Burn-out and employability rates are impacted by the level of job autonomy and workload among Dutch gastroenterologists.

BACKGROUND: Increasing burn-out rates among gastroenterologists make it necessary to find ways to prevent burn-out and to stimulate their ability and willingness to continue working (i.e., their employability). Understanding their antecedents might help organizations to prevent burn-out and to enhance employability among this occupational group. OBJECTIVE: The purpose of this study is to provide insight in the relationship between job characteristics and job crafting behavior on the one hand and job outcomes (burn-out symptoms and employability) on the other hand. METHODS: Data from two surveys in 2020 and 2021 were collected in a longitudinal study among 238 Dutch gastroenterologists. The data were analyzed with multiple linear regression analyses and paired-samples t-tests. RESULTS: Job characteristics, specifically job aspects that require sustained physical and/or psychological effort or skills (i.e., job demands), are important predictors of burn-out symptoms among gastroenterologists. Specifically, high quantitative and emotional workload are significantly related to more burn-out symptoms. No strong relationship was found between job crafting and burn-out symptoms. Furthermore, job aspects that reduce the negative impact of these demanding aspects and that help to achieve work goals (i.e., job resources), and job demands to some extent, significantly predict employability. In particular, high job autonomy is related to higher employability, and high quantitative workload is associated with lower employability. Job crafting does not significantly affect employability. Furthermore, levels of burn-out symptoms and employability differed only little across time. CONCLUSION: In gastroenterologists, a high quantitative workload and emotional workload are associated with a higher burn-out risk, while low job autonomy and high quantitative workload are associated with more negative perceptions of employability. To prevent burn-out and to create positive perceptions of employability, it is important to take these aspects into account.

Microbiota composition and mucosal immunity in patients with asymptomatic diverticulosis and controls.

INTRODUCTION: The etiology of diverticulosis is still poorly understood. However, in patients with diverticulitis, markers of mucosal inflammation and microbiota alterations have been found. The aim of this study was to evaluate potential differences of the gut microbiota composition and mucosal immunity between patients with asymptomatic diverticulosis and controls. METHODS: We performed a prospective study on patients who underwent routine colonoscopy for causes not related to diverticular disease or inflammatory bowel disease. Participants were grouped based on the presence or absence of diverticula. Mucosal biopsies were obtained from the sigmoid and transverse colon. Microbiota composition was analyzed with IS-pro, a 16S-23S based bacterial profiling technique. To predict if patients belonged to the asymptomatic diverticulosis or control group a partial least squares discriminant analysis (PLS-DA) regression model was used. Inflammation was assessed by neutrophil and lymphocyte counts within the taken biopsies. RESULTS: Forty-three patients were enrolled. Intestinal microbiota profiles were highly similar within individuals for all phyla. Between individuals, microbiota profiles differed substantially but regardless of the presence (n = 19) of absence (n = 24) of diverticula. Microbiota diversity in both sigmoid and transverse colon was similar in all participants. We were not able to differentiate between diverticulosis patients and controls with a PLS-DA model. Mucosal lymphocyte counts were comparable among both groups; no neutrophils were detected in any of the studied biopsies. CONCLUSIONS: Microbiota composition and inflammatory markers were comparable among asymptomatic diverticulosis patients and controls. This suggests that the gut microbiota and mucosal inflammation do not play a major role in the pathogenesis of diverticula formation.

Assessment of serum matrix metalloproteinases MMP-2 and MMP-9 after human liver transplantation: increased serum MMP-9 level in acute rejection.

BACKGROUND: Alterations in synthesis and breakdown of extracellular matrix components play a role in acute rejection after orthotopic liver transplantation (OLT). Matrix metalloproteinases (MMPs) are capable of degrading basement membranes and are involved in the process of tissue remodelling in inflammation and liver fibrosis. METHODS: We examined MMP-2 and MMP-9 in serum of 33 patients before and during 1 year after OLT, in 60 controls as well as in some specimens of cirrhotic liver and control liver tissue. RESULTS: Serum MMP-2 levels before OLT were significantly higher compared with controls and decreased approximately 50% after OLT. Also, the MMP-2 content of cirrhotic liver specimens was significantly higher compared with normal liver. MMP-9 in serum and liver tissue of patients were similar to controls, but serum levels showed a peak at 1 week after OLT. At this time-point, total and active/inhibitor-complexed MMP-9 was significantly higher in patients with rejection (n=13) compared with those without rejection (n=20). The relative amount of MMP-9 in the active/inhibitor-complexed form did not differ between each group over time. Immunohistochemical staining at 1 week after OLT showed increased numbers of MMP-9-positive inflammatory cells in the portal triads of patients with rejection. CONCLUSIONS: Patients with acute allograft rejection have elevated serum levels of MMP-9 1 week after OLT, which was most likely derived from inflammatory cells. An increased MMP-2 serum level and liver tissue content was found in patients with cirrhosis, which decreased after OLT. These observations indicate active involvement of MMP-2 and -9 in end-stage liver disease and OLT.

