![128466-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-04/128466-Thumbnail%20Image.png?versionId=uRWVC7pSD_LRS3Vd7QdQFrgdJ.mypnUx&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240616/us-west-2/s3/aws4_request&X-Amz-Date=20240616T222705Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=d58a1cb61c7828c5a04f5a386a6bd934b1406b657c23df302619919f57ba4818&itok=4zq2VK0C)
It has long been accepted that modern reproductive patterns are likely contributors to breast cancer susceptibility because of their influence on hormones such as estrogen and the importance of these hormones in breast cancer. We conducted a meta-analysis to assess whether this ‘evolutionary mismatch hypothesis’ can explain susceptibility to both estrogen receptor positive (ER-positive) and estrogen receptor negative (ER-negative) cancer. Our meta-analysis includes a total of 33 studies and examines parity, age of first birth and age of menarche broken down by estrogen receptor status. We found that modern reproductive patterns are more closely linked to ER-positive than ER-negative breast cancer. Thus, the evolutionary mismatch hypothesis for breast cancer can account for ER-positive breast cancer susceptibility but not ER-negative breast cancer.
![128468-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-04/128468-Thumbnail%20Image.png?versionId=7FOH50Bln343U0n1uJzAFCDl73h7Nk_D&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240616/us-west-2/s3/aws4_request&X-Amz-Date=20240616T223649Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=008101b6280ee3e054ca3a5c17028af5d18d5e82702aa50b34ab00d819377bb7&itok=x8tQg1oH)
In a meta-analysis published by myself and co-authors, we report differences in the life history risk factors for estrogen receptor negative (ER−) and estrogen receptor positive (ER+) breast cancers. Our meta-analysis did not find the association of ER− breast cancer risk with fast life history characteristics that Hidaka and Boddy suggest in their response to our article. There are a number of possible explanations for the differences between their conclusions and the conclusions we drew from our meta-analysis, including limitations of our meta-analysis and methodological challenges in measuring and categorizing estrogen receptor status. These challenges, along with the association of ER+ breast cancer with slow life history characteristics, may make it challenging to find a clear signal of ER− breast cancer with fast life history characteristics, even if that relationship does exist. The contradictory results regarding breast cancer risk and life history characteristics illustrate a more general challenge in evolutionary medicine: often different sub-theories in evolutionary biology make contradictory predictions about disease risk. In this case, life history models predict that breast cancer risk should increase with faster life history characteristics, while the evolutionary mismatch hypothesis predicts that breast cancer risk should increase with delayed reproduction. Whether life history tradeoffs contribute to ER− breast cancer is still an open question, but current models and several lines of evidence suggest that it is a possibility.
![155731-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-09/155731-Thumbnail%20Image.png?versionId=3cFqoJKGCIxwhNwKJQec_bJ4fO.AZLcV&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240616/us-west-2/s3/aws4_request&X-Amz-Date=20240616T004940Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=e5fca4cb6645a7d9dd2c8fd55466a36f93c13b39604f08b42795f2430fb01e6d&itok=_FJIz06M)
The eddy covariance technique is well established to measure energy, water, and carbon fluxes and is used to quantify and compare flux measurements over different land surfaces. Results reveal that in an urban setting, paved surfaces exhibit the largest sensible and lowest latent heat fluxes in an urban environment, while a mesic landscape exhibits the largest latent heat fluxes, due to heavy irrigation. Irrigation impacts flux sensitivity to precipitation input, where latent heat fluxes increase with precipitation in xeric and parking lot landscapes, but do not impact the mesic system. In a semiarid managed rangeland, past management strategies and disturbance histories impact vegetation distribution, particularly the distribution of mesquite trees. At the site with less mesquite coverage, evapotranspiration (ET) is greater, due to greater grass cover. Both sites are generally net sinks of CO2, which is largely dependent on moisture availability, while the site with greater mesquite coverage has more respiration and generally greater gross ecosystem production (GEP). Initial impacts of brush management reveal ET and GEP decrease, due to the absence of mesquite trees. However the impact appears to be minimal by the end of the productive season. Overall, this dissertation advances the understanding of land cover change impacts on surface energy, water, and carbon fluxes in semiarid ecosystems.
