Using Ce-Qual-W2 to Model A Contaminant Spill Into the Wachusett Reservoir

This research was done to understand the potential fate and transport of a contaminant spill into the Wachusett Reservoir utilizing the model CE-QUAL-W2 V3.6. The Wachusett Reservoir, located in central Massachusetts, is the main water supply for the Boston, MA metropolitan area. The reservoir has a capacity of approximately 65 billion gallons and receives about half of its total inflow from the Quabbin Reservoir, which has a capacity of 412 billion gallons. Water is transferred from the Quabbin Reservoir to the western end of the Wachusett Reservoir intermittently through the Quabbin Aqueduct typically from June through November to meet higher water demands, maintain the water level, and mitigate water quality concerns in Wachusett. The largest outflow from the Wachusett Reservoir is the Cosgrove drinking water intake, located at the most eastern end of the waterbody. CE-QUAL-W2 is a two-dimensional, longitudinal and vertical, hydrodynamic and water quality model. The model is suitable for simulating water quality and hydrodynamics in Wachusett because the reservoir is relatively long and narrow. Therefore, longitudinal and vertical gradients in velocities, temperatures, and constituents are much larger than lateral gradients. For this study, a model of the reservoir was developed for the year 2009 using inputs for meteorology, bathymetry, initial flow and constituent conditions, inflow quantity and quality, outflow quantity, and outlet descriptions. The 2009 simulation was successfully created and calibrated to match temperature and specific conductivity profile measurements in the reservoir. Models for the years 2003-2008 had been created and calibrated during previous UMass research by Matthews (2007), Sojkowski (2011), and Devonis (2011). The calibrated CE-QUAL models for the years 2003-2009, verified by the temperature and specific conductivity profiles, were used to simulate potential contaminant spills into the Wachusett Reservoir. Contaminant spills were modeled as a conservative substance to study the effects of seasonal change, various spill densities (temperatures), and turning the Quabbin transfer on and off. Spill dates for each season were chosen based on days with similar meteorological conditions. The approximate contaminant spill arrival time, maximum relative concentrations, and behavior at the Cosgrove Intake were observed and compared for various analyzed scenarios. During the spring and the fall seasons, the density of a contaminant spill does not typically have an effect on the arrival time or relative concentration of the contaminant at the Cosgrove Intake. Spring spills arrive between 2 and 7 days after the spill occurred, reaching an average maximum relative concentration of 1.0 to 2.9. Fall spills typically arrive between 4 and 11 days with an average maximum concentration of approximately 1.0 to 1.2. During the summer months, when the reservoir is stratified, contaminant spill behavior is more variable, arrival time is usually later, and the average maximum relative concentration is greater. The average arrival times for warm, medium, and cold spills during the summer are 8.4, 11.6, and 12.3 days respectively. The average maximum relative concentration at the Cosgrove for warm spills is 1.9, while for medium and cold spills the average are about 2.6 during the summer months. Impacts of the Quabbin transfer on spill behavior and relative contaminant concentration were also investigated for the spring, summer, and fall. Turning the Quabbin Aqueduct off after a spill in the summer, when it is normally on, generally does not impact the arrival time of the contaminant at the Cosgrove. However, turning the Quabbin transfer off reduces the variability in the concentration of the contaminant at the intake. Changes in the Quabbin transfer during the spring and the fall have minimal impacts on contaminant arrival time and behavior. A combined two year model developed from the data for years 2008 and 2009 demonstrates that a conservative contaminant can remain in the reservoir for more than three times the mean hydraulic residence time of 206 days. In contrast, a contaminant with a first order decay rate of 0.02 day-1 results in a 99% decay of contaminant concentration in the outflow after one mean hydraulic residence time. Model results for decaying contaminants show that relatively rapid decay rates (0.10 to 0.66 day-1) are needed to decrease the peak outflow concentration by 99% for a range of peak concentration arrival times of 7 to 46 days for all simulated model years. Additionally, a combined two year model is useful producing more realistic boundary conditions for a 3-D model of the North Basin in the Wachusett Reservoir

Measurement of Weight in Clinical Trials: Is One Day Enough?

