Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[EX Q]: Lack of the yeast Rrm3p DNA helicase causes replication defects at multiple sites within ribosomal DNA (rDNA), including at the replication fork barrier (RFB). These defects were unaltered in rrm3 sir2 cells. When the RFB binding Fob1p was deleted, rrm3-generated defects at the RFB were eliminated, but defects at other rDNA sites were not affected. Thus, specific protein-DNA complexes make replication Rrm3p-dependent. Because rrm3-induced increases in recombination and cell cycle length were only partially suppressed in rrm3 fob1 cells, which still required checkpoint and fork restart activities for viability, non-RFB rrm3-induced defects contribute to rDNA fragility and genome instability.
[EX A]: What is the effect of the absence of Saccharomyces cerevisiae Rrm3p?

[EX Q]: To determine the validity of the rapid antigen test (RAT) OSOM StrepA Genzyme for the diagnosis of acute pharyngitis caused by group A beta-haemolytic strep (GABHS). Diagnostic techniques survey. Urban primary care centre, Spain. All patients over 14 years old seen in 6 surgeries with sore throat and 2 or more Centor criteria: pharyngotonsillar exudate, tender laterocervical nodes, absence of coughing, and/or history or presence of fever. Pharyngeal swabs were taken from all the patients, one for RAT and another to send for culture in the microbiology department. A total of 182 patients were evaluable, with a mean age of 30.6 (12.1) years of which 116 were women (63.7%); 63 patients had 2 Centor criteria; 83 had 3 and 36, the 4 criteria. The culture was positive in 102 patients (56%), with GABHS showing infection in forty (22%; 95% confidence interval [CI], 21.2-22.8). Group C Streptococcus was isolated in 26 patients (14.3%). GABHS was higher among patients with four Centor criteria (38.9% vs 25.3% observed among those with 3 criteria and 7.9% with 2 criteria; P<.001). Sensitivity of RAT was 95%, with a specificity of 93%, a positive predictive value of 79.2% and a negative predictive value of 98.5%. These results show the usefulness of RAT for diagnosing streptococcal pharyngitis. Its use should be spread to all primary care practices.
[EX A]: Centor criteria are used for which disease?

[EX Q]: Spinocerebellar ataxia type 3 is a neurodegenerative disorder caused by the expansion of the polyglutamine repeat region within the ataxin-3 protein. The mutant protein forms intracellular aggregates in the brain. However, the cellular mechanisms causing toxicity are still poorly understood and there are currently no effective treatments. In this study we show that administration of a rapamycin ester (cell cycle inhibitor-779, temsirolimus) improves motor performance in a transgenic mouse model of spinocerebellar ataxia type 3. Temsirolimus inhibits mammalian target of rapamycin and hence upregulates protein degradation by autophagy. Temsirolimus reduces the number of aggregates seen in the brains of transgenic mice and decreases levels of cytosolic soluble mutant ataxin-3, while endogenous wild-type protein levels remain unaffected. Temsirolimus is designed for long-term use in patients and therefore represents a possible therapeutic strategy for the treatment of spinocerebellar ataxia type 3. Using this disease model and treatment paradigm, we employed a microarray approach to investigate transcriptional changes that might be important in the pathogenesis of spinocerebellar ataxia type 3. This identified ubiquitin specific peptidase-15, which showed expression changes at both the messenger ribonucleic acid and protein level. Ubiquitin specific peptidase-15 levels were also changed in mice expressing another mutant polyglutamine protein, huntingtin. In total we identified 16 transcripts that were decreased in transgenic ataxin-3 mice that were normalized following temsirolimus treatment. In this mouse model with relatively mild disease progression, the number of transcripts changed was low and the magnitude of these changes was small. However, the importance of these transcriptional alterations in the pathogenesis of spinocerebellar ataxia type 3 remains unclear.
[EX A]:
Which is the protein implicated in Spinocerebellar ataxia type 3?