Optimal Temporal Filtering of the Cosmic-Ray Neutron Signal to Reduce Soil Moisture Uncertainty.

Cosmic ray neutron sensors (CRNS) are increasingly used to determine field-scale soil moisture (SM). Uncertainty of the CRNS-derived soil moisture strongly depends on the CRNS count rate subject to Poisson distribution. State-of-the-art CRNS signal processing averages neutron counts over many hours, thereby accounting for soil moisture temporal dynamics at the daily but not sub-daily time scale. This study demonstrates CRNS signal processing methods to improve the temporal accuracy of the signal in order to observe sub-daily changes in soil moisture and improve the signal-to-noise ratio overall. In particular, this study investigates the effectiveness of the Moving Average (MA), Median filter (MF), Savitzky-Golay (SG) filter, and Kalman filter (KF) to reduce neutron count error while ensuring that the temporal SM dynamics are as good as possible. The study uses synthetic data from four stations for measuring forest ecosystem-atmosphere relations in Africa (Gorigo) and Europe (SMEAR II (Station for Measuring Forest Ecosystem-Atmosphere Relations), Rollesbroich, and Conde) with different soil properties, land cover and climate. The results showed that smaller window sizes (12 h) for MA, MF and SG captured sharp changes closely. Longer window sizes were more beneficial in the case of moderate soil moisture variations during long time periods. For MA, MF and SG, optimal window sizes were identified and varied by count rate and climate, i.e., estimated temporal soil moisture dynamics by providing a compromise between monitoring sharp changes and reducing the effects of outliers. The optimal window for these filters and the Kalman filter always outperformed the standard procedure of simple 24-h averaging. The Kalman filter showed its highest robustness in uncertainty reduction at three different locations, and it maintained relevant sharp changes in the neutron counts without the need to identify the optimal window size. Importantly, standard corrections of CRNS before filtering improved soil moisture accuracy for all filters. We anticipate the improved signal-to-noise ratio to benefit CRNS applications such as detection of rain events at sub-daily resolution, provision of SM at the exact time of a satellite overpass, and irrigation applications.

Towards diversity in genomics: The emergence of neurogenomics in Africa?

There is a high burden of mental and neurological disorders in Africa. Nevertheless, there appears to be an under-representation of African ancestry populations in large-scale genomic studies. Here, we evaluated the extent of under-representation of Africans in neurogenomic studies in the GWAS Catalog. We found 569 neurogenomic studies, of which 88.9% were exclusively focused on people with European ancestry and the remaining 11.1% having African ancestry cases included. In terms of population, only 1.2% of the total populations involved in these 569 GWAS studies were of African descent. Further, most of the individuals in the African ancestry category were identified to be African-Americans/Afro-Caribbeans, highlighting the huge under-representation of homogenous African populations in large-scale neurogenomic studies. Efforts geared at establishing strong collaborative ties with European/American researchers, maintaining freely accessible biobanks and establishing comprehensive African genome data repositories to track African genome variations are critical for propelling neurogenomics/precision medicine in Africa.

The concept of alpha-synuclein as a prion-like protein: ten years after.

Parkinson's disease is characterized by the loss of nigrostriatal dopaminergic signaling and the presence of alpha-synuclein aggregates (also called Lewy bodies and neurites) throughout the brain. In 2003, Braak and colleagues created a staging system for Parkinson's disease describing the connection between the alpha-synuclein pathology and disease severity. Later, they suggested that the pathology might initially be triggered by exogenous insults targeting the gut and olfactory system. In 2008, we and other groups documented Lewy pathology in grafted neurons in people with Parkinson's disease who had been transplanted over a decade prior to autopsy. We proposed that the Lewy pathology in the grafted neurons was the result of permissive templating or prion-like spread of alpha-synuclein pathology from neurons in the host to those in the grafts. During the following ten years, several studies described the transmission of alpha-synuclein pathology between neurons, both in cell culture and in experimental animals. Recent research has also begun to identify underlying molecular mechanisms. Collectively, these experimental studies tentatively support the idea that the progression from one Braak stage to the next is the consequence of prion-like propagation of Lewy pathology. However, definitive proof that intercellular propagation of alpha-synuclein pathology occurs in Parkinson's disease cases has proven difficult to secure. In this review, we highlight several open questions that currently prevent us from concluding with certainty that prion-like transfer of alpha-synuclein contributes to the progression of Parkinson's disease.

