ABSTRACT
BACKGROUND: Residency is the fundation for high-quality medical care and also for career development of young urologists. In 2015 the GeSRU (German Society of Residents in Urology) carried out the first nationwide survey among young physicians in urology and described the status quo of their residency. This revised follow-up examination draws an updated picture of the training and working conditions of residents in urology and assesses the development. METHODS: In 2020 the GeSRU conducted an online-based survey of all residents in urology; therefore, the 2015 questionnaire was expanded. The model of the professional gratification crisis was used again. RESULTS: A total of 332 questionnaires were analyzed. Major findings have not changed since 2015. The daily working routine is characterized by high pace and workload and economic considerations. Family- and research-friendly working conditions are largely lacking. 35% of the respondents draw professional consequences. The psychosocial strain remains very high and conveys a risk for physicians' health and patients' quality of care. CONCLUSION: These results demonstrate that there are still systemically immanent burdens for residents in urology, which require adjustments to the working and training conditions. A structured, transparent curriculum for urological residency, remuneration and time for training and models which enable work-life balance should be established.
Subject(s)
Internship and Residency , Urology , Germany , Humans , Surveys and Questionnaires , Urology/education , Work-Life BalanceABSTRACT
BACKGROUND: In current hospital-based urological care, economic pressure and its influence on urological working and further training conditions are a main point of criticism among young urologists. Against the background of a growing need for young talent in our specialist discipline, there is an urgent need for action. With the introduction of the lower limits for nursing staff, there is now a threat of a reduction in the number of physicians with the aim of reducing costs for business reasons. OBJECTIVE: A mandatory staffing ratio is often mentioned to counteract the downsizing in German clinics. The role of the lower staffing limit is explained in the following article. MATERIALS AND METHODS: We have analyzed the current draft laws of the federal government, as well as position papers and statements from federal political representatives such as the Marburger Bund, Bundesverband Deutscher Urologen and the German Medical Association (Bundesärztekammer) since 2018. RESULTS AND CONCLUSION: The analysis of current developments in nursing policy shows that the first step is a needs-based assessment of personnel and subsequent financing in the clinic setting. With adequate staffing, as in the traffic light scheme of the German Medical Association, not only would clinics position themselves as attractive employers and training centers for large parts of the urological medical profession, but would also significantly improve working conditions, patient care and patient safety. Medical training must remain an essential part of everyday hospital life.
Subject(s)
Physicians , Hospitals , Humans , Patient Safety , Urologists , WorkforceABSTRACT
Currently, continuing medical evaluation takes place in Germany-but not nationally or regularly, and without national standards. Therefore, comparisons between different clinics and trainers can currently not be drawn. Survey modes, such as those that have existed in Switzerland for decades, could provide a constructive basis in the assessment of the current continuing medical education of urology residents and subsequently facilitate the discussion on improvements. This requires constructive cooperation of all involved, without attributing the responsibility only to the educators. Models of rewarding good continuing education should also be found.
