Impact of obesity on morbidity and oncologic outcomes after total mesorectal excision for mid and low rectal cancer.

BACKGROUND: A recent meta-analysis showed that obesity increased the conversion rate and postoperative morbidity of rectal cancer surgery, but did not influence pathological results. However, this meta-analysis included patients with cancer of the upper rectum and had many biases. The aim of the present retrospective study was to investigate the impact of obesity, defined as a body mass index (BMI) ≥ 30 kg/m2, on postoperative morbidity and short- and long-term oncologic outcomes of total mesorectal excision for mid and low rectal cancer in consecutive patients. METHODS: This study included all eligible patients who were operated on for mid and lower rectal cancer between 1999 and 2018 in our hospital. We compared 90-day postoperative morbidity and mortality, and short- and long-term oncologic outcomes between obese and non-obese patients. RESULTS: Three hundred and ninety patients [280 males, mean age 65.7 ± 11.3 years, 59 obese individuals (15.1%)] were included. There was no difference in the 90-day mortality rate between obese and non-obese groups (p = 0.068). There was a difference in the overall 90-day morbidity rate between the obese and non-obese groups that disappeared after propensity score matching of the patients. There was no difference in short-term oncological parameters, with a median follow-up of 43 (20-84) months, and there were no significant differences in disease-free and overall survival between obese and non-obese patients (p = 0.42 and p = 0.11, respectively). CONCLUSIONS: Obesity does not affect the 90-day morbidity rate, or short- and long-term oncologic results in patients operated on for mid and lower rectal cancer.

Nocturnal city lighting elicits a macroscale response from an insect outbreak population.

Anthropogenic environmental change affects organisms by exposing them to enhanced sensory stimuli that can elicit novel behavioural responses. A pervasive feature of the built environment is artificial nocturnal lighting, and brightly lit urban areas can influence organism abundance, distribution and community structure within proximate landscapes. In some cases, the attractive or disorienting effect of artificial light at night can draw animals into highly unfavourable habitats, acting as a macroscale attractive ecological sink. Despite their significance for animal ecology, identifying cases of these phenomena and determining their effective scales and the number of organisms impacted remains challenging. Using an integrated set of remote-sensing observations, we quantify the effect of a large-scale attractive sink on nocturnal flights of an outbreak insect population in Las Vegas, USA. At the peak of the outbreak, over 45 million grasshoppers took flight across the region, with the greatest numbers concentrating over high-intensity city lighting. Patterns of dusk ascent from vegetated habitat toward urban areas suggest a daily pull toward a time-varying nocturnal attractive sink. The strength of this attractor varies with grasshopper density. These observations provide the first macroscale characterization of the effects of nocturnal urban lighting on the behaviour of regional insect populations and demonstrate the link between insect perception of the built environment and resulting changes in spatial and movement ecology. As human-induced environmental change continues to affect insect populations, understanding the impacts of nocturnal light on insect behaviour and fitness will be vital to developing robust large-scale management and conservation strategies.

Retrospective study of thoracotomy performed in a French level 1-trauma center.

OBJECTIVE: Resuscitative thoracotomy, a potentially life-saving procedure, is used exceptionally, and essentially for penetrating trauma. Most of the available literature is American while reports from Europe are sparse. We report our experience in a French level 1-trauma center. MATERIAL AND METHODS: Patient records (patient age, gender, mechanism of injury, indication for emergency thoracotomy, anatomic injuries, interventions and survival) for all patients who underwent emergency thoracotomy between January 2005 and December 2015 were analyzed. RESULTS: Twenty-two patients (19 males) underwent emergency thoracotomy. Median age was 27.5 (12-67) years. Twelve were performed for blunt trauma (55%) and 10 for penetrating injuries (45%). Thirteen patients presented with cardiac arrest, while nine had deep and refractory hypotension. Overall, survival was 32% (n=7). There were no survivors in the blunt trauma group while seven of ten with penetrating injuries survived. All patients presenting with cardiac arrest died. CONCLUSION: The survival rate in this French retrospective study was in accordance with the literature.

Congenic BB.SHR rat provides evidence for effects of a chromosome 4 segment (D4Mit6-Npy approximately 1 cm) on total serum and lipoprotein lipid concentration and composition after feeding a high-fat, high-cholesterol diet.

Congenic BB.SHR (previously referred to as BB.LL) rats were generated by transferring the segment of chromosome 4 flanked by the D4Mit6 and Spr loci from the spontaneously hypertensive rat (SHR/Mol) onto the genetic background of the diabetes-prone BB/OK rat. In this study, the influence of the above-mentioned region of chromosome 4 on triglyceride, cholesterol, and phospholipid phenotypes after a high-fat, high-cholesterol diet was examined by comparison of BB.SHR congenic rats with BB/OK rats. BB/OK and BB.SHR had comparable concentrations of basal and postdietary serum insulin, as well as of basal total serum triglycerides and had an identical body weight and food intake at the beginning of the test period. However, after 4 weeks on the test diet, BB.SHR rats were significantly heavier than BB/OK rats and had significantly higher food intake and lower total serum triglyceride concentrations. The basal serum leptin level was significantly lower, but postdietary serum leptin concentration did not show a significant difference between the 2 strains. Furthermore, significantly higher basal total serum cholesterol and phospholipid levels were observed in BB.SHR rats, but this difference disappeared after feeding the high-fat, high-cholesterol diet. Postdietary high-density lipoprotein (HDL)(2) cholesterol and phospholipid levels were significantly elevated in BB.SHR rats when compared with BB/OK rats. The 2 strains also differed slightly, but significantly, with respect to the other HDL phospholipid concentrations. In addition to previously described differences between BB/OK and BB.SHR rats, the results of this study clearly show the impact of genes, lying within the transferred segment, on serum lipid phenotypes after high-fat, high-cholesterol diet.

