The best temperature range to acquire reliable thermal infrared spectra from orbit.

Solar System bodies undergo to daily and periodical variations of temperature that mainly depend on their closeness to the Sun. It is known that mineral expansion and contraction due to such variations modify the thermal infrared spectra acquired on solid surfaces. Therefore, it becomes crucial to know the best temperature range at which the acquisition itself should be carried out to get reliable information on the mineralogy of such bodies. Here we provide the thermal expansion of olivine between 20 and 298 K determined by X-ray diffraction. Our data reveal the non-linear behaviour of silicates that undergo to low temperatures, where volume variations appear positively correlated with temperatures. Subtle bond-length variations occurring at low temperatures are then expected to minimally affect vibrational absorption positions. We suggest that thermal infrared spectra of those Solar-System surfaces that are not exceeding 300 K provide reliable information about not only the silicate mineral identification but also on their chemical composition, regardless of the instantaneous temperature.

Impact shock origin of diamonds in ureilite meteorites.

The origin of diamonds in ureilite meteorites is a timely topic in planetary geology as recent studies have proposed their formation at static pressures >20 GPa in a large planetary body, like diamonds formed deep within Earth's mantle. We investigated fragments of three diamond-bearing ureilites (two from the Almahata Sitta polymict ureilite and one from the NWA 7983 main group ureilite). In NWA 7983 we found an intimate association of large monocrystalline diamonds (up to at least 100 µm), nanodiamonds, nanographite, and nanometric grains of metallic iron, cohenite, troilite, and likely schreibersite. The diamonds show a striking texture pseudomorphing inferred original graphite laths. The silicates in NWA 7983 record a high degree of shock metamorphism. The coexistence of large monocrystalline diamonds and nanodiamonds in a highly shocked ureilite can be explained by catalyzed transformation from graphite during an impact shock event characterized by peak pressures possibly as low as 15 GPa for relatively long duration (on the order of 4 to 5 s). The formation of "large" (as opposed to nano) diamond crystals could have been enhanced by the catalytic effect of metallic Fe-Ni-C liquid coexisting with graphite during this shock event. We found no evidence that formation of micrometer(s)-sized diamonds or associated Fe-S-P phases in ureilites require high static pressures and long growth times, which makes it unlikely that any of the diamonds in ureilites formed in bodies as large as Mars or Mercury.

Graphite-Based Geothermometry on Almahata Sitta Ureilitic Meteorites.

The thermal history of carbon phases, including graphite and diamond, in the ureilite meteorites has implications for the formation, igneous evolution, and impact disruption of their parent body early in the history of the Solar System. Geothermometry data were obtained by micro-Raman spectroscopy on graphite in Almahata Sitta (AhS) ureilites AhS 72, AhS 209b and AhS A135A from the University of Khartoum collection. In these samples, graphite shows G-band peak centers between 1578 and 1585 cm-1 and the full width at half maximum values correspond to a crystallization temperature of 1266 °C for graphite for AhS 209b, 1242 °C for AhS 72, and 1332 °C for AhS A135A. Recent work on AhS 72 and AhS 209b has shown graphite associated with nanodiamonds and argued that this assemblage formed due to an impact-event. Our samples show disordered graphite with a crystalline domain size ranging between about 70 and 140 nm. The nanometric grain-size of the recrystallized graphite indicates that it records a shock event and thus argues that the temperatures we obtained are related to such an event, rather than the primary igneous processing of the ureilite parent body.

Structure refinement using precession electron diffraction tomography and dynamical diffraction: tests on experimental data.

The recently published method for the structure refinement from three-dimensional precession electron diffraction data using dynamical diffraction theory [Palatinus et al. (2015). Acta Cryst. A71, 235-244] has been applied to a set of experimental data sets from five different samples - Ni2Si, PrVO3, kaolinite, orthopyroxene and mayenite. The data were measured on different instruments and with variable precession angles. For each sample a reliable reference structure was available. A large series of tests revealed that the method provides structure models with an average error in atomic positions typically between 0.01 and 0.02 Å. The obtained structure models are significantly more accurate than models obtained by refinement using kinematical approximation for the calculation of model intensities. The method also allows a reliable determination of site occupancies and determination of absolute structure. Based on the extensive tests, an optimal set of the parameters for the method is proposed.

Clinical guidelines and definitions of autoinflammatory diseases: contrasts and comparisons with autoimmunity-a comprehensive review.

Autoinflammatory diseases (AIDs) and autoimmune diseases (ADs) are characterized by an aberrant chronic activation of the immune system which causes tissue inflammation and damage in genetically predisposed individuals. Pathogenetic mechanisms underlying this damage differ between these two types of diseases; in AIDs, the innate immune system is directly responsible for tissue inflammation, while in ADs it works by activating the adaptive immune system, which becomes the main effector of the inflammatory process. Despite the fact that AIDs have only been recently defined, they are older than ADs. The innate immune system is found in plants and animals, and it developed earlier than the adaptive immune system, which first appeared in jawed vertebrates. According to genetic background and clinical, serological, and radiological findings, AIDs and ADs might be considered as a single spectrum of disorders, with a wide range of manifestations. Indeed, autoinflammatory-like diseases have been reported in simple organisms such as Drosophila melanogaster and Caenorhabditis elegans. We analyzed here the main pathogenetic and clinical features of these two groups of diseases mostly dealing with their similarities and differences.

