2,438 research outputs found
Perspective: Vitamin D deficiency and COVIDā19 severity ā plausibly linked by latitude, ethnicity, impacts on cytokines, ACE2 and thrombosis
Background
SARSāCoVā2 coronavirus infection ranges from asymptomatic through to fatal COVIDā19 characterized by a ācytokine stormā and lung failure. Vitamin D deficiency has been postulated as a determinant of severity.
Objectives
To review the evidence relevant to vitamin D and COVIDā19.
Methods
Narrative review.
Results
Regression modelling shows that more northerly countries in the Northern Hemisphere are currently (May 2020) showing relatively high COVIDā19 mortality, with an estimated 4.4% increase in mortality for each 1 degree latitude north of 28 degrees North (P = 0.031) after adjustment for age of population. This supports a role for ultraviolet B acting via vitamin D synthesis. Factors associated with worse COVIDā19 prognosis include old age, ethnicity, male sex, obesity, diabetes and hypertension and these also associate with deficiency of vitamin D or its response. Vitamin D deficiency is also linked to severity of childhood respiratory illness. Experimentally, vitamin D increases the ratio of angiotensināconverting enzyme 2 (ACE2) to ACE, thus increasing angiotensin II hydrolysis and reducing subsequent inflammatory cytokine response to pathogens and lung injury.
Conclusions
Substantial evidence supports a link between vitamin D deficiency and COVIDā19 severity but it is all indirect. Communityābased placeboācontrolled trials of vitamin D supplementation may be difficult. Further evidence could come from study of COVIDā19 outcomes in large cohorts with information on prescribing data for vitamin D supplementation or assay of serum unbound 25(OH) vitamin D levels. Meanwhile, vitamin D supplementation should be strongly advised for people likely to be deficient
Coupling molecular spin states by photon-assisted tunneling
Artificial molecules containing just one or two electrons provide a powerful
platform for studies of orbital and spin quantum dynamics in nanoscale devices.
A well-known example of these dynamics is tunneling of electrons between two
coupled quantum dots triggered by microwave irradiation. So far, these
tunneling processes have been treated as electric dipole-allowed
spin-conserving events. Here we report that microwaves can also excite
tunneling transitions between states with different spin. In this work, the
dominant mechanism responsible for violation of spin conservation is the
spin-orbit interaction. These transitions make it possible to perform detailed
microwave spectroscopy of the molecular spin states of an artificial hydrogen
molecule and open up the possibility of realizing full quantum control of a two
spin system via microwave excitation.Comment: 13 pages, 9 figure
Internal representations, external representations and ergonomics: towards a theoretical integration
No evidence for association between SLC11A1 and visceral leishmaniasis in India.
BACKGROUND: SLC11A1 has pleiotropic effects on macrophage function and remains a strong candidate for infectious disease susceptibility. 5' and/or 3' polymorphisms have been associated with tuberculosis, leprosy, and visceral leishmaniasis (VL). Most studies undertaken to date were under-powered, and none has been replicated within a population. Association with tuberculosis has replicated variably across populations. Here we investigate SLC11A1 and VL in India. METHODS: Nine polymorphisms (rs34448891, rs7573065, rs2276631, rs3731865, rs17221959, rs2279015, rs17235409, rs17235416, rs17229009) that tag linkage disequilibrium blocks across SLC11A1 were genotyped in primary family-based (313 cases; 176 families) and replication (941 cases; 992 controls) samples. Family- and population-based analyses were performed to look for association between SLC11A1 variants and VL. Quantitative RT/PCR was used to compare SLC11A1 expression in mRNA from paired splenic aspirates taken before and after treatment from 24 VL patients carrying different genotypes at the functional promoter GTn polymorphism (rs34448891). RESULTS: No associations were observed between VL and polymorphisms at SLC11A1 that were either robust to correction for multiple testing or replicated across primary and replication samples. No differences in expression of SLC11A1 were observed when comparing pre- and post-treatment samples, or between individuals carrying different genotypes at the GTn repeat. CONCLUSIONS: This is the first well-powered study of SLC11A1 as a candidate for VL, which we conclude does not have a major role in regulating VL susceptibility in India.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are
Agency, qualia and life: connecting mind and body biologically
Many believe that a suitably programmed computer could act for its own goals and experience feelings. I challenge this view and argue that agency, mental causation and qualia are all founded in the unique, homeostatic nature of living matter. The theory was formulated for coherence with the concept of an agent, neuroscientific data and laws of physics. By this method, I infer that a successful action is homeostatic for its agent and can be caused by a feeling - which does not motivate as a force, but as a control signal. From brain research and the locality principle of physics, I surmise that qualia are a fundamental, biological form of energy generated in specialized neurons. Subjectivity is explained as thermodynamically necessary on the supposition that, by converting action potentials to feelings, the neural cells avert damage from the electrochemical pulses. In exchange for this entropic benefit, phenomenal energy is spent as and where it is produced - which precludes the objective observation of qualia
Electrically driven single electron spin resonance in a slanting Zeeman field
The rapidly rising fields of spintronics and quantum information science have
led to a strong interest in developing the ability to coherently manipulate
electron spins. Electron spin resonance (ESR) is a powerful technique to
manipulate spins that is commonly achieved by applying an oscillating magnetic
field. However, the technique has proven very challenging when addressing
individual spins. In contrast, by mixing the spin and charge degrees of freedom
in a controlled way through engineered non-uniform magnetic fields, electron
spin can be manipulated electrically without the need of high-frequency
magnetic fields. Here we realize electrically-driven addressable spin rotations
on two individual electrons by integrating a micron-size ferromagnet to a
double quantum dot device. We find that the electrical control and spin
selectivity is enabled by the micro-magnet's stray magnetic field which can be
tailored to multi-dots architecture. Our results demonstrate the feasibility of
manipulating electron spins electrically in a scalable way.Comment: 25 pages, 6 figure
Would the field of cognitive neuroscience be advanced by sharing functional MRI data?
