Miracle-dz/UniFAR-FTUs huggingface dataset:
Genetic mapping of two loci affecting DDT resistance in the malaria vector Anopheles gambiae

Resistance to the insecticide DDT in the mosquito vectors of malaria has severely hampered efforts to control this disease and has contributed to the increase in prevalence of malaria cases seen in recent years. Over 90% of the 300–500 million annual cases of malaria occur in Africa, where the major vector is Anopheles gambiae. DDT resistance in the ZAN/U strain of An. gambiae is associated with an increased metabolism of the insecticide, catalysed by members of the glutathione S‐transferase (GST) enzyme family, but the molecular mechanism underlying this metabolic resistance is not known. Genetic crosses show that resistance is autosomal and semidominant. We have used microsatellite markers to identify two quantitative trait loci (QTL), which together explain over 50% of the variance in susceptibility to DDT in the ZAN/U strain of An. gambiae. The first locus, rtd1, is on chromosome 3 between markers H341 and H88 and has a recessive effect with respect to susceptibility. The second locus, rtd2 is on chromosome 2L, close to marker H325 and has an additive genetic effect. The markers flanking these two QTL have been physically mapped to An. gambiae polytene chromosomes. They do not coincide with any of the GST genes that have been cloned and mapped in this species. Characterization of these QTL will lead to a clearer understanding of the mechanisms of metabolic resistance to DDT.
Letter by Kielstein et al regarding article, "High-dose allopurinol improves endothelial function by profoundly reducing vascular oxidative stress and not by lowering uric acid".

To the Editor: We read with interest the paper by George and colleagues1 about the benefit of high-dose allopurinol on endothelial dysfunction in patients with class II or III heart failure. The authors suggest that on the basis of the steep dose–response relationship between allopurinol and endothelial function, a dose of 600 mg/d yields the most improvement in endothelial function. We are concerned about the implications of …
Does Size Matter? Atmospheric CO2 May Be a Stronger Driver of Stomatal Closing Rate Than Stomatal Size in Taxa That Diversified under Low CO2

One strategy for plants to optimize stomatal function is to open and close their stomata quickly in response to environmental signals. It is generally assumed that small stomata can alter aperture faster than large stomata. We tested the hypothesis that species with small stomata close faster than species with larger stomata in response to darkness by comparing rate of stomatal closure across an evolutionary range of species including ferns, cycads, conifers, and angiosperms under controlled ambient conditions (380 ppm CO2; 20.9% O2). The two species with fastest half-closure time and the two species with slowest half-closure time had large stomata while the remaining three species had small stomata, implying that closing rate was not correlated with stomatal size in these species. Neither was response time correlated with stomatal density, phylogeny, functional group, or life strategy. Our results suggest that past atmospheric CO2 concentration during time of taxa diversification may influence stomatal response time. We show that species which last diversified under low or declining atmospheric CO2 concentration close stomata faster than species that last diversified in a high CO2 world. Low atmospheric [CO2] during taxa diversification may have placed a selection pressure on plants to accelerate stomatal closing to maintain adequate internal CO2 and optimize water use efficiency.
Approaches for Setting-up Multi-Stakeholder Platforms for Agricultural Research and Development