Activation of the immune system and coronary artery disease: the role of anti-endothelial cell antibodies.

On the basis of the role of immuno-mediated inflammation in atherosclerosis we investigated, (1) the prevalence of anti-endothelial cell antibodies (AECA) in ischaemic heart disease (IHD); (2) if beta2-glycoprotein I (beta2-GPI) was the target antigen of AECA; (3) the relationship between AECA, tissue factor (TF) and tissue factor pathway inhibitor (TFPI). In 93 consecutive IHD patients undergoing percutaneous transluminal coronary angioplasty (PTCA) and 105 controls AECA were detected by ELISA on human umbilical vein endothelial cells (HUVEC). AECA positive sera were evaluated for anti-beta2-GPI antibodies by ELISA. TF and TFPI plasma levels were assessed by ELISA. Twelve of 93 (12.9%) IHD patients and only one of 105 controls (0.95%) were AECA positive. The prevalence of AECA was higher in unstable angina (UA) than in effort angina (EA) (P=0.01). Three of 12 AECA positive sera resulted positive for anti-beta2-GPI and showed a marked decrease in EC-binding when tested on HUVEC cultured in serum-free medium. The binding was restored by the addition of beta2-GPI. TF and TFPI levels were similar in AECA positive and AECA negative patients. The rate of angiographically documented clinical recurrences was 66.7% in the AECA positive and 14.8% in the AECA negative group (P=0.0004) with a significant relationship between restenosis and AECA (P<0.0001), unchanged by the inclusion of cardiovascular risk factors in the regression model. Our results suggest a 'role' for AECA in the immune-mediated inflammation in UA beta2-GPI is not the only AECA target antigen. AECA are not responsible for high TF and TFPI levels. The high rate of clinical recurrences after PTCA, confirmed by angiography, in AECA positive patients is in line with such a role and suggests further large-scale 'ad hoc' studies.

High prevalence of anti-beta2 glycoprotein I antibodies in patients with ischemic heart disease.

Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. As concerns the relationship between anti-beta2 glycoprotein I antibodies (anti-beta2-GPI) and ischemic heart disease (IHD), it was investigated in only one coronary primary prevention study. We investigated the prevalence of anti-beta2-GPI in a well characterized group of patients with different clinical manifestation of IHD. Sera from 37 patients (mean age 62.7 +/- 9.9) with IHD (20 with unstable angina-UA and 17 with effort angina-EA) and from 40 healthy subjects, matched for age and sex, were tested for the presence of IgG and IgM anti-beta2-GPI using an ELISA technique. Eleven/37 patients (29.7%) resulted positive for anti-beta2-GPI. A positivity for IgG anti-beta2-GPI was found in 10 patients, 1 patient was positive for IgM and 1 for both isotypes. The prevalence of anti-beta2-GPI in the control group resulted significantly lower (2.5%; p < 0.005) than in patients with IHD. Positivity for anti-beta2-GPI was found in 9/20 (45%) patients with UA and only in 2/17 patients (11.8%) with EA (p = 0.0365). IgG anti-beta2-GPI levels (median 7.7U/ml, range 2.6-24.1) were significantly higher in patients with UA compared to patients with EA (median 4.6 U/ml, range 2.3-11.5; p = 0.02) and controls (median 3.15 U/ml, range 2.3-9.0; p < 0.0001); also IgM levels resulted higher in patients with unstable angina. A positivity for anti-beta2-GPI was observed in 4/13 patients (30.8%) with a previous myocardial infarction (MI) and in 7/24 (29.2%) patients without a previous MI. Our findings suggest that anti-beta2-GPI could represent an expression of the T-cell activation detectable in patients with unstable angina. The lack of a significant difference in the prevalence of these antibodies in patients with or without a previous MI suggests that anti-beta2-GPI are not induced by tissue necrosis.

Some anti-thyroperoxidase antibodies positive sera give a pANCA pattern on ethanol-fixed human neutrophils: cross-reactivity or false positives?

Fifty-six sera from patients with autoimmune thyroiditis and 33 sera from patients with MPO-ANCA were examined in order to ascertain whether a cross reactivity between MPO-ANCA and anti-thyroperoxidase (aTPO) was present. Sera from 20 healthy donors aTPO and aMPO negative were used as control. About 95% of heat inactivated sera from patients with autoimmune thyroiditis and from controls gave positive results (atypical pANCA pattern) on ethanol-fixed neutrophils. The prevalence of positive results was significantly lower when unheated aTPO positive sera were used (17.8%). On the other hand, only 9% of sera with MPO-ANCA were positive on cryostatic sections of human thyroid. Indirect immunofluorescence tests (IF) on human