During the past two decades, the advent of functional magnetic resonance imaging (fMRI) has fundamentally changed our understanding of brain-behavior relationships. However, the data from any one study add only incrementally to the big picture. This fact raises important questions about the dominant practice of performing studies in isolation. To what extent are the findings from any single study reproducible? Are researchers who lack the resources to conduct a fMRI study being needlessly excluded? Is pre-existing fMRI data being used effectively to train new students in the field? Here, we will argue that greater sharing and synthesis of raw fMRI data among researchers would make the answers to all of these questions more favorable to scientific discovery than they are today and that such sharing is an important next step for advancing the field of cognitive neuroscience
Reasoning deficits among illicit drug users are associated with aspects of cannabis use
Background. Deficits in deductive reasoning have been observed among ecstasy/polydrug users. The present study seeks to investigate dose-related effects of specific drugs and whether these vary with the cognitive demands of the task. Methods. One hundred and five participants (mean age 21.33, S.D. 3.14; 77 females, 28 males) attempted to generate solutions for eight one-model syllogisms and one syllogism for which there was no valid conclusion (NVC). All of the one model syllogisms generated at least one valid conclusion and six generated two valid conclusions. In these six cases one of the conclusions was classified as common and the other as non-common. Results. The number of valid common inferences was negatively associated with aspects of short term cannabis use and with measures of IQ. The outcomes observed were more than simple post intoxication effects since cannabis use in the 10 days immediately before testing was unrelated to reasoning performance. Following adjustment for multiple comparisons, the number of non-common valid inferences was not significantly associated with any of the drug use measures. Conclusions. Recent cannabis use appears to impair the processes associated with generating valid common inferences while not affecting the production of non-common inferences. It is possible, therefore, that the two types of inference may recruit different executive resources which may differ in their susceptibility to cannabis-related effects
Daily life stress and the cortisol awakening response : testing the anticipation hypothesis
Acknowledgments We thank Paul Stewart for his contribution to data collection and Dr Matthew Jones for programming the handheld computers. Author Contributions Conceived and designed the experiments: WS DJP. Performed the experiments: DJP. Analyzed the data: WS. Wrote the paper: WS DJP.Peer reviewedPublisher PD
Enhanced pre-synaptic glutamate release in deep-dorsal horn contributes to calcium channel alpha-2-delta-1 protein-mediated spinal sensitization and behavioral hypersensitivity
Nerve injury-induced expression of the spinal calcium channel alpha-2-delta-1 subunit (CavĪ±2Ī“1) has been shown to mediate behavioral hypersensitivity through a yet identified mechanism. We examined if this neuroplasticity modulates behavioral hypersensitivity by regulating spinal glutamatergic neurotransmission in injury-free transgenic mice overexpressing the CavĪ±2Ī“1 proteins in neuronal tissues. The transgenic mice exhibited hypersensitivity to mechanical stimulation (allodynia) similar to the spinal nerve ligation injury model. Intrathecally delivered antagonists for N-methyl-D-aspartate (NMDA) and Ī±-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptors, but not for the metabotropic glutamate receptors, caused a dose-dependent allodynia reversal in the transgenic mice without changing the behavioral sensitivity in wild-type mice. This suggests that elevated spinal CavĪ±2Ī“1 mediates allodynia through a pathway involving activation of selective glutamate receptors. To determine if this is mediated by enhanced spinal neuronal excitability or pre-synaptic glutamate release in deep-dorsal horn, we examined wide-dynamic-range (WDR) neuron excitability with extracellular recording and glutamate-mediated excitatory postsynaptic currents with whole-cell patch recording in deep-dorsal horn of the CavĪ±2Ī“1 transgenic mice. Our data indicated that overexpression of CavĪ±2Ī“1 in neuronal tissues led to increased frequency, but not amplitude, of miniature excitatory post synaptic currents mediated mainly by AMPA/kainate receptors at physiological membrane potentials, and also by NMDA receptors upon depolarization, without changing the excitability of WDR neurons to high intensity stimulation. Together, these findings support a mechanism of CavĪ±2Ī“1-mediated spinal sensitization in which elevated CavĪ±2Ī“1 causes increased pre-synaptic glutamate release that leads to reduced excitation thresholds of post-synaptic dorsal horn neurons to innocuous stimuli. This spinal sensitization mechanism may mediate at least partially the neuropathic pain states derived from increased pre-synaptic CavĪ±2Ī“1 expression
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