The Penetration of Solar Radiation into Granular Carbon Dioxide and Water Ices of Varying Grain Sizes on Mars

The penetration depth of broad spectrum solar irradiation over the wavelength range 300 nm – 1100 nm has been experimentally measured for water and carbon dioxide ices of different grain size ranges. Both of these ice compositions are found on the surface of Mars, and have been observed as surface frosts, snow deposits and ice sheets. The e‐folding scale of snow and slab ice has been previously measured, but understanding the behaviour between these end‐member states is important for modelling the thermal behaviour and surface processes associated with ice deposits on Mars, such as grain growth and slab formation via sintering, and carbon dioxide jetting leading to the formation of araneiforms. We find the penetration depth increases in a predictable way with grain size, and an empirical model is given to fit this data, varying with both ice composition and grain size

The Penetration of Solar Radiation into Water and Carbon Dioxide Snow, with reference to Mars

The depth to which solar radiation can penetrate through ice is an important factor in understanding surface‐atmosphere interactions for icy planetary surfaces. Mars hosts both water and carbon dioxide ice on the surface and in the subsurface. At high latitudes during autumn and winter carbon dioxide condenses to form the seasonal polar cap. This has been both modelled and observed to, in part, occur as snowfall. As snow accumulates, the thermal properties of the surface are changed, whether the underlying surface was rocky, regolith or a solid ice sheet. This results in a change (usually increase) in albedo, affecting the proportion of the incident solar energy reflected, or transmitted below the surface of the snow layer. The depth to which light can penetrate through this layer is an important parameter in heat transfer models for the Martian surface, and is often quantified using the e‐folding scale. We present the first measurements of the e‐folding scale in pure carbon dioxide snow for the wavelengths 300 nm to 1100 nm alongside new measurements of water snow

Eye movement recordings to investigate a supranuclear component in chronic progressive external ophthalmoplegia: a cross-sectional study

Background It has been postulated that eye movement disorders in chronic progressive external ophthalmoplegia (CPEO) have a neurological as well as a myopathic component to them. Aim To investigate whether there is a supranuclear component to eye movement disorders in CPEO using eye movement recordings. Methods Saccade and smooth pursuit (SP) characteristics together with vestibulo-ocular reflex (VOR) gain and VOR suppression (VORS) gain in 18 patients with CPEO and 34 normal patients were measured using Eyelink II video-oculography. Results The asymptotic values of the peak velocity main sequence curves were reduced in the CPEO group compared to those of normal patients, with a mean of 161°/s (95% CI 126°/s to 197°/s) compared with 453°/s (95% CI 430 to 475°/s), respectively. Saccadic latency was longer in CPEO (263 ms; 95% CI 250 to 278), compared to controls (185 ms; 95% CI 181 to 189). Smooth pursuit and VOR gains were impaired in CPEO, although this could be explained by non-supranuclear causes. VORS gain was identical in the two groups. Conclusions This study does not support a supranuclear component to the ophthalmoplegia of CPEO, although the increased latencies observed may warrant further investigation

Age-related mitochondrial DNA depletion and the impact on pancreatic beta cell function

Type 2 diabetes is characterised by an age-related decline in insulin secretion. We previously identified a 50% age-related decline in mitochondrial DNA (mtDNA) copy number in isolated human islets. The purpose of this study was to mimic this degree of mtDNA depletion in MIN6 cells to determine whether there is a direct impact on insulin secretion. Transcriptional silencing of mitochondrial transcription factor A, TFAM, decreased mtDNA levels by 40% in MIN6 cells. This level of mtDNA depletion significantly decreased mtDNA gene transcription and translation, resulting in reduced mitochondrial respiratory capacity and ATP production. Glucose-stimulated insulin secretion was impaired following partial mtDNA depletion, but was normalised following treatment with glibenclamide. This confirms that the deficit in the insulin secretory pathway precedes K+ channel closure, indicating that the impact of mtDNA depletion is at the level of mitochondrial respiration. In conclusion, partial mtDNA depletion to a degree comparable to that seen in aged human islets impaired mitochondrial function and directly decreased insulin secretion. Using our model of partial mtDNA depletion following targeted gene silencing of TFAM, we have managed to mimic the degree of mtDNA depletion observed in aged human islets, and have shown how this correlates with impaired insulin secretion. We therefore predict that the age-related mtDNA depletion in human islets is not simply a biomarker of the aging process, but will contribute to the age-related risk of type 2 diabetes

Precession of a Freely Rotating Rigid Body. Inelastic Relaxation in the Vicinity of Poles

When a solid body is freely rotating at an angular velocity ${\bf \Omega}$, the ellipsoid of constant angular momentum, in the space $\Omega_1, \Omega_2, \Omega_3$, has poles corresponding to spinning about the minimal-inertia and maximal-inertia axes. The first pole may be considered stable if we neglect the inner dissipation, but becomes unstable if the dissipation is taken into account. This happens because the bodies dissipate energy when they rotate about any axis different from principal. In the case of an oblate symmetrical body, the angular velocity describes a circular cone about the vector of (conserved) angular momentum. In the course of relaxation, the angle of this cone decreases, so that both the angular velocity and the maximal-inertia axis of the body align along the angular momentum. The generic case of an asymmetric body is far more involved. Even the symmetrical prolate body exhibits a sophisticated behaviour, because an infinitesimally small deviation of the body's shape from a rotational symmetry (i.e., a small difference between the largest and second largest moments of inertia) yields libration: the precession trajectory is not a circle but an ellipse. In this article we show that often the most effective internal dissipation takes place at twice the frequency of the body's precession. Applications to precessing asteroids, cosmic-dust alignment, and rotating satellites are discussed.Comment: 47 pages, 1 figur

