Danse et littérature

To elaborate on the connections between dance and literature means to be confronted with the eternal dilemma between speech and action, between words which enables communication and gestures which enhance it. And whereas many points are in common between the two forms of art - search of shape, construction, rhythm, as well as in vocabulary, step alphabet, ballet grammar, modern dance syntax for dance - noteworthy differences still persist. On one hand, the writer carries out a solitary work free from boundaries and builds an imaginary world with self-imagined rules; on the other, the choreographer is a team leader, which means to be confronted with the real world of the dancers and their bodies or the technical features of the performance.To elaborate on the connections between dance and literature means to be confronted with the eternal dilemma between speech and action, between words which enables communication and gestures which enhance it. And whereas many points are in common between the two forms of art - search of shape, construction, rhythm, as well as in vocabulary, step alphabet, ballet grammar, modern dance syntax for dance - noteworthy differences still persist. On one hand, the writer carries out a solitary work free from boundaries and builds an imaginary world with self-imagined rules; on the other, the choreographer is a team leader, which means to be confronted with the real world of the dancers and their bodies or the technical features of the performance

Enacting Anti-Racist Visualities Through Photo-Dialogues on Race in Paris

Purpose Grounded in experience of co-organizing a two-day photography-based workshop in Paris, this paper explores how photo-dialogues can facilitate anti-racist pedagogy and generative discussions about how race and racism function in marketplace contexts. Design/methodology/approach This paper draws on the authors\u27 involvement in a cross-national and cross-disciplinary team of scholars who worked with local community stakeholders—including activists, artists and practitioners—to discuss, theorize and photo-document issues regarding race and racism in the Parisian marketplace. Findings This paper contributes to the literature on visual culture studies and critical race studies as it demonstrates the potentials of photography combined with dialogue to challenge the White supremacy over archiving and visuality in the context of urban spaces. This new methodology is an opportunity to reflect on archetypes of visuality that depart from the traditional Parisian flâneur to be consistent with and reinforce anti-racist stances. Originality/value Photography and visual methods often play peripheral roles in anti-racist education across various disciplines and research areas, including critical marketplace studies. This paper expands understanding of the potentials of using photographic methods as part of critical and anti-racist work related to racial and racist dynamics, including issues regarding power, White supremacy and public space. It outlines the use of photographic dialogues in a context (Paris, France) where discussion of race is regularly societally discouraged. Thus, this work shifts the focus away from decontextualized research that regards race as an object, to specifically foreground understandings of racialized experiences and how the photographic gaze produces and is produced by racialized viewers

Developmental programming by maternal obesity: Lessons from animal models

Funder: Medical Research Council; Id: http://dx.doi.org/10.13039/501100000265Funder: British Heart Foundation; Id: http://dx.doi.org/10.13039/501100000274Abstract: The obesity epidemic has led to more women entering pregnancy overweight or obese. In addition to adverse short‐term outcomes, maternal obesity and/or gestational diabetes predispose offspring to developing obesity, type 2 diabetes and cardiovascular disease in adulthood through developmental programming. Human epidemiological studies, although vital in identifying associations, are often unable to address causality and mechanistic studies can be limited by the lack of accessibility of key metabolic tissues. Furthermore, multi‐generational studies take many years to complete. Integration of findings from human studies with those from animal models has therefore been critical in moving forward this field that has been termed the ‘Developmental Origins of Health and Disease’. This review summarises the evidence from animal models and highlights how animal models provide valuable insight into the maternal factors responsible for developmental programming, potential critical developmental windows, sexual dimorphism, molecular mechanisms and age‐related offspring outcomes throughout life. Moreover, we describe how animal models are vital to explore clinically relevant interventions to prevent adverse offspring outcomes in obese or glucose intolerant pregnancy, such as antioxidant supplementation, exercise and maternal metformin treatment

Preparing for Crew-Control of Surface Robots from Orbit

Since 2010, the European Space Agency (ESA) and the National Aeronautics and Space Administration (NASA) have been developing robots that can be remotely operated on planetary surfaces by astronauts in orbiting spacecraft. A primary objective of this work has been to test telerobotic technologies that are needed for future deep-space human exploration missions. Specifically, ESA's Multi-Purpose End-To-End Robotic Operations Network (METERON) project and NASA's Human Exploration Telerobotics (HET) project are complementary initiatives that aim to validate communications, operations and robotic systems through a range of ground and flight experiments with humans and robots in the loop. Several experiments have already been successfully completed and others are now in preparation for flight

Maternal Metformin Intervention during Obese Glucose-Intolerant Pregnancy Affects Adiposity in Young Adult Mouse Offspring in a Sex-Specific Manner.