Neuroscience-related research in Ghana: a systematic evaluation of direction and capacity.

Neurological and neuropsychiatric diseases account for considerable healthcare, economic and social burdens in Ghana. In order to effectively address these burdens, appropriately-trained scientists who conduct high-impact neuroscience research will be needed. Additionally, research directions should be aligned with national research priorities. However, to provide information about current neuroscience research productivity and direction, the existing capacity and focus need to be identified. This would allow opportunities for collaborative research and training to be properly explored and developmental interventions to be better targeted. In this study, we sought to evaluate the existing capacity and direction of neuroscience-related research in Ghana. To do this, we examined publications reporting research investigations authored by scientists affiliated with Ghanaian institutions in specific areas of neuroscience over the last two decades (1995-2015). 127 articles that met our inclusion criteria were systematically evaluated in terms of research foci, annual publication trends and author affiliations. The most actively-researched areas identified include neurocognitive impairments in non-nervous system disorders, depression and suicide, epilepsy and seizures, neurological impact of substance misuse, and neurological disorders. These studies were mostly hospital and community-based surveys. About 60% of these articles were published in the last seven years, suggesting a recent increase in research productivity. However, data on experimental and clinical research outcomes were particularly lacking. We suggest that future investigations should focus on the following specific areas where information was lacking: large-scale disease epidemiology, effectiveness of diagnostic platforms and therapeutic treatments, and the genetic, genomic and molecular bases of diseases.

Developing Science Communication in Africa: Undergraduate and Graduate Students should be Trained and Actively Involved in Outreach Activity Development and Implementation.

Despite recent improvements in scientific research output from Africa, public understanding of science in many parts of the continent remains low. Science communication there is faced with challenges such as (i) lack of interest among some scientists, (ii) low availability of training programs for scientists, (iii) low literacy rates among the public, and (iv) multiplicity of languages. To address these challenges, new ways of training and motivating scientists to dialogue with non-scientists are essential. Developing communication skills early in researchers' scientific career would be a good way to enhance their public engagement abilities. Therefore, a potentially effective means to develop science communication in Africa would be to actively involve trainee scientists (i.e., undergraduate and graduate students) in outreach activity development and delivery. These students are often enthusiastic about science, eager to develop their teaching and communication skills, and can be good mentors to younger students. Involving them in all aspects of outreach activity is, therefore, likely to be a productive implementation strategy. However, science communication training specifically for students and the involvement of these students in outreach activity design and delivery are lacking in Africa. Here, we argue that improving the training and involvement of budding scientists in science communication activities would be a good way to bridge the wide gap between scientists and the African public.

Serum leptin levels in patients with chronic kidney disease and hypertensive heart disease: An observational cross-sectional study.

Background and Aim: Adipocytes secrete a peptide hormone called leptin, which plays a crucial role in controlling appetite and energy expenditure. Alterations in leptin concentrations are associated with CKD-related cardiovascular problems such as hypertensive heart disease (HHD). Despite the link, data on the precise function of leptin in people with CKD and HHD is scant. Methods: An observational cross-sectional study involving a total of 108 participants (72 CKD patients with HHD and 36 healthy controls). Their demographic and anthropometric information was collected using a standardized questionnaire. Certain clinical measures such as blood pressure and body mass index (BMI) were assessed. Fasting blood samples were analyzed for levels of plasma glucose (FPG), lipids, creatinine, and leptin. Data were analyzed with SPSS v23. Results: Leptin, FPG, creatinine and triglyceride levels were all significantly higher in CKD patients with HHD compared to controls (p < 0.01 for all). Furthermore, advanced CKD status (being in stage 5), having a 6-year diagnosis of HHD, being female, having a higher BMI, and elevation in levels of HDL and FPG contributed significantly to the variance in serum leptin levels in the case group (ß = 0.37, 0.22, 0.19, 0.18, 0.27, 0.28; p < 0.05 for all). In the control group, the female gender had the biggest unique effect on circulating leptin levels, followed by BMI and eGFR (ß = 0.71, 0.34, -0.22; p < 0.01 for all). Conclusion: Patients with CKD who also had HHD reported considerably higher circulating leptin levels. Significantly higher blood leptin levels were shown to be associated with CKD stage 5 in the case group. These results are consistent with the role of leptin in the metabolic complexity seen in CKD patients. There needs to be more research into treatments that aim to lower leptin levels in CKD patients with HHD.

