City of Commerce Tree Canopy Prioritization

EXECUTIVE SUMMARY In 2019, the Loyola Marymount University Center for Urban Resilience (CURes) partnered with TreePeople to conduct a tree canopy prioritization in the City of Commerce. This process utilized high resolution, high accuracy tree canopy data as a foundation to engage the public in identifying their priorities for tree planting in the city. Analysis of the tree canopy data, acquired through a previous project between CURes and TreePeople, showed that the City of Commerce only has 5% tree canopy cover. This is in contrast to 25% cover in the City of Los Angeles, and 18% tree canopy cover found countywide. The analyses also found that Commerce has great opportunity to increase its tree canopy, with 51% of the land area of the city shown to be Possible Tree Canopy. CURes and TreePeople held two planning meetings with the City of Commerce and conducted multiple forms of outreach to engage community participation in a “tree summit,” which took place in November, 2019. Participants were introduced to the numerous ways that their city could benefit from increased tree canopy, engaged in a discussion about their personal experiences and values around trees, and were invited to take a survey to choose their top ten priorities for tree planting. Overall, 33 surveys were collected, with the large majority (88%) of respondents indicating that they were residents of Commerce and a smaller number (42%) indicating that they worked in Commerce. Respondents had the opportunity to vote to prioritize 17 specific tree benefits across seven categories. Participants identified “Improve Air Quality and Reduce Noise” and “Beautify Neighborhoods” as their top priority categories for tree planting. Among the specific benefits, the highest priorities were Access to Parks, Air Quality, Heat, Low Tree Canopy, and Schools. Each of the benefits voted on by participants was associated with a spatial variable (e.g. “Heat” was associated with high-resolution surface temperature data available through NASA). Using the results from the survey, priority weightings were calculated for each spatial variable, and these priorities were mapped using the Possible Tree Canopy data as a guide. Thus, the resulting maps showed the priority locations for tree planting in the City of Commerce that were already identified by the tree canopy assessment as Possible Tree Canopy. The prioritization map revealed that highest priority areas of Commerce are in the northern and central parts of the City. In addition to the maps, tables were produced to provide rankings for each individual parcel in the Possible Tree Canopy boundaries. These datasets include a comprehensive listing of 2,168 Residential Parcels, 909 Road Segments, and 4 Parks in the City of Commerce. Together, the products of this tree canopy prioritization project can guide the City of Commerce in its urban forestry planning. In the near term, TreePeople will use these data to inform a planting of over 1,000 trees, most concentrated in parks, streets, and residential giveaways. In the longer term, the City can use these data to guide future tree planting strategies.https://digitalcommons.lmu.edu/cures_reports/1001/thumbnail.jp

Characterization of the human STAT5A and STAT5B promoters: evidence of a positive and negative mechanism of transcriptional regulation

AbstractWe recently published the genomic characterization of the STAT5A and STAT5B paralogous genes that are located head to head in the 17q21 chromosome and share large regions of sequence identity. We here demonstrate by transient in vitro transfection that STAT5A and STAT5B promoters are able to direct comparable levels of transcription. The expression of basal promoters is enhanced after Sp1 up-regulation in HeLa and SL2 cells while DNA methylation associated to the recruitment of MeCP2 methyl CpG binding protein down-regulates STAT5A and B promoters by interfering with Sp1-induced transcription. In addition, cross-species sequence comparison identified a bi-directional negative cis-acting regulatory element located in the STAT5 intergenic region

Ovarian dysfunction and FMR1 alleles in a large Italian family with POF and FRAXA disorders: case report

BACKGROUND: The association between premature ovarian failure (POF) and the FMR1 repeat number (41> CGG(n)< 200) has been widely investigated. Current findings suggest that the risk estimation for POF can be calculated in the offspring of women with pre-mutated FMR1 alleles. CASE PRESENTATION: We describe the coexistence in a large Italian kindred of Fragile X syndrome and familial POF in females with ovarian dysfunctions who carried normal or expanded FMR1 alleles. Genetic analysis of the FMR1 gene in over three generations of females revealed that six carried pre-mutated alleles (61–200), of which two were also affected by POF. However a young woman, who presented a severe ovarian failure with early onset, carried normal FMR1 alleles (<40). The coexistence within the same family of two dysfunctional ovarian conditions, one FMR1-related and one not FMR1-related, suggests that the complexity of familial POF conditions is larger than expected. CONCLUSION: Our case study represents a helpful observation and will provide familial cases with heterogeneous etiology that could be further studied when candidate genes in addition to the FMR1 premutation will be available

