To accurately estimate near-surface (2 m) air temperatures in a mountainous region for hydrologic prediction models and other investigations of environmental processes, the authors evaluated daily and seasonal variations (with the consideration of different weather types) of surface air temperature lapse rates at a spatial scale of 10 000 km 2 in south-central Idaho. Near-surface air temperature data (T max , T min , and T avg ) from 14 meteorological stations were used to compute daily lapse rates from January 1989 to December 2004 for a medium-elevation study area in south-central Idaho. Daily lapse rates were grouped by month, synoptic weather type, and a combination of both (seasonal-synoptic). Daily air temperature lapse rates show high variability at both daily and seasonal time scales. Daily T max lapse rates show a distinct seasonal trend, with steeper lapse rates (greater decrease in temperature with height) occurring in summer and shallower rates (lesser decrease in temperature with height) occurring in winter. Daily T min and T avg lapse rates are more variable and tend to be steepest in spring and shallowest in midsummer. Different synoptic weather types also influence lapse rates, although differences are tenuous. In general, warmer air masses tend to be associated with steeper lapse rates for maximum temperature, and drier air masses have shallower lapse rates for minimum temperature. The largest diurnal range is produced by dry tropical conditions (clear skies, high solar input). Cross-validation results indicate that the commonly used environmental lapse rate [typically assumed to be Ϫ0.65°C (100 m) Ϫ1] is solely applicable to maximum temperature and often grossly overestimates T min and T avg lapse rates. Regional lapse rates perform better than the environmental lapse rate for T min and T avg , although for some months rates can be predicted more accurately by using monthly lapse rates. Lapse rates computed for different months, synoptic types, and seasonal-synoptic categories all perform similarly. Therefore, the use of monthly lapse rates is recommended as a practical combination of effective performance and ease of implementation.

The BRMS1 metastasis suppressor interacts with the protein AT-rich interactive domain 4A (ARID4A, RBBP1) as part of SIN3⅐histone deacetylase chromatin remodeling complexes. These transcriptional co-repressors regulate diverse cell phenotypes depending upon complex composition. To define BRMS1 complexes and their roles in metastasis suppression, we generated BRMS1 mutants (BRMS1 mut ) and mapped ARID4A interactions. BRMS1L174D disrupted direct interaction with ARID4A in yeast two-hybrid genetic screens but retained an indirect association with ARID4A in MDA-MB-231 and -435 human breast cancer cell lines by co-immunoprecipitation. Deletion of the first coiled-coil domain (BRMS1 ⌬CC1 ) did not disrupt direct interaction in yeast two-hybrid screens but did prevent association by co-immunoprecipitation. These results suggest altered complex composition with BRMS1 mut . Although basal transcription repression was impaired and the pro-metastatic protein osteopontin was differentially down-regulated by BRMS1 L174D and BRMS1 ⌬CC1 , both down-regulated the epidermal growth factor receptor and suppressed metastasis in MDA-MB-231 and -435 breast cancer xenograft models. We conclude that BRMS1 mut , which modifies the composition of a SIN3⅐histone deacetylase chromatin remodeling complex, leads to altered gene expression profiles. Because metastasis requires the coordinate expression of multiple genes, down-regulation of at least one important gene, such as the epidermal growth factor receptor, had the ability to suppress metastasis. Understanding which interactions are necessary for particular biochemical/ cellular functions may prove important for future strategies targeting metastasis.The ability of a cancer cell to complete all steps of the metastatic cascade requires diverse tumor-host interactions that are dependent on the coordinate expression of specific genes both intrinsically and extrinsically (1-3). The metastasis suppressor BRMS1 3 has been shown to regulate the expression of multiple genes leading to the suppression of metastasis in multiple model systems, including human breast carcinoma (4, 5), melanoma (6), and ovarian carcinoma (7), without preventing orthotopic tumor growth. Specifically, down-regulation of the pro-metastatic genes osteopontin (OPN) and urokinase-type plasminogen activator has been linked to BRMS1 expression (8, 9). Gap junctional intercellular communication is restored by BRMS1 through a change in connexin expression (10). Microarray and proteomic analyses have also been performed showing multiple changes in gene and protein expression when BRMS1 was introduced (11-13). Clinically, loss of BRMS1 protein has been correlated with progesterone receptor expression and inversely correlated with HER2 expression in breast cancer patients (14).BRMS1 has been proposed to regulate transcription of genes by interaction with a large SIN3⅐HDAC chromatin remodeling complex through interaction with the protein AT-rich interactive domain 4A (ARID4A) that suppresses basal transcription in vivo using a Gal...

A novel method assessed the quality of bicycle travel throughout a community. Most previous research on the quality of bicycle travel assessed bicycle suitability, that is, the perceived comfort and safety of a linear section of bikeway. Assessment of bikeability (as defined by authors), however, considers comfort and safety of the entire bikeway network for access to important destinations, and there is ample research concerning the related concept of accessibility. A proposed calculation for bikeability was developed on the basis of a common accessibility equation and was demonstrated through a case study of three capital investment scenarios. The analysis used a geographic information system. Engineers and planners can follow a similar procedure to the one used in the calculation development to prioritize improvement projects or to communicate the benefits of new projects.

Breast cancer metastasis suppressor 1 (BRMS1) is a member of the mSin3-HDAC transcription co-repressor complex. However, the proteins associated with BRMS1 have not been fully identified. Yeast two-hybrid screen, immuno-affinity chromatography, and co-immunoprecipitation experiments were performed to identify BRMS1 interacting proteins (BIPs). In addition to known core mSin3 transcriptional complex components RBBP1 and mSDS3, BRMS1 interacted with other proteins including three chaperones: DNAJB6 (MRJ), Hsp90, and Hsp70. Hsp90 is a known target of HDAC6 and reversible acetylation is one of the mechanisms that is implicated in regulation of Hsp90 chaperone complex activity. BRMS1 interacted with class II HDACs, HDAC 4, 5, and 6. We further found that BRMS1 is stabilized by Hsp90, and its turnover is proteasome dependent. The stability of BRMS1 protein may be important in maintaining the functional role of BRMS1 in metastasis suppression.