kyphoscoliosis. In this study we investigated the efficacy of neonatal enzyme replacement therapy (ERT), alone or in combination with oral simvastatin (ERT + SIM) for attenuating cervical spine disease progression in MPS I, using a canine model. Four groups were studied: normal controls; MPS I untreated; MPS I ERT‐treated; and MPS I ERT + SIM–treated. Animals were euthanized at age 1 year. Intervertebral disc condition and spinal cord compression were evaluated from magnetic resonance imaging (MRI) images and plain radiographs, vertebral bone condition and odontoid hypoplasia were evaluated using micro–computed tomography (µCT), and epiphyseal cartilage to bone conversion was evaluated histologically. Untreated MPS I animals exhibited more advanced disc degeneration and more severe spinal cord compression than normal animals. Both treatment groups resulted in partial preservation of disc condition and cord compression, with ERT + SIM not significantly better than ERT alone. Untreated MPS I animals had significantly lower vertebral trabecular bone volume and mineral density, whereas ERT treatment resulted in partial preservation of these properties. ERT + SIM treatment demonstrated similar, but not greater, efficacy. Both treatment groups partially normalized endochondral ossification in the vertebral epiphyses (as indicated by absence of persistent growth plate cartilage), and odontoid process size and morphology. These results indicate that ERT begun from a very early age attenuates the severity of cervical spine disease in MPS I, particularly for the vertebral bone and odontoid process, and that additional treatment with simvastatin does not provide a significant additional benefit over ERT alone. © 2014 American Society for Bone and Mineral Research.  相似文献   
65.
Familial tumoral calcinosis is characterized by ectopic calcifications due to persistent hyperphosphatemia. The most common genetic cause of the disease is mutations in GALNT3, encoding a glycosyltransferase involved in a posttranslational modification of fibroblast growth factor 23 (FGF23). The Galnt3 knockout mouse we developed was hyperphosphatemic due to low intact Fgf23 levels, but did not develop any apparent calcifications on a standard rodent diet. We therefore tested the hypothesis that a further challenge with a high phosphate diet could induce ectopic calcifications in Galnt3 knockout mice. Mice were fed either normal (0.6%) or high (1.65%) phosphate diet for 20 weeks beginning from weaning at 3 weeks. The high phosphate diet did not affect serum phosphorus concentration. However, regardless of the dietary phosphate contents, serum phosphorus levels were consistently elevated in Galnt3 knockout mice. The mice on the high phosphate diet had slightly low serum calcium, but significantly high alkaline phosphatase, parathyroid hormone (PTH), and calcium in the kidney. Although none of Galnt3 knockout mice on the normal phosphate diet developed calcifications, calcifications appeared in approximately one‐half of the mice on the high phosphate diet by 12 weeks. Calcified masses were most often found around the neck and on the back and as large as 9.9 mm in length. These data indicate that dietary phosphate load has major impact on the development of ectopic calcifications in tumoral calcinosis. © 2014 American Society for Bone and Mineral Research.  相似文献   
66.
67.
本文探讨了物理治疗行业的历史发展、相关的职业、工作和就业特征,专业教育体系并对未来的发展进行了展望.  相似文献   
68.
69.
Automatic segmentation of 3D micro-CT coronary vascular images   总被引:1,自引:0,他引:1  
Although there are many algorithms available in the literature aimed at segmentation and model reconstruction of 3D angiographic images, many are focused on characterizing only a part of the vascular network. This study is motivated by the recent emerging prospects of whole-organ simulations in coronary hemodynamics, autoregulation and tissue oxygen delivery for which anatomically accurate vascular meshes of extended scale are highly desirable. The key requirements of a reconstruction technique for this purpose are automation of processing and sub-voxel accuracy. We have designed a vascular reconstruction algorithm which satisfies these two criteria. It combines automatic seeding and tracking of vessels with radius detection based on active contours. The method was first examined through a series of tests on synthetic data, for accuracy in reproduced topology and morphology of the network and was shown to exhibit errors of less than 0.5 voxel for centerline and radius detections, and 3 degrees for initial seed directions. The algorithm was then applied on real-world data of full rat coronary structure acquired using a micro-CT scanner at 20 microm voxel size. For this, a further validation of radius quantification was carried out against a partially rescanned portion of the network at 8 microm voxel size, which estimated less than 10% radius error in vessels larger than 2 voxels in radius.  相似文献   
70.
Objective To evaluate the specificity, sensitivity, and accuracy of pain intensity assessments (0–10) conducted by registered nurses (RN) and clinical nurse assistants (CAN) as compared to those conducted by the palliative care consultant (PCC).Patients and methods We performed a retrospective review of charts of patients who had received palliative care consult between April 2002 and August 2002. Data on patient demographic, date of palliative care consult, and date and intensity of pain assessment were collected. A numerical rating scale from 0 (no pain) to 10 (worst pain) was used to assess pain intensity. The data were included for analysis if the pain intensity assessment was performed during the same shift by all three care providers (RN, CNA, and PCC).Results Forty-one charts were found to include a complete pain assessment performed by the RN, CNA, and PCC. The agreement of pain intensity between the PCC and both the RN and CNA was poor. For a diagnosis of moderate-to-severe pain, the RNs intensity assessment had a specificity of 90% but a sensitivity of 45%, and the CNAs intensity assessment had a specificity of 100% but a sensitivity of only 30%. The Spearman correlation coefficient between the intensity assessments performed by the PCC and the RN was 0.56 (p=0.00) and between those by the PCC and the CNA 0.22 (p=0.15).Conclusion Lack of agreement between pain intensity assessments performed by the PCC and bedside nurse suggests possible inconsistencies in the way the assessments were performed. Better education on how to perform standard pain intensity assessment is needed.  相似文献   
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