Crossover of the patient satisfaction surveys, adverse events and patient complaints for continuous improvement in radiotherapy department.

OBJECTIVE: The patient's needs and expectations can be assessed through satisfaction surveys, adverse event declarations and records of complaints. By cross-referencing individual complaints, satisfaction surveys and the adverse events received, we could get valuable information. The objective is to identify common elements of work between these different sources to improve care. METHODS: A retrospective analysis of patients' complaints, surveys and adverse events was carried out in order to highlight common improvement items between these three sources of information. RESULTS: A satisfaction survey was given to the patients at the end of their treatment, who filled it out and left it in the 'ad hoc' letterbox. At the end of December 2019, 4695 questionnaires had been collected (response rate 37%). In addition, since 2014, 1369 patients (∼20 patients per month) have been interviewed 'face to face' by the research nurse who assesses their satisfaction using open questions. At the same time, a collection of complaints and adverse events was carried out. All these data have been analysed and cross-checked in order to highlight areas for improvement and strengthen the safety and quality of care in our department. CONCLUSIONS: Collect and analyse satisfaction surveys, unexpected events and complaints constitute in our opinion, an effective tool to achieve patient empowerment. We aim for the patients to become a real player in their safety and involve in the overall effort to improve the quality of their radiotherapy treatment by reporting what does not meet their expectations.

Comparison between the WHO-CFICPS and the PRISMA classification of safety-related events in a radiation oncology department.

INTRODUCTION: Describing Safety-Related Events (SREs) in a radiotherapy (RT) department and comparing WHO-CFICPS (World Health Organization's Conceptual Framework For The International Classification For Patient Safety) and PRISMA (Prevention and Recovery Information System for Monitoring and Analysis) methods for classifying SREs. METHODS: From February 2017 to October 2020, two Quality Managers (QMs) randomly classified 1173 SREs using 13 incident types of WHO-CFICPS. The same two QMs, reclassified the same SREs according to 20 PRISMA incident codes. Statistical analysis was performed to assess the association between the 13 incident types of WHO-CFICPS and the 20 PRISMA codes. The chi-squared and post-hoc tests using adjusted standardized residuals were applied to detect the association between the two systems. RESULTS: There was a significant association between WHO-CFICPS incident types and PRISMA codes (P < 0.001). Ninety-two percent of all SREs were categorized using 4 of 13 WHO-CFICPS incident types including Clinical Process/Procedure (n = 448, 38.2%), Clinical Administration (n = 248, 21.1%), Documentation (n = 226, 19.2%) and Resources/Organizational Management (n = 15,613.3%). According to PRISMA classification, 14 of the 20 codes were used to describe the same SREs. PRISMA captured 41 Humans Skill Slips from 226 not better defined WHO-CFICPS Documentation Incidents, 38 Human Rule-based behaviour Qualification from not better defined 447 Clinical Process/Procedure and 40 Organization Management priority events from 156 not better defined WHO-CFICPS Resources/Organizational Management events (P < 0.001). CONCLUSION: Although there was a significant association between WHO-CFICPS and PRISMA, The PRISMA method provides a more detailed insight into SREs compared to WHO-CFICPS in a RT department.

Effects of granulocyte-colony-stimulating factor on progenitor cell mobilization and heart perfusion and function in normal mice.

BACKGROUND AIMS: Mobilization of stem cells and progenitor cells from the bone marrow (BM) into the peripheral blood (PB) by granulocyte-colony-stimulating factor (G-CSF) is being investigated for cardiac regeneration in ischemic heart disease. However, hematopoietic (HPC), mesenchymal (MPC) and endothelial (EPC) progenitor mobilization have not been optimized and the effect of G-CSF on myocardial perfusion and cardiac function in a normal heart has never been studied. METHODS: Normal mice were injected daily for 1-10 days with subcutaneous recombinant human G-CSF. PB and BM were evaluated for HPC and EPC by flow cytometry and HPC and MPC by hematopoietic (CFU-GM) and mesenchymal (CFU-F) colony assays. Echocardiography, microSPECT imaging, cardiac catheterization and immunohistochemistry were performed in mice treated for 10 days. RESULTS: HPC and CFU-GM in PB peaked after 2 days, CFU-F after 4 days and EPC after 3 days. Thereafter, while HPC temporally decreased before showing a second peak, EPC remained detectable only at low levels. In BM, hematopoietic stem cells (HSC) and CFU-GM did not increase much overall but peaked twice on days 2 and 7. EPC (peak on day 7) production increased in the BM, but CFU-F formation declined considerably after day 2. G-CSF enhanced myocardial perfusion and vascularization but impaired hemodynamic performance of the heart through apparently increased ventricular wall rigidity. CONCLUSIONS: G-CSF induces the mobilization of HPC, EPC and CFU-F progenitors in PB according to very different patterns, and has a significant impact on perfusion and function of the normal heart.

Spontaneous and granulocyte–colony-stimulating factor-enhanced marrow response and progenitor cell mobilization in mice after myocardial infarction.