Effects of Methylphenidate on the Dopamine Transporter and Beyond.

The dopamine transporter (DAT) is the main target of methylphenidate (MPH), which remains the number one drug prescribed worldwide for the treatment of Attention-Deficit Hyperactivity Disorder (ADHD). In addition, abnormalities of the DAT have been widely associated with ADHD. Based on clinical and preclinical studies, the direction of DAT abnormalities in ADHD are, however, still unclear. Moreover, chronic treatment of MPH has been shown to increase brain DAT expression in both animals and ADHD patients, suggesting that findings of overexpressed levels of DAT in ADHD patients are possibly attributable to the effects of long-term MPH treatment rather than the pathology of the condition itself. In this chapter, we will discuss some of the effects exerted by MPH, which are related to its actions on catecholamine protein targets and brain metabolites, together with genes and proteins mediating neuronal plasticity. For this purpose, we present data from biochemical, proton nuclear magnetic resonance spectroscopy (1H-NMR) and gene/protein expression studies. Overall, results of the studies discussed in this chapter show that MPH has a complex biological/pharmacological action well beyond the DAT.

A novel automated morphological analysis of Iba1+ microglia using a deep learning assisted model.

There is growing evidence for the key role of microglial functional state in brain pathophysiology. Consequently, there is a need for efficient automated methods to measure the morphological changes distinctive of microglia functional states in research settings. Currently, many commonly used automated methods can be subject to sample representation bias, time consuming imaging, specific hardware requirements and difficulty in maintaining an accurate comparison across research environments. To overcome these issues, we use commercially available deep learning tools Aiforia® Cloud (Aifoira Inc., Cambridge, MA, United States) to quantify microglial morphology and cell counts from histopathological slides of Iba1 stained tissue sections. We provide evidence for the effective application of this method across a range of independently collected datasets in mouse models of viral infection and Parkinson's disease. Additionally, we provide a comprehensive workflow with training details and annotation strategies by feature layer that can be used as a guide to generate new models. In addition, all models described in this work are available within the Aiforia® platform for study-specific adaptation and validation.

Estimation of the return periods of maxima rainfall and floods at the Pra River Catchment, Ghana, West Africa using the Gumbel extreme value theory.

The Pra river catchment in Ghana is adversely affected by perennial flooding from high-intensity rainfall events. To aid in flood management at the catchment, the Gumbel extreme value distribution has been used to estimate the return periods of maxima rainfall, flood, and consecutive dry and wet days (CDD and CWD) for a period of 5 to 100 years. The results revealed an expected increase in maxima rainfall, CDD and CWD. Maxima rainfall favours the south of the catchment while the CDD decreases northward. Furthermore, an increase in the magnitude of CWD observed at the centre of the catchment had a maximum of approximately 30 days for the 100 year return period, while lower flood volumes had a higher recurrence of 50% to 100% for 1 to 2 year return periods. The inclusion of a projected increase in anthropogenic activities and climate factors at the catchment will slightly affect the magnitude of these variables for the various return periods. Nonetheless, the findings in this study will be of essential input to policy implementation of the Integrated Water Resource Management Plan for river catchments in Ghana, West Africa.

Specific immune modulation of experimental colitis drives enteric alpha-synuclein accumulation and triggers age-related Parkinson-like brain pathology.