MRX87 family with Aristaless X dup24bp mutation and implication for polyAlanine expansions

<p>Abstract</p> <p>Background</p> <p>Cognitive impairments are heterogeneous conditions, and it is estimated that 10% may be caused by a defect of mental function genes on the X chromosome. One of those genes is <it>Aristaless related homeobox </it>(<it>ARX</it>) encoding a polyA-rich homeobox transcription factor essential for cerebral patterning and its mutations cause different neurologic disorders. We reported on the clinical and genetic analysis of an Italian family with X-linked mental retardation (XLMR) and intra-familial heterogeneity, and provided insight into its molecular defect.</p> <p>Methods</p> <p>We carried out on linkage-candidate gene studies in a new MRX family (MRX87). All coding regions and exon-intron boundaries of ARX gene were analysed by direct sequencing.</p> <p>Results</p> <p>MRX87 patients had moderate to profound cognition impairment and a combination of minor congenital anomalies. The disease locus, MRX87, was mapped between DXS7104 and DXS1214, placing it in Xp22-p21 interval, a hot spot region for mental handicap. An in frame duplication of 24 bp (ARXdup24) in the second polyAlanine tract (polyA_II) in ARX was identified.</p> <p>Conclusion</p> <p>Our study underlines the role of ARXdup24 as a critical mutational site causing mental retardation linked to Xp22. Phenotypic heterogeneity of MRX87 patients represents a new observation relevant to the functional consequences of polyAlanine expansions enriching the puzzling complexity of ARXdup24-linked diseases.</p

Twelve Variants Polygenic Score for Low-Density Lipoprotein Cholesterol Distribution in a Large Cohort of Patients With Clinically Diagnosed Familial Hypercholesterolemia With or Without Causative Mutations

: Background A significant proportion of individuals clinically diagnosed with familial hypercholesterolemia (FH), but without any disease-causing mutation, are likely to have polygenic hypercholesterolemia. We evaluated the distribution of a polygenic risk score, consisting of 12 low-density lipoprotein cholesterol (LDL-C)-raising variants (polygenic LDL-C risk score), in subjects with a clinical diagnosis of FH. Methods and Results Within the Lipid Transport Disorders Italian Genetic Network (LIPIGEN) study, 875 patients who were FH-mutation positive (women, 54.75%; mean age, 42.47±15.00 years) and 644 patients who were FH-mutation negative (women, 54.21%; mean age, 49.73±13.54 years) were evaluated. Patients who were FH-mutation negative had lower mean levels of pretreatment LDL-C than patients who were FH-mutation positive (217.14±55.49 versus 270.52±68.59 mg/dL, P<0.0001). The mean value (±SD) of the polygenic LDL-C risk score was 1.00 (±0.18) in patients who were FH-mutation negative and 0.94 (±0.20) in patients who were FH-mutation positive (P<0.0001). In the receiver operating characteristic analysis, the area under the curve for recognizing subjects characterized by polygenic hypercholesterolemia was 0.59 (95% CI, 0.56-0.62), with sensitivity and specificity being 78% and 36%, respectively, at 0.905 as a cutoff value. Higher mean polygenic LDL-C risk score levels were observed among patients who were FH-mutation negative having pretreatment LDL-C levels in the range of 150 to 350 mg/dL (150-249 mg/dL: 1.01 versus 0.91, P<0.0001; 250-349 mg/dL: 1.02 versus 0.95, P=0.0001). A positive correlation between polygenic LDL-C risk score and pretreatment LDL-C levels was observed among patients with FH independently of the presence of causative mutations. Conclusions This analysis confirms the role of polymorphisms in modulating LDL-C levels, even in patients with genetically confirmed FH. More data are needed to support the use of the polygenic score in routine clinical practice