Multi-phase volcanic resurfacing at Loki Patera on Io.

The Jovian moon Io hosts the most powerful persistently active volcano in the Solar System, Loki Patera. The interior of this volcanic, caldera-like feature is composed of a warm, dark floor covering 21,500 square kilometres surrounding a much cooler central 'island'. The temperature gradient seen across areas of the patera indicates a systematic resurfacing process, which has been seen to occur typically every one to three years since the 1980s. Analysis of past data has indicated that the resurfacing progressed around the patera in an anti-clockwise direction at a rate of one to two kilometres per day, and that it is caused either by episodic eruptions that emplace voluminous lava flows or by a cyclically overturning lava lake contained within the patera. However, spacecraft and telescope observations have been unable to map the emission from the entire patera floor at sufficient spatial resolution to establish the physical processes at play. Here we report temperature and lava cooling age maps of the entire patera floor at a spatial sampling of about two kilometres, derived from ground-based interferometric imaging of thermal emission from Loki Patera obtained on 8 March 2015 ut as the limb of Europa occulted Io. Our results indicate that Loki Patera is resurfaced by a multi-phase process in which two waves propagate and converge around the central island. The different velocities and start times of the waves indicate a non-uniformity in the lava gas content and/or crust bulk density across the patera.

Clinical and laboratory findings in referrals for mitochondrial DNA analysis.

BACKGROUND: Increasingly, mutations of mitochondrial DNA (mtDNA) are being considered when investigating the aetiology of neurological diseases in childhood. However, they are often difficult to predict clinically. METHOD: Mitochondrial DNA analysis was carried out on 190 children from 1992 to 1996. Most patients were screened for large scale rearrangements and point mutations at nucleotide positions 3243, 3271, 8344, and 8993. RESULTS: Mutations were found in only 15 patients (7.9%) and were either large scale rearrangements (seven patients) or point mutations at nucleotide position 3243 (eight patients). Other point mutations were screened for depending on the clinical picture. The age of symptom onset was significantly older in children with an mtDNA mutation (mean 7.0 years) compared with children without a mutation (mean 2.8 years). Neither Leigh's syndrome (28 cases) nor severe infantile lactic acidosis (12 cases) was associated with mtDNA mutation. Only three clinical features were significantly associated with an mtDNA mutation: progressive external ophthalmoplegia, myopathy, and pigmentary retinopathy. Family history was valuable: the point mutation at nucleotide 3243 (but not the large scale rearrangements) was associated with maternal inheritance; and consanguinity was not associated with mtDNA mutations. The only investigation that provided specific evidence of an underlying mtDNA mutation was histochemical staining of muscle biopsy specimens. The large scale mutations associated with Kearns-Sayre syndrome and progressive external ophthalmoplegia were found in DNA from muscle only, not leucocyte DNA; whereas point mutations were found in leucocyte DNA. CONCLUSIONS: Even among children seen at a neurogenetic referral centre, mtDNA mutations were very uncommon. Muscle biopsy was the only investigation to provide evidence of mtDNA abnormality.

Variations in the 3 micron spectrum across the Orion Bar: polycyclic aromatic hydrocarbons and related molecules.

Long-slit spectra across the Orion Bar reveal significant differences in the spatial behavior of the components of the 3 microns polycyclic aromatic hydrocarbon (PAH) spectrum. The strong PAH band at 3.29 microns generally decreases exponentially with distance from the ionization front into the molecular cloud (scale height approximately 12"), although excesses appear approximately 10" and 20" behind the ionization front, close to layers of H2 and CO emission, respectively. The 3.40 microns PAH feature separates into two components with very different spatial distributions. The main component (at 3.395 microns), along with the 3.51 microns band and the PAH plateau (3.3-3.6 microns), shows excess emission approximately 10" and approximately 20" behind the ionization front, stronger than the excesses in the 3.29 microns band. The extra component of the 3.40 microns band, which peaks at approximately 3.405 microns, has a spatial distribution very similar to the H2 emission. Aromatic C-H stretches in PAHs most likely produce the 3.29 microns feature. Aliphatic C-H stretches in either attached methyl side-groups or superhydrogenated PAHs, or perhaps both, could produce the complicated spectral and spatial structure at 3.40 microns.

