G313.3+00.3: A New Planetary Nebula discovered by the Australia Telescope Compact Array and the Spitzer Space Telescope

We present a new planetary nebula, first identified in images from the Australia Telescope Compact Array, although not recognized at that time. Recent observations with the Spitzer Space Telescope during the GLIMPSE Legacy program have rediscovered the object. The high-resolution radio and infrared images enable the identification of the central star or its wind, the recognition of the radio emission as thermal, and the probable presence of polycylic aromatic hydrocarbons in and around the source. These lead to the conclusion that G313.3+00.3 is a planetary nebula. This object is of particular interest because it was discovered solely through radio and mid-infrared imaging, without any optical (or near-infrared) confirmation, and acts as a proof of concept for the discovery of many more highly extinguished planetary nebulae. G313.3+00.3 is well-resolved by both the instruments with which it was identified, and suffers extreme reddening due to its location in the Scutum-Crux spiral arm.Comment: 18 pages, LaTeX (aastex), incl. 8 PostScript (eps) figures and 1 table. Accepted by ApJ (Part 1

Acute Kawasaki Disease: Not Just for Kids

Kawasaki Disease is a small-to-medium-vessel vasculitis that preferentially affects children. Kawasaki Disease can occur in adults, but the presentation may differ from that observed in children. Typical findings in both adults and children include fever, conjunctivitis, pharyngitis, and skin erythema progressing to a desquamating rash on the palms and soles. Adults more frequently present with cervical adenopathy (93% of adults vs. 15% of children), hepatitis (65% vs. 10%), and arthralgia (61% vs. 24–38%). In contrast, adults are less frequently affected by meningitis (10% vs. 34%), thrombocytosis (55% vs. 100%), and coronary artery aneurysms (5% vs. 18–25%). We report a case of acute Kawasaki Disease in a 24-year-old man who presented with rash, fever, and arthritis. He was successfully treated with high-dose aspirin and intravenous immunoglobulin (IVIG). Our case highlights the importance of considering Kawasaki Disease in adults presenting with symptoms commonly encountered in a general medical practice

Immortalized pathological human myoblasts: towards a universal tool for the study of neuromuscular disorders

<p>Abstract</p> <p>Background</p> <p>Investigations into both the pathophysiology and therapeutic targets in muscle dystrophies have been hampered by the limited proliferative capacity of human myoblasts. Isolation of reliable and stable immortalized cell lines from patient biopsies is a powerful tool for investigating pathological mechanisms, including those associated with muscle aging, and for developing innovative gene-based, cell-based or pharmacological biotherapies.</p> <p>Methods</p> <p>Using transduction with both telomerase-expressing and cyclin-dependent kinase 4-expressing vectors, we were able to generate a battery of immortalized human muscle stem-cell lines from patients with various neuromuscular disorders.</p> <p>Results</p> <p>The immortalized human cell lines from patients with Duchenne muscular dystrophy, facioscapulohumeral muscular dystrophy, oculopharyngeal muscular dystrophy, congenital muscular dystrophy, and limb-girdle muscular dystrophy type 2B had greatly increased proliferative capacity, and maintained their potential to differentiate both <it>in vitro </it>and <it>in vivo </it>after transplantation into regenerating muscle of immunodeficient mice.</p> <p>Conclusions</p> <p>Dystrophic cellular models are required as a supplement to animal models to assess cellular mechanisms, such as signaling defects, or to perform high-throughput screening for therapeutic molecules. These investigations have been conducted for many years on cells derived from animals, and would greatly benefit from having human cell models with prolonged proliferative capacity. Furthermore, the possibility to assess <it>in vivo </it>the regenerative capacity of these cells extends their potential use. The innovative cellular tools derived from several different neuromuscular diseases as described in this report will allow investigation of the pathophysiology of these disorders and assessment of new therapeutic strategies.</p

Genetic architecture distinguishes systemic juvenile idiopathic arthritis from other forms of juvenile idiopathic arthritis: Clinical and therapeutic implications

Objectives Juvenile idiopathic arthritis (JIA) is a heterogeneous group of conditions unified by the presence of chronic childhood arthritis without an identifiable cause. Systemic JIA (sJIA) is a rare form of JIA characterised by systemic inflammation. sJIA is distinguished from other forms of JIA by unique clinical features and treatment responses that are similar to autoinflammatory diseases. However, approximately half of children with sJIA develop destructive, long-standing arthritis that appears similar to other forms of JIA. Using genomic approaches, we sought to gain novel insights into the pathophysiology of sJIA and its relationship with other forms of JIA. Methods We performed a genome-wide association study of 770 children with sJIA collected in nine countries by the International Childhood Arthritis Genetics Consortium. Single nucleotide polymorphisms were tested for association with sJIA. Weighted genetic risk scores were used to compare the genetic architecture of sJIA with other JIA subtypes. Results The major histocompatibility complex locus and a locus on chromosome 1 each showed association with sJIA exceeding the threshold for genome-wide significance, while 23 other novel loci were suggestive of association with sJIA. Using a combination of genetic and statistical approaches, we found no evidence of shared genetic architecture between sJIA and other common JIA subtypes. Conclusions The lack of shared genetic risk factors between sJIA and other JIA subtypes supports the hypothesis that sJIA is a unique disease process and argues for a different classification framework. Research to improve sJIA therapy should target its unique genetics and specific pathophysiological pathways

