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PurposeTo explore the current state of teleradiology practice, defined as the interpretation of imaging examinations at a different facility from where the examination was performed.MethodsA national survey addressing radiologists’ habits, attitudes, and perceptions regarding teleradiology was distributed by e-mail to a random sample of ACR members in early 2019.ResultsAmong 731 of 936 respondents who indicated a non-teleradiologist primary work setting, 85.6% reported performing teleradiology within the past 10 years and 25.4% reported that teleradiology represents a majority of their annual imaging volumes; 84.4% performed teleradiology for internal examinations and 45.7% for external examinations; 46.2% performed teleradiology for rural areas and 37.2% for critical access hospitals; 91.3% performed teleradiology during weekday normal business hours and 44.5% to 79.6% over evening, overnight, and weekend hours. In all, 76.9% to 86.2% perceived value from teleradiology for geographic, after-hours, and multispecialty coverage, as well as reduced interpretation turnaround times. The most common challenges for teleradiology were electronic health record access (62.8%), quality assurance (53.8%), and technologist proximity (48.4%). The strategy most commonly considered useful for improving teleradiology was technical interpretation standards (33.3%). Radiologists in smaller practices were less likely to perform teleradiology or performed teleradiology for lower fractions of work, were less likely to experience coverage advantages of teleradiology, and reported larger implementation challenges, particularly relating to electronic health records and prior examination access.ConclusionDespite historic concerns, teleradiology is widespread throughout modern radiology practice, helping practices achieve geographic, after-hours, and multispecialty coverage; reducing turnaround times; and expanding underserved access. Nonetheless, quality assurance of offsite examinations remains necessary. IT integration solutions could help smaller practices achieve teleradiology’s benefits.  相似文献   
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OBJECTIVE—To assess physiological cardiac adaptation in adolescent professional soccer players.
SUBJECTS AND DESIGN—Over a 32 month period 172 teenage soccer players were screened by echocardiography and ECG at a tertiary referral cardiothoracic centre. They were from six professional soccer teams in the north west of England, competing in the English Football League. One was excluded because of an atrial septal defect. The median age of the 171 players assessed was 16.7 years (5th to 95th centile range: 14-19) and median body surface area 1.68 m2 (1.39-2.06 m2).
MAIN OUTCOME MEASURES—Standard echocardiographic measurements were compared with predicted mean, lower, and upper limits in a cohort of normal controls after matching for age and surface area. Univariate regression analysis was used to assess the correlation between echocardiographic variables and the age and surface area of the soccer player cohort. ECG findings were also assessed.
RESULTS—All mean echocardiographic variables were greater than predicted for age and surface area matched controls (p < 0.001). All variables except left ventricular septal and posterior wall thickness showed a modest linear correlation with surface area (r = 0.2 to 0.4, p < 0.001); however, left ventricular mass was the only variable that was significantly correlated with age (r = 0.2, p < 0.01). Only six players (3.5%) had structural anomalies, none of which required further evaluation. All had normal left ventricular systolic function. Sinus bradycardia was found in 65 (39%). The Solokow-Lyon voltage criteria for left ventricular hypertrophy were present in 85 (50%) and the Romhilt-Estes points score (five or more) in 29 (17%). Repolarisation changes were present in 19 (11%), mainly in the inferior leads.
CONCLUSIONS—Chamber dimensions, left ventricular wall thickness and mass, and aortic root size were all greater than predicted for controls after matching for age and surface area. Sinus bradycardia and the ECG criteria for left ventricular hypertrophy were common but there was poor correlation with echocardiographic left ventricular hypertrophy. The type of hypertrophy found reflected the combined endurance and strength based training undertaken.


Keywords: cardiac morphology; professional soccer players; echocardiography; ECG findings  相似文献   
15.
The cytoskeleton in Chediak-Higashi syndrome fibroblasts   总被引:2,自引:0,他引:2  
The Chediak-Higashi syndrome (CHS) trait is expressed in cultured human skin fibroblasts as an abnormal perinuclear concentration of moderately enlarged lysosomes. The cytoskeleton of CHS fibroblasts appears intact. Microtubules are normal in number and morphology, as assessed by colchicine binding studies, antitubulin immunofluorescence, and electron microscopy. Deformability by shear force is unaltered and microfilaments are abundant. However, CHS lysosomes appear to interact abnormally with the cytoskeleton, since the perinculear aggregation partially disperses after depolymerization of cell microtubules with colchicine. These results suggest that CHS is associated with a defect of either the lysosomal membrane itself or of lysosomal membrane- microtubule interaction.  相似文献   
16.