Deficiency of respiratory chain complex I is a common cause of Leigh disease.

We reviewed the clinical features and etiologies of Leigh disease in 66 patients from 60 pedigrees. Biochemical or molecular defects were identified in 50% of all pedigrees, and in 74% of the 19 pedigrees with pathologically proved Leigh disease. Isolated deficiency of respiratory chain complex I was found in 7 patients, though the complex was only assayed in 25 patients, making this the second most common biochemical abnormality after complex IV deficiency. Mutations at residue 8993 of mitochondrial DNA were found in only 2 patients. No correlation was found between the clinical features and etiologies. No defects were identified in the 8 patients with normal lactate concentrations in the cerebrospinal fluid.

Pearson's marrow/pancreas syndrome: haematological features associated with deletion and duplication of mitochondrial DNA.

Pearson's marrow/pancreas syndrome (PS) is a rare, often fatal, disorder of infancy that is characterized by impaired bone marrow, exocrine pancreatic, hepatic and renal function. Large-scale rearrangements of mitochondrial DNA (mtDNA) are present in blood. We report a patient with PS who has predominantly impaired haemopoiesis manifesting as sideroblastic anaemia, vacuolization of bone marrow precursors, and neutropenia. 77% of bone marrow mtDNA was rearranged (64% deleted an 13% duplicated). We suggest that rearrangements of mtDNA should be sought in all infants presenting with sideroblastic anaemia.

Binding of Ca2+ to calmodulin and its tryptic fragments: theory and experiment.

The Ca(2+)-binding constant of the protein calmodulin is determined experimentally at different pH and varying salt concentration. By comparison to statistical mechanical simulation results, it is shown that the shift in binding constant upon addition of salt is almost quantitatively due to electrostatic interactions. Specific interactions as well as effects due to structural rearrangements of the protein seem to be less important, indicating a structurally rather conserved protein upon addition of salt and changes in pH. The tryptic fragments of calmodulin also bind calcium with high affinity, and the electrostatic effects seem likewise to dominate the binding constant shifts in these systems. It is also shown that the chemical potential of free calcium ions, which is normally dominated by the salt, is strongly influenced by the highly charged calmodulin molecule. This complicates a detailed comparison at low salt concentration, since it requires very accurate information on the salt and protein concentrations, which normally are not available.

Electrostatic interactions in protein solution--a comparison between Poisson-Boltzmann and Monte Carlo calculations.

The accuracy of the Poisson-Boltzmann (PB) approximation and its linearized version is investigated by comparison to results obtained from Monte Carlo simulations. The dependence of the calcium binding constant of the protein calbindin as a function of salt concentration and mutation is used as a test case. The protein is modeled as a collection of charged and neutral spheres immersed in the electrolyte solution. The PB equation is solved using a finite difference technique on a grid in a spherical polar coordinate system, which is the preferred choice for a globular protein like calbindin. Both MC and PB give quantitative agreement with experimental results. The linearized PB equation is almost as accurate, but it becomes less reliable in systems with divalent ions. However, the linearized PB equation fails to describe the concentration profiles for cations and anions outside the protein even in a 1:1 salt solution.

Ion-binding properties of calbindin D9k: a Monte Carlo simulation study.

Monte Carlo simulations are used to calculate the binding constant of two Ca2+ ions to the protein bovine calbindin D9k. The change in binding constant with respect to mutation of charged amino acids, presence of various electrolytes, protein concentration, solution pH, and competitive binding of monovalent ions is investigated. Each of these factors may have a large influence on the binding constant. The simulations are performed in a dielectric continuum model, the so-called primitive model of electrolyte theory, with a fixed protein structure and a uniform dielectric permittivity. The calculated binding constants are in excellent agreement with experimental data and describe changes in the binding constant over six orders of magnitude.