In order to facilitate improved returns to research and development in African agriculture, the innovation systems approach which engenders the involvement of multiple stakeholders in its innovation pathway, has been proposed. Despite the potential of this approach, the understanding of its implementation and particularly of the process of setting up its multi-stakeholder platform is still largely lacking. Yet, this platform is critical to the success and sustainability of the operations of the platform. This article introduces the concept of Integrated Agricultural Research for Development (IAR4D) and the constituent Innovation Platform (IP) as a workable multistakeholders approach for sustainable agricultural research and development. The IAR4D approach entails a multi-sectoral orientation to agricultural problem diagnosis and draws on integrated approaches using 'hard' and 'soft' sciences to provide solutions, while maximizing available resources. IAR4D is premised on the innovation systems approach and requires systemic interaction among all stakeholders around specific commodities or production systems. The procedure for the establishment of an IP requires a value chain analysis of the commodity of interest, followed by a systematic engagement of the identified stakeholders to the platform. The stakeholders in a balanced IP will cut across the private and the public sectors with distinct engagement of the non-traditional stakeholders as input dealers, financial institutions, policy makers, etc. The activity of a typical IP could be kick-started by joint development of a business plan and its proactive implementation in a partnership mood. A functional IP will normally experience series of iterative learning at the interphase of which innovation is generated. The set-up of multistakeholders platform in IAR4D mode has potentials to function effectively as a model for regional and national ARD planning.
New Models of Worker Representation

Albert Einstein was reputed to have said that continuing to do the same thing over and over again and expecting different results was the definition of insanity. He wasn’t referring to the labor movement, but it would seem to be an apt assessment of how poorly the idea of collective bargaining has fared since at least Ronald Reagan’s election. In truth, union membership and political influence were in decline before the PATCO strike. But it was not until AFL-CIO President Richard Trumka came to Chicago in 2013 and declared that “the basic system of worker representation is failing to meet the needs of America’s working men and women by every critical measure” that old models of union behavior were no longer the default organizing mode. Some unions had always been creative about how they behaved, and many used innovative techniques to win organizing campaigns and good labor agreements. It’s not that everything that organized labor was doing was failing—just too much of it. The fault of labor’s retrenchment lay in many areas. First among them was that the political climate turned decidedly hostile. Labor’s enemies were diverse but united behind a “union-free” ideology. Legal protections for union organizing and bargaining were never robust, but since the 1970s, federal attacks on the National Labor Relations Board and state restrictions on publicand private-sector unionism have degraded respect for “industrial democracy. ” Additionally, trade agreements shipped millions of union jobs someplace else, and fiscal policy shifted increased shares of wealth into fewer already well-provisioned hands, which squeezed the life out of public budgets, further eroding the benefits of unionization. As the external threats multiplied, however, organized labor mostly accepted concessions and, more fatefully, defaulted to the familiar practice of accepting changes over which it had no influence. When the ground was collapsing underfoot, the labor movement assumed a fortress mentality. Live to fight another day became the battle cry of a badly damaged army of workers. Perhaps the biggest loss was the conceptual flattening of collective bargaining. From a powerful process for creating economic prosperity and democratic problem solving, collective bargaining was reduced to an inconvenience. While employers had mostly only learned to tolerate what they couldn’t avoid, the idea of democracy in the workplace had once held out the promise that all labor could be valued and that the rules we work under could contribute to a broadly shared prosperity. But truthfully, it seems that only unions and groups that stand for workers see the future in such inclusive shades. Yet despite repeated predictions of labor’s ultimate demise, unions have proven to be remarkably durable institutions. Fight remains. The cause is no less right. But how 579766 LSJXXX10.1177/0160449X15579766Labor Studies JournalBruno research-article2015
Respiratory Syncytial Virus Predisposes Mice to Augmented Allergic Airway Responses Via IL-13-Mediated Mechanisms1

The development of severe childhood asthma may be influenced by several factors including environmental and infectious stimuli. The causal relationship between infectious viral responses, such as respiratory syncytial virus (RSV), and severe asthma during early childhood is unclear. In these studies, the ability for an initial RSV infection to exacerbate and promote a more severe asthmatic-type response was investigated by combining established murine models of disease. We examined the ability of RSV to induce exacerbation of allergic disease over a relatively long period, leading to development of severe airway responses including airway inflammation and hyperreactivity. The preferential production of IL-13 during a primary RSV infection appears to play a critical role for the exacerbation of cockroach allergen-induced disease. The depletion of IL-13 during RSV infections inhibited the exacerbation and acceleration of severe allergen-induced airway hyperreactivity. This was indicated by decreases in airway hyperreactivity and changes in lung chemokine production. These data suggest that the airway responses during asthma can be greatly affected by a previous RSV infection, even when infection occurs before allergen sensitization. Overall, infection of the airways with RSV can induce an IL-13-dependent change in airway function and promotes an environment that contributes to the development of severe allergic asthmatic responses.
Urinary Volatile Compounds as Biomarkers for Lung Cancer: A Proof of Principle Study Using Odor Signatures in Mouse Models of Lung Cancer

