An estimation of the endoscopist's musculoskeletal injury risk for right and left lateral decubitus positions during colonoscopy: a field-based ergonomic study

Background Colonoscopy exposes endoscopists to awkward postures and prolonged forces, which increases their risk of musculoskeletal injury. Patient positioning has a significant impact on the ergonomics of colonoscopy. Recent trials have found the right lateral decubitus position is associated with quicker insertion, higher adenoma detection rates, and greater patient comfort compared to the left lateral decubitus position. However, this patient position is perceived as more strenuous by endoscopists. Methods Nineteen endoscopists were observed performing colonoscopies during a series of four-hour endoscopy clinics. Durations of each patient position (right lateral decubitus, left lateral decubitus, prone, and supine) were recorded for all observed procedures (n = 64). Endoscopist injury risk was estimated by a trained researcher for the first and last colonoscopies of the shifts (n = 34) using Rapid Upper Limb Assessment (RULA), an observational ergonomic tool that estimates risk of musculoskeletal injury by scoring postures of the upper body and factors such as muscle use, force, and load. The total RULA scores were compared with a Wilcoxon Signed-Rank test for patient position (right and left lateral decubitus) and time (first and last procedures) with significance taken at p < 0.05. Endoscopist preferences were also surveyed. Results The right lateral decubitus position was associated with significantly higher RULA scores than the left lateral decubitus position (median 5 vs. 3, p < 0.001). RULA scores were not significantly different between the first and last procedures of the shifts (median 5 vs. 5, p = 0.816). 89% of endoscopists preferred the left lateral decubitus position, primarily due to superior ergonomics and comfort. Conclusion RULA scores indicate an increased risk of musculoskeletal injury in both patient positions, with greater risk in the right lateral decubitus position

Strain-specific modifier genes of Cecr2-associated exencephaly in mice: genetic analysis and identification of differentially expressed candidate genes

Kooistra MK, Leduc RYM, Dawe CE, Fairbridge NA, Rasmussen J, Man JHY, Bujold M, Juriloff D, King-Jones K, McDermid HE. Strain-specific modifier genes of Cecr2-associated exencephaly in mice: genetic analysis and identification of differentially expressed candidate genes. Physiol Genomics 44: 35-46, 2012. First published November 1, 2011; doi:10.1152/physiolgenomics.00124.2011.-Although neural tube defects (NTDs) are common in humans, little is known about their multifactorial genetic causes. While most mouse models involve NTDs caused by a single mutated gene, we have previously described a multigenic system involving susceptibility to NTDs. In mice with a mutation in Cecr2, the cranial NTD exencephaly shows strain-specific differences in penetrance, with 74% penetrance in BALB/cCrl and 0% penetrance in FVB/N. Whole genome linkage analysis showed that a region of chromosome 19 was partially responsible for this difference in penetrance. We now reveal by genetic analysis of three subinterval congenic lines that the chromosome 19 region contains more than one modifier gene. Analysis of embryos showed that although a Cecr2 mutation causes wider neural tubes in both strains, FVB/N embryos overcome this abnormality and close. A microarray analysis comparing neurulating female embryos from both strains identified differentially expressed genes within the chromosome 19 region, including Arhgap19, which is expressed at a lower level in BALB/cCrl due to a stop codon specific to that substrain. Modifier genes in this region are of particular interest because a large portion of this region is syntenic to human chromosome 10q25, the site of a human susceptibility locus

Loss of CD24 in Mice Leads to Metabolic Dysfunctions and a Reduction in White Adipocyte Tissue

<div><p>CD24 is a glycophosphatidylinositol (GPI)-linked cell surface receptor that is involved in regulating the survival or differentiation of several different cell types. CD24 has been used to identify pre-adipocytes that are able to reconstitute white adipose tissue (WAT) <i>in vivo</i>. Moreover, we recently found that the dynamic upregulation of CD24 <i>in vitro</i> during early phases of adipogenesis is necessary for mature adipocyte development. To determine the role of CD24 in adipocyte development <i>in vivo</i>, we evaluated the development of the inguinal and interscapular subcutaneous WAT and the epididymal visceral WAT in mice with a homozygous deletion of CD24 (CD24KO). We observed a significant decrease in WAT mass of 40% to 74% in WAT mass from both visceral and subcutaneous depots in male mice, with no significant effect in female mice, compared to wild-type (WT) sex- and age-matched controls. We also found that CD24KO mice had increased fasting glucose and free fatty acids, decreased fasting insulin, and plasma leptin. No major differences were observed in the sensitivity to insulin or glucose, or in circulating triglycerides, total cholesterol, HDL-cholesterol, or LDL-cholesterol levels between WT and CD24KO mice. Challenging the CD24KO mice with either high sucrose (35%) or high fat (45%) diets that promote increased adiposity, increased WAT mass and fasting insulin, adiponectin and leptin levels, as well as reduced the sensitivity to insulin and glucose, to the levels of WT mice on the same diets. The CD24-mediated reduction in fat pad size was due to a reduction in adipocyte cell size in all depots with no significant reduction pre-adipocyte or adipocyte cell number. Thus, we have clearly demonstrated that the global absence of CD24 affects adipocyte cell size <i>in vivo</i> in a sex- and diet-dependent manner, as well as causing metabolic disturbances in glucose homeostasis and free fatty acid levels.</p></div