![128801-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-04/128801-Thumbnail%20Image.png?versionId=ZODU4dE5MixXhDc8LTk8p.jpYtsBQSPL&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240616/us-west-2/s3/aws4_request&X-Amz-Date=20240616T201501Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=c5aa172314ce5350e56726d1d28ba1ded1eb16dbd17d1abfefb95a96ff06d557&itok=ewWJORTf)
Cancer therapy selects for cancer cells resistant to treatment, a process that is fundamentally evolutionary. To what extent, however, is the evolutionary perspective employed in research on therapeutic resistance and relapse? We analyzed 6,228 papers on therapeutic resistance and/or relapse in cancers and found that the use of evolution terms in abstracts has remained at about 1% since the 1980s. However, detailed coding of 22 recent papers revealed a higher proportion of papers using evolutionary methods or evolutionary theory, although this number is still less than 10%. Despite the fact that relapse and therapeutic resistance is essentially an evolutionary process, it appears that this framework has not permeated research. This represents an unrealized opportunity for advances in research on therapeutic resistance.
![128657-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-04/128657-Thumbnail%20Image.png?versionId=3mZOy0vmLZFBalPt0_j.GTRLNS52xEZV&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240616/us-west-2/s3/aws4_request&X-Amz-Date=20240616T013210Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=cf0189b0330b34df55bc3a8f6e7fbc0b946abd16ea8f6efcf96229308e635712&itok=pYxA0fAE)
This study examines the spatial and temporal patterns of the surface urban heat island (SUHI) intensity in the Phoenix metropolitan area and the relationship with land use land cover (LULC) change between 2000 and 2014. The objective is to identify specific regions in Phoenix that have been increasingly heated and cooled to further understand how LULC change influences the SUHI intensity. The data employed include MODerate-resolution Imaging Spectroradiometer (MODIS) land surface temperature (LST) 8-day composite June imagery, and classified LULC maps generated using 2000 and 2014 Landsat imagery. Results show that the regions that experienced the most significant LST changes during the study period are primarily on the outskirts of the Phoenix metropolitan area for both daytime and nighttime. The conversion to urban, residential, and impervious surfaces from all other LULC types has been identified as the primary cause of the UHI effect in Phoenix. Vegetation cover has been shown to significantly lower LST for both daytime and nighttime due to its strong cooling effect by producing more latent heat flux and less sensible heat flux. We suggest that urban planners, decision-makers, and city managers formulate new policies and regulations that encourage residential, commercial, and industrial developers to include more vegetation when planning new construction.
![141489-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-06/141489-Thumbnail%20Image.png?versionId=Lv8jucEq1BCpM8mpAo9U0QlSpbbFxHjx&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240615/us-west-2/s3/aws4_request&X-Amz-Date=20240615T171010Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=86e1dae13e6f22d0af45e6e732e224c6465de2d20e65d84b961e47b8be10f55d&itok=cM88he-j)
Background: Autism spectrum disorders (ASD) are complex neurobiological disorders that impair social interactions and communication and lead to restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. The causes of these disorders remain poorly understood, but gut microbiota, the 1013 bacteria in the human intestines, have been implicated because children with ASD often suffer gastrointestinal (GI) problems that correlate with ASD severity. Several previous studies have reported abnormal gut bacteria in children with ASD. The gut microbiome-ASD connection has been tested in a mouse model of ASD, where the microbiome was mechanistically linked to abnormal metabolites and behavior. Similarly, a study of children with ASD found that oral non-absorbable antibiotic treatment improved GI and ASD symptoms, albeit temporarily. Here, a small open-label clinical trial evaluated the impact of Microbiota Transfer Therapy (MTT) on gut microbiota composition and GI and ASD symptoms of 18 ASD-diagnosed children.
