Conférences ecclésiastiques du Diocese d'Angers, sur les actes humains : tenues pendant l'Année 1760, [et] les suivantes ... /

Mode of access: Internet.

Conférences ecclésiastiques du Diocese d'Angers, sur les états : tenues pendant l'année 1760, [et] les suivantes ... /

Mode of access: Internet.

Conférences ecclésiastiques du Diocese d'Angers, sur les états : tenues pendant l'année 1760, [et] les suivantes ... /

Mode of access: Internet.

Conférences ecclésiastiques du Diocese d'Angers, sur les Péchés; tenues pendant l'Année 1760, & les suivantes par l'ordre de ... Jacques de Grasse, evêque d'Angers /

Mode of access: Internet.

Obras de don Nicolas y don Leand

Mode of access: Internet.

Obras postumas de d. Nicolas Fernandez de Moratin /

"Vida del autor [por su hijo, don Leandro Fernández de Moratin,": p. i-liv.

Galerie auxonnaise; ou, Revue générale des auxonnais dignes de mémoire; comprenant la réimpression des biographies de Maillard du Mesle, intendant des îles de France et de Bourbon, et de Madame Gardel, première danseuse de l'Académie royale de musique.

Mode of access: Internet.

Obras postumas de d. Nicolas Fernandez de Moratin.

"Vida del autor [por su hijo, don Leandro Fernández de Moratin,": p. i-liv.

Celebrating difference/censoring difference? : Marie Chouinard’s bODY rEMIX

This paper examines performances that defy established representations of disease, deformity and bodily difference. Historically, the ‘deformed’ body has been cast – onstage and in sideshows – as flawed, an object of pity, or an example of the human capacity to overcome. Such representations define the boundaries of the ‘normal’ body by displaying its Other. They bracket the ‘abnormal’ body off as an example of deviance from the ‘norm’, thus, paradoxically, decreasing the social and symbolic visibility (and agency) of disabled people. Yet, in contemporary theory and culture, these representations are reappropriated – by disabled artists, certainly, but also as what Carrie Sandahl has called a ‘master trope’ for representing a range of bodily differences. In this paper, I investigate this phenomenon. I analyse French Canadian choreographer Marie Chouinard’s bODY rEMIX/gOLDBERG vARIATIONS, in which 10 able-bodied dancers are reborn as bizarre biotechnical mutants via the use of crutches, walkers, ballet shoes and barres as prosthetic pseudo-organs. These bodies defy boundaries, defy expectations, develop new modes of expression, and celebrate bodily difference. The self-inflicted pain dancers experience during training is cast as a ‘disablement’ that is ultimately ‘enabling’. I ask what effect encountering able bodies celebrating ‘dis’ or ‘diff’ ability has on audiences. Do we see the emergence of a once-repressed Other, no longer silenced, censored or negated? Or does using ‘disability’ to express the dancers’ difference and self-determination usurp a ‘trope’ by which disabled people themselves might speak back to the dominant culture, creating further censorship?

Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010 : a systematic analysis for the Global Burden of Disease Study 2010

Background Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Methods Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Findings Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350 000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient −0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Interpretation Rates of YLDs per 100 000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Funding Bill & Melinda Gates Foundation.

Regional chromosomal assignment of human renin gene to 1q12→qter and use in linkage studies in Charcot-Marie-Tooth disease

The gene for renin, previously mapped to human chromosome 1, was further localized to 1q12 → qter using human-mouse somatic cell hybrid DNAs. The renin DNA probe used (λ HR5) could detect a HindIII restriction fragment length polymorphism. When used in studies of 12 informative families, no linkage could be found between the renin and Charcot-Marie-Tooth disease. Furthermore, an association of any renin allele with hypertension was not apparent.

Chromosome I linkage studies in Charcot-Marie-Tooth neuropathy type I

Charcot-Marie-Tooth neuropathy type 1 (CMT1) is an autosomal dominant disorder of peripheral nerve. The gene for CMT1 was originally localized to chromosome 1 by linkage to the Duffy blood group, but it has since been shown that not all CMT1 pedigrees show this linkage. We report here the results of linkage studies using five chromosome 1 markers - Duffy (Fy), antithrombin III (AT3), renin (REN), β-nerve growth factor (NGFB), and salivary amylase (AMY1) - in 16 CMT1 pedigrees. The total lod scores exclude close linkage of CMT1 to any of these markers. However, individual families show probable linkage of CMT1 to Duffy, AT3, and/or AMY1. No linkage was indicated with REN or NGFB. These results indicate that possible location of a CMT1 gene between the AMY1 and AT3 loci at p21 and q23, respectively, on chromosome 1 and support the theory that there is at least one other CMT1 gene.

Heterogeneity evidence and linkage studies on Charcot-Marie-Tooth disease

Charcot-Marie-Tooth neuropathy type 1 (CMT1) is an autosomal dominant disorder originally localized to chromosome 1 by linkage to the Duffy blood group. Studies have since shown that the disorder may be heterogeneous, as not all families show this linkage. We tested genetic heterogeneity by the HOMOG computer program in 15 CMT1 pedigrees informative for Duffy. We detected no evidence for heterogeneity in this sample, but when we combined results with previously published lod scores, heterogeneity was statistically significant. Twelve of the 15 families studied did not show linkage to Duffy. We found six of these families to be informative for a chromosome 19 marker, apolipoprotein CII(ApoC2). Despite a previous report showing probable linkage of a non-Duffy-linked CMT1 pedigree to two chromosome 19 markers, we did not detect significant linkage of ApoC2 to CMT1 in these families.

Isolation and use of chromosome 1 probes for linkage studies on Charcot-Marie-Tooth disease

Nine probes were isolated from a human chromosome 1 enriched library and mapped to regions of chromosome 1 using somatic cell hybrid lines. One clone, LR67, which mapped 1q12→q23 detected a BglI RFLP. This probe, as well as 4 other known chromosome 1 markers, α-spectrin, Factor XIIIB, DR10 and DR78, were used for linkage studies in 15 Charcot-Marie-Tooth disease (CMT1) families. Close linking of CMT1 to any of the 5 markers was not indicated. Total lod scores excluded linkage of CMT1 to LR67 and to DR10 at 5 cM or less, to DR78 and 10 cM or less, α-spectrin at 15 cM or less and Factor XIIIB at 20 cM or less. Possible linkage, however, was shown between LR67 and CMT1 at a distance of 30 cM. Also linkage at a distance of 5 cM was detected between this probe and α-spectrin.