A potential strategy for diagnosing lung cancer, the leading cause of cancer-related death, is to identify metabolic signatures (biomarkers) of the disease. Although data supports the hypothesis that volatile compounds can be detected in the breath of lung cancer patients by the sense of smell or through bioanalytical techniques, analysis of breath samples is cumbersome and technically challenging, thus limiting its applicability. The hypothesis explored here is that variations in small molecular weight volatile organic compounds (“odorants”) in urine could be used as biomarkers for lung cancer. To demonstrate the presence and chemical structures of volatile biomarkers, we studied mouse olfactory-guided behavior and metabolomics of volatile constituents of urine. Sensor mice could be trained to discriminate between odors of mice with and without experimental tumors demonstrating that volatile odorants are sufficient to identify tumor-bearing mice. Consistent with this result, chemical analyses of urinary volatiles demonstrated that the amounts of several compounds were dramatically different between tumor and control mice. Using principal component analysis and supervised machine-learning, we accurately discriminated between tumor and control groups, a result that was cross validated with novel test groups. Although there were shared differences between experimental and control animals in the two tumor models, we also found chemical differences between these models, demonstrating tumor-based specificity. The success of these studies provides a novel proof-of-principle demonstration of lung tumor diagnosis through urinary volatile odorants. This work should provide an impetus for similar searches for volatile diagnostic biomarkers in the urine of human lung cancer patients.
Inhibition of tissue angiotensin-converting enzyme with quinapril reduces hypoxic pulmonary hypertension and pulmonary vascular remodeling.

BACKGROUND Angiotensin II may contribute to hypoxic pulmonary hypertension via its vasoconstrictor and growth-stimulatory effects on vascular smooth muscle cells (VSMCs). Therefore, the use of ACE inhibitors might reduce hypoxic pulmonary hypertension by decreasing pulmonary vasomotor tone or vascular remodeling. METHODS AND RESULTS Pulmonary hemodynamics and vascular remodeling were compared in chronically hypoxic (FIO2 = 0.10) rats treated with 0, 1, and 10 mg.kg-1.d-1 quinapril, a potent tissue ACE inhibitor, both during and after the development of pulmonary hypertension. Quinapril reduced the development of pulmonary hypertension after 12 days of hypoxia from 26 +/- 1 to 19 +/- 1 mm Hg (P < .05). When started in established pulmonary hypertension, quinapril reduced pulmonary artery pressure and total pulmonary resistance index from 29 +/- 1 to 25 +/- 1 mm Hg and from 0.136 +/- 0.01 to 0.101 +/- 0.005 mm Hg . mL-1.min-1 per kg, respectively (P < .05). Chronically hypoxic rats showed a small pulmonary vasoconstrictor response that was not affected by quinapril. In contrast, percent medial thickness in alveolar duct blood vessels was reduced by quinapril treatment both in developing and in established pulmonary hypertension (10.0 +/- 0.2% versus 8.9 +/- 0.1% [P < .05] and 11.2 +/- 0.2% versus 9.1 +/- 0.2% [P < .05], respectively). 5'-Bromo-deoxyuridine-positive VSMCs were detected in 56 +/- 3% of hypoxic control pulmonary resistance vessels versus 41 +/- 3% of vessels after quinapril treatment (P < .05). CONCLUSIONS Pulmonary ACE and angiotensin II contribute to the development and maintenance of hypoxic pulmonary hypertension in rats. ACE inhibition with quinapril reduces the development of hypoxic pulmonary hypertension and in part reverses established pulmonary hypertension, most likely via inhibition of pulmonary VSMC proliferation and/or growth.
Understanding Grief: An Introduction