BACKGROUND AIMS: Hematopoietic (HPC), mesenchymal (MPC) and/or endothelial (EPC) progenitor cells are being studied to repair the myocardium after acute or chronic ischemia. We examined marrow response to myocardial infarction (MI) and the ability of granulocyte­colony-stimulating factor (G-CSF) to enhance mobilization of HPC, MPC and EPC in peripheral blood (PB) and bone marrow (BM) of MI mice. METHODS: We induced MI in C57Bl/6 mice, while sham-operated (SO) animals were similarly operated on but without coronary artery ligation. Animals were treated with either saline or G-CSF, from day −5 to day +5 after MI or from day 0 to day +5. Progenitor cell numbers in PB and BM were evaluated by fluorescence-activated cell sorting (FACS) analysis and cell culture. RESULTS: White blood cells (WBC) decreased in BM and increased in PB after MI; G-CSF amplified this effect in BM but not in PB. HPC numbers decreased in BM after MI, while HPC and granulocyte­macrophage colony-forming units (GM-CFU) increased in PB only after G-CSF treatment, and more prominently so in MI than in SO mice. MPC and fibroblast­colony-forming units (F-CFU) as well as EPC were mobilized into the PB after MI and further after G-CSF treatment. Plasma troponin T concentrations decreased after G-CSF treatment. CONCLUSIONS: BM is globally affected by acute MI, but not simple body injury, with intense mobilization of marrow MPC and EPC into the PB but inhibition of HPC. Progenitor cell entry into the PB may be paralleled by depletion of their BM pools. G-CSF is required for HPC mobilization and enhances MPC and EPC entry into the PB.

Myocardial infarct size quantification in mice by SPECT using a novel algorithm independent of a normal perfusion database.

BACKGROUND: There is a growing interest in developing non-invasive imaging techniques permitting infarct size (IS) measurements in mice. The aim of this study was to validate the high-resolution rodent Linoview single photon emission computed tomography (SPECT) system for non-invasive measurements of IS in mice by using a novel algorithm independent of a normal database, in comparison with histology. METHODS: Eleven mice underwent a left coronary artery ligature. Seven days later, animals were imaged on the SPECT 2h30 after injection of 173 ± 27 MBq of Tc-99m-sestamibi. Mice were subsequently killed, and their hearts were excised for IS determination with triphenyltetrazolium chloride (TTC) staining. SPECT images were reconstructed using the expectation maximization maximum likelihood algorithm, and the IS was calculated using a novel algorithm applied on the 20-segment polar map provided by the commercially available QPS software (Cedars-Sinai Medical Center, CA, USA). This original method is attractive by the fact that it does not require the implementation of a normal perfusion database. RESULTS: Reconstructed images allowed a clear delineation of the left ventricles borders in all mice. No significant difference was found between mean IS determined by SPECT and by TTC staining [37.9 ± 17.5% vs 35.6 ± 17.2%, respectively (P = 0.10)]. Linear regression analysis showed an excellent correlation between IS measured on the SPECT images and IS obtained with TTC staining (y = 0.95x + 0.03 (r = 0.97; P < 0.0001)), without bias, as demonstrated by the Bland-Altman plot. CONCLUSION: Our results demonstrate the accuracy of the method for the measurement of myocardial IS in mice with the Linoview SPECT system.

Bone marrow-derived myofibroblasts are the providers of pro-invasive matrix metalloproteinase 13 in primary tumor.

Carcinoma-associated fibroblasts are key contributors of the tumor microenvironment that regulates carcinoma progression. They consist of a heterogeneous cell population with diverse origins, phenotypes, and functions. In the present report, we have explored the contribution of bone marrow (BM)-derived cells to generate different fibroblast subsets that putatively produce the matrix metalloproteinase 13 (MMP13) and affect cancer cell invasion. A murine model of skin carcinoma was applied to mice, irradiated, and engrafted with BM isolated from green fluorescent protein (GFP) transgenic mice. We provide evidence that one third of BM-derived GFP(+) cells infiltrating the tumor expressed the chondroitin sulfate proteoglycan NG2 (pericytic marker) or α-smooth muscle actin (α-SMA, myofibroblast marker), whereas almost 90% of Thy1(+) fibroblasts were originating from resident GFP-negative cells. MMP13producing cells were exclusively α-SMA(+) cells and derived from GFP(+) BM cells. To investigate their impact on tumor invasion, we isolated mesenchymal stem cells (MSCs) from the BM of wild-type and MMP13-deficient mice. Wild-type MSC promoted cancer cell invasion in a spheroid assay, whereas MSCs obtained from MMP13-deficient mice failed to. Our data support the concept of fibroblast subset specialization with BM-derived α-SMA(+) cells being the main source of MMP13, a stromal mediator of cancer cell invasion.

Systematic chromosomal aberrations found in murine bone marrow-derived mesenchymal stem cells.

Mesenchymal stem cells (MSCs) are studied as a cellular source for the treatment of various diseases. In this work, we isolated and cultivated murine bone marrow-derived MSCs. After a first observation of a solid tumor in a mouse injected with these cells, we systematically explored their chromosomal stability. We observed in all the cytogenetically analyzed cases gross chromosomal alterations every time the MSCs went through the senescence crisis while the lymphocytes from the same animals showed a normal chromosome count. This observation was confirmed in different mouse strains, with different culture protocols, and even in short-term cultures after a hematopoietic cell negative immunodepletion performed in order to accelerate the isolation procedure. Therefore, we conclude that murine MSCs display high chromosomal instability and can generate tumors, and that care must be taken before using them for the evaluation of MSC therapeutic potential.