Assessing Energy Efficiency in Massachusetts

On behalf of the Conservation Law Foundation, this report, prepared by the Applied Economics Clinic (AEC), investigates how well Massachusetts' energy efficiency programs are reaching under-served communities and hard-to-reach families. In 2017, Massachusetts' "Mass Save" energy efficiency programs ranked number one in the annual efficiency scorecard produced by the American Council for an Energy-Efficient Economy (ACEEE) for the seventh consecutive year. Mass Save's ranking is not, however, a good indicator of whether or not low-income households are getting the services they need. At present, it is not possible to answer this question completely because Mass Save program administrators have access to - but do not include in publicly available statistics - information regarding low-income households, under-served communities and hard-to-reach families. Working with limited data, AEC found that there are substantial differences in energy savings among Massachusetts' towns, and lower-income communities are receiving lower efficiency savings. This report presents maps and other figures showing differences in efficiency savings, income, and other community characteristics like language abilities and renter status for both Massachusetts towns and neighborhoods within Boston

Amyloid-β-Acetylcholinesterase complexes potentiate neurodegenerative changes induced by the Aβ peptide. Implications for the pathogenesis of Alzheimer's disease

The presence of amyloid-β (Aβ) deposits in selected brain regions is a hallmark of Alzheimer's disease (AD). The amyloid deposits have "chaperone molecules" which play critical roles in amyloid formation and toxicity. We report here that treatment of rat hippocampal neurons with Aβ-acetylcholinesterase (Aβ-AChE) complexes induced neurite network dystrophia and apoptosis. Moreover, the Aβ-AChE complexes induced a sustained increase in intracellular Ca2+ as well as a loss of mitochondrial membrane potential. The Aβ-AChE oligomers complex also induced higher alteration of Ca2+ homeostasis compared with Aβ-AChE fibrillar complexes. These alterations in calcium homeostasis were reversed when the neurons were treated previously with lithium, a GSK-3β inhibitor; Wnt-7a ligand, an activator for Wnt Pathway; and an N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801), demonstrating protective roles for activation of the Wnt signaling pathway as well as for NMDA-receptor inhibition. Our results indicate that the Aβ-AChE complexes enhance Aβ-dependent deregulation of intracellular Ca2+ as well as mitochondrial dysfunction in hippocampal neurons, triggering an enhanced damage than Aβ alone. From a therapeutic point of view, activation of the Wnt signaling pathway, as well as NMDAR inhibition may be important factors to protect neurons under Aβ-AChE attack

Structure-Function Relationships of the Follicle-Stimulating Hormone Receptor

The follicle-stimulating hormone receptor (FSHR) plays a crucial role in reproduction. This structurally complex receptor is a member of the G-protein coupled receptor (GPCR) superfamily of membrane receptors. As with the other structurally similar glycoprotein hormone receptors (the thyroid-stimulating hormone and luteinizing hormone-chorionic gonadotropin hormone receptors), the FSHR is characterized by an extensive extracellular domain, where binding to FSH occurs, linked to the signal specificity subdomain or hinge region. This region is involved in ligand-stimulated receptor activation whereas the seven transmembrane domain is associated with receptor activation and transmission of the activation process to the intracellular loops comprised of amino acid sequences, which predicate coupling to effectors, interaction with adapter proteins, and triggering of downstream intracellular signaling. In this review, we describe the most important structural features of the FSHR intimately involved in regulation of FSHR function, including trafficking, dimerization, and oligomerization, ligand binding, agonist-stimulated activation, and signal transduction

Assessing Health Research and Innovation Impact: Evolution of a Framework and Tools in Alberta, Canada

Publicly funded research and innovation (R&I) organizations around the world are facing increasing demands to demonstrate the impacts of their investments. In most cases, these demands are shifting from academically based outputs to impacts that benefit society. Funders and other organizations are grappling to understand and demonstrate how their investments and activities are achieving impact. This is compounded with challenges that are inherent to impact assessment, such as having an agreed understanding of impact, the time lag from research to impact, establishing attribution and contribution, and consideration of diverse stakeholder needs and values. In response, many organizations are implementing frameworks and using web-based tools to track and assess academic and societal impact. This conceptual analysis begins with an overview of international research impact frameworks and emerging tools that are used by an increasing number of public R&I funders to demonstrate the value of their investments. From concept to real-world, this paper illustrates how one organization, Alberta Innovates, used the Canadian Academy of Health Sciences (CAHS) impact framework to guide implementation of its fit-for-purpose impact framework with an agnostic international six-block protocol. The implementation of the impact framework at Alberta Innovates is also supported by adopting emerging web-based tools. Drawing on the lessons learned from this continuous organizational endeavor to assess and measure R&I impact, we present preliminary plans for developing an impact strategy for Alberta Innovates that can be applied across sectors, including energy, environment and agriculture, and may possibly be adopted by other international funders

Levofloxacin pharmacokinetics in saliva as measured by a mobile microvolume UV spectrophotometer among people treated for rifampicin-resistant TB in Tanzania

