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Importance Guidelines recommend avoiding unnecessary laboratory tests to minimise risks of anaemia in hospitalised patients as well as reduce costs, but there are costs to skipping routine labs including missing acute kidney injury.Objective Quantify the costs and benefits of routine labs in dollar costs as well as mortality.Evidence review This is a retrospective analysis of 48 204 admissions at University of Kentucky Hospitals and simulates different strategies for skipping labs.Findings In a simplified estimate of pure dollar costs, the costs of daily labs appear to outweigh the costs of missing acute kidney injury.Conclusions and relevance In both dollar costs and the number of patients with mortality effects, the benefits of randomly skipping labs appear to significantly outweigh the costs, but the costs are not insignificant.

In Saccharomyces cerevisiae exit from mitosis requires the Cdc14 phosphatase to reverse CDK-mediated phosphorylation. Cdc14 is released from the nucleolus by the Cdc14 early anaphase release (FEAR) and mitotic exit network (MEN) pathways. In meiosis, the FEAR pathway is essential for exit from anaphase I. The MEN component Cdc15 is required for the formation of mature spores. To analyze the role of Cdc15 during sporulation, a conditional mutant in which CDC15 expression was controlled by the CLB2 promoter was used. Cdc15-depleted cells proceeded normally through the meiotic divisions but were unable to properly disassemble meiosis II spindles. The morphology of the prospore membrane was aberrant and failed to capture the nuclear lobes. Cdc15 was not required for Cdc14 release from the nucleoli, but it was essential to maintain Cdc14 released and for its nucleo-cytoplasmic transport. However, cells carrying a CDC14 allele with defects in nuclear export (Cdc14-[DELTA]NES) were able to disassemble the spindle and to complete spore formation, suggesting that the Cdc14 nuclear export defect was not the cause of the phenotypes observed in cdc15 mutants.

Meiosis I in Saccharomyces cerevisiae is dependent upon the motor protein Kar3. Absence of Kar3p in meiosis results in an arrest in prophase I. Cik1p and Vik1p are kinesin-associated proteins known to modulate the function of Kar3p in the microtubule-dependent processes of karyogamy and mitosis. Experiments were performed to determine whether Cik1p and Vik1p are also important for the function of Kar3p during meiosis. The meiotic phenotypes of a cik1 mutant were found to be similar to those of kar3 mutants. Cells without Cik1p exhibit a meiotic defect in homologous recombination and synaptonemal complex formation. Most cik1 mutant cells, like kar3 mutants, arrest in meiotic prophase; however, in cik1 mutants this arrest is less severe. These data are consistent with the model that Gik1p is necessary for some, but not all, of the roles of Kar3p in meiosis I. vik1 mutants sporulate at wild-type levels, but have reduced spore viability. This loss in viability is partially attributable to vegetative chromosome loss in vik1 diploids. Cellular localization experiments reveal that Kar3p, Gik1p, and Vik1p are present throughout meiosis and are consistent with Cik1p and Vik1p having different meiotic roles.

The role of the yeast motor protein, KAR3, in the passage through meiosis I was investigated through interhomologue recombination measurements and analysis of double-strand breaks. Results have shown that KAR3 recombinant mutant, Kar3p, acted in meiotic prophase to mediate homologous chromosome interactions. The rough alignment demonstrated by the mutant homologues was believed to be a precondition for efficient synapsis.

A model for analyzing the segregation of homologous chromosomes undergoing phase I meiosis has been developed. The model was tested using DNA sequences from Saccharomyces cerevisiae. Specifically, it was used to determine which DNA sequences moved away from each other during meiosis and to identify possible relationships between movement and chromosome size, recombination initiation and crossing over. Results showed that chromosome size and recombination initiation had negligible influence on the segregation of noncrossover chromosomes.

Errors in meiosis I were studied to detect diploids that give rise to disomes. A characterization of dominant allele SID1-1 was presented. Quantitation of meiotic segregation was done using the tetrad plating technique. Results showed that the SID1-1 effect does not cause any alteration in chromosome structure but decreased the incidence of complementary choromosome segregation in mitosis. Three types of segregational errors occurred in SID1-1 diploids and incidence increased in the wild types. SID1-1 errors were related to defective sister-chromatid association.

The meiotic recombinations in artificial chromosomes composed mainly of bacteriophage lambda and minichromosome derivatives of Saccharomyces cerevisiae chromosome III were studied. The results showed that artificial chromosomes undergo very low frequencies of meiotic recombination. However, when a short fragment of yeast chromosome VIII was inserted within the right arm of the artificial chromosome, meiotic recombination frequencies mimicked the wild type levels of the short fragment. These findings were similar to those observed in the minichromosome experiments. These results indicate that meiotic recombination is regulated locally, rather than from afar.