Risk Management in Biobanks

The administration of risks is usually an important corner stone of professional operations. Nevertheless, specifically for biobanking organizations, risk recognition, control, management, and easing are inevitably extremely critical elements of everyday operations. The costly kind of unique samples/cell lines, data and also other high-pitched value biobanking products and services such as cell-based drugs, and biologically active pharmaceutical materials call for tremendously precise planning—including the full spectrum of risks. In this chapter, we have included the common risks in biobanking and the management way and methods of risks in a biobanking institution

Manifestation of Non-Alcoholic Fatty Liver Disease/Non-Alcoholic Steatohepatitis in Different Dietary Mouse Models

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), which are usually associated with obesity and metabolic syndrome, are considerable health and economic issues due to the rapid increase of their prevalence in Western society. Histologically, the diseases are characterised by steatosis, hepatic inflammation, and if further progressed, fibrosis. Dietary-induced mouse models are widely used in investigations of the development and progression of NAFLD and NASH; these models attempt to mimic the histological and metabolic features of the human diseases. However, the majority of dietary mouse models fail to reflect the whole pathophysiological spectrum of NAFLD and NASH. Some models exhibit histological features similar to those seen in humans while lacking the metabolic context, while others resemble the metabolic conditions leading to NAFLD in humans but fail to mimic the whole histological spectrum, including progression from steatosis to liver fibrosis, and thus fail to mimic NASH. This review summarises the advantages and disadvantages of the different dietary-induced mouse models of NAFLD and NASH, with a focus on the genetic background of several commonly used wild-type mouse strains as well as gender and age, which influence the development and progression of these liver diseases

Hepatic Response of Magnesium-Restricted Wild Type Mice

Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the hepatic inflammatory response was quantified by determining hepatic IL-6, TNFα, and MCP-1. Magnesium-restriction resulted in at least a 2-fold significant reduction of serum magnesium levels compared to the high-fat-diet fed and control mice, whereas the hepatic magnesium content was decreased due to high-fat-diet feeding. No changes in metabolic markers in magnesium-restricted mice were observed, while the cholesterol content was elevated in high-fat-diet fed mice. Magnesium-restricted mice additionally featured inflammation and enlarged hepatocytes in liver histology. Furthermore, magnesium-restricted and high-fat-diet fed mice exhibited elevated hepatic TNFα levels compared to control mice. Accordingly, our data suggest that magnesium is involved in hepatic inflammatory processes and hepatocyte enlargement, key histological features of human NAFLD, and may therefore contribute to development and progression of the disease

Susceptibility of Different Mouse Wild Type Strains to Develop Diet-Induced NAFLD/AFLD-Associated Liver Disease.

Although non-alcoholic and alcoholic fatty liver disease have been intensively studied, concerning pathophysiological mechanisms are still incompletely understood. This may be due to the use of different animal models and resulting model-associated variation. Therefore, this study aimed to compare three frequently used wild type mouse strains in their susceptibility to develop diet-induced features of non-alcoholic/alcoholic fatty liver disease. Fatty liver disease associated clinical, biochemical, and histological features in C57BL/6, CD-1, and 129Sv WT mice were induced by (i) high-fat diet feeding, (ii) ethanol feeding only, and (iii) the combination of high-fat diet and ethanol feeding. Hepatic and subcutaneous adipose lipid profiles were compared in CD-1 and 129Sv mice. Additionally hepatic fatty acid composition was determined in 129Sv mice. In C57BL/6 mice dietary regimens resulted in heterogeneous hepatic responses, ranging from pronounced steatosis and inflammation to a lack of any features of fatty liver disease. Liver-related serum biochemistry showed high deviations within the regimen groups. CD-1 mice did not exhibit significant changes in metabolic and liver markers and developed no significant steatosis or inflammation as a response to dietary regimens. Although 129Sv mice showed no weight gain, this strain achieved most consistent features of fatty liver disease, apparent from concentration alterations of liver-related serum biochemistry as well as moderate steatosis and inflammation as a result of all dietary regimens. Furthermore, the hepatic lipid profile as well as the fatty acid composition of 129Sv mice were considerably altered, upon feeding the different dietary regimens. Accordingly, diet-induced non-alcoholic/alcoholic fatty liver disease is most consistently promoted in 129Sv mice compared to C57BL/6 and CD-1 mice. As a conclusion, this study demonstrates the importance of genetic background of used mouse strains for modeling diet-induced non-alcoholic/alcoholic fatty liver disease

Data from: "ABC" - the Awareness-Body-Chart: a New Tool Assessing Body Awareness

Background: Despite the importance of body awareness for health and well-being there is still a lack of valid assessment tools to scan proper body awareness. To respond to the limitations of questionnaires (reading/interpretation problems of subjects) the Awareness-Body-Chart (ABC) was designed to assess body awareness by colouring 51 regions according to their awareness. The objective of this study was to investigate the psychometric characteristics of the ABC. Methods: In a questionnaire-study, 106 students in Graz (79 females, 27 males, age median 21 (IQR 20 - 23) years) filled in the ABC, furthermore a German body awareness questionnaire „KEKS", and the Beck Depression Inventory II. Factor structure, internal consistency, and retest reliability of the ABC were investigated. Correlations of the ABC with the KEKS and the Beck Depression Inventory II and comparisons of subgroups were conducted. Results: Through factor analyses, 14 factors with clear assignments to body parts could be categorized: cranium, face, cervical/lumbar region, chest/abdomen, back, shoulder, upper arm, lower arm/elbow, hand, genital area, thigh/hip, knee, lower leg, and foot. The 14 body parts and the total score showed acceptable to high Cronbach's alphas (α = .64 - .97). The test-retest reliability showed values between ρ = .71 and ρ = .96. The correlation of the ABC and KEKS (r = .66, p < .001) confirmed validity. Further indications of validity could be seen in comparisons of subgroups and in correlations with the Beck Depression Inventory II. Conclusion: The ABC proved good psychometric properties with acceptable to high internal consistency, acceptable to high retest reliability and high construct validity. It is an easy-to-use tool for clinical settings and research. The ABC opens new insights into body awareness-patterns of various subgroups

Determination of hepatic lipid profile of regimen treated CD-1 and 129Sv mice.

<p>Hepatic lipid content was determined out of livers from regimen fed CD-1 and 129Sv mice by a semi-quantitative chromatographic method and is shown as relative amount compared to untreated counterparts. (A) TG levels were increased in both mouse strains, with elevated hepatic TG storage in 129Sv mice compared to CD-1 mice. (B) Free cholesterol was only altered in some of the regimen treated 129Sv mice, including decreased free cholesterol in feeding group EtOH 14 weeks and increased free cholesterol in HF + EtOH fed for 7 and 9 weeks. (C) CE as well as (D) CER levels were increased in all feeding groups of either strain, with higher CE content in 129Sv mice compared to CD-1 mice. (E) PC levels were not altered in CD-1 mice, while HF feeding for 7 weeks caused elevated PC content and HF + EtOH feeding for 7 weeks caused decreased PC levels. (F) PE content was similar in both strains, with no alterations between untreated and regimen treated mice. Values are given as means with standard deviations and relevant significant differences are marked by an asterisk (Mann-Whitney U test, <i>P</i> values of <0.05).</p

Medians and interquartile ranges of histopathological features of steatosis, ballooning, and inflammation as well as NAS of regimen treated C57BL/6, CD-1, and 129Sv mice.

<p>Medians and interquartile ranges of histopathological features of steatosis, ballooning, and inflammation as well as NAS of regimen treated C57BL/6, CD-1, and 129Sv mice.</p