Background: In some people with Parkinson's disease (PD), α-synuclein (αSyn) accumulation may begin in the enteric nervous system (ENS) decades before development of brain pathology and disease diagnosis. Objective: To determine how different types and severity of intestinal inflammation could trigger αSyn accumulation in the ENS and the subsequent development of αSyn brain pathology. Methods: We assessed the effects of modulating short- and long-term experimental colitis on αSyn accumulation in the gut of αSyn transgenic and wild type mice by immunostaining and gene expression analysis. To determine the long-term effect on the brain, we induced dextran sulfate sodium (DSS) colitis in young αSyn transgenic mice and aged them under normal conditions up to 9 or 21 months before tissue analyses. Results: A single strong or sustained mild DSS colitis triggered αSyn accumulation in the submucosal plexus of wild type and αSyn transgenic mice, while short-term mild DSS colitis or inflammation induced by lipopolysaccharide did not have such an effect. Genetic and pharmacological modulation of macrophage-associated pathways modulated the severity of enteric αSyn. Remarkably, experimental colitis at three months of age exacerbated the accumulation of aggregated phospho-Serine 129 αSyn in the midbrain (including the substantia nigra), in 21- but not 9-month-old αSyn transgenic mice. This increase in midbrain αSyn accumulation is accompanied by the loss of tyrosine hydroxylase-immunoreactive nigral neurons. Conclusions: Our data suggest that specific types and severity of intestinal inflammation, mediated by monocyte/macrophage signaling, could play a critical role in the initiation and progression of PD.

Chronic methylphenidate preferentially alters catecholamine protein targets in the parietal cortex and ventral striatum.

The psychostimulant methylphenidate (MPH) is the primary drug treatment for attention deficit hyperactivity disorder (ADHD) in children. MPH is well known to acutely block the dopamine (DAT) and noradrenaline (NET) transporters. Its effect on additional catecholamine targets is however less known. This study was aimed at comparing the effects of acute (2 mg/kg, i.p.) and chronic (2 mg/kg twice daily for 2 weeks) MPH treatment to young rats on key catecholamine protein targets in brain regions implicated in the symptoms and treatment of ADHD. For this purpose, the density of DAT, NET, the vesicular monoamine transporter 2 (VMAT2), the rate limiting enzyme for catecholamine synthesis tyrosine hydroxylase (TH) and the dopamine D1 receptor were measured in frontal (FC), parietal cortex (PCx) and the dorsal (DS) and ventral (VS) striatum. The data demonstrate that the effects of MPH depend on duration of treatment and brain region investigated. With the exception of DAT in the VS our results indicate that chronic but not acute administration of MPH increases levels of DAT, NET, TH, VMAT2 and D1. These effects were further more prominent in the VS over DS and in the PCx compared to the FC. In addition, chronic MPH enhanced DAT levels in the left DS but not in right side. To summarize, this study shows new evidence that chronic MPH to young rats preferentially alters catecholamine targets in PCx and VS over DS and FC. The effect of chronic MPH to increase levels of DAT, NET and VMAT2 suggests that the drug might long-term loose some of its acute action to increase extracellular levels of dopamine and noradrenaline. In conclusion, these findings provide novel insights into the mechanism of action by MPH in the treatment of ADHD and further suggest that the long-term effectiveness of the stimulant drug could be limited.

The impact of rain events on CO2 emissions from contrasting land use systems in semi-arid West African savannas.

In the future the Sudanian savanna - one of West Africa's high-potential "bread baskets" - will likely face shorter rainy seasons with more extreme rains and droughts. That could have serious impacts on the vegetation and its carbon dioxide (CO2) exchange with potentially increasing CO2 emissions accelerating climate warming. Understanding how the CO2 fluxes in this area respond to environmental variables, in particular rain events, is essential, but available data are scarce. In this study, we monitored net ecosystem exchange (NEE) of CO2, rainfall and other environmental parameters during four years at three savannas. Savannas were characterized by different vegetation due to different land use: i) woody and nearly pristine, ii) mixture of cropland and grassland and iii) intensive grazing. The impact of rain events on CO2 exchange for these contrasting ecosystems were analyzed for single rain events (short-term) and on a yearly time scale (long-term) using three eddy covariance towers. We found that the woody pristine savanna site was a prominent sink of CO2 (-864 to -1299 g CO2 m-2 y-1) while the degraded sites were net CO2 sources (118 to 605 g CO2 m-2 y-1) with a complicated relation with annual rainfall amounts. The NEE responses to single rain events revealed that daytime rain systematically decreased the sink strengths at all sites, which might be associated with decreased light availability. At the degraded sites, additional factors increasing CO2 losses were rain duration and dry spell length. The observed patterns of immediate CO2 flux responses to rainfall at differently used savannas indicate strong internal feedbacks between vegetation and land use changes and raise the question whether the CO2 sink strengths might be overestimated with possible implications for global CO2 budgets. Sustainable adaptation strategies need to be developed for West Africa.

