Cultural Resources Investigations for the Proposed Espada Road Widening Project City of San Antonio Bexar County, Texas

Between February 2014 and October 2015, Atkins North America, Inc. (Atkins), conducted cultural resources investigations for the City of San Antonio’s (COSA’s) proposed Espada Road Widening Project. The project area extends from Southeast Interstate Loop 410 to approximately 137 meters (450 feet) west of the intersection of East Ashley Road and Espada Road, a distance of approximately 1.6 kilometers (1.0 mile), comprising 7.99 acres (3.2 hectares). The project area was subjected to an intensive pedestrian survey, which was supplemented by mechanical trenching. In total, 27 shovel tests and 9 backhoe trenches were placed in locations across the Area of Potential Effects (APE), with particular emphasis on areas potentially containing remnants of distribution laterals extending from the Espada Acequia. Although the locations of a few of the acequia laterals were visible from the surface, most have been backfilled and affected by modern disturbances. Mechanical trenching was employed in an attempt to catch the acequia laterals in cross-section, but no such features were observed. No new archaeological resources were identified during the survey. An archival review hypothesized the presence of three acequia laterals extending into the parcel immediately south of Rilling Road. Because the property currently houses a construction yard and no excavation was possible, the parcel could not be examined at the time of the surveys. Therefore, Atkins recommends that any construction within that section of the APE be monitored by a qualified archaeologist. Atkins also recommends monitoring the property at the northern end of Espada Road, where an outfall will be located. Due to the APE’s proximity to existing archaeological site 41BX260 at that location, excavation within that portion of the APE should be monitored as well

Disparities of Care for African-Americans and Caucasians with Community-Acquired Pneumonia: A Retrospective Cohort Study

Background\ud African-Americans admitted to U.S. hospitals with community-acquired pneumonia (CAP) are more likely than Caucasians to experience prolonged hospital length of stay (LOS), possibly due to either differential treatment decisions or patient characteristics.\ud \ud Methods\ud We assessed associations between race and outcomes (Intensive Care Unit [ICU] variables, LOS, 30-day mortality) for African-American or Caucasian patients over 65 years hospitalized in the Veterans Health Administration (VHA) with CAP (2002-2007). Patients admitted to the ICU were analyzed separately from those not admitted to the ICU. VHA patients who died within 30 days of discharge were excluded from all LOS analyses. We used chi-square and Fisher's exact statistics to compare dichotomous variables, the Wilcoxon Rank Sum test to compare age by race, and Cox Proportional Hazards Regression to analyze hospital LOS. We used separate generalized linear mixed-effect models, with admitting hospital as a random effect, to examine associations between patient race and the receipt of guideline-concordant antibiotics, ICU admission, use of mechanical ventilation, use of vasopressors, LOS, and 30-day mortality. We defined statistical significance as a two-tailed p ≤ 0.0001.\ud \ud Results\ud Of 40,878 patients, African-Americans (n = 4,936) were less likely to be married and more likely to have a substance use disorder, neoplastic disease, renal disease, or diabetes compared to Caucasians. African-Americans and Caucasians were equally likely to receive guideline-concordant antibiotics (92% versus 93%, adjusted OR = 0.99; 95% CI = 0.81 to 1.20) and experienced similar 30-day mortality when treated in medical wards (adjusted OR = 0.98; 95% CI = 0.87 to 1.10). African-Americans had a shorter adjusted hospital LOS (adjusted HR = 0.95; 95% CI = 0.92 to 0.98). When admitted to the ICU, African Americans were as likely as Caucasians to receive guideline-concordant antibiotics (76% versus 78%, adjusted OR = 0.99; 95% CI = 0.81 to 1.20), but experienced lower 30-day mortality (adjusted OR = 0.82; 95% CI = 0.68 to 0.99) and shorter hospital LOS (adjusted HR = 0.84; 95% CI = 0.76 to 0.93).\ud \ud Conclusions\ud Elderly African-American CAP patients experienced a survival advantage (i.e., lower 30-day mortality) in the ICU compared to Caucasians and shorter hospital LOS in both medical wards and ICUs, after adjusting for numerous baseline differences in patient characteristics. There were no racial differences in receipt of guideline-concordant antibiotic therapies

Ebola virus epidemiology, transmission, and evolution during seven months in Sierra Leone

The 2013-2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission and offered important information for outbreak response. Here, we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission

Expanding the diversity of mycobacteriophages: insights into genome architecture and evolution.