The Nature and Experience of Grief. Attachment, Loss and Grief. Theories and Models of Grief. The Social Context of Grief. Cultural and Religious Aspects of Death and Dying. Grief and Relationship With the Deceased: Kinship. Complicated Grief. The Wider Context of Grief: Loss of Pets and Loss of Self. Recommended Reading and Websites.
Sequential Circuit Design for Embedded Cryptographic Applications Resilient to Adversarial Faults

In the relatively young field of fault-tolerant cryptography, the main research effort has focused exclusively on the protection of the data path of cryptographic circuits. To date, however, we have not found any work that aims at protecting the control logic of these circuits against fault attacks, which thus remains the proverbial Achilles' heel. Motivated by a hypothetical yet realistic fault analysis attack that, in principle, could be mounted against any modular exponentiation engine, even one with appropriate data path protection, we set out to close this remaining gap. In this paper, we present guidelines for the design of multifault-resilient sequential control logic based on standard Error-Detecting Codes (EDCs) with large minimum distance. We introduce a metric that measures the effectiveness of the error detection technique in terms of the effort the attacker has to make in relation to the area overhead spent in implementing the EDC. Our comparison shows that the proposed EDC-based technique provides superior performance when compared against regular N-modular redundancy techniques. Furthermore, our technique scales well and does not affect the critical path delay.
Deep Sparse Coding Using Optimized Linear Expansion of Thresholds

We address the problem of reconstructing sparse signals from noisy and compressive measurements using a feed-forward deep neural network (DNN) with an architecture motivated by the iterative shrinkage-thresholding algorithm (ISTA). We maintain the weights and biases of the network links as prescribed by ISTA and model the nonlinear activation function using a linear expansion of thresholds (LET), which has been very successful in image denoising and deconvolution. The optimal set of coefficients of the parametrized activation is learned over a training dataset containing measurement-sparse signal pairs, corresponding to a fixed sensing matrix. For training, we develop an efficient second-order algorithm, which requires only matrix-vector product computations in every training epoch (Hessian-free optimization) and offers superior convergence performance than gradient-descent optimization. Subsequently, we derive an improved network architecture inspired by FISTA, a faster version of ISTA, to achieve similar signal estimation performance with about 50% of the number of layers. The resulting architecture turns out to be a deep residual network, which has recently been shown to exhibit superior performance in several visual recognition tasks. Numerical experiments demonstrate that the proposed DNN architectures lead to 3 to 4 dB improvement in the reconstruction signal-to-noise ratio (SNR), compared with the state-of-the-art sparse coding algorithms.
Endoplasmic reticulum stress induces autophagy in renal proximal tubular cells.

BACKGROUND Autophagy, an intracellular self-degradation system conserved throughout eukaryotes, plays an important role in a variety of biological processes, including cell death, development, cancer, defence against infection and neurodegeneration. However, little information about autophagy in renal tubular cells is available. We investigated the relationship of autophagy with endoplasmic reticulum (ER) stress in proximal tubular cells. METHODS Immortalized rat proximal tubular cells were exposed to the classic ER stress inducers tunicamycin or brefeldin A. Autophagy was detected mainly by immunoblot analysis of LC3, a widely used marker of autophagy, and also by immunofluorescent cytochemistry of LC3 and electron microscopy. Biological significance of the phenomenon was studied using bafilomycin A1, an inhibitor of autophagosome degradation. Signal transduction pathways following ER stress were also investigated using inhibitors of the MAPK pathway. RESULTS Both ER stress inducers significantly increased LC3-II as a marker of autophagy in immunoblot analysis. Immunocytochemistry of LC3 and electron microscopy also showed activation of autophagy by ER stress. Inhibition by bafilomycin A1 showed that autophagy following ER stress fulfilled its intrinsic function, namely degradation of cytoplasmic components. Further, use of the MEK 1/2 inhibitor U0126, which inhibits ER stress-induced autophagy induction and ERK activation, showed that ERK, a MAPK family member, was necessary to the induction of autophagy. CONCLUSIONS For the first time, we demonstrate the induction of autophagy following ER stress in renal tubules, and clarify its mechanism. These findings serve as the foundation for further investigation into autophagy in renal diseases.
Xath5 regulates neurogenesis in the Xenopus olfactory placode

