In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Input: Consider Input: Interfering with the activity of polo-like kinases can lead to the formation of monopolar spindles. Polo-like kinases also regulate mitotic entry, activation of the anaphase-promoting complex and the necessary preconditions for cytokinesis. Similarities between the phenotypes of the Drosophila mutants asp and polo point towards a common role in spindle pole function. The abnormal spindles of asp mutants are bipolar but have disorganized broad poles at which -tubulin has an abnormal distribution. Moreover, the synergism or of polo1 aspE3 double mutants indicates a possible involvement of these genes in a common process. Asp is a microtubule-associated protein of relative molecular mass 220,000 (Mr 220K) found at the face of the centrosome that contacts spindle microtubules. In partially purified centrosomes, it is required with -tubulin to organize microtubule asters. Here, we show that Asp is the previously identified Mr 220K substrate of Polo kinase. Polo phosphorylates Asp in vitro, converting it into an MPM2 epitope. Polo and Asp proteins immunoprecipitate together and exist as part of a 2538S complex. Extracts of polo-derived embryos are unable to restore the ability of salt-stripped centrosomes to nucleate microtubule asters. This can be rescued by addition of phosphorylated Asp or active Polo kinase.

Output: Polo kinase and Asp are needed to promote the mitotic organizing activity of centrosomes

Input: Consider Input: CONTEXT Gastroesophageal reflux (GER) has not previously been widely regarded as a hereditary disease. A few reports have suggested, however, that a genetic component may contribute to the incidence of GER, especially in its severe or chronic forms.
OBJECTIVE To identify a genetic locus that cosegregates with a severe pediatric GER phenotype in families with multiple affected members.
DESIGN A genome-wide scan of families affected by severe pediatric GER using polymorphic microsatellite markers spaced at an average of 8 centimorgans (cM), followed by haplotyping and by pairwise and multipoint linkage analyses.
SETTING General US community, with research performed in a university tertiary care hospital. SUBJECTS Affected and unaffected family members from 5 families having multiple individuals affected by severe pediatric GER, identified through a patient support group.
MAIN OUTCOME MEASURES Determination of inheritance patterns and linkage of a genetic locus with the severe pediatric GER phenotype by logarithm-of-odds (lod) score analysis, considering a lod score of 3 or greater as evidence of linkage.
RESULTS In these families, severe pediatric GER followed an autosomal dominant hereditary pattern with high penetrance. A gene for severe pediatric GER was mapped to a 13-cM region on chromosome 13q between microsatellite markers D13S171 and D13S263. A maximum multifamily 2-point lod score of 5.58 and a maximum multifamily multipoint lod score of 7.15 were obtained for marker D13S1253 at map position 35 cM when presumptively affected persons were modeled as unknown (a maximum multipoint score of 4.88 was obtained when presumptively affected persons were modeled as unaffected).
CONCLUSION These data suggest that a gene for severe pediatric GER maps to chromosome 13q14. JAMA. 2000;284:325-334

Output: Mapping of a gene for severe pediatric gastroesophageal reflux to chromosome 13q14.

Input: Consider Input: The first experimental vaccination against ticks was carried out 60 years ago. Since then, progress has been slow, although the recent commercial release of a recombinant vaccine against Boophilus microplus is significant. The nature of naturally acquired protective immunity against ticks is poorly understood, particularly in the important, domesticated ruminant hosts. Characterization of the antigens of naturally acquired immunity remains limited, although more has been achieved with 'concealed' antigens. Crucial questions remain about the true impact of tick-induced immunosuppression and the effect of immunity on the transmission of tick-borne diseases, despite some fascinating and important recent results, as discussed here by Peter Willadsen and Frans Jongejan.
Output: Immunology of the tick-host interaction and the control of ticks and tick-borne diseases.