Background: Early detection and correction of low fluoroquinolone exposure may improve treatment of MDR-TB. Objectives: To explore a recently developed portable, battery-powered, UV spectrophotometer for measuring levofloxacin in saliva of people treated for MDR-TB. Methods: Patients treated with levofloxacin as part of a regimen for MDR-TB in Northern Tanzania had serum and saliva collected concurrently at 1 and 4 h after 2 weeks of observed levofloxacin administration. Saliva levofloxacin concentrations were quantified in the field via spectrophotometry, while serum was analysed at a regional laboratory using HPLC. A Bayesian population pharmacokinetics model was used to estimate the area under the concentration-time curve (AUC(0-24)). Subtarget exposures of levofloxacin were defined by serum AUC(0-24) Results: Among 45 patients, 11 (25.6%) were women and 16 (37.2%) were living with HIV. Median AUC(0- 24) in serum was 140 (IQR = 102.4-179.09) mg.h/L and median AUC(0- 24) in saliva was 97.10 (IQR = 74.80-121.10) mg.h/L. A positive linear correlation was observed with serum and saliva AUC(0-24), and a receiver operating characteristic curve constructed to detect serum AUC(0- 24) below 80mg.h/L demonstrated excellent prediction [AUC 0.80 (95% CI = 0.62-0.94)]. Utilizing a saliva AUC(0- 24) cut-off of 91.6mg.h/L, the assay was 88.9% sensitive and 69.4% specific in detecting subtarget serum AUC(0- 24) values, including identifying eight of nine patients below target. Conclusions: Portable UV spectrophotometry as a point-of-care screen for subtarget levofloxacin exposure was feasible. Use for triage to other investigation or personalized dosing strategy should be tested in a randomized study

Tratamiento por Electrocoagulación para la remoción de índigo carmín presente en agua

En el presente estudio se evaluaron las condiciones óptimas del proceso de electrocoagulación (EC) para su aplicación en la remoción del colorante índigo carmín(IC) presente en agua. Se utilizaron soluciones acuosas de diferentes concentraciones iniciales de 100, 200 y 300 mg/L del colorante. Se determinó la densidad de corriente (DC) óptima para cada una de las concentraciones de partida. Se encontró que, al aumentar la concentración inicial del índigo carmín, la DC óptima utilizada fue mayor, para un tiempo de tratamiento de 40 minutos. Los porcentajes de remoción de color obtenidos fueron 65, 61 y 54% partiendo de concentraciones inicial de 100, 200 y 300 mg/L respectivamente

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Cerebral microbleeds and intracranial haemorrhage risk in patients anticoagulated for atrial fibrillation after acute ischaemic stroke or transient ischaemic attack (CROMIS-2):a multicentre observational cohort study

Background: Cerebral microbleeds are a potential neuroimaging biomarker of cerebral small vessel diseases that are prone to intracranial bleeding. We aimed to determine whether presence of cerebral microbleeds can identify patients at high risk of symptomatic intracranial haemorrhage when anticoagulated for atrial fibrillation after recent ischaemic stroke or transient ischaemic attack. Methods: Our observational, multicentre, prospective inception cohort study recruited adults aged 18 years or older from 79 hospitals in the UK and one in the Netherlands with atrial fibrillation and recent acute ischaemic stroke or transient ischaemic attack, treated with a vitamin K antagonist or direct oral anticoagulant, and followed up for 24 months using general practitioner and patient postal questionnaires, telephone interviews, hospital visits, and National Health Service digital data on hospital admissions or death. We excluded patients if they could not undergo MRI, had a definite contraindication to anticoagulation, or had previously received therapeutic anticoagulation. The primary outcome was symptomatic intracranial haemorrhage occurring at any time before the final follow-up at 24 months. The log-rank test was used to compare rates of intracranial haemorrhage between those with and without cerebral microbleeds. We developed two prediction models using Cox regression: first, including all predictors associated with intracranial haemorrhage at the 20% level in univariable analysis; and second, including cerebral microbleed presence and HAS-BLED score. We then compared these with the HAS-BLED score alone. This study is registered with ClinicalTrials.gov, number NCT02513316. Findings: Between Aug 4, 2011, and July 31, 2015, we recruited 1490 participants of whom follow-up data were available for 1447 (97%), over a mean period of 850 days (SD 373; 3366 patient-years). The symptomatic intracranial haemorrhage rate in patients with cerebral microbleeds was 9·8 per 1000 patient-years (95% CI 4·0–20·3) compared with 2·6 per 1000 patient-years (95% CI 1·1–5·4) in those without cerebral microbleeds (adjusted hazard ratio 3·67, 95% CI 1·27–10·60). Compared with the HAS-BLED score alone (C-index 0·41, 95% CI 0·29–0·53), models including cerebral microbleeds and HAS-BLED (0·66, 0·53–0·80) and cerebral microbleeds, diabetes, anticoagulant type, and HAS-BLED (0·74, 0·60–0·88) predicted symptomatic intracranial haemorrhage significantly better (difference in C-index 0·25, 95% CI 0·07–0·43, p=0·0065; and 0·33, 0·14–0·51, p=0·00059, respectively). Interpretation: In patients with atrial fibrillation anticoagulated after recent ischaemic stroke or transient ischaemic attack, cerebral microbleed presence is independently associated with symptomatic intracranial haemorrhage risk and could be used to inform anticoagulation decisions. Large-scale collaborative observational cohort analyses are needed to refine and validate intracranial haemorrhage risk scores incorporating cerebral microbleeds to identify patients at risk of net harm from oral anticoagulation. Funding: The Stroke Association and the British Heart Foundation