Low-energy particle events associated with sector boundaries

Onsets of some 40 to 45 low-energy proton events during the years 1957–1969 coincided in time with transits of well-defined sector boundaries across the Earth. These events can be interpreted as long-lived proton streams filling up some of the magnetic sectors, indicating an acceleration of protons which is not associated with typical proton-producing flares. The sharp onsets of these particle streams, as well as a deficiency of flare-associated particle events shortly before the boundary transit, indicate that in some cases magnetic sector boundaries can inhibit transverse propagation of low-energy particles in the solar corona or in interplanetary space.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43744/1/11207_2004_Article_BF00155310.pd

“Help! I Need Somebody”: Music as a global resource for obtaining wellbeing goals in times of crisis

Health and self-regulatio

Adaptation de la symbiose légumineuse / rhizobia au déficit en phosphore et impact sur sa biodisponibilité dans le sol

International audienc

Serodiagnosis of tuberculosis using nine in silico predicted B-cell epitopes peptides derived from Mycobacterium tuberculosis proteins

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Evaluation of a multi-antigen test based on B-cell epitope peptides for the serodiagnosis of pulmonary tuberculosis

SETTING: Two sample panels: 1) 20 pulmonary tuberculosis (PTB) patients and 10 healthy subjects from a country with a low incidence of TB (Italy); and 2) 47 PTB patients and 26 healthy subjects from a country with a high incidence of TB (Morocco). OBJECTIVE: To identify a combination of Mycobacterium tuberculosis peptides useful for the serodiagnosis of active PTB. METHODS: Fifty-seven B-cell epitope peptides of M. tuberculosis were evaluated by immunoenzymatic assay and the data were analysed using logistic regression analysis and the random forest method. RESULTS: The best discriminating peptide between PTB patients and healthy subjects from the sample of the low TB incidence country was the 23 amino acid peptide of the Rv3878 protein. The sensitivity and specificity were respectively 65% and 100%. The same peptide had a sensitivity and specificity of respectively 47% and 100% for the sample from the high TB incidence country. The best combination of peptides was a pool of nine peptides which had a sensitivity of 70.2% and a specificity of 100% in the high TB incidence country. CONCLUSIONS: The 9-peptide pool can be useful in identifying patients with active PTB

A founder deletion in the TRPM1 gene associated with congenital stationary night blindness and myopia is highly prevalent in Ashkenazi Jews

Congenital stationary night blindness (CSNB) is a disease affecting the night vision of individuals. Previous studies identified TRPM1 as a gene involved in reduced night vision. Homozygous deletion of TRPM1 was the cause of CSNB in several children in 6 Ashkenazi Jewish families, thereby prompting further investigation of the carrier status within the families as well as in large cohorts of unrelated Ashkenazi and Sephardi individuals. Affected children were tested with a CSNB next-generation (NextGen) sequencing panel. A deletion of TRPM1 exons 2 through 7 was detected and confirmed by PCR and sequence analysis. A TaqMan-based assay was used to assess the frequency of this deletion in 18266 individuals of Jewish descent. High-throughput amplicon sequencing was performed on 380 samples to determine the putative deletion-flanking founder haplotype. Heterozygous TRPM1 deletions were found in 2.75% (1/36) of Ashkenazi subjects and in 1.22% (1/82) individuals of mixed Ashkenazi/Sephardic origin. The homozygous deletion frequency in our data was 0.03% (1/4025) and was only found in Ashkenazi Jewish individuals. Homozygous deletion of exons 2–7 in TRPM1 is a common cause of CSNB and myopia in many Ashkenazi Jewish patients. This deletion is a founder Ashkenazi Jewish deletion. A genetic mutation found in Ashkenazi Jewish population causes an eye disease that leads to poor vision in dim light. Yoel Hirsch and Martin M. Johansson from Dor Yeshorim, together with colleagues determined the genetic etiology of congenital stationary night blindness (CSNB) in children from six Ashkenazi families. Each affected child harbored two mutant versions of TRPM1 , a gene involved in the transmission of light-elicited signals within the retina of the eye. Notably, all the children had the same large chunk of DNA missing from the gene. The researchers next screened for this genetic deletion in >18,000 individuals of Jewish descent, finding single copies of the mutation in 2.75% of Ashkenazi subjects. The findings should help doctors better diagnose CSNB and care for Jewish patients with eyesight problems