Quantitative trait loci influencing hepatic copper in rats.

Significant differences in liver copper content have been observed between rat inbred strains. To define loci controlling this trait, the offspring (n = 190) from an (LEW/OlaHsd x BC/CpbU) F(2)-intercross was genetically analyzed. From each F(2) animal, liver copper content was determined and genomic DNA was screened with polymorphic DNA markers. We found a major quantitative trait locus (QTL) for liver copper content in females on chromosome 2 and in males on chromosome 10. Both QTLs accounted for approximately 20% of the genetic variance. In addition, suggestive linkage for liver copper content was found on rat chromosomes 1, 8, 10, 12, 14, and 19. The regions on these chromosomes contain genes that are responsible for 9.0-15.5% of the genetic variance of liver copper content.

A rat linkage map based on BC x LEW intercross.

A genetic linkage map consisting of 258 polymorphic loci has been constructed on the basis of an F2 intercross between the BC/CpbU and LEW/OlaHsd inbred rat strains. When compared to previously published maps a discrepancy was found for rat chromosome 7. The map spans a sex-averaged genetic length of 1790 cM and has an average marker spacing of 7.7 cM. It was estimated that this genetic map is linked to about 90% of the DNA in the rat genome. Because LEW/OlaHsd and BC/CpbU strains differ for dietary cholesterol susceptibility and hepatic copper content, the map is considered to be a valuable tool for studying the genetic background of these complex traits.

Sequencing and chromosomal assignment of the rat endothelial-derived lipase gene (Lipg).

Part of the nucleotide sequence of the Lipg gene in the rat was established using primers based on the mRNA sequence described in the mouse. The rat intron sequence served as a template for designing primers for the specific amplification of rat Lipg. A rat-hamster radiation hybrid (RH) panel was used for chromosomal assignment of the rat Lipg gene. The Lipg gene was found to be located on rat chromosome 18 in the vicinity of the marker D18Mit11; a region reported to be homologous with both human and mouse chromosome 18.

Chromosomal localization of genes involved in biosynthesis, metabolism or transport of cholesterol in the rat.

Several genes involved in biosynthesis, transport or metabolism of cholesterol have been localized on rat chromosomes by using a radiation hybrid (RH) panel. The genes, coding for squalene epoxidase (Sqle), mevalonate kinase (Mvk), and farnesyl diphosphate farnesyl transferase 1 (Fdft1) which are involved in cholesterol biosynthesis, have been mapped on chromosome 7, 12, and 15, respectively. The genes coding for phospholipid transfer protein (Pltp), sterol carrier protein-2 (Scp2), ATP binding cassette reporter A7 (Abca7), scavenger receptor class B, type 1 (Cd36l1), steroidogenic acute regulatory protein (Star), and lecithin:cholesterol acyl transferase (Lcat), which are involved in the transfer and/or metabolism of cholesterol, have been mapped on chromosome 3, 5, 7, 12, 16, and 19, respectively. Each of the genes Scp2, Sqle and Fdft1 maps close to a QTL for serum total cholesterol in rat, suggesting that these three genes might represent candidate genes for the previously mapped QTLs.

Y-chromosome transfer induces changes in blood pressure and blood lipids in SHR.

Previous studies with chromosome-Y consomic strains of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats suggest that a quantitative trait locus for blood pressure regulation exists on chromosome Y. To test this hypothesis in the SHR-Brown Norway (BN) model and to study the effects of chromosome Y on lipid and carbohydrate metabolism, we produced a new consomic strain of SHR carrying the Y chromosome transferred from the BN rat. We found that replacing the SHR Y chromosome with the BN Y chromosome resulted in significant decreases in systolic and diastolic blood pressures in the SHR.BN-Y consomic strain (P<0.05). To elicit possible dietary-induced variation in lipid and glucose metabolism between the SHR progenitor and chromosome-Y consomic strains, we fed rats a high-fructose diet for 15 days in addition to the normal diet. On the high-fructose diet, the SHR.BN-Y consomic rats exhibited significantly increased levels of serum triglycerides and decreased levels of serum HDL cholesterol versus the SHR progenitor rats. Glucose tolerance and insulin/glucose ratios, however, were similar in both strains on both normal and high-fructose diets. These findings provide direct evidence that a gene or genes on chromosome Y contribute to the pathogenesis of spontaneous hypertension in the SHR-BN model. These results also indicate that transfer of the Y chromosome from the BN rat onto the SHR background exacerbates dietary-induced dyslipidemia in SHR. Thus, genetic variation in genes on the Y chromosome may contribute to variation in blood pressure and lipid levels and may influence the risk for cardiovascular disease.