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Previous studies reveal that the primary distribution of the current density is sharply enhanced at the edge of a disk electrode submerged into a semi-infinite space of conductive solution. The current enhancement will cause the double layer capacitance at the periphery of the electrode to be charged much faster compared to the center, and can also lead to severe corrosion at the edge. While several studies focused on the geometric design of the electrode to reduce this enhancement, we explore the feasibility of achieving similar effect by shaping the edges of the current input. The simulation uses finite element analysis software to solve the system of partial differential equations and results show that the edge enhancement could be greatly reduced without significantly changing the input efficacy of current and/or charge.

Background:  We previously found that activation of the glial cell line‐derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) reduces ethanol‐drinking behaviors. In this study, we set out to assess the contribution of endogenous GDNF or its receptor GFRα1 to the regulation of ethanol‐related behaviors.Methods:  GDNF and GFRα1 heterozygote mice (HET) and their wild‐type littermate controls (WT) were used for the studies. Ethanol‐induced hyperlocomotion, sensitization, and conditioned place preference (CPP), as well as ethanol consumption before and after a period of abstinence were evaluated. Blood ethanol concentration (BEC) was also measured.Results:  We observed no differences between the GDNF HET and WT mice in the level of locomotor activity or in sensitization to ethanol‐induced hyperlocomotion after systemic injection of a nonhypnotic dose of ethanol and in BEC. However, GDNF and GFRα1 mice exhibited increased place preference to ethanol as compared with their WT littermates. The levels of voluntary ethanol or quinine consumption were similar in the GDNF HET and WT mice, however, a small but significant increase in saccharin intake was observed in the GDNF HET mice. No changes were detected in voluntary ethanol, saccharin or quinine consumption of GFRα1 HET mice as compared with their WT littermates. Interestingly, however, both the GDNF and GFRα1 HET mice consumed much larger quantities of ethanol after a period of abstinence from ethanol as compared with their WT littermates. Furthermore, the increase in ethanol consumption after abstinence was found to be specific for ethanol as similar levels of saccharin intake were measured in the GDNF and GFRα1 HET and WT mice after abstinence.Conclusions:  Our results suggest that endogenous GDNF negatively regulates the rewarding effect of ethanol and ethanol‐drinking behaviors after a period of abstinence.

Abstract Background Environmental factors such as temperature, rainfall, and vegetation cover play a critical role in malaria transmission. However, quantifying the relationships between environmental factors and measures of disease burden relevant for public health can be complex as effects are often non-linear and subject to temporal lags between when changes in environmental factors lead to changes in malaria incidence. The study investigated the effect of environmental covariates on malaria incidence in high transmission settings of Uganda. Methods This study leveraged data from seven malaria reference centres (MRCs) located in high transmission settings of Uganda over a 24-month period. Estimates of monthly malaria incidence (MI) were derived from MRCs’ catchment areas. Environmental data including monthly temperature, rainfall, and normalized difference vegetation index (NDVI) were obtained from remote sensing sources. A distributed lag nonlinear model was used to investigate the effect of environmental covariates on malaria incidence. Results Overall, the median (range) monthly temperature was 30 °C (26–47), rainfall 133.0 mm (3.0–247), NDVI 0.66 (0.24–0.80) and MI was 790 per 1000 person-years (73–3973). Temperature of 35 °C was significantly associated with malaria incidence compared to the median observed temperature (30 °C) at month lag 2 (IRR: 2.00, 95% CI: 1.42–2.83) and the increased cumulative IRR of malaria at month lags 1–4, with the highest cumulative IRR of 8.16 (95% CI: 3.41–20.26) at lag-month 4. Rainfall of 200 mm significantly increased IRR of malaria compared to the median observed rainfall (133 mm) at lag-month 0 (IRR: 1.24, 95% CI: 1.01–1.52) and the increased cumulative IRR of malaria at month lags 1–4, with the highest cumulative IRR of 1.99(95% CI: 1.22–2.27) at lag-month 4. Average NVDI of 0.72 significantly increased the cumulative IRR of malaria compared to the median observed NDVI (0.66) at month lags 2–4, with the highest cumulative IRR of 1.57(95% CI: 1.09–2.25) at lag-month 4. Conclusions In high-malaria transmission settings, high values of environmental covariates were associated with increased cumulative IRR of malaria, with IRR peaks at variable lag times. The complex associations identified are valuable for designing strategies for early warning, prevention, and control of seasonal malaria surges and epidemics.

