Most, but not all, departments accounted for academic productivity in their compensation system. Most programs used the chair's discretion to determine academic bonuses, but several departments had developed point systems. There are common themes with regard to this issue, including the importance of the academic mission, the need for clinical revenues, the value of flexibility and transparency, and the importance of culture and leadership.
Increased phosphorus (P) availability under flooded, anaerobic conditions may accelerate P loss from soils to water bodies. Existing knowledge on P release to floodwater from flooded soils is limited to summer conditions and/or room temperatures. Spring snowmelt runoff, which occurs under cold temperatures with frequent freeze-thaw events, is the dominant mode of P loss from agricultural lands to water bodies in the Canadian Prairies. This research examined the effects of temperature on P dynamics under flooded conditions in a laboratory study using five agricultural soils from Manitoba, Canada. The treatments were (a) freezing for 1 wk at −20 • C, thawing and flooding at 4 ± 1 • C (frozen, cold); (b) flooding unfrozen soil at 4 ± 1 • C (unfrozen, cold); and (c) flooding unfrozen soil at 20 ± 2 • C (warm). Pore water and surface water were collected weekly over 8 wk and analyzed for dissolved reactive phosphorus (DRP), pH, calcium, magnesium, iron (Fe), and manganese (Mn). Soils under warm flooding showed enhanced P release with significantly higher DRP concentrations in pore and surface floodwater compared with cold flooding of frozen and unfrozen soils.The development of anaerobic conditions was slow under cold flooding with only a slight decrease in Eh, whereas under warm flooding Eh declined sharply, favoring reductive dissolution reactions releasing P, Fe, and Mn. Pore water and floodwater DRP concentrations were similar between frozen and unfrozen soil under cold flooding, suggesting that one freeze-thaw event prior to flooding had minimal effect on P release under simulated snowmelt conditions. Abbreviations: DAF, days after flooding; DRP, dissolved reactive phosphorus.
The hormonally responsive prolactin-inducible protein (PIP) gene is expressed in benign and malignant breast tumor tissues and in such normal exocrine organs as sweat, salivary, and lacrimal glands. In this communication we report the regional chromosome localization of the PIP gene locus to chromosome 7 by Southern hybridization to DNA from human-hamster somatic cell hybrids, and to 7q32-36 by in situ hybridization.
The Prader-Willi (PWS) and Angelman syndromes (AS) share the same apparent cytogenetic and molecular lesions of 15q11-13 and yet exhibit distinct clinical phenotypes. The etiology of PWS or AS appears to depend on the parental origin of the aberrant chromosome 15. Substantial clinical overlap has not been reported between deletion-positive PWS and AS patients. In the present study, we report the clinical, cytogenetic, and molecular findings in three AS patients. The first patient is a mentally retarded woman with a visible deletion of 15q11-13 with typical craniofacial, behavioral, and neurologic changes of AS. This patient is hyperphagic, and she is moderately obese for her height. Her hands and feet are small. These manifestations are more characteristic of PWS and not of AS. The molecular studies showed deletions of maternal origin for five distal PWCR loci. The most proximal locus, D15S18, was not deleted. These findings are identical to those found in our third AS patient who does not have any PWS features. To the best of our knowledge, this is the first report of concurrence of hyperphagia with consequent obesity and the AS phenotype in a patient with a del 15(q11-13) of maternal origin. These clinical findings suggest that overlap in the symptoms of PWS and AS can occur. Our second AS patient presents with atypical molecular findings in that he cannot be classed into any of the three proposed sub-groups of AS patients and may be representative of a fourth sub-group of AS patients.
The Prader-Willi chromosome region (PWCR) in Prader-Willi syndrome patients was analyzed by using genomic DNA probes mapping to 15q11.2-q12. The present report includes analysis of dosage by RFLP and densitometric studies, and analysis of restriction patterns. Twelve Prader-Willi syndrome (PWS) patients were studied: 5 had deletions of 15q11-q13, one had an unbalanced translocation, and 6 were karyotypically normal. Four genomic DNA probes were used: pML34 (D15S9); pTD3-21 (D15S10); IR4-3 (D15S11), a subclone of IR4; and IR10-1 (D15S12), a subclone of IR10 (Donolon et al.: Proc Natl Acad Sci USA 83:4408-4412, 1986). The results presented demonstrate that molecular rearrangements have occurred in 10 of the 12 PWS patients investigated and that the specific rearrangements differ from patient to patient. Patients with apparently similar cytogenetic deletions differ at the molecular level with deletions and/or duplications of various loci. The present study reports molecular alterations within the PWCR in PWS patients reported as cytogenetically normal. However, the 6 karyotypically normal patients are a heterogeneous group with molecular rearrangements ranging from none detected to deletions and/or duplications. These molecular studies suggest that a physical disruption of the PWCR causes the PWS not only in those patients reported to have a cytogenetic aberration but also in those identified as apparently karyotypically normal. The question remains as to whether the PWS patients in whom a molecular abnormality has not been detected have an autosomal recessive form of PWS, a molecular disruption which has not yet been detected, or another mechanism producing an apparently identical phenotype. The order of the 4 loci on chromosome 15 is hypothesized to be cen----D15S9----D15S12----D15S11----D15S10.
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