Loss of One Engrailed1 Allele Enhances Induced α-Synucleinopathy.

BACKGROUND: Parkinson's disease (PD) is a synucleinopathy that has multiple neuropathological characteristics, with nigrostriatal dopamine system degeneration being a core feature. Current models of PD pathology typically fail to recapitulate several attributes of the pathogenic process and neuropathology. We aimed to define the effects of combining a mouse model exhibiting multiple PD-like changes with intrastriatal injections of α-synuclein (α-syn) pre-formed fibril (PFFs) aggregates. We employed the heterozygous Engrailed 1 (En1+/-) mouse that features several pathophysiological hallmarks of clinical PD. OBJECTIVE: To test the hypothesis that the neuropathological changes in the En1+/- mice will promote formation of α-syn aggregates following intrastriatal injections of pathogenic human α-syn PFFs. METHODS: We unilaterally injected PFFs into the striata of 1-month-old En1+/- and control wild-type mice and euthanized animals at 3 months for post-mortem analysis. RESULTS: Using immunohistochemistry and unbiased stereology, we established that PFF-injected En1+/- mice exhibited a near-threefold increase in pS129-α-syn-positive neurons in the substantia nigra compared to PFF-injected wild-type mice. The PFF-injected En1+/- mice also displayed significant increases in pS129-α-syn-positive neurons in the amygdala and ventral tegmental area; regions of known PD pathology with projections to the striatum. Additionally, we observed amplified pS129-α-syn-positive aggregation in En1+/- mice in multiple cortical regions. CONCLUSIONS: Following intrastriatal injection of PFFs, absence of an En1 allele leads to additional aggregation of pathological α-syn, potentially due to En1-loss mediated nigrostriatal impairment. We propose that further development of this double-hit model could result in a PD mouse model that predicts which experimental therapies will be effective in PD.

Methylphenidate alters monoaminergic and metabolic pathways in the cerebellum of adolescent rats.

Abnormalities in the cerebellar circuitry have been suggested to contribute to some of the symptoms associated with attention deficit hyperactivity disorder (ADHD). The psychostimulant methylphenidate (MPH) is the major drug for treating this condition. Here, the effects of acute (2.0 mg/kg and 5.0 mg/kg) and chronic (2.0 mg/kg, twice daily for 15 days) MPH treatments were investigated in adolescent (35-40 days old) rats on monoaminergic and metabolic markers in the cerebellum. Data acquired indicates that acute MPH treatment (2.0 mg/kg) decreased cerebellar vesicular monoamine transporter (VMAT2) density, while chronic treatment caused an increase. In contrast, protein levels of tyrosine hydroxylase (TH) and the dopamine D1 receptor were not significantly altered by neither acute nor chronic MPH treatment. In addition, while chronic but not acute MPH treatment significantly enhanced dopamine turnover (DOPAC/dopamine) in the cerebellum, levels of dopamine and homovanillic acid (HVA) were not altered. Acute MPH (5.0 mg/kg) significantly modified levels of a range of cerebellar metabolites with similar trends also detected for the lower dose (2.0 mg/kg). In this regard, acute MPH tended to decrease cerebellar metabolites associated with energy consumption and excitatory neurotransmission including glutamate, glutamine, N-acetyl aspartate, and inosine. Conversely, levels of some metabolites associated with inhibitory neurotransmission, including GABA and glycine were reduced by acute (5.0 mg/kg) MPH, together with acetate, aspartate and hypoxanthine. In conclusion, this study demonstrated that MPH alters cerebellar biochemistry, and that this effect depends on both dose and duration of treatment. The therapeutic significance of these results requires further investigation.

Targeting energy metabolism via the mitochondrial pyruvate carrier as a novel approach to attenuate neurodegeneration.

