The Economic Contribution of Instream Flows to the Lower Connecticut River Watershed, New England, USA

River recreation is a rapidly expanding source of economic productivity. Angler spending has been used as the basis for estimating the regional economic estimates of local income and jobs in several water-limited systems of the western United States and Mexico. However, the contribution of outdoor recreation to the economies of regions that do not experience water scarcity continues to be underappreciated. This paper estimates the economic contribution of angling to the lower Connecticut River Watershed (CRW) economy. The authors draw upon existing angler expenditure, river flow and geographic information system (GIS) data to relate anger use of the lower CRW and expenditures to river flows. The authors then translate angler expenditures into state income and employment using a regional economic multiplier. The results show that fishing expenditures of $62.8 million per year equate to$74.2 million annually in supply chain revenues which supports 1660 jobs. The authors identified a significant positive relationship between fishing intensity and river flow rates, which suggests that decreasing current water diversions on the lower CRW by just 25% would add an additional $37 million and 638 jobs to Connecticut’s economy. The findings demonstrate that investments in managing the health the CRW through flow restoration can have large economic and ecological pay-offs

Computational identification and experimental validation of PPRE motifs in NHE1 and MnSOD genes of Human

Background: Activation of PPARs has been reported to inhibit the proliferation of malignant cells from different lineages. They are involved in transcription regulation of genes upon activation by a ligand. The binding of PPARs to the promoter sequence either represses or activates the gene. Hence, PPARs represent promising targets for cancer treatment because of their anti-proliferative and pro-apoptotic activities. Here we computationally identified PPAR binding regions in NHE1 and MnSOD. We further validated the predictions in vitro. Results: Our results computationally predicted the presence of 2 PPRE motifs in NHE1 and 3 PPRE motifs in MnSOD. We experimentally confirmed the true motifs and their regulation by PPAR. Conclusion: Our results suggest that both NHE1 and MnSOD have PPRE binding motif in their upstream/promoter region and hence are regulated by PPAR upon ligand binding.Singapore. National Medical Research Council (Grant R-183-000-204-213

Electrical properties of extended defects in strain relaxed GeSn

We report the electrical properties of 60 degrees dislocations originating from the +1.2% lattice mismatch between an unintentionally doped, 315 nm thick Ge0.922Sn0.078 layer (58% relaxed) and the underlying Ge substrate, using deep level transient spectroscopy. The 60 degrees dislocations are found to be split into Shockley partials, binding a stacking fault. The dislocations exhibit a band-like distribution of electronic states in the bandgap, with the highest occupied defect state at similar to E-V + 0.15 eV, indicating no interaction with point defects in the dislocation's strain field. A small capture cross-section of 1.5 x 10(-19) cm(2) with a capture barrier of 60 meV is observed, indicating a donor-like nature of the defect-states. Thus, these dislocation-states are not the source of unintentional p-type doping in the Ge0.922Sn0.078 layer. Importantly, we show that the resolved 60 degrees dislocation-states act as a source of leakage current by thermally generating minority electrons via the Shockley-ReadHall mechanism

Source/Drain Materials for Ge nMOS Devices : Phosphorus Activation in Epitaxial Si, Ge, Ge1-xSnx and SiyGe1-x-ySnx

This paper benchmarks various epitaxial growth schemes based on n-type group-IV materials as viable source/drain candidates for Ge nMOS devices. Si:P grown at low temperature on Ge, gives an active carrier concentration as high as 3.5 x 10(20) cm(-3) and a contact resistivity down to 7.5 x 10(-9) Omega.cm(2). However, Si:P growth is highly defective due to large lattice mismatch between Si and Ge. Within the material stacks assessed, one option for Ge nMOS source/drain stressors would be to stack Si:P, deposited at contact level, on top of a selectively grown n-SiyGe1-x-ySnx at source/drain level, in line with the concept of Si passivation of n-Ge surfaces to achieve low contact resistivities as reported in literature (Martens et al. 2011 Appl. Phys. Lett., 98, 013 504). The saturation in active carrier concentration with increasing P (or As)-doping is the major bottleneck in achieving low contact resistivities for as-grown Ge or SiyGe1-x-ySnx. We focus on understanding various dopant deactivation mechanisms in P-doped Ge and Ge1-xSnx alloys. First principles simulation results suggest that P deactivation in Ge and Ge1-xSnx can be explained both by P-clustering and donor-vacancy complexes. Positron annihilation spectroscopy analysis, suggests that dopant deactivation in P-doped Ge and Ge1-xSnx is primarily due to the formation of P-n-V and SnmPn-V clusters. (C) 2020 The Author(s). Published on behalf of The Electrochemical Society by IOP Publishing Limited.Peer reviewe

Diagnosis and Management of Radiation Necrosis in Patients With Brain Metastases

The use of radiotherapy, either in the form of stereotactic radiosurgery (SRS) or whole-brain radiotherapy (WBRT), remains the cornerstone for the treatment of brain metastases (BM). As the survival of patients with BM is being prolonged, due to improved systemic therapy (i.e., for better extra-cranial control) and increased use of SRS (i.e., for improved intra-cranial control), patients are clinically manifesting late effects of radiotherapy. One of these late effects is radiation necrosis (RN). Unfortunately, symptomatic RN is notoriously hard to diagnose and manage. The features of RN overlap considerably with tumor recurrence, and misdiagnosing RN as tumor recurrence may lead to deleterious treatment which may cause detrimental effects to the patient. In this review, we will explore the pathophysiology of RN, risk factors for its development, and the strategies to evaluate and manage RN

Requirement of NOX2 and Reactive Oxygen Species for Efficient RIG-I-Mediated Antiviral Response through Regulation of MAVS Expression

The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNβ and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS

Racism as a determinant of health: a systematic review and meta-analysis

Despite a growing body of epidemiological evidence in recent years documenting the health impacts of racism, the cumulative evidence base has yet to be synthesized in a comprehensive meta-analysis focused specifically on racism as a determinant of health. This meta-analysis reviewed the literature focusing on the relationship between reported racism and mental and physical health outcomes. Data from 293 studies reported in 333 articles published between 1983 and 2013, and conducted predominately in the U.S., were analysed using random effects models and mean weighted effect sizes. Racism was associated with poorer mental health (negative mental health: r = -.23, 95% CI [-.24,-.21], k = 227; positive mental health: r = -.13, 95% CI [-.16,-.10], k = 113), including depression, anxiety, psychological stress and various other outcomes. Racism was also associated with poorer general health (r = -.13 (95% CI [-.18,-.09], k = 30), and poorer physical health (r = -.09, 95% CI [-.12,-.06], k = 50). Moderation effects were found for some outcomes with regard to study and exposure characteristics. Effect sizes of racism on mental health were stronger in cross-sectional compared with longitudinal data and in non-representative samples compared with representative samples. Age, sex, birthplace and education level did not moderate the effects of racism on health. Ethnicity significantly moderated the effect of racism on negative mental health and physical health: the association between racism and negative mental health was significantly stronger for Asian American and Latino(a) American participants compared with African American participants, and the association between racism and physical health was significantly stronger for Latino(a) American participants compared with African American participants.<br /