The aims of the present study were: to determine the diagnostic accuracy of objectively measured, self-reported and recalled body mass index (BMI) for osteoporosis and osteopenia; to determine the diagnostic costs, in terms of bone mineral density (BMD) measurements, per osteoporotic or osteopenic patient detected, using different BMI tests; and to determine the extent to which the results can be used within the framework of the current screening program for breast cancer in The Netherlands. Within the framework of a cross-sectional study on the prevalence of osteoporosis in the south of The Netherlands, 1155 postmenopausal women aged 50-80 years were asked for their present height and their weight at age 20-30 years. Subsequently their actual weight, height and BMD of the lumbar spine (DXA) were measured. The BMD cutoff was 0.800 g/cm2 for osteoporosis and 0.970 g/cm2 for low BMD (osteoporosis + osteopenia). After receiver operating characteristic analysis, age was cut off at 60 years and BMI at 27 kg/m2. Diagnostic accuracies of objectively measured, self-reported and recalled BMI were evaluated using predictive values (PV) and odds ratios. The resulting 'true positive' and 'false positive' rates were used to calculate diagnostic costs (i.e., DXA) for each osteoporotic patient or low-BMD patient detected. The prevalence of osteoporosis in the study population was 25%, that of low BMD 65%. Only the age-BMI tests 'age > or = 60, BMI < or = 27' showed PVs for osteoporosis (31-41%) and for low BMD (71-81%) that were higher than the prior probabilities for these conditions. Related odds ratios were 2.14-3.18 (osteoporosis) and 1.87-3.04 (low BMD). The objective BMI test detected 50% of the osteoporotic patients. Using the self-reported BMI test and the recalled BMI test, detection rates increased to 55% and 69%, respectively. Concomitant costs per osteoporotic patient detected rose by 24%. Detection of patients with a low BMD increased from 38% for objective BMI and 42% for self-reported BMI to 60% for recalled BMI. Related costs increased by 11%. If all women over 50 years of age (irrespective of their BMI) were to be referred for BMD measurement, costs per osteoporotic patient or low-BMD patient detected would be 304 and 116 Euros, respectively. Only in women over 60 years does a BMI below 27 kg/m2 provide a better prediction of the presence of osteoporosis or low BMD than could be expected solely on the basis of the relevant prevalences in postmenopausal women aged 50-80 years. If the use of BMI for the detection of osteoporotic or low-BMD patients is still considered, measuring weight and just asking for a person's height will do. Although age and BMI are the strongest risk factors for osteoporosis, they are of less significance when used for screening the population for osteoporosis. More research is needed before age and BMI can be included in any screening program. As regards practical considerations alone, measurements of BMD could be implemented within the screening program for breast cancer.

Abstract:In the past decade, the number of the studies conducted on the effects of resistance training on circadian rhythm of endocrine hormones is increasing exponentially. The aim of this report is to explore the current and prevailing studies in an attempt to elucidate the findings of resistance training on circadian rhythm of endocrine hormones. Analysis of the available research from 2001 until 2015 demonstrated a wide variety of methodologies and sampled populations. However, all sampled studies made use of a pre-test, post-test experimental design taking place during the day. In addition, the primary hormones assessed were testosterone and cortisol, sampled via saliva. Collectively the sampled studies demonstrated that resistance training is capable of affecting the circadian rhythm of endocrine hormone secretion. However, it must be noted that these alterations were primary following training and the alterations transient in nature, with endocrine responses returning to normal circadian rhythm ranges via natural feedback mechanisms.

End‐stage chronic liver disease is a major cause of mortality worldwide. Irrespective of the underlying cause, most chronic liver diseases are characterized by fibrosis, hepatocellular necrosis, inflammation, ductular reactions and proliferation of the liver progenitor cells. Vast differences exist between experimental models that mimic these processes, and their identification is fundamental for translational research. However, the underlying differences in the molecular mechanism driving liver injury in different models remains largely unknown due to our inability to visualize the initiation and progression of liver injury in vivo in mice. Recently we have introduced quantitative Liver Intravital Microscopy (qLIM) that enables real‐time assessment of bile transport and blood‐bile barrier (BBlB) integrity in the intact liver of live mice (Pradhan‐Sundd et al., Gastroenterology, 2018) to visualize injury progression in two widely used experimental models of chronic liver injury ‐the choline‐deficient ethionine‐supplemented (CDE) or 3, 5‐diethoxycarbonyl 1, 4‐dihydrocollidine (DDC) diet, respectively. qLIM analysis revealed that chronic liver injury involves physical breach of BBlB, mixing of blood with bile and loss of bile transport across hepatocytes in both CDE and DDC diet fed mice. Mechanistically we showed an association of disruption of the BBlB and loss of various tight junctional proteins with sustained inflammation and apoptotic cell death (Pradhan‐Sundd et al., Gastroenterology, 2018). Thus, we hypothesized that blocking Caspase ‐1 induced inflammatory response can inhibit the loss of BBlB and thus postpone the chronic liver injury initiation in these diet fed mice. Indeed, mice with deletion of caspase‐1 displayed reduced liver injury, ductular reaction, fibrosis, inflammation, and apoptosis after two weeks of CDE and DDC diet. Remarkably, qLIM analysis showed intact blood biliary barrier at day 4 and 6 of CDE and DDC fed mice suggestive of delay in injury initiation. Furthermore, we demonstrate that the recovery from CDE and DDC diet induced liver injury is significantly accelerated in caspase‐1 KO mouse. We also found upregulation several tight junctional claudins in the liver upon caspase ‐1 knockdown. Current investigation is underway to analyse the regulation of tight junctional claudins by Caspase‐1. These findings may lead insight to disease progression and possible treatment of diet induced chronic liver injury.