Helix‐loop‐helix (HLH) genes function as important regulators of neurogenesis in both the peripheral and central nervous systems. The olfactory system is an ideal tissue in which to study the role of these genes in regulating the acquisition of neuronal cell fate, particularly that of the olfactory receptor neuron (ORN). Here we describe the expression of several basic HLH (bHLH) and repeat HLH (rHLH) factors during olfactory placode development in Xenopus laevis. Our work reveals that a combination of both bHLH and rHLH genes are sequentially expressed within the nascent olfactory placode during normal development. Moreover, overexpression of the bHLH factor, Xenopus atonal homologue 5 (Xath5), promotes olfactory neural fate independent of cellular proliferation within a restricted domain at the anterior of the embryo. Collectively, our data argue that HLH genes are expressed in a cascade during olfactory placode development and that the activity of an atonal homologue, Xath5, can promote ORN fate but only in the appropriate developmental context. © 2002 Wiley‐Liss, Inc.
Adverse events arising from a palliative care survey

Development of evidence-based practice requires investigation of the attitudes and needs of patients, families and healthcare professionals, particularly for sensitive subject areas. Cystic fibrosis (CF) is a recessively inherited life-limiting disorder resulting in early death. Patients with this condition generally expect that lung transplantation will be an available treatment option; however, this is uncertain. A dual approach to care that involves both preparing patients for transplant assessment, while simultaneously exploring acceptable palliative care options is needed. A survey amongst patients with CF, their families and health carers was conducted to understand their attitudes and needs in relation to end-of-life care. The survey encompassed five separate domains, with a total of 60 questions requiring approximately 20 min to complete. Of the 200 surveys sent to patients, 82 (41%) completed responses were received. The Institutional Ethics Committee received six complaints from families of seven patients (3.5% of those surveyed). This article explores the nature of the adverse responses to the survey. The majority of complaints were received from family members rather than from patients. Complaints described dissatisfaction with the topic, little warning about the study and felt it to be inappropriate for their family member’s level of health. Survey instruments used to determine attitudes and needs in relation to end-of-life patient care are likely to elicit adverse responses that should be reported in a similar way to other investigational studies. Also arising from adverse responses and the complaint process, is the impact of criticism on study researchers.
Future Large-Scale Memristive Device Crossbar Arrays: Limits Imposed by Sneak-Path Currents on Read Operations

Passive crossbar arrays based upon memristive devices, at crosspoints, hold great promise for the future high-density and non-volatile memories. The most significant challenge facing memristive device based crossbars today is the problem of sneak-path currents. In this paper, we investigate a memristive device with intrinsic rectification behavior to suppress the sneak-path currents in crossbar arrays. The device model is implemented in Verilog-A language and is simulated to match device characteristics readily available in the literature. Then, we systematically evaluate the read operation performance of large-scale crossbar arrays utilizing our proposed model in terms of read margin and power consumption while considering different crossbar sizes, interconnect resistance values, HRS/LRS (High Resistance State/Low Resistance State) values, rectification ratios and different read-schemes. The outcomes of this study are understanding the trade-offs among read margin, power consumption, read-schemes and most importantly providing a guideline for circuit designers to improve the performance of a memory based crossbar structure. In addition, read operation performance comparison of the intrinsic rectifying memristive device model with other memristive device models are studied.