Questionnaire study to gain an insight into the manufacturing and fitting process of artificial eyes in children: an ocularist perspective

Purpose To gain an insight into the manufacturing and fitting of artificial eyes in children and potential improvements to the process. Method An online qualitative survey was distributed to 39 ocularists/prosthetists in Europe and Canada. Participants were recruited through purposive sampling, specifically maximum variation sampling from the researcher’s contacts and an online search. Results The findings highlighted the current impression technique as being the most difficult yet most important part of the current process for both the ocularist and child patient. Negatively affecting obtaining a good impression, the child patients distress can be reduced by their parents by providing encouragement, reassurance, practicing the insertion and removal of the artificial eye and being matter of fact. Whilst improvements to the current process provided mixed views, the incorporation of current technology was perceived as not being able to meet the requirements to produce aesthetically pleasing artificial eyes. Conclusion The current artificial eye process can be seen as an interaction with its success being dependent on the child patient’s acceptance and adjustment which is dependent on the factors associated to the process. Investigation into the needs of the patient and whether technology can improve the process are the next steps in its advancement

ANO10 mutations cause ataxia and coenzyme Q(10) deficiency

Inherited ataxias are heterogeneous disorders affecting both children and adults, with over 40 different causative genes, making molecular genetic diagnosis challenging. Although recent advances in next-generation sequencing have significantly improved mutation detection, few treatments exist for patients with inherited ataxia. In two patients with adult-onset cerebellar ataxia and coenzyme Q10 (CoQ10) deficiency in muscle, whole exome sequencing revealed mutations in ANO10, which encodes anoctamin 10, a member of a family of putative calcium-activated chloride channels, and the causative gene for autosomal recessive spinocerebellar ataxia-10 (SCAR10). Both patients presented with slowly progressive ataxia and dysarthria leading to severe disability in the sixth decade. Epilepsy and learning difficulties were also present in one patient, while retinal degeneration and cataract were present in the other. The detection of mutations in ANO10 in our patients indicate that ANO10 defects cause secondary low CoQ10 and SCAR10 patients may benefit from CoQ10 supplementation

Exposure of Monocytic Cells to Lipopolysaccharide Induces Coordinated Endotoxin Tolerance, Mitochondrial Biogenesis, Mitophagy, and Antioxidant Defenses

In order to limit the adverse effects of excessive inflammation, anti-inflammatory responses are stimulated at an early stage of an infection, but during sepsis these can lead to deactivation of immune cells including monocytes. In addition, there is emerging evidence that the up-regulation of mitochondrial quality control mechanisms, including mitochondrial biogenesis and mitophagy, is important during the recovery from sepsis and inflammation. We aimed to describe the relationship between the compensatory immune and mitochondrial responses that are triggered following exposure to an inflammatory stimulus in human monocytic cells. Incubation with lipopolysaccharide resulted in a change in the immune phenotype of THP-1 cells consistent with the induction of endotoxin tolerance, similar to that seen in deactivated septic monocytes. After exposure to LPS there was also early evidence of oxidative stress, which resolved in association with the induction of antioxidant defenses and the stimulation of mitochondrial degradation through mitophagy. This was compensated by a parallel up-regulation of mitochondrial biogenesis that resulted in an overall increase in mitochondrial respiratory activity. These observations improve our understanding of the normal homeostatic responses that limit the adverse cellular effects of unregulated inflammation, and which may become ineffective when an infection causes sepsis

Mapping gene associations in human mitochondria using clinical disease phenotypes

Nuclear genes encode most mitochondrial proteins, and their mutations cause diverse and debilitating clinical disorders. To date, 1,200 of these mitochondrial genes have been recorded, while no standardized catalog exists of the associated clinical phenotypes. Such a catalog would be useful to develop methods to analyze human phenotypic data, to determine genotype-phenotype relations among many genes and diseases, and to support the clinical diagnosis of mitochondrial disorders. Here we establish a clinical phenotype catalog of 174 mitochondrial disease genes and study associations of diseases and genes. Phenotypic features such as clinical signs and symptoms were manually annotated from full-text medical articles and classified based on the hierarchical MeSH ontology. This classification of phenotypic features of each gene allowed for the comparison of diseases between different genes. In turn, we were then able to measure the phenotypic associations of disease genes for which we calculated a quantitative value that is based on their shared phenotypic features. The results showed that genes sharing more similar phenotypes have a stronger tendency for functional interactions, proving the usefulness of phenotype similarity values in disease gene network analysis. We then constructed a functional network of mitochondrial genes and discovered a higher connectivity for non-disease than for disease genes, and a tendency of disease genes to interact with each other. Utilizing these differences, we propose 168 candidate genes that resemble the characteristic interaction patterns of mitochondrial disease genes. Through their network associations, the candidates are further prioritized for the study of specific disorders such as optic neuropathies and Parkinson disease. Most mitochondrial disease phenotypes involve several clinical categories including neurologic, metabolic, and gastrointestinal disorders, which might indicate the effects of gene defects within the mitochondrial system. The accompanying knowledgebase (http://www.mitophenome.org/) supports the study of clinical diseases and associated genes