Plasma MMP-2 and MMP-9 and their inhibitors TIMP-1 and TIMP-2 during human orthotopic liver transplantation. The effect of aprotinin and the relation to ischemia/reperfusion injury.

Uncontrolled activation of matrix metalloproteinases (MMPs) can result in tissue injury and inflammation, yet little is known about the activation of MMPs during orthotopic liver transplantation (OLT). OLT is associated with increased fibrinolytic activity due to elevated plasmin generation. The serine-protease plasmin not only causes degradation of fibrin clots but is also thought, amongst others, to play a role in the activation of some matrix metalloproteinases. We therefore studied the evolution of MMP-2 and -9 plasma concentrations during OLT and the effect of serine-protease inhibition by aprotinin on the level and activation of these MMPs. In a group of 24 patients who participated in a randomized, double-blind, placebo-controlled study we determined serial MMP-2 and MMP-9 plasma levels during transplantation using ELISA (total MMP), activity assays (activatable MMP) and zymography. In addition, the MMP-inhibitors TIMP-1 and TIMP-2 were assessed by ELISA. The putative regulating factors tumor necrosis factor alpha (TNF-alpha) and tissue-type plasminogen activator (t-PA) were assessed as well. Patients were administered high-dose aprotinin, regular-dose aprotinin or placebo during surgery. Plasma TIMP-1, TIMP-2 and MMP-2 level gradually decreased during transplantation. Approximately two-thirds of total MMP-2 appeared to be in its activatable proMMP form. No release of MMP-2 from the graft could be detected. In contrast, plasma levels of MMP-9 increased sharply during the anhepatic and postreperfusion periods. Peak MMP-9 levels of about eight times above baseline were found at 30 minutes after reperfusion. Most MMP-9 appeared to be in its active/inhibitor-complexed form. No significant differences were observed between the three treatment groups. However, in patients with more severe ischemia/reperfusion (I/R) injury the MMP-9 concentration, particularly of the active/inhibitor-complexed form, remained high at 120 minutes postreperfusion compared to patients with no or mild I/R injury. The decrease in plasma levels of MMP-2, TIMP-1 and TIMP-2 during OLT occurred irrespective of the severity of the I/R injury. There was a significant correlation between MMP-9 and t-PA levels, but not with TNF-alpha. In conclusion, OLT is associated with a sharp increase of MMP-9 during the anhepatic and postreperfusion periods, which coincided with the changes in t-PA. MMP-2, TIMP-1 and TIMP-2 gradually decreased during OLT. The composition of these MMPs was not altered by the use of aprotinin, suggesting that serine-protease/plasmin-independent pathways are responsible for MMP regulation during OLT. In addition, only MMP-9 seems to be involved in I/R injury during human liver transplantation.

Assessment of the clinical significance of serum matrix metalloproteinases MMP-2 and MMP-9 in patients with various chronic liver diseases and hepatocellular carcinoma.

Matrix metalloproteinases (MMPs) have the ability to degrade basement membranes and may thus play an important role in extracellular matrix turnover in liver fibrosis and carcinogenesis. Serum levels of MMPs have been suggested as diagnostic markers in these processes. We measured serum MMP-2 and MMP-9 by ELISA in 91 patients with chronic liver disease, including 25 patients with hepatocellular carcinoma (HCC), and in 60 controls. MMP-2 was significantly higher in patients with chronic liver disease compared to controls, and increased with Child-Pugh class. There was a significant correlation between MMP-2 and liver function (bilirubin, albumin, and prothrombin time), and a strong opposite correlation between MMP-9 and these parameters. MMP-2 levels in patients with HCC were significantly higher than in controls, but comparable to patients with chronic liver disease without this malignancy. MMP-9 yielded no significant differences between patients with or without HCC and controls. Serum MMP-2 and to a lesser extent MMP-9 correlate with the severity of liver disease and may reflect changes in extracellular matrix remodeling. Due to a considerable overlap in patients with chronic liver disease with or without HCC, MMP-2 and MMP-9 can not be used as a diagnostic marker for HCC.