Subject(s)
Education, Medical, Continuing/standards , Urology/education , Germany , Humans , Quality Assurance, Health Care , Surveys and Questionnaires , Switzerland , Urology/standardsABSTRACT
Left ventricular dilation and myocardial remodeling are hallmarks of dilated cardiomyopathy (DCM). It is assumed that left ventricular dilation is caused by the disintegration of the collagenous network by increased collagenolytic activity of matrix metalloproteinases (MMPs) and their adequate tissue inhibitors (TIMPs). In this study the myocardial MMP-1 and TIMP-1 mRNA expressions were investigated by using real-time quantitative PCR analysis from right septal endomyocardial biopsies of patients with dilated cardiomyopathy (n = 46) and control subjects (n = 11). The volume density (Vv%) of collagen was measured morphometrically. Classification was done according to LV diameters [left ventricular enddiastolic diameter (LVEDD, cm) calculated to body surface area (BSA, m(2))] into three DCM groups: group I (LVEDD-BSA > 2.7-3.0 cm/m(2)), group II ( > 3.0-3.6 cm/m(2)), group III ( > 3.6 cm/m(2)), controls (< 2.7 cm/m(2)). Compared with controls, the MMP-1 expression in patients with DCM was significantly increased (119.2 +/- 45.2 vs. 1.3 +/- 0.4; p < 0.001) as was TIMP-1 expression (9.6 +/- 1.2 vs. 1.3 +/- 0.4; p < 0.01). Moreover the MMP-1 and TIMP-1 expression varied according to LV diameter: group I (MMP-1: 8.7 +/- 3.5; p = 0.33; TIMP- 1: 4.5 +/- 1.2; p < 0.01); group II (MMP-1: 211.4 +/- 86.0; p < 0.001; TIMP-1: 12.5 +/- 1.9 ; p < 0.001); group III (MMP-1: 38.8 +/- 22.6; p < 0.01; TIMP-1: 8.1 +/- 1.7; p < 0.001). Compared with controls, the collagen level in DCMPt. was significantly increased: 5.0 +/- 0.6 vol% vs 1.2 +/- 0.2 vol% p < 0.001 and correlates with LV diameter. This study reveals that the overexpression of MMP-1, which is associated with an increased ratio of MMP-1/TIMP-1 in DCM, indicates an activated collagenolytic system while replacement fibrosis is accumulating. The MMP-1 overexpression is mainly found in moderately dilated DCM hearts (group II) indicating the dynamic process of LV dilation and the importance of collagenases in the early phase of LV remodeling.
Subject(s)
Cardiomyopathy, Dilated/metabolism , Endocardium/metabolism , Heart Ventricles/metabolism , Matrix Metalloproteinase 1/metabolism , Tissue Inhibitor of Metalloproteinase-1/metabolism , Biomarkers/metabolism , Cardiomyopathy, Dilated/genetics , Humans , Male , Matrix Metalloproteinase 1/genetics , Middle Aged , RNA, Messenger/metabolism , Tissue Inhibitor of Metalloproteinase-1/geneticsABSTRACT
OBJECTIVES: The hypothesis of impaired collagenolysis in patients with hypertrophic cardiomyopathy (HCM) was tested by measuring serum markers of type-I collagen metabolism. These markers were correlated with echocardiographic parameters of diastolic function. BACKGROUND: HCM is a common disease in the adult population with a wide range of clinical manifestations. Left ventricular hypertrophy and increased intramyocardial collagen content are known to cause diastolic dysfunction in patients with HCM. METHODS: In 26 patients with HCM and 38 control subjects (aged: 57+/-3 and 54+/-2 years, p=n.s.) serum levels of collagenolytic matrixmetalloproteinase-1 (MMP-1) and its inhibitor TIMP-1, the markers for collagen type-I synthesis (PICP) and degradation (ICTP) were determined by ELISA and RIA. Diastolic function were determined by Doppler echocardiography. RESULTS: Free TIMP-1 was elevated in HCM compared to controls (216,78+/-9,89 vs 183.77+/-7.57 ng/ml ; p=0.006) as well as PICP (165.92+/-10.26 vs 114.57+/-6.38 mug/l; p<0.001). Free MMP-1 was significantly lower in HCM (1.13+/-0.20 vs 2.33+/-0.34; p=0.01). ICTP did not differ. The MMP-1/TIMP-1 ratio was significantly lower in HCM (0.006+/-0.001 vs 0.012+/-0.001, p=0.003). PICP correlated positively with diastolic E/A ratio (r=0.389; p=0.05) and septal thickness (r=0.484; p=0.01). CONCLUSIONS: Serum marker of collagen synthesis (PICP) is increased in patients with HCM. Increased marker for inhibition of collagenolysis (TIMP-1) and a disturbed balance of collagen synthesis and degradation (ratio) with a predominance of inhibition of collagenolysis indicates collagen accumulation (fibrosis), which explains passive diastolic dysfunction in patients with HCM.