Impaired fat mass accumulation in CD24KO affects all WAT depots and is rescued by adiposity-promoting diets.

<p>Male CD24KO and wild-type mice were fed <b>A-B</b>. standard chow diet (chow), <b>C-D.</b> high sucrose diet (HSD), or <b>E-F.</b> high fat diet (HFD) for 5 weeks starting at 4 weeks of age. <b>A, C, E.</b> Relative body length, total weight, and weights of liver, interscapular (Int.) brown adipose tissue (BAT), Int. white adipose tissue (WAT), inguinal (Ing.) WAT, epididymal (Epi.) WAT are shown. Data are relative to the mean of the WT chow fed group and are shown as box-and-whisker plots. Statistical significance was determined by Wilcoxon rank sum, n = 5–9, *P<0.05, **P<0.01. <b>B, D, F.</b> Representative images of whole WAT from Int, Ing, and Epi WAT depots from 9-week-old CD24KO and WT male mice. Scale bar = 1 cm</p

CD24KO male mice have reduced fat and increased lean and bone weight compared to wild-type male mice.

<p><b>A.</b> Total fat weight, <b>B.</b> percent fat weight, <b>C.</b> total lean weight, <b>D.</b> percent lean weight, <b>E.</b> bone weight, <b>F.</b> percent bone weight, and <b>G.</b> estimated total body weight from dual X-ray absorptiometry (DEXA) scans of male wild-type C57BL/6 and CD24KO mice at 5, 9, and 12 weeks of age on standard show diet. Trend lines display the Loess conditional means and squares represent individual animals. Statistical significance determined by repeated measures ANOVA, n = 6, interaction effects between genotype (G) and time (T) are indicated as P(G*T), main effects of genotype are shown as P(G) and the effect of time within each genotype is shown as P(G[T]).</p

CD24KO male mice show altered glucose and insulin tolerance that is affected by adiposity-promoting diets.

<p>Male CD24KO and WT C57BL/6 mice were fed <b>A-B</b>. standard chow diet (chow), <b>C-D</b>. high sucrose diet (HSD), and <b>E-F.</b> high fat diet (HFD), as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0141966#pone.0141966.g002" target="_blank">Fig 2</a>. <b>A, C, E.</b> Blood glucose was determined after a 6 h fast and then 15 min, 30 min, 60 min, and 120 min following intraperitoneal injection of 2 mg/g glucose for glucose tolerance test. <b>B, E, F.</b> Blood glucose was determined after a 4 h fast and then 15 min, 30 min, 60 min, and 120 min following intraperitoneal injection of 1 mU/g bovine insulin for insulin tolerance test. Trend lines display the Loess conditional means and squares represent individual animals. The total glucose load (Total) and the glucose response from control levels (Response) for <b>G.</b> GTT and <b>H.</b> ITT were determined and compared between genotypes by Wilcoxon rank sum, *P<0.05, ^#P = 0.09, n = 7–9 animals per group for glucose tolerance and 6–8 for insulin tolerance.</p

Indicators of glucose and lipid metabolism in fasted WAT and CD24KO mice at 9 weeks of age after being fed high caloric diets for 5 weeks.

<p>mean ±sem, n = 6,</p><p>^†n = 6 to 9,</p><p>^‡n = 4 to 6.</p><p>^aMain effect of genotype at P<0.05.</p><p>^bMain effect of diet at P<0.05.</p><p>^cInteraction between genotype and diet at P<0.05 by linear mixed model analysis including 9-week-old mice on chow diet.</p><p>*P<0.05 <i>a priori</i> analysis by Wilcoxon rank sum test between WT and CD24KO within each diet</p><p>^§detection threshold of 62.5 pg/mL.</p><p>Indicators of glucose and lipid metabolism in fasted WAT and CD24KO mice at 9 weeks of age after being fed high caloric diets for 5 weeks.</p