Sanfordhyde1980
The results were validated quantitatively on 2D MPR images. An accuracy of 95.265±0.4551% was achieved through volumetric overlap computation. Through pairedt-test, at α=5%, statistical values were p=0.6769, and t=0.4169 which infer that there was no much significant difference. CONCLUSION The combination of different validation techniques was applied to check the robustness of colon segmentation method, and good results were achieved with this approach. Through quantitative validation, the results were accepted at α=5%. BACKGROUND Orthognathic surgery is useful for correction of dental malocclusion and improvement of facial appearance. The FACE-Q is a patient-reported outcome instrument for evaluation of surgical and psychosocial effect. The purposes of this study were to conduct a linguistic validation of all FACE-Q scales to Mandarin Chinese, to test the orthognathic surgery-related scales for reliability and validity, and to evaluate the effect of orthognathic surgery. METHODS All FACE-Q scales and checklists were translated from English to Mandarin Chinese according to international recommendations forward translations, backward translation, and cognitive interviews. Psychometric testing of orthognathic surgery-related scales of translated version was administered to patients with facial deformities and history of orthognathic surgery (n = 53; 17 scales) or no history of orthognathic surgery (n = 44; 11 scales), and control subjects (n = 57; 11 scales). RESULTS All FACE-Q scales and checklists were linguistically validated into Mandarin Chinese. The contents were confirmed valid among Mandarin Chinese-speaking population. The FACE-Q scales had excellent internal consistency (Cronbach's alpha >0.70) and discriminated (p less then 0.05) well between patients before and after orthognathic surgeries and normal subjects. CONCLUSIONS This study discovered significant benefit of orthognathic surgery on improving facial appearance and psychosocial function, as compared with the non-surgical patients and normal controls. BACKGROUND Papillary thyroid carcinoma occasionally presents with concomitant hyperparathyroidism; however, the clinical significance has not been well established. This study aimed to evaluate the long-term cancer prognosis following a multimodality therapy. METHODS We conducted a case-control study using prospectively maintained data from a medical center thyroid cancer database between 1980 and 2013. The study cohort comprised patients with concomitant papillary thyroid carcinoma and hyperparathyroidism. Patients with papillary thyroid carcinoma only were matched using the propensity score method. Therapeutic outcomes, including the non-remission rate of papillary thyroid carcinoma and patient mortality, were compared. RESULTS We identified 27 study participants from 2537 patients with papillary thyroid carcinoma, with 10 patients having primary hyperparathyroidism and 17 having renal hyperparathyroidism. Eighty-five percent of the cohort was found to have tumor-node-metastasis stage I disease. During a mean follow-up of 7.7 years, we identified 3 disease non-remission and 4 mortality events. The non-remission risk did not increase (hazard ratio [HR], 1.66; 95% confidence interval [CI], 0.43-6.40; p = 0.47); however, the overall mortality risk significantly increased (HR, 4.43; 95% CI, 1.11-17.75; p = 0.04). All mortality events were not thyroid cancer related, including two identified cardiovascular diseases. CONCLUSIONS Patients with papillary thyroid carcinoma who present with concomitant hyperparathyroidism are usually diagnosed at an early cancer stage with compatible therapeutic outcomes. However, hyperparathyroidism-related comorbidity may decrease long-term survival. BACKGROUND This study used novel human neurophysiologic models to investigate whether the mechanism of rate-sensitive H-reflex depression lies in the pre-synaptic or post-synaptic locus in humans. We hypothesized that pre-synaptic inhibition would suppress Ia afferents and H-reflexes without suppressing alpha motor neurons or motor evoked potentials (MEPs). In contrast, post-synaptic inhibition would suppress alpha motor neurons, thereby reducing H-reflexes and MEPs. METHODS We recruited 23 healthy adults with typical rate-sensitive H-reflex depression, 2 participants with acute sensory-impaired spinal cord injury (SCI) (to rule out influence of sensory stimulation on supra-spinal excitability), and an atypical cohort of 5 healthy adults without rate-sensitive depression. After a single electrical stimulation to the tibial nerve, we administered either a testing H-reflex or a testing MEP at 50-5000 ms intervals. RESULTS Testing MEPs were not diminished in healthy subjects with or without typical rate-sensitive H-reflex depression, or in subjects with sensory-impaired SCI. MEP responses were similar in healthy subjects with versus without rate-sensitive H-reflex depression. CONCLUSIONS Results from these novel in vivo human models support a pre-synaptic locus of rate-sensitive H-reflex depression for the first time in humans. Spinal reflex excitability can be modulated separately from descending corticospinal influence. AZD1152-HQPA Each represents a potential target for neuromodulatory intervention. BACKGROUND CDGSH iron sulfur domain-containing protein 1 (CISD-1) belongs to the CISD protein family that is evolutionary conserved across different species. In mammals, CISD-1 protein has been implicated in diseases such as cancers and diabetes. As a tractable model organism to study disease-associated proteins, we employed Caenorhabditis elegans in this study with an aim to establish a model for interrogating the functional relevance of CISD-1 in human metabolic conditions. METHODS We first bioinformatically identified the human Cisd-1 homologue in worms. We then employed N2 wild-type and cisd-1(tm4993) mutant to investigate the consequences of CISD-1 loss-of-function on 1) the expression pattern of CISD-1, 2) mitochondrial morphology pattern, 3) mitochondrial function and bioenergetics, and 4) the effects of anti-diabetes drugs. RESULTS We first identified C. elegans W02B12.15 gene as the human Cisd-1 homologous gene, and pinpointed the localization of CISD-1 to the outer membrane of mitochondria. As compared with the N2 wild-type worm, cisd-1(tm4993) mutant exhibited a higher proportion of hyperfused form of mitochondria.