Abstract Background. Future distribution of dengue risk is usually predicted based on predicted climate changes using general circulation models (GCMs). However, it is hard to validate the GCM results and assess the uncertainty of the predictions. Observed changes in climate may be very different from GCM results. Methods.We collected Aedes albopictus surveillance data and observed climate records from about 90 meteorological stations for the period 1970–2021. We analyzed the trends of climate change in China and made predictions on future climate for the years 2050 and 2080 based on trend analyses. We analyzed the relationship between climatic variables and the prevalence of Ae. albopictusin different months/seasons. We built a series of machine learning classification tree models to predict the monthly/seasonal Ae. albopictus distribution based on the average climate from 1970 to 2000 and assessed the contributions of different climatic variables to the Ae. albopictus distribution. Using these models, we projected the future distributions of Ae. albopictus for the years of 2050 and 2080. Results. The study included Ae. albopictus surveillance from 259 sites in China and found that winter to early spring (November–February) temperatures were strongly correlated with Ae. albopictus prevalence – the higher the temperature the higher the prevalence, while precipitation in summer (June–September) was important predictors for Ae. albopictus prevalence. The machine learning tree models predicted the current prevalence of Ae. albopictus with high agreement (accuracy > 90% and Kappa agreement > 80% for all months). Overall, winter temperature contributed the most to Ae. albopictus distribution, followed by summer precipitation. Increase in temperature was observed in most places in China and rates of annual change varied substantially among sites, with the highest increase in temperature occurring from February to April (annual increase of 1.4 – 4.7ºC for monthly mean, 0.6 – 4.0ºC for monthly minimum, and 1.3 – 4.3ºC for monthly maximum temperature) and the lowest in November and December. Temperature increases were lower in the tropics/subtropics compared to the high-latitude areas. The projected temperatures in 2050 and 2080 by this study were about 1~1.5°C higher than projected by GCMs. The estimated current Ae. albopictus risk distribution had a northern boundary of north-central China and the southern edge of northeastern China, with a risk period of June–September. The projected future Ae. albopictus risks in 2050 and 2080 cover nearly all of China, with an expanded risk period of April–October. The current at-risk population was estimated to be 960 million and the future at-risk population was projected to be 1.2 billion. Conclusions.The magnitude of climate change in China is likely to surpass the GCM predictions. Future dengue risks will expand to cover nearly all of China if the current climate trends continue.

The relationship between alcohol consumption, sensitivity, and tolerance is an important question that has been addressed in humans and rodent models. Studies have shown that alcohol consumption and risk of abuse may correlate with (1) increased sensitivity to the stimulant effects of alcohol, (2) decreased sensitivity to the depressant effects of alcohol, and (3) increased alcohol tolerance. However, many conflicting results have been observed. To complement these studies, we utilized a different organism and approach to analyze the relationship between ethanol consumption and other ethanol responses. Using a set of 20 Drosophila melanogaster mutants that were isolated for altered ethanol sensitivity, we measured ethanol-induced hyperactivity, ethanol sedation, sedation tolerance, and ethanol consumption preference. Ethanol preference showed a strong positive correlation with ethanol tolerance, consistent with some rodent and human studies, but not with ethanol hyperactivity or sedation. No pairwise correlations were observed between ethanol hyperactivity, sedation, and tolerance. The evolutionary conservation of the relationship between tolerance and ethanol consumption in flies, rodents, and humans indicates that there are fundamental biological mechanisms linking specific ethanol responses.

Recent studies have correlated kinetic energy (KE) and viscous dissipation rate (VDR) in the left ventricle (LV) with heart health. These studies have relied on 4D-flow imaging or computational fluid dynamics modeling, which are able to measure, or compute, all 3 components (3C) of the blood flow velocity in 3 dimensional (3D) space. This richness of data is difficult to acquire clinically. Alternatively, color Doppler echocardiography (CDE) is more widespread clinically, but only measures a single radial component of velocity and typically only over a planar section. Because of this limitation, prior CDE-based studies have first reconstructed a second component of velocity in the measurement plane prior to evaluating VDR or KE. Herein, we propose 1C-based surrogates of KE and VDR that can be derived directly from the radial component of the flow velocity in the LV. Our results demonstrate that the proposed 1C-based surrogates of KE and VDR are generally as well-correlated with the true KE and VDR values as surrogates that use reconstructed 2C flow data. Moreover, the correlation of these 1C-based surrogates with the true values indicate that CDE (3D in particular) may be useful in evaluating these metrics in practice.

Background and PurposeVarenicline, a neuronal nicotinic acetylcholine receptor (nAChR) modulator, decreases ethanol consumption in rodents and humans. The proposed mechanism of action for varenicline to reduce ethanol consumption has been through modulation of dopamine (DA) release in the nucleus accumbens (NAc) via α4*‐containing nAChRs in the ventral tegmental area (VTA). However, presynaptic nAChRs on dopaminergic terminals in the NAc have been shown to directly modulate dopaminergic signalling independently of neuronal activity from the VTA. In this study, we determined whether nAChRs in the NAc play a role in varenicline's effects on ethanol consumption.Experimental ApproachRats were trained to consume ethanol using the intermittent‐access two‐bottle choice protocol for 10 weeks. Ethanol intake was measured after varenicline or vehicle was microinfused into the NAc (core, shell or core‐shell border) or the VTA (anterior or posterior). The effect of varenicline treatment on DA release in the NAc was measured using both in vivo microdialysis and in vitro fast‐scan cyclic voltammetry (FSCV).Key ResultsMicroinfusion of varenicline into the NAc core and core‐shell border, but not into the NAc shell or VTA, reduced ethanol intake following long‐term ethanol consumption. During microdialysis, a significant enhancement in accumbal DA release occurred following systemic administration of varenicline and FSCV showed that varenicline also altered the evoked release of DA in the NAc.Conclusion and ImplicationsFollowing long‐term ethanol consumption, varenicline in the NAc reduces ethanol intake, suggesting that presynaptic nAChRs in the NAc are important for mediating varenicline's effects on ethanol consumption.