Background. Weight is typically measured on a single day in research studies. This practice assumes negligible day-to-day weight variability, although little evidence exists to support this assumption. We compared the precision of measuring weight on one versus two days among control participants in the Weight Loss Maintenance trial. Methods. Trained staff measured weight on two separate days at baseline, 12 months, and 30 months (2004–2007). We calculated the standard deviation (SD) of mean weight change from baseline to the 12- and 30-month visits using (a) the first and (b) both daily weights from each visit and conducted a variance components analysis (2009). Results. Of the 316 participants with follow-up measurements, mean (SD) age was 55.8 (8.5) years, BMI was 30.8 (4.5) kg/m2, 64% were women, 36% were black, and 50% were obese. At 12 months, the SD of mean weight change was 5.1 versus 5.0 kg using one versus two days of weight measurements (P = .76), while at 30 months the corresponding SDs were 6.3 and 6.3 kg (P = .98). We observed similar findings within subgroups of BMI, sex, and race. Day-to-day variability within individuals accounted for <1% of variability in weight. Conclusions. Measurement of weight on two separate days has no advantage over measurement on a single day in studies with well-standardized weight measurement protocols

The Distribution and Origin of Smooth Plains on Mercury

Orbital images from the MESSENGER spacecraft show that ~27% of Mercury's surface is covered by smooth plains, the majority (greater than 65%) of which are interpreted to be volcanic in origin. Most smooth plains share the spectral characteristics of Mercury's northern smooth plains, suggesting they also share their magnesian alkali-basalt-like composition. A smaller fraction of smooth plains interpreted to be volcanic in nature have a lower reflectance and shallower spectral slope, suggesting more ultramafic compositions, an inference that implies high temperatures and high degrees of partial melting in magma source regions persisted through most of the duration of smooth plains formation. The knobby and hummocky plains surrounding the Caloris basin, known as Odin-type plains, occupy an additional 2% of Mercury’s surface. The morphology of these plains and their color and stratigraphic relationships suggest that they formed as Caloris ejecta, although such an origin is in conflict with a straightforward interpretation of crater size-frequency distributions. If some fraction is volcanic, this added area would substantially increase the abundance of relatively young effusive deposits inferred to have more mafic compositions. Smooth plains are widespread on Mercury, but they are more heavily concentrated in the north and in the hemisphere surrounding Caloris. No simple relationship between plains distribution and crustal thickness or radioactive element distribution is observed. A likely volcanic origin for some older terrain on Mercury suggests that the uneven distribution of smooth plains may indicate differences in the emplacement age of large-scale volcanic deposits rather than differences in crustal formational process

Lymphocyte proliferation to mycobacterial antigens is detectable across a spectrum of HIV-associated tuberculosis

<p>Abstract</p> <p>Background</p> <p>Identifying novel TB diagnostics is a major public health priority. We explored the diagnostic characteristics of antimycobacterial lymphocyte proliferation assays (LPA) in HIV-infected subjects with latent or active TB.</p> <p>Methods</p> <p>HIV-infected subjects with bacille Calmette Guérin (BCG) scars and CD4 counts ≥ 200 cells/mm³entering a TB booster vaccine trial in Tanzania had baseline in vivo and in vitro immune tests performed: tuberculin skin tests (TST), LPA and five day assays of interferon gamma (IFN-γ) release. Assay antigens were early secreted antigenic target 6 (ESAT-6), antigen 85 (Ag85), and <it>Mycobacterium tuberculosis </it>whole cell lysate (WCL). Subjects were screened for active TB at enrollment by history, exam, sputum smear and culture. We compared antimycobacterial immune responses between subjects with and without latent or active TB at enrollment.</p> <p>Results</p> <p>Among 1885 subjects screened, 635 had latent TB and 13 had active TB. Subjects with latent TB were more likely than subjects without TB to have LPA responses to ESAT-6 (13.2% vs. 5.5%, P < 0.0001), Ag85 (18.7% vs. 3.1%, P < 0.0001), and WCL (45.7% vs. 17.1%, P < 0.0001). Subjects with active TB also were more likely than those without active TB to have detectable LPA responses to ESAT-6 (38.5% vs. 8.1%, P = 0.0001), Ag85 (46.2% vs. 8.5%, P < 0.0001), and WCL (61.5% vs. 27.0%, P = 0.0053). In subjects with a positive TST, LPA responses to ESAT-6, Ag85 and WCL were more common during active TB (p < 0.0001 for all tests). In diagnosing active TB, in vivo and in vitro tests of mycobacterial immune responses had sensitivity and specificity as follows: TST 84.6% and 65.5%, ESAT-6 LPA 38.5% and 92.0%, Ag85 LPA 46.2% and 91.5%, and WCL LPA 61.5% and 73.0%. Detectable LPA responses were more common in patients with higher CD4 counts, and higher HIV viral loads.</p> <p>Conclusion</p> <p>Lymphoproliferative responses to mycobacteria are detectable during HIV-associated active TB, and are less sensitive but more specific than TST.</p> <p>Trial registration</p> <p>ClinicalTrials.gov Identifier NCT00052195.</p

