A gene atlas of the mouse and human protein-encoding transcriptomes.

The tissue-specific pattern of mRNA expression can indicate important clues about gene function. High-density oligonucleotide arrays offer the opportunity to examine patterns of gene expression on a genome scale. Toward this end, we have designed custom arrays that interrogate the expression of the vast majority of protein-encoding human and mouse genes and have used them to profile a panel of 79 human and 61 mouse tissues. The resulting data set provides the expression patterns for thousands of predicted genes, as well as known and poorly characterized genes, from mice and humans. We have explored this data set for global trends in gene expression, evaluated commonly used lines of evidence in gene prediction methodologies, and investigated patterns indicative of chromosomal organization of transcription. We describe hundreds of regions of correlated transcription and show that some are subject to both tissue and parental allele-specific expression, suggesting a link between spatial expression and imprinting.

Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization.

MLL fusion proteins are oncogenic transcription factors that are associated with aggressive lymphoid and myeloid leukemias. We constructed an inducible MLL fusion, MLL-ENL-ERtm, that rendered the transcriptional and transforming properties of MLL-ENL strictly dependent on the presence of 4-hydroxy-tamoxifen. MLL-ENL-ERtm-immortalized hematopoietic cells required 4-hydroxy-tamoxifen for continuous growth and differentiated terminally upon tamoxifen withdrawal. Microarray analysis performed on these conditionally transformed cells revealed Hoxa9 and Hoxa7 as well as the Hox coregulators Meis1 and Pbx3 among the targets upregulated by MLL-ENL-ERtm. Overexpression of the Hox repressor Bmi-1 inhibited the growth-transforming activity of MLL-ENL. Moreover, the enforced expression of Hoxa9 in combination with Meis1 was sufficient to substitute for MLL-ENL-ERtm function and to maintain a state of continuous proliferation and differentiation arrest. These results suggest that MLL fusion proteins impose a reversible block on myeloid differentiation through aberrant activation of a limited set of homeobox genes and Hox coregulators that are consistently expressed in MLL-associated leukemias.

Do third-party plans really pay for CVS care?

Until specific CPT and ICD-9 codes are created and approved for CVS, and until there is uniform agreement that CVS is a true medical anomaly (or not), each practitioner will have to decide on how to bill for the signs and symptoms of Computer Vision Syndrome. If the practitioner chooses to view CVS as a medical problem, then the same guidelines and rules for all other patients should be followed with appropriate documentation using CPT and ICD-9 coding. If the practitioner chooses to consider CVS solely as an optical problem, this is a "noncovered" service and the patient or any applicable optical plan will be responsible for payment. One final note: each practitioner who tests for CVS will also have to determine if there is a separate fee for CVS testing. If the practitioner considers CVS to be a medical problem, it may be applicable to include testing for Computer Vision Syndrome as an incidental test to the medical office visit. If the practitioner chooses to consider CVS to be purely an optical problem, it may be appropriate to add an appropriate charge to the noncovered examination. Whatever the decision is, there must be consistency from patient to patient.