Several molecular pathways are currently being targeted in attempts to develop disease-modifying therapies to slow down neurodegeneration in Parkinson's disease. Failure of cellular energy metabolism has long been implicated in sporadic Parkinson's disease and recent research on rare inherited forms of Parkinson's disease have added further weight to the importance of energy metabolism in the disease pathogenesis. There exists a new class of anti-diabetic insulin sensitizers in development that inhibit the mitochondrial pyruvate carrier (MPC), a protein which mediates the import of pyruvate across the inner membrane of mitochondria. Pharmacological inhibition of the MPC was recently found to be strongly neuroprotective in multiple neurotoxin-based and genetic models of neurodegeneration which are relevant to Parkinson's disease. In this review, we summarize the neuroprotective effects of MPC inhibition and discuss the potential putative underlying mechanisms. These mechanisms involve augmentation of autophagy via attenuation of the activity of the mammalian target of rapamycin (mTOR) in neurons, as well as the inhibition of neuroinflammation, which is at least partly mediated by direct inhibition of MPC in glia cells. We conclude that MPC is a novel and potentially powerful therapeutic target that warrants further study in attempts to slow Parkinson's disease progression.

Medicinal Plants Used in the Treatment of Mental and Neurological Disorders in Ghana.

ETHNOPHARMACOLOGICAL RELEVANCE: Mental and neurological disorders are a serious public health challenge globally, particularly in developing countries where cultural factors and limited access to standard healthcare have led to a reliance on traditional medicines. However, ethnopharmacological characterization of traditional medicines used to treat these diseases is lacking. In this study, an ethnobotanical description of plant species used in treating mental and neurological disorders in Ghana and an update of their experimentally validated pharmacological relevance are provided. MATERIALS AND METHODS: Two hundred herbalists agreed to participate but sixty-six specialized in treating mental and neurological disorders were interviewed on their traditional medical practice. Literature review was conducted to verify the experimentally validated pharmacological importance of the reported plants. RESULTS: Thirty-two plant species belonging to twenty-eight families were identified. Most plant species had either analgesic (50%), anxiolytic (18.8%), or anticonvulsant (15.6%) properties. Others had reported sedative, anti-Alzheimer's disease, motor coordination, antipsychotic, antidepressant, cognitive enhancement, and neuroprotective properties. While Ageratum conyzoides L. (Asteraceae) and Ocimum gratissimum L. (Lamiaceae) were the most commonly mentioned species with analgesic properties, Lantana camara L. (Verbenaceae) was the most-reported anxiolytic product, with Cymbopogon citratus DC. (Gramineae), Mangifera indica L., Tetrapleura tetraptera Schum Taub. (Fabaceae), and Persea Americana Mill (Lauraceae) being the most studied anticonvulsants. CONCLUSIONS: This study provides the first report specifically on medicinal plants used in treating mental and neurological disorders in Ghana. Most of the identified plants have been scientifically confirmed to possess neuro- and psychopharmacological properties and may serve as templates for drug development.

Chronic methylphenidate regulates genes and proteins mediating neuroplasticity in the juvenile rat brain.

Methylphenidate (MPH) is the front-line psychostimulant medication prescribed for alleviating the symptoms associated with attention deficit hyperactivity disorder (ADHD) in children. Here, we investigated the effects of chronic MPH (2.0mg/kg, twice daily for 15days) exposure to young rats (20-25days old at start of treatment) on the expression of genes and proteins associated with neuroplasticity, such as activity regulated cytoskeleton-associated protein (Arc), insulin receptor substrate protein 53 (IRSp53), cell division control protein 42 (Cdc42), and actin-related protein 2 (Arp2). Chronic MPH increased Arc expression in areas of the cerebrum including, the striatum, nucleus accumbens and hippocampus. In addition, chronic MPH also increased the expression of IRSp53 in the striatum, while Cdc42 and Arp2 were specifically increased in the nucleus accumbens. Conversely, chronic MPH decreased Arc and IRSp53 protein expression in the cerebellum, indicating differential effects of the drug in cerebral areas relative to the cerebellum. Overall, our results indicate that chronic MPH treatment increases expression of genes and proteins associated with dendritic spine formation and neuronal plasticity in target areas of the cerebrum while it decreases the expression in the cerebellum.

