Detection and characterization of antimicrobial resistant bacteria from imported reptile and amphibian meat products

Meat from food-producing animals play an important role in the dissemination of antimicrobial resistant bacteria. Active surveillance programs target major agricultural animals but do not include niche food products. In the current investigation, we sought to (1) Identify bacterial pathogens from imported reptile and amphibian meat products and determine the presence of broad spectrum β-lactamase and colistin resistance genes, (2) determine the antimicrobial resistance profiles of Macrococcus caseolyticus isolated from imported meat products and (3) develop a culture medium for the selective isolation of M. caseolyticus. Fifty-three imported reptile and amphibian meat products were purchased from markets in Vancouver, BC and Saskatoon, SK. We found that 41.5% (22/53) of the products carried antimicrobial resistant bacteria with identifiable extended spectrum β-lactamase (ESBL), AmpC β-lactamase, carbapenemase and mobile colistin resistance genes. Seventy-one isolates from 7 genera of Enterobacteriaceae were recovered (from 41 of the 53 products), with none of the Salmonella isolates resistant to any of the antimicrobials tested. One multidrug resistant E. coli, isolated from a soft shell turtle, produced the CTX-M-55 enzyme and possessed the mcr-1 gene conferring mobile colistin resistance. An NDM-1 carbapenemase-producing Acinetobacter spp. was also isolated from a dried turtle carapace. Gram-positive bacteria resembling Staphylococcus aureus were isolated from imported meat samples and identified as Macrococcus caseolyticus; a commensal bacterium found from animal skin and food products. All isolates were resistant to the β-lactam class of drugs, including meropenem, and possessed the mecB gene conferring methicillin resistance. As the ecological distribution of M. caseolyticus in nature is largely unknown, we developed a selective culture medium to help facilitate targeted prevalence studies. Of the prepared selective media challenged, colistin nalidixic acid (CNA) blood agar with ampicillin 0.5µg/ml and meropenem 0.5µg/ml worked the best. This medium facilitated the growth of M. caseolyticus while inhibiting the growth of Gram-negative and most Gram-positive bacteria except for Enterococcus spp. This is the first study to determine the prevalence of antimicrobial resistance and identify ESBL, AmpC β-lactamase, carbapenemase, methicillin and colistin resistance genes from imported reptile and amphibian meat products. More research is required to evaluate the magnitude of the risk that these products have to public health

Smoking-related cancer in military veterans: retrospective cohort study of 57,000 veterans and 173,000 matched non-veterans

Background: Serving military personnel are more likely to smoke, and to smoke more heavily, than civilians. The aim of our study was to examine whether veterans have an increased risk of a range of smoking-related cancers compared with non-veterans, using a large, national cohort of veterans. Methods: We conducted a retrospective cohort study of 57,000 veterans resident in Scotland and 173,000 age, sex and area of residence matched civilians. We used Cox proportional hazard models to compare the risk of any cancer, lung cancer and other smoking-related cancers overall, by sex and by birth cohort, adjusting for the potential confounding effect of socioeconomic deprivation. Results: Over a mean of 29 years follow-up, 445 (0.79 %) veterans developed lung cancer compared with 1106 (0.64 %) non-veterans (adjusted hazard ratio 1.16, 95 % confidence intervals 1.04–1.30, p = 0.008). Other smoking-related cancers occurred in 737 (1.31 %) veterans compared with 1883 (1.09 %) non-veterans (adjusted hazard ratio 1.18, 95 % confidence intervals 1.08–1.29, p < 0.001). A significantly increased risk was observed among veterans born 1950–1954 for lung cancer and 1945–1954 for other smoking-related cancers. The risk of lung cancer was decreased among veterans born 1960 onwards. In comparison, there was no difference in the risk of any cancer overall (adjusted hazard ratio 0.98, 95 % confidence intervals 0.94–1.01, p = 0.171), whilst younger veterans were at reduced risk of any cancer (adjusted hazard ratio 0.88, 95 % confidence intervals 0.81–0.97, p = 0.006). Conclusions: Military veterans living in Scotland who were born before 1955 are at increased risk of smoking-related cancer compared with non-veterans, but younger veterans are not. The differences may reflect changing patterns of smoking behaviour over time in military personnel which may, in turn, be linked to developments in military health promotion policy and a changing military operational environment, as well as to wider societal factors

Smoking-related cancer in military veterans: retrospective cohort study of 57,000 veterans and 173,000 matched non-veterans