A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function

Description of familial keloids in five pedigrees: evidence for autosomal dominant inheritance and phenotypic heterogeneity

<p>Abstract</p> <p>Background</p> <p>Familial keloids have been reported, having either autosomal dominant or autosomal recessive inheritance. We wished to determine the inheritance pattern and phenotype of keloids among multigenerational families, as a prelude to a positional mapping strategy to identify candidate genes.</p> <p>Methods</p> <p>We studied three African American families, one Afro-Caribbean family and one Asian-American family. Phenotyping including assessing all patients for the presence, distribution, and appearance of keloids, together with the timing of keloid onset and provocative factors. The clinical trial was registered at clinicaltrials.gov (NCT 00005802).</p> <p>Results</p> <p>Age of keloid onset varied considerably within families, but commonly occurred by the second decade. The fraction of affected individuals was 38%, 45%, 62%, 67% and 73% among the five families respectively. Keloid severity and morphology differed within and between families. A novel finding is that certain families manifest keloids in distinct locations, with one family showing an excess of extremity keloids and two families showing an excess of axilla-groin keloids.</p> <p>Conclusion</p> <p>Familial keloids appear to most commonly manifest autosomal dominant or semidominant inheritance, and there may be familial patterns of keloid distribution.</p

HIV Testing and Treatment with the Use of a Community Health Approach in Rural Africa.

BACKGROUND: Universal antiretroviral therapy (ART) with annual population testing and a multidisease, patient-centered strategy could reduce new human immunodeficiency virus (HIV) infections and improve community health. METHODS: We randomly assigned 32 rural communities in Uganda and Kenya to baseline HIV and multidisease testing and national guideline-restricted ART (control group) or to baseline testing plus annual testing, eligibility for universal ART, and patient-centered care (intervention group). The primary end point was the cumulative incidence of HIV infection at 3 years. Secondary end points included viral suppression, death, tuberculosis, hypertension control, and the change in the annual incidence of HIV infection (which was evaluated in the intervention group only). RESULTS: A total of 150,395 persons were included in the analyses. Population-level viral suppression among 15,399 HIV-infected persons was 42% at baseline and was higher in the intervention group than in the control group at 3 years (79% vs. 68%; relative prevalence, 1.15; 95% confidence interval [CI], 1.11 to 1.20). The annual incidence of HIV infection in the intervention group decreased by 32% over 3 years (from 0.43 to 0.31 cases per 100 person-years; relative rate, 0.68; 95% CI, 0.56 to 0.84). However, the 3-year cumulative incidence (704 incident HIV infections) did not differ significantly between the intervention group and the control group (0.77% and 0.81%, respectively; relative risk, 0.95; 95% CI, 0.77 to 1.17). Among HIV-infected persons, the risk of death by year 3 was 3% in the intervention group and 4% in the control group (0.99 vs. 1.29 deaths per 100 person-years; relative risk, 0.77; 95% CI, 0.64 to 0.93). The risk of HIV-associated tuberculosis or death by year 3 among HIV-infected persons was 4% in the intervention group and 5% in the control group (1.19 vs. 1.50 events per 100 person-years; relative risk, 0.79; 95% CI, 0.67 to 0.94). At 3 years, 47% of adults with hypertension in the intervention group and 37% in the control group had hypertension control (relative prevalence, 1.26; 95% CI, 1.15 to 1.39). CONCLUSIONS: Universal HIV treatment did not result in a significantly lower incidence of HIV infection than standard care, probably owing to the availability of comprehensive baseline HIV testing and the rapid expansion of ART eligibility in the control group. (Funded by the National Institutes of Health and others; SEARCH ClinicalTrials.gov number, NCT01864603.)