1H NMR-based metabolomics reveals neurochemical alterations in the brain of adolescent rats following acute methylphenidate administration.

The psychostimulant methylphenidate (MPH) is increasingly used in the treatment of attention deficit hyperactivity disorder (ADHD). While there is little evidence for common brain pathology in ADHD, some studies suggest a right hemisphere dysfunction among people diagnosed with the condition. However, in spite of the high usage of MPH in children and adolescents, its mechanism of action is poorly understood. Given that MPH blocks the neuronal transporters for dopamine and noradrenaline, most research into the effects of MPH on the brain has largely focused on these two monoamine neurotransmitter systems. Interestingly, recent studies have demonstrated metabolic changes in the brain of ADHD patients, but the impact of MPH on endogenous brain metabolites remains unclear. In this study, a proton nuclear magnetic resonance (1H NMR)-based metabolomics approach was employed to investigate the effects of MPH on brain biomolecules. Adolescent male Sprague Dawley rats were injected intraperitoneally with MPH (5.0 mg/kg) or saline (1.0 ml/kg), and cerebral extracts from the left and right hemispheres were analysed. A total of 22 variables (representing 13 distinct metabolites) were significantly increased in the MPH-treated samples relative to the saline-treated controls. The upregulated metabolites included: amino acid neurotransmitters such as GABA, glutamate and aspartate; large neutral amino acids (LNAA), including the aromatic amino acids (AAA) tyrosine and phenylalanine, both of which are involved in the metabolism of dopamine and noradrenaline; and metabolites associated with energy and cell membrane dynamics, such as creatine and myo-inositol. No significant differences in metabolite concentrations were found between the left and right cerebral hemispheres. These findings provide new insights into the mechanisms of action of the anti-ADHD drug MPH.

Biological control via "ecological" damping: An approach that attenuates non-target effects.

In this work we develop and analyze a mathematical model of biological control to prevent or attenuate the explosive increase of an invasive species population, that functions as a top predator, in a three-species food chain. We allow for finite time blow-up in the model as a mathematical construct to mimic the explosive increase in population, enabling the species to reach "disastrous", and uncontrollable population levels, in a finite time. We next improve the mathematical model and incorporate controls that are shown to drive down the invasive population growth and, in certain cases, eliminate blow-up. Hence, the population does not reach an uncontrollable level. The controls avoid chemical treatments and/or natural enemy introduction, thus eliminating various non-target effects associated with such classical methods. We refer to these new controls as "ecological damping", as their inclusion dampens the invasive species population growth. Further, we improve prior results on the regularity and Turing instability of the three-species model that were derived in Parshad et al. (2014). Lastly, we confirm the existence of spatiotemporal chaos.

Disregard of neurological impairments associated with neglected tropical diseases in Africa.

Neglected tropical diseases (NTDs) affect people in the bottom billion poorest in the world. These diseases are concentrated in rural areas, conflict zones and urban slums in Africa and other tropical areas. While the World Health Organization recognizes seventeen priority NTDs, the list of conditions present in Africa and elsewhere that are eligible to be classified as NTDs is much longer. Although NTDs are generally marginalized, their associated neurological burden has been almost completely disregarded. However, reports indicate that trichuriasis, schistosomiasis and hookworm infection, among others, cause impairments in memory and cognition, negatively affecting school attendance rates and educational performance particularly among children, as well as agricultural productivity among adults. Consequently, the neurological impairments have substantial influence on education and economic productivity, thus aggravating and perpetuating poverty in affected societies. However, inadequate research, policy and public health attention has been paid to the neurological burdens associated with NTDs. In order to appropriately address these burdens, we recommend the development of policy interventions that focus on the following areas: (i) the introduction of training programs to develop the capacity of scientists and clinicians in research, diagnostic and treatment approaches (ii) the establishment of competitive research grant schemes to fund cutting-edge research into these neurological impairments, and (iii) the development of public health interventions to improve community awareness of the NTD-associated neurological problems, possibly enhancing disease prevention and expediting treatment.