Background: Serving military personnel are more likely to smoke, and to smoke more heavily, than civilians. The aim of our study was to examine whether veterans have an increased risk of a range of smoking-related cancers compared with non-veterans, using a large, national cohort of veterans. Methods: We conducted a retrospective cohort study of 57,000 veterans resident in Scotland and 173,000 age, sex and area of residence matched civilians. We used Cox proportional hazard models to compare the risk of any cancer, lung cancer and other smoking-related cancers overall, by sex and by birth cohort, adjusting for the potential confounding effect of socioeconomic deprivation. Results: Over a mean of 29 years follow-up, 445 (0.79 %) veterans developed lung cancer compared with 1106 (0.64 %) non-veterans (adjusted hazard ratio 1.16, 95 % confidence intervals 1.04–1.30, p = 0.008). Other smoking-related cancers occurred in 737 (1.31 %) veterans compared with 1883 (1.09 %) non-veterans (adjusted hazard ratio 1.18, 95 % confidence intervals 1.08–1.29, p < 0.001). A significantly increased risk was observed among veterans born 1950–1954 for lung cancer and 1945–1954 for other smoking-related cancers. The risk of lung cancer was decreased among veterans born 1960 onwards. In comparison, there was no difference in the risk of any cancer overall (adjusted hazard ratio 0.98, 95 % confidence intervals 0.94–1.01, p = 0.171), whilst younger veterans were at reduced risk of any cancer (adjusted hazard ratio 0.88, 95 % confidence intervals 0.81–0.97, p = 0.006). Conclusions: Military veterans living in Scotland who were born before 1955 are at increased risk of smoking-related cancer compared with non-veterans, but younger veterans are not. The differences may reflect changing patterns of smoking behaviour over time in military personnel which may, in turn, be linked to developments in military health promotion policy and a changing military operational environment, as well as to wider societal factors

Recent developments on the role of epigenetics in obesity and metabolic disease

The increased prevalence of obesity and related comorbidities is a major public health problem. While genetic factors undoubtedly play a role in determining individual susceptibility to weight gain and obesity, the identified genetic variants only explain part of the variation. This has led to growing interest in understanding the potential role of epigenetics as a mediator of gene-environment interactions underlying the development of obesity and its associated comorbidities. Initial evidence in support of a role of epigenetics in obesity and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which reported epigenetic changes in key metabolically important tissues following high-fat feeding and epigenetic differences between lean and obese animals and by human studies which showed epigenetic changes in obesity and T2DM candidate genes in obese/diabetic individuals. More recently, advances in epigenetic methodologies and the reduced cost of epigenome-wide association studies (EWAS) have led to a rapid expansion of studies in human populations. These studies have also reported epigenetic differences between obese/T2DM adults and healthy controls and epigenetic changes in association with nutritional, weight loss, and exercise interventions. There is also increasing evidence from both human and animal studies that the relationship between perinatal nutritional exposures and later risk of obesity and T2DM may be mediated by epigenetic changes in the offspring. The aim of this review is to summarize the most recent developments in this rapidly moving field, with a particular focus on human EWAS and studies investigating the impact of nutritional and lifestyle factors (both pre- and postnatal) on the epigenome and their relationship to metabolic health outcomes. The difficulties in distinguishing consequence from causality in these studies and the critical role of animal models for testing causal relationships and providing insight into underlying mechanisms are also addressed. In summary, the area of epigenetics and metabolic health has seen rapid developments in a short space of time. While the outcomes to date are promising, studies are ongoing, and the next decade promises to be a time of productive research into the complex interactions between the genome, epigenome, and environment as they relate to metabolic disease.Susan J. van Dijk, Ross L. Tellam, Janna L. Morrison, Beverly S. Muhlhausler, and Peter L. Mollo

Performance evaluation of serial photolithography clusters: Queueing models, throughput and workload sequencing,” in

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The Grizzly, November 12, 1982

Nobel Prize Winner at Ursinus • Tray Contest at Wismer • Life in the Fast Lane • International Accord Signed • Berry Brings About Changes • Eclectic Exhibit • President\u27s Corner • Registrar Announces Finals Schedule • Stallone Knocked Out in First Blood • From Bar to Bard • UPB Bus to New Market • No Encore, Please • Immersion Excursion • USGA Notes • Frostburg Freezes UC in ECAC Playoffs • Field Hockey Ends Season at .500 • Career Options Presented • Grizzlies Drop Season Finale to Widener • Harriers Take Second in MAC Meethttps://digitalcommons.ursinus.edu/grizzlynews/1088/thumbnail.jp

Placental glucocorticoid receptor isoforms in a sheep model of maternal allergic asthma

Maternal asthma increases the risk of adverse pregnancy outcomes and may affect fetal growth and placental function by differential effects on the expression of glucocorticoid receptor (GR) isoforms, leading to altered glucocorticoid signalling. Our aim was to examine the effect of maternal asthma on placental GR profiles using a pregnant sheep model of asthma. Nine known GR isoforms were detected. There was a significant increase in the expression of placental GR isoforms that are known to have low trans-activational activity in other species including GR A, GR P and GRγ which may result in a pro-inflammatory environment in the presence of allergic asthma

Cutting Edge: NLRP12 Controls Dendritic and Myeloid Cell Migration To Affect Contact Hypersensitivity

Nucleotide-binding domain leucine-rich repeat (NLR) proteins are regulators of inflammation and immunity. Although first described 8 y ago, a physiologic role for NLRP12 has remained elusive until now. We find that murine Nlrp12, an NLR linked to atopic dermatitis and hereditary periodic fever in humans, is prominently expressed in dendritic cells (DCs) and neutrophils. Nlrp12-deficient mice exhibit attenuated inflammatory responses in two models of contact hypersensitivity that exhibit features of allergic dermatitis. This cannot be attributed to defective Ag processing/presentation, inflammasome activation, or measurable changes in other inflammatory cytokines. Rather, Nlrp12(-/-) DCs display a significantly reduced capacity to migrate to draining lymph nodes. Both DCs and neutrophils fail to respond to chemokines in vitro. These findings indicate that NLRP12 is important in maintaining neutrophils and peripheral DCs in a migration-competent state