Prevalence, Clinical Staging and Risk for Blood-Borne Transmission of Chagas Disease among Latin American Migrants in Geneva, Switzerland

Chagas disease, a parasitic disease caused by Trypanosoma cruzi, is a leading cause of cardiac and digestive tract disorders in Mexico, Central and South America. An increasing number of cases have recently been reported in North America and Europe due to international human migration, but data outside Latin America remains scarce. This study showed that Chagas disease is an emerging health problem in Switzerland, affecting a substantial proportion of Latin American migrants (13%). Persons at increased risk of infection were Bolivian, older than 35 years or had a mother infected with T. cruzi. Early signs of cardiac or digestive tract disease were found in one out of six infected patients. The risk of local transmission by blood transfusion or organ transplant was illustrated by the frequent willingness expressed by patients to donate blood or organs in Switzerland. The authors recommend the screening of persons at risk of infection and the diffusion of appropriate information to the medical community to increase awareness of this emerging health problem. Considering that affected persons frequently lack health insurance in Switzerland, a facilitated access to medical care is an important step towards better recognition and management of Chagas disease

Influenza Virus Ribonucleoprotein Complexes Gain Preferential Access to Cellular Export Machinery through Chromatin Targeting

In contrast to most RNA viruses, influenza viruses replicate their genome in the nucleus of infected cells. As a result, newly-synthesized vRNA genomes, in the form of viral ribonucleoprotein complexes (vRNPs), must be exported to the cytoplasm for productive infection. To characterize the composition of vRNP export complexes and their interplay with the nucleus of infected cells, we affinity-purified tagged vRNPs from biochemically fractionated infected nuclei. After treatment of infected cells with leptomycin B, a potent inhibitor of Crm1-mediated export, we isolated vRNP export complexes which, unexpectedly, were tethered to the host-cell chromatin with very high affinity. At late time points of infection, the cellular export receptor Crm1 also accumulated at the same regions of the chromatin as vRNPs, which led to a decrease in the export of other nuclear Crm1 substrates from the nucleus. Interestingly, chromatin targeting of vRNP export complexes brought them into association with Rcc1, the Ran guanine exchange factor responsible for generating RanGTP and driving Crm1-dependent nuclear export. Thus, influenza viruses gain preferential access to newly-generated host cell export machinery by targeting vRNP export complexes at the sites of Ran regeneration

Migrant health in French Guiana: Are undocumented immigrants more vulnerable?

<p>Abstract</p> <p>Background</p> <p>Few data exist on the health status of the immigrant population in French Guiana. The main objective of this article was to identify differences in its health status in relation to that of the native-born population.</p> <p>Methods</p> <p>A representative, population-based, cross-sectional survey was conducted in 2009 among 1027 adults living in Cayenne and St-Laurent du Maroni. Health status was assessed in terms of self-perceived health, chronic diseases and functional limitations. The migration variables were immigration status, the duration of residence in French Guiana and the country of birth. Logistic regression models were conducted.</p> <p>Results</p> <p>Immigrants account for 40.5% and 57.8% of the adult population of Cayenne and St-Laurent du Maroni, respectively. Most of them (60.7% and 77.5%, respectively) had been living in French Guiana for more than 10 years. A large proportion were still undocumented or had a precarious legal status. The undocumented immigrants reported the worst health status (OR = 3.18 [1.21-7.84] for self-perceived health, OR = 2.79 [1.22-6.34] for a chronic disease, and OR = 2.17 [1.00-4.70] for a functional limitation). These differences are partially explained by socioeconomic status and psychosocial factors. The country of birth and the duration of residence also had an impact on health indicators.</p> <p>Conclusion</p> <p>Data on immigrant health are scarce in France, and more generally, immigrant health problems have been largely ignored in public health policies. Immigrant health status is of crucial interest to health policy planners, and it is especially relevant in French Guiana, considering the size of the foreign-born population in that region.</p

Negative perceptions of aging and decline in walking speed: A self-fulfilling prophecy

Introduction Walking speed is a meaningful marker of physical function in the aging population. While it is a primarily physical measure, experimental studies have shown that merely priming older adults with negative stereotypes about aging results in immediate declines in objective walking speed. What is not clear is whether this is a temporary experimental effect or whether negative aging stereotypes have detrimental effects on long term objective health. We sought to explore the association between baseline negative perceptions of aging in the general population and objective walking speed 2 years later. Method 4,803 participations were assessed over 2 waves of The Irish Longitudinal Study on Ageing (TILDA), a prospective, population representative study of adults aged 50+ in the Republic of Ireland. Wave 1 measures – which included the Aging Perceptions Questionnaire, walking speed and all covariates - were taken between 2009 and 2011. Wave 2 measures – which included a second measurement of walking speed and covariates - were collected 2 years later between March and December 2012. Walking speed was measured as the number of seconds to complete the Timed Up-And-Go (TUG) task. Participations with a history of stroke, Parkinson’s disease or an MMSE < 18 were excluded. Results After full adjustment for all covariates (age, gender, level of education, disability, chronic conditions, medications, global cognition and baseline TUG) negative perceptions of aging at baseline were associated with slower TUG speed 2 years later (B=.03, 95% CI = .01 to 05, p< .01). Conclusions Walking speed has previously been considered to be a consequence of physical decline but these results highlight the direct role of psychological state in predicting an objective aging outcome. Negative perceptions about aging are a potentially modifiable risk factor of some elements of physical decline in aging