BackgroundMetformin is commonly used to treat gestational diabetes mellitus. This study investigated the effect of maternal metformin intervention during obese glucose-intolerant pregnancy on the gonadal white adipose tissue (WAT) of 8-week-old male and female mouse offspring.MethodsC57BL/6J female mice were provided with a control (Con) or obesogenic diet (Ob) to induce pre-conception obesity. Half the obese dams were treated orally with 300 mg/kg/d of metformin (Ob-Met) during pregnancy. Gonadal WAT depots from 8-week-old offspring were investigated for adipocyte size, macrophage infiltration and mRNA expression of pro-inflammatory genes using RT-PCR.ResultsGestational metformin attenuated the adiposity in obese dams and increased the gestation length without correcting the offspring in utero growth restriction and catch-up growth caused by maternal obesity. Despite similar body weight, the Ob and Ob-Met offspring of both sexes showed adipocyte hypertrophy in young adulthood. Male Ob-Met offspring had increased WAT depot weight (p p p F4/80 (p ConclusionsMaternal metformin intervention during obese pregnancy causes excessive adiposity, adipocyte hyperplasia and WAT inflammation in male offspring, highlighting sex-specific effects of prenatal metformin exposure on offspring WAT

Effects of maternal diet-induced obesity on metabolic disorders and age-associated miRNA expression in the liver of male mouse offspring

Objective: This study investigated the effect of maternal obesity on aged-male offspring liver phenotype and hepatic expression of a programmed miRNA. Methods: A mouse model (C57BL/6 J) of maternal diet-induced obesity was used to investigate fasting-serum metabolites, hepatic lipid content, steatosis, and relative mRNA levels (RT-PCR) and protein expression (Western blotting) of key components involved in hepatic and mitochondrial metabolism in 12-month-old offspring. We also measured hepatic lipid peroxidation, mitochondrial content, fibrosis stage, and apoptosis in the offspring. To investigate potential mechanisms leading to the observed phenotype, we also measured the expression of miR-582 (a miRNA previously implicated in liver cirrhosis) in 8-week-old and 12-month-old offspring. Results: Body weight and composition was similar between 8-week-old offspring, however, 12-month-old offspring from obese mothers had increased body weight and fat mass (19.5 ± 0.8 g versus 10.4 ± 0.9 g, p < 0.001), as well as elevated serum levels of LDL and leptin and hepatic lipid content (21.4 ± 2.1 g versus 12.9 ± 1.8 g, p < 0.01). This was accompanied by steatosis, increased Bax/Bcl-2 ratio, and overexpression of p-SAPK/JNK, Tgfβ1, Map3k14, and Col1a1 in the liver. Decreased levels of Bcl-2, p-AMPKα, total AMPKα and mitochondrial complexes were also observed. Maternal obesity was associated with increased hepatic miR-582-3p (p < 0.001) and miR-582-5p (p < 0.05). Age was also associated with an increase in both miR-582-3p and miR-582-5p, however, this was more pronounced in the offspring of obese dams, such that differences were greater in 12-month-old animals (−3p: 7.34 ± 1.35 versus 1.39 ± 0.50, p < 0.0001 and −5p: 4.66 ± 1.16 versus 1.63 ± 0.65, p < 0.05). Conclusion: Our findings demonstrate that maternal diet-induced obesity has detrimental effects on offspring body composition as well as hepatic phenotype that may be indicative of accelerated-ageing phenotype. These whole-body and cellular phenotypes were associated with age-dependent changes in expression of miRNA-582 that might contribute mechanistically to the development of metabolic disorders in the older progeny

Serum bile acid measurements in women of European and South Asian ethnicity with or without gestational diabetes mellitus: A cohort study

Objective Investigation of serum bile acid profiles in pregnancies complicated by gestational diabetes mellitus (GDM) in a multi‐ethnic cohort of women who are lean or obese. Design Prospective cohort study. Setting UK multicentre study. Population Fasting serum from participants of European or South Asian self‐reported ethnicity from the PRiDE study, between 23 and 31 weeks of gestation. Methods Bile acids were measured using ultra‐performance liquid chromatography‐tandem mass spectrometry. Log‐transformed data were analysed using linear regression in STATA/IC 15.0. Main outcome measures Total bile acids (TBAs), C4, fasting glucose and insulin. Results The TBAs were 1.327‐fold (1.105–1.594) increased with GDM in European women ( P = 0.003). Women with GDM had 1.162‐fold (1.002–1.347) increased levels of the BA synthesis marker C4 ( P = 0.047). In South Asian women, obesity (but not GDM) increased TBAs 1.522‐fold (1.193–1.942, P = 0.001). Obesity was associated with 1.420‐fold (1.185–1.702) increased primary/secondary BA ratio ( P Conclusions Serum BA homeostasis in late gestation depends on body mass index and GDM in ethnicity‐specific ways. This suggests ethnicity‐specific aetiologies may contribute to metabolic risk in European and South Asian women, with the relationship between BAs and insulin resistance of greater importance in European women. Further studies into ethnicity‐specific precision medicine for GDM are required

Effects of maternal diet-induced obesity on metabolic disorders and age-associated miRNA expression in the liver of male mouse offspring.

