TASK DEFINITION: Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
PROBLEM: Facioscapulohumeral muscular dystrophy (FSHD) is a primary muscle disorder with autosomal dominant inheritance. FSHD was mapped to chromosome 4 locus q35, but the gene is not yet known. It is characterised by progressive, often asymmetric, selective muscular weakness and great clinical variability. The aim of the study was to analyze 62 FSHD cases from 44 Polish families in which the diagnosis was confirmed by DNA analyses. FSHD diagnosis was based on the clinical findings and standardized investigations confirming primary muscular involvement (EMG, muscle biopsy). DNA analysis was based on EcoRI/BlnI restriction enzyme digestion followed by hybridization with P13E-11 molecular probe. In our material, we have found a relatively large percentage (41%) of big deletions (EcoRI/BlnI fragment of 10-15 kb [kilo bases]), which in the majority of cases (67%) was present in isolated cases. In 10 families (23%) the phenotype was assessed as severe. These are cases with the onset before the age of 10 and fast progression. "Middle sized" deletions (EcoRI/BlnI fragment of 16-29 kb) were prevalent in familial cases and present in 57% of families. "Small" deletion was found in one family (EcoRI/BlnI fragment of 30 kb). Somatic mosaicism was confirmed in one case. De novo mutations were shown in 11% of the examined families. The results of this study indicate that the bigger the deletion, the more severe the FSHD course, however there are some exceptions. A similar relationship has been shown by previous research. Molecular analyses are particularly important in atypical and sporadic cases. It is the first genetic presentation of a group of patients' with this kind of dystrophy in the Polish population.

SOLUTION: What is the mode of inheritance of Facioscapulohumeral muscular dystrophy (FSHD)?

PROBLEM: Jan Muhlstein (born 3 July 1949 in Most, Czechoslovakia) is a journalist, German Jewish activist and the former chair of the Union of Progressive Jews in Germany.

SOLUTION: Which language or languages is Jan Muhlstein fluent in?

PROBLEM: Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene are present in lung adenocarcinomas that respond to the EGFR inhibitors gefitinib and erlotinib. Two types of mutations account for approximately 90% of mutated cases: short in-frame deletions in exon 19 and a specific point mutation in exon 21 at codon 858 (L858R). Screening for these mutations has been based mainly on direct sequencing. We report here the development and validation of polymerase chain reaction-based assays for these two predominant types of EGFR mutations. The assay for exon 19 mutations is based on length analysis of fluorescently labeled polymerase chain reaction products, and the assay for the exon 21 L858R mutation is based on a new Sau96I restriction site created by this mutation. Using serial dilutions of DNAs from lung cancer cell lines harboring either exon 19 or 21 mutations, we detected these mutations in the presence of up to approximately 90% normal DNA. In a test set of 39 lung cancer samples, direct sequencing detected mutations in 25 cases whereas our assays were positive in 29 cases, including 4 cases in which mutations were not apparent by sequencing. These assays offer higher sensitivity and ease of scoring and eliminate the need for sequencing, providing a robust and accessible approach to the rapid identification of most lung cancer patients likely to respond to EGFR inhibitors.

SOLUTION:
Mutations in which gene determine response to both erlotinib and gefitinib?