Purpose: With the introduction of new treatment devices, such as a multileaf collimator (MLC) and dynamic wedge (DW), therapists have an increased responsibility to ensure correct treatment. Simultaneously, three-dimensional treatment planning (3DTP) has led to an increased number of portals and table movements. To counteract this challenge and maintain efficiency, a comprehensive record and verify (R&V) system is mandatory. We evaluated a commercial system (Varis) for reliability, ease of use, efficiency, and integration with our planning systems.
Methods and Materials: Some key elements of the Varis system are: integration of MLC and DW; auto setup for MLC, jaw, collimator, gantry, and limited table parameters; direct download of simulation beam data; and a regimented field scheduling system that prescribes all beam data for particular fractions. Evaluation of the system was driven by treatment time analysis, error rates, and an increased workload. These issues were governed by how we disseminated duties and how the system accommodated or changed our processes.
Results: Most data entry is performed by our dosimetry staff. Data can be downloaded from the simulator, but more patients now move from CT simulation and/or 3DTP to the treatment machine. Varis does not link to these systems. The physics staff confirms all entries to correct data entry errors. The workload for dosimetrists increased by an average of 8 minutes/patient entry; physics time increased by 7 minutes/patient entry; the weekly electronic chart check takes approximately 3 minutes/patient. Therapists who used Varis efficiently showed a slight decrease in treatment times, attributed to MLC integration and auto-setup. Some therapists experienced a decrease in efficiency, because of unfamiliarity and excess intervention. On a positive note, notable events have decreased by a factor of 10 since full initiation. Unfortunately, the remaining errors are often the result of a therapist relying on incorrect electronic information.
Conclusion: The Varis R&V system has had an impact on our clinic’s process and efficiency. Checking of all beam data and related field scheduling have helped reduce errors and misconceptions. We feel a dual-energy machine can be operated with two experienced therapists and an up-to-date R&V system more accurately and efficiently than with three therapists working without an integrated R&V. We anticipate future Varis releases will further promote efficiency and accuracy. 相似文献
Obesity is a multifactorial disease and is associated with an increased risk of developing metabolic syndrome and co-morbidities. Dysregulated expansion of the adipose tissue during obesity induces local tissue hypoxia, altered secretory profile of adipokines, cytokines and chemokines, altered profile of local tissue inflammatory cells leading to the development of low-grade chronic inflammation. Low grade chronic inflammation is considered to be the underlying mechanism that increases the risk of developing obesity associated comorbidities. The glucocorticoid induced protein annexin A1 and its N-terminal peptides are anti-inflammatory mediators involved in resolving inflammation. The aim of the current study was to investigate the role of annexin A1 in obesity and associated inflammation. To achieve this aim, the current study analysed data from two feasibility studies in clinical populations: (1) bariatric surgery patients (Pre- and 3 months post-surgery) and (2) Lipodystrophy patients. Plasma annexin A1 levels were increased at 3-months post-surgery compared to pre-surgery (1.2 ± 0.1 ng/mL, n = 19 vs. 1.6 ± 0.1 ng/mL, n = 9, p = 0.009) and positively correlated with adiponectin (p = 0.009, r = 0.468, n = 25). Plasma annexin A1 levels were decreased in patients with lipodystrophy compared to BMI matched controls (0.2 ± 0.1 ng/mL, n = 9 vs. 0.97 ± 0.1 ng/mL, n = 30, p = 0.008), whereas CRP levels were significantly elevated (3.3 ± 1.0 µg/mL, n = 9 vs. 1.4 ± 0.3 µg/mL, n = 31, p = 0.0074). The roles of annexin A1 were explored using an in vitro cell based model (SGBS cells) mimicking the inflammatory status that is observed in obesity. Acute treatment with the annexin A1 N-terminal peptide, AC2-26 differentially regulated gene expression (including PPARA (2.8 ± 0.7-fold, p = 0.0303, n = 3), ADIPOQ (2.0 ± 0.3-fold, p = 0.0073, n = 3), LEP (0.6 ± 0.2-fold, p = 0.0400, n = 3), NAMPT (0.4 ± 0.1-fold, p = 0.0039, n = 3) and RETN (0.1 ± 0.03-fold, p < 0.0001, n = 3) in mature obesogenic adipocytes indicating that annexin A1 may play a protective role in obesity and inflammation. However, this effect may be overshadowed by the continued increase in systemic inflammation associated with rapid tissue expansion in obesity. 相似文献