Abstract-Epidemiological studies in humans, as well as experimental studies in animal models, have shown an association between visceral obesity and dyslipidemia, insulin resistance, and type 2 diabetes mellitus. Recently, attention has been focused on the excessive accumulation of triglycerides (TG) in the liver as part of this syndrome. In this review, important principles of the pathophysiological involvement of the liver in the metabolic syndrome obtained in rodent models are summarized. We focus on non-alcoholic causes of steatosis, because the animal experiments we refer to did not include alcohol as an experimental condition. In general, there is continuous cycling and redistribution of non-oxidized fatty acids between different organs. The amount of TG in an intrinsically normal liver is not fixed but can readily be increased by nutritional, metabolic, and endocrine interactions involving TG/free fatty acid (FFA) partitioning and TG/FFA metabolism. Several lines of evidence indicate that hepatic TG accumulation is also a causative factor involved in hepatic insulin resistance. Complex interactions between endocrine, metabolic, and transcriptional pathways are involved in TG-induced hepatic insulin resistance. Therefore, the liver participates passively and actively in the metabolic derangements of the metabolic syndrome. We speculate that similar mechanisms may also be involved in human pathophysiology. Key Words: lipoprotein metabolism Ⅲ glucose metabolism Ⅲ fatty acid metabolism Ⅲ insulin resistance Ⅲ mouse models E pidemiological studies in humans have documented an association between visceral obesity and cardiovascular risk factors such as dyslipidemia, insulin resistance, and type 2 diabetes mellitus. [1][2][3][4] Recently, attention has been focused on the excessive accumulation of triglycerides (TG) within the liver as part of this metabolic syndrome. It appears that fat accumulation in the liver is associated with several features of insulin resistance even in normal-weight and moderately overweight subjects. 5 Nonetheless, from these observations in humans it remains unclear to what extent hepatic steatosis is a cause rather than a consequence of the metabolic syndrome.This issue is difficult to solve, because the liver is not readily accessible in humans. Therefore, in the present review we focus on mouse models with variations in liver TG content induced by targeted interventions to elucidate the role of liver steatosis in metabolic diseases like dyslipidemia, insulin resistance, and type 2 diabetes mellitus. Although alcohol-induced liver steatosis was already described by Thomas Addison in 1845, it is appreciated only since 1962 that steatosis can also occur without the use of alcohol, so-called non-alcoholic steatosis. 6 The current review focuses on non-alcoholic causes of steatosis, because the animal experiments we refer to did not include alcohol as an experimental condition. We briefly describe factors involved in body TG homeostasis, intrahepatic and extrahepatic factors causing stea...

Many factors determine the performance and success of delivery room management of newborn babies. Improving the quality of care in this challenging surrounding has an important impact on patient safety and on perinatal morbidity and mortality. Video recording (VR) offers the advantage to record and store work as done rather than work as recalled. It provides information about adherence to algorithms and guidelines, and technical, cognitive and behavioural skills. VR is feasible for education and training, improves team performance and results of research led to changes of international guidelines. However, studies thus far have not provided data regarding whether delivery room video recording affects long-term team performance or clinical outcomes. Privacy is a concern because data can be stored and individuals can be identified. We describe the current state of clinical practice in highand low-resource settings, discuss ethical and medical-legal issues and give recommendations for implementation with the aim of improving the quality of care and outcome of vulnerable babies.

No abstract

Background Iron deficiency (ID) and anaemia in Inflammatory Bowel Disease (IBD) are associated with reduced quality of life, worse disease outcomes, and an increase in healthcare costs. In the European guidelines, anaemia is listed as one of the treatment goals. The data on the prevalence of anaemia and ID are inconsistent. Therefore, we evaluated the prevalence of ID, anaemia, and potential risk factors in a large Dutch outpatient population. Methods Between January and November 2021, consecutive adult outpatients with IBD, who did not have significant comorbidities associated with anaemia, were included in this study across 16 general, teaching, and academic hospitals within the Netherlands. Besides demographic and clinical data, relevant biochemical parameters such as haemoglobin (Hb), Mean Corpuscular Volume (MCV), iron indices, and inflammatory markers (e.g., C-reactive protein (CRP) and faecal calprotectin (FCP)) were extracted from medical records. Active IBD was defined by either CRP >5mg/L or FCP >150mg/g. ID was defined by ferritin <100µg/L in case of inflammation and <30µg/L in quiescent IBD, or transferrin saturation <20%. The Dutch national reference range was used to define anaemia: Hb <7.5mmol/L or <8.5mmol/L for females and males, respectively. The data were analysed by stratifying patients into Crohn’s Disease (CD) and Ulcerative Colitis (UC) groups, with the latter also including patients with IBD-unclassified (IBDU). Results In total, 2197 patients (1271 CD, 849 UC, and 77 IBDU) were included in the study. The overall prevalence of anaemia, iron-deficiency anaemia (IDA), and ID was: 18.0%, 12.2%, and 43.4%, respectively. The prevalence of all three conditions did not differ between the CD and UC groups (P>0.05). Severe anaemia (Hb<6.2 mmol/L) was observed only in 28 patients. ID was more frequently observed in biochemically active IBD compared with quiescent IBD (70.8% versus 23.9%; P<0.001). Female gender, younger age, low MCV, and a twofold increase in biochemical inflammation were associated with ID development in multivariable analysis: Log2FCP [OR 1.39; 95% CI: 1.29–1.50; P<0.001] and Log2platelets [OR 1.85; 95% CI: 1.16–2.95; P<0.01]. In multivariable analysis, low ferritin and MCV, inflammation, older age, and male gender were associated with a higher risk of anaemia; however, disease location or behaviour did not affect the risk of developing anaemia or ID. Conclusion One in five ambulatory IBD patients presents with anaemia that is primarily caused by ID. Inflammation increases the risk of ID and anaemia regardless of IBD type or disease location. High ID prevalence suggests the need for screening and treatment optimisation.