Mycobacteriophages are viruses that infect mycobacterial hosts such as Mycobacterium smegmatis and Mycobacterium tuberculosis. All mycobacteriophages characterized to date are dsDNA tailed phages, and have either siphoviral or myoviral morphotypes. However, their genetic diversity is considerable, and although sixty-two genomes have been sequenced and comparatively analyzed, these likely represent only a small portion of the diversity of the mycobacteriophage population at large. Here we report the isolation, sequencing and comparative genomic analysis of 18 new mycobacteriophages isolated from geographically distinct locations within the United States. Although no clear correlation between location and genome type can be discerned, these genomes expand our knowledge of mycobacteriophage diversity and enhance our understanding of the roles of mobile elements in viral evolution. Expansion of the number of mycobacteriophages grouped within Cluster A provides insights into the basis of immune specificity in these temperate phages, and we also describe a novel example of apparent immunity theft. The isolation and genomic analysis of bacteriophages by freshman college students provides an example of an authentic research experience for novice scientists

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Brain multiplexes reveal morphological connectional biomarkers fingerprinting late brain dementia states

Accurate diagnosis of mild cognitive impairment (MCI) before conversion to Alzheimer’s disease (AD) is invaluable for patient treatment. Many works showed that MCI and AD affect functional and structural connections between brain regions as well as the shape of cortical regions. However, ‘shape connections’ between brain regions are rarely investigated -e.g., how morphological attributes such as cortical thickness and sulcal depth of a specific brain region change in relation to morphological attributes in other regions. To fill this gap, we unprecedentedly design morphological brain multiplexes for late MCI/AD classification. Specifically, we use structural T1-w MRI to define morphological brain networks, each quantifying similarity in morphology between different cortical regions for a specific cortical attribute. Then, we define a brain multiplex where each intra-layer represents the morphological connectivity network of a specific cortical attribute, and each inter-layer encodes the similarity between two consecutive intra-layers. A significant performance gain is achieved when using the multiplex architecture in comparison to other conventional network analysis architectures. We also leverage this architecture to discover morphological connectional biomarkers fingerprinting the difference between late MCI and AD stages, which included the right entorhinal cortex and right caudal middle frontal gyrus

Multimodal and Multiscale Deep Neural Networks for the Early Diagnosis of Alzheimer’s Disease using structural MR and FDG-PET images

Alzheimer’s Disease (AD) is a progressive neurodegenerative disease where biomarkers for disease based on pathophysiology may be able to provide objective measures for disease diagnosis and staging. Neuroimaging scans acquired from MRI and metabolism images obtained by FDG-PET provide in-vivo measurements of structure and function (glucose metabolism) in a living brain. It is hypothesized that combining multiple different image modalities providing complementary information could help improve early diagnosis of AD. In this paper, we propose a novel deep-learning-based framework to discriminate individuals with AD utilizing a multimodal and multiscale deep neural network. Our method delivers 82.4% accuracy in identifying the individuals with mild cognitive impairment (MCI) who will convert to AD at 3 years prior to conversion (86.4% combined accuracy for conversion within 1–3 years), a 94.23% sensitivity in classifying individuals with clinical diagnosis of probable AD, and a 86.3% specificity in classifying non-demented controls improving upon results in published literature

The impact of PICALM genetic variations on reserve capacity of posterior cingulate in AD continuum

Phosphatidylinositolbinding clathrin assembly protein (PICALM) gene is one novel genetic player associated with late-onset Alzheimer’s disease (LOAD), based on recent genome wide association studies (GWAS). However, how it affects AD occurrence is still unknown. Brain reserve hypothesis highlights the tolerant capacities of brain as a passive means to fight against neurodegenerations. Here, we took the baseline volume and/or thickness of LOAD-associated brain regions as proxies of brain reserve capacities and investigated whether PICALM genetic variations can influence the baseline reserve capacities and the longitudinal atrophy rate of these specific regions using data from Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset. In mixed population, we found that brain region significantly affected by PICALM genetic variations was majorly restricted to posterior cingulate. In sub-population analysis, we found that one PICALM variation (C allele of rs642949) was associated with larger baseline thickness of posterior cingulate in health. We found seven variations in health and two variations (rs543293 and rs592297) in individuals with mild cognitive impairment were associated with slower atrophy rate of posterior cingulate. Our study provided preliminary evidences supporting that PICALM variations render protections by facilitating reserve capacities of posterior cingulate in non-demented elderly

Early role of vascular dysregulation on late-onset Alzheimer's disease based on multifactorial data-driven analysis

Multifactorial mechanisms underlying late-onset Alzheimer's disease (LOAD) are poorly characterized from an integrative perspective. Here spatiotemporal alterations in brain amyloid-β deposition, metabolism, vascular, functional activity at rest, structural properties, cognitive integrity and peripheral proteins levels are characterized in relation to LOAD progression. We analyse over 7,700 brain images and tens of plasma and cerebrospinal fluid biomarkers from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Through a multifactorial data-driven analysis, we obtain dynamic LOAD–abnormality indices for all biomarkers, and a tentative temporal ordering of disease progression. Imaging results suggest that intra-brain vascular dysregulation is an early pathological event during disease development. Cognitive decline is noticeable from initial LOAD stages, suggesting early memory deficit associated with the primary disease factors. High abnormality levels are also observed for specific proteins associated with the vascular system's integrity. Although still subjected to the sensitivity of the algorithms and biomarkers employed, our results might contribute to the development of preventive therapeutic interventions