LaDuca  FM; Bettigole  RE; Bell  WR; Robson  EB 《Blood》1986,68(4):927-937
The contribution of von Willebrand factor (vWF)-platelet binding to platelet-collagen interaction was examined in vitro. The binding of vWF to platelets was mediated and regulated by ristocetin. Subthreshold concentrations of ristocetin (less than or equal to 1 mg/mL), insufficient to cause ristocetin-induced platelet aggregation (RIPA), were added to platelet-rich plasma (PRP) prior to the addition of collagen. The collagen-induced platelet aggregation (CIPA) was modified by ristocetin and the degree of alteration was dependent on the ristocetin concentration. Response as a function of ristocetin concentration was designated the Collagen-Platelet Aggregation Response (CoI-PAR). In normal PRP the CoI-PAR was a progressive inhibition followed by decreasing inhibition and then an enhanced response. The enhanced response occurred over a narrow range of ristocetin concentrations (0.8 to 1.0 mg/mL). In the absence of vWF (severe von Willebrand's disease, Type I, vWF less than 1%) the CoI-PAR was a progressive, eventually complete inhibition with no enhanced response (with ristocetin concentrations up to 3.0 mg/mL). With addition of vWF to this PRP an enhanced response was observed at a ristocetin concentration inversely proportional to the vWF level. PRP from a patient with severe Hemophilia A showed a response within the normal range. Subthreshold ristocetin did not cause plasma protein precipitation or platelet release of 3H-serotonin, nor induce micro platelet aggregate formation. Digestion of platelet membrane glycoproteins (GP(s] with chymotrypsin demonstrated that upon removal of GPI, RIPA was absent, CIPA retained and the CoI-PAR was progressive inhibition, with no enhancement. With removal of GPs I, II, and III, RIPA, CIPA, and the CoI-PAR were absent. A dose-response 125I-vWF- platelet binding occurred with increasing ristocetin concentrations which was unchanged by the addition of collagen. These results demonstrated that ristocetin-platelet association inhibited CIPA, and vWF-platelet binding enhanced platelet-collagen adhesion and platelet aggregation. The in vitro-enhanced CIPA represents a vWF-dependent aggregation of sufficient magnitude to overcome the inhibitory effect of ristocetin. These studies demonstrate an influential interaction of ristocetin, vWF, and collagen with the platelet membrane and imply an important hemostatic contribution of vWF-platelet binding in platelet- collagen interaction.  相似文献   
17.
Simmonds  RE; Ireland  H; Kunz  G; Lane  DA 《Blood》1996,88(11):4195-4204
Protein S is a protein C-dependent and independent inhibitor of the coagulation cascade. Deficiency of protein S is an established risk factor for venous thromboembolism. We have used a strategy of specific amplification of the coding regions and intron/exon boundaries of the active protein S gene (PROS1) and direct single-strand solid phase sequencing, to seek mutations in 35 individuals with phenotypic protein S deficiency. Nineteen point mutations (16 novel) in 19 probands (or relatives of probands) with venous thromboembolism are reported here. Fifteen of the 19 mutations were expected to be causal and included 10 missense mutations (Lys9Glu, Glu26Ala, Gly54Glu, Cys145Tyr, Cys200Ser, Ser283Pro, Gly340Asp, Cys408Ser, Ser460Pro, and Cys625Arg). Three of the 15 mutations resulted in premature stop codons (delete T 635 producing a stop codon at position 126, Lys368stop and Tyr595stop) and two were at intron/exon boundaries (+1 G to A in intron d and +3 A to C in intron j). Of the remaining four mutations, three were within intronic sequence and one was a silent mutation within the coding region and did not alter amino acid composition. In two of the 10 missense mutations, reduced plasma protein S activity compared with antigen level suggested the presence of variant (type II) protein S.  相似文献   
18.
目的:分析载脂蛋白B(apoB)基因EcoRI、XbaI、MspI位点和载脂蛋白AI(apoAI)基因-75bp、+83bp位点多态性与哈萨克族人冠心病的关系.方法:采用聚合酶链式反应-限制性片段长度多态性分析法检测185例哈萨克族冠心病患者和216例哈萨克族非冠心病对照者的这些位点多态性.结果:①TC、TG及apoA...  相似文献   
19.
目的 应用彩色多普勒超声寻找移植肾急性排异反应较为特异的诊断指标.方法 经移植肾穿刺活检证实的急性排异反应患者42例,经长期随访(1年以上)和临床检查证实的功能稳定期患者115例.对两组移植肾长径、宽径、厚径、实质厚度以及主肾动脉和弓状动脉的阻力指数(RI)进行统计学比较;选取肾体积增大,锥体肿大回声减低、RI<0.7、RI≥0.7及RI≥0.8作为诊断标准,按诊断试验评价原则分别计算灵敏度、特异度、误诊率、漏诊率和符合率;并绘制ROC曲线,确定诊断界值.结果 两组的移植肾长径、宽径、厚径及实质厚度差异有统计学意义(P<0.05);急性排异反应组肾内血流灌注减少,肾动脉舒张期血流速度明显下降,RI明显增高,与移植肾功能稳定期比较差异有统计学意义(P<0.05);各诊断标准对应的灵敏度分别为55.30%,55.20%,42.10%,57.90%和31.60%;特异度分别为71.30%、87.10%、25.70%、74.20%、98.20%.结论 肾体积增大、肾锥体肿大、回声减低、RI升高对诊断移植肾急性排异反应有特异性.  相似文献   
20.
In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects.  相似文献   
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