Results: MTT involved a 2-week antibiotic treatment, a bowel cleanse, and then an extended fecal microbiota transplant (FMT) using a high initial dose followed by daily and lower maintenance doses for 7–8 weeks. The Gastrointestinal Symptom Rating Scale revealed an approximately 80% reduction of GI symptoms at the end of treatment, including significant improvements in symptoms of constipation, diarrhea, indigestion, and abdominal pain. Improvements persisted 8 weeks after treatment. Similarly, clinical assessments showed that behavioral ASD symptoms improved significantly and remained improved 8 weeks after treatment ended. Bacterial and phage deep sequencing analyses revealed successful partial engraftment of donor microbiota and beneficial changes in the gut environment. Specifically, overall bacterial diversity and the abundance of Bifidobacterium, Prevotella, and Desulfovibrio among other taxa increased following MTT, and these changes persisted after treatment stopped (followed for 8 weeks).
Conclusions: This exploratory, extended-duration treatment protocol thus appears to be a promising approach to alter the gut microbiome and virome and improve GI and behavioral symptoms of ASD. Improvements in GI symptoms, ASD symptoms, and the microbiome all persisted for at least 8 weeks after treatment ended, suggesting a long-term impact.
![141505-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-06/141505-Thumbnail%20Image.png?versionId=s4hP9hf6YahxPAqct7IFHbBdH2yQP1Cv&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240615/us-west-2/s3/aws4_request&X-Amz-Date=20240615T214124Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=8338f660733e76fdd46f611210bedf49e182869a5494455a3529a84ba4f63452&itok=fmDsoT1_)
High proportions of autistic children suffer from gastrointestinal (GI) disorders, implying a link between autism and abnormalities in gut microbial functions. Increasing evidence from recent high-throughput sequencing analyses indicates that disturbances in composition and diversity of gut microbiome are associated with various disease conditions. However, microbiome-level studies on autism are limited and mostly focused on pathogenic bacteria. Therefore, here we aimed to define systemic changes in gut microbiome associated with autism and autism-related GI problems. We recruited 20 neurotypical and 20 autistic children accompanied by a survey of both autistic severity and GI symptoms. By pyrosequencing the V2/V3 regions in bacterial 16S rDNA from fecal DNA samples, we compared gut microbiomes of GI symptom-free neurotypical children with those of autistic children mostly presenting GI symptoms. Unexpectedly, the presence of autistic symptoms, rather than the severity of GI symptoms, was associated with less diverse gut microbiomes. Further, rigorous statistical tests with multiple testing corrections showed significantly lower abundances of the genera Prevotella, Coprococcus, and unclassified Veillonellaceae in autistic samples. These are intriguingly versatile carbohydrate-degrading and/or fermenting bacteria, suggesting a potential influence of unusual diet patterns observed in autistic children. However, multivariate analyses showed that autism-related changes in both overall diversity and individual genus abundances were correlated with the presence of autistic symptoms but not with their diet patterns. Taken together, autism and accompanying GI symptoms were characterized by distinct and less diverse gut microbial compositions with lower levels of Prevotella, Coprococcus, and unclassified Veillonellaceae.
![141208-Thumbnail Image.png](https://d1rbsgppyrdqq4.cloudfront.net/s3fs-public/styles/width_400/public/2021-06/141208-Thumbnail%20Image.png?versionId=T1eOs3b0gCDVi.xJODIE8SHDNH57GS_4&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Credential=AKIASBVQ3ZQ42ZLA5CUJ/20240615/us-west-2/s3/aws4_request&X-Amz-Date=20240615T234305Z&X-Amz-SignedHeaders=host&X-Amz-Expires=120&X-Amz-Signature=abc45c3f97cb80facec694d9baa9979f2cf8b0004ff2a0d1858a919ebd734813&itok=uVB1YJr7)