OBJECTIVE: This study investigated the effect of maternal obesity on aged-male offspring liver phenotype and hepatic expression of a programmed miRNA. METHODS: A mouse model (C57BL/6 J) of maternal diet-induced obesity was used to investigate fasting-serum metabolites, hepatic lipid content, steatosis, and relative mRNA levels (RT-PCR) and protein expression (Western blotting) of key components involved in hepatic and mitochondrial metabolism in 12-month-old offspring. We also measured hepatic lipid peroxidation, mitochondrial content, fibrosis stage, and apoptosis in the offspring. To investigate potential mechanisms leading to the observed phenotype, we also measured the expression of miR-582 (a miRNA previously implicated in liver cirrhosis) in 8-week-old and 12-month-old offspring. RESULTS: Body weight and composition was similar between 8-week-old offspring, however, 12-month-old offspring from obese mothers had increased body weight and fat mass (19.5 ± 0.8 g versus 10.4 ± 0.9 g, p < 0.001), as well as elevated serum levels of LDL and leptin and hepatic lipid content (21.4 ± 2.1 g versus 12.9 ± 1.8 g, p < 0.01). This was accompanied by steatosis, increased Bax/Bcl-2 ratio, and overexpression of p-SAPK/JNK, Tgfβ1, Map3k14, and Col1a1 in the liver. Decreased levels of Bcl-2, p-AMPKα, total AMPKα and mitochondrial complexes were also observed. Maternal obesity was associated with increased hepatic miR-582-3p (p < 0.001) and miR-582-5p (p < 0.05). Age was also associated with an increase in both miR-582-3p and miR-582-5p, however, this was more pronounced in the offspring of obese dams, such that differences were greater in 12-month-old animals (-3p: 7.34 ± 1.35 versus 1.39 ± 0.50, p < 0.0001 and -5p: 4.66 ± 1.16 versus 1.63 ± 0.65, p < 0.05). CONCLUSION: Our findings demonstrate that maternal diet-induced obesity has detrimental effects on offspring body composition as well as hepatic phenotype that may be indicative of accelerated-ageing phenotype. These whole-body and cellular phenotypes were associated with age-dependent changes in expression of miRNA-582 that might contribute mechanistically to the development of metabolic disorders in the older progeny

Maternal diet-induced obesity programmes cardiac dysfunction in male mice independently of post-weaning diet.

AIMS: Obesity during pregnancy increases risk of cardiovascular disease (CVD) in the offspring and individuals exposed to over-nutrition during fetal life are likely to be exposed to a calorie-rich environment postnatally. Here, we established the consequences of combined exposure to a maternal and post-weaning obesogenic diet on offspring cardiac structure and function using an established mouse model of maternal diet-induced obesity. METHODS AND RESULTS: The impact of the maternal and postnatal environment on the offspring metabolic profile, arterial blood pressure, cardiac structure, and function was assessed in 8-week-old C57BL/6 male mice. Measurement of cardiomyocyte cell area, the transcriptional re-activation of cardiac fetal genes as well as genes involved in the regulation of contractile function and matrix remodelling in the adult heart were determined as potential mediators of effects on cardiac function. In the adult offspring: a post-weaning obesogenic diet coupled with exposure to maternal obesity increased serum insulin (P < 0.0001) and leptin levels (P < 0.0001); maternal obesity (P = 0.001) and a post-weaning obesogenic diet (P = 0.002) increased absolute heart weight; maternal obesity (P = 0.01) and offspring obesity (P = 0.01) caused cardiac dysfunction but effects were not additive; cardiac dysfunction resulting from maternal obesity was associated with re-expression of cardiac fetal genes (Myh7: Myh6 ratio; P = 0.0004), however, these genes were not affected by offspring diet; maternal obesity (P = 0.02); and offspring obesity (P = 0.05) caused hypertension and effects were additive. CONCLUSIONS: Maternal diet-induced obesity and offspring obesity independently promote cardiac dysfunction and hypertension in adult male progeny. Exposure to maternal obesity alone programmed cardiac dysfunction, associated with hallmarks of pathological left ventricular hypertrophy, including increased cardiomyocyte area, upregulation of fetal genes, and remodelling of cardiac structure. These data highlight that the perinatal period is just as important as adult-onset obesity in predicting CVD risk. Therefore, early developmental periods are key intervention windows to reduce the prevalence of CVD.This work was supported by the Medical Research Council (MRC_MC_UU_12012/4), the British Heart Foundation (FS/12/64/30001 to E.L., PG/14/20/ 30769 and RG/17/12/33167) and São Paulo Research Foundation (2017/03525-8 to J.A.F.)

T4-Related Bacteriophage LIMEstone Isolates for the Control of Soft Rot on Potato Caused by ‘Dickeya solani’

The bacterium ‘Dickeya solani’, an aggressive biovar 3 variant of Dickeya dianthicola, causes rotting and blackleg in potato. To control this pathogen using bacteriophage therapy, we isolated and characterized two closely related and specific bacteriophages, vB_DsoM_LIMEstone1 and vB_DsoM_LIMEstone2. The LIMEstone phages have a T4-related genome organization and share DNA similarity with Salmonella phage ViI. Microbiological and molecular characterization of the phages deemed them suitable and promising for use in phage therapy. The phages reduced disease incidence and severity on potato tubers in laboratory assays. In addition, in a field trial of potato tubers, when infected with ‘Dickeya solani’, the experimental phage treatment resulted in a higher yield. These results form the basis for the development of a bacteriophage-based biocontrol of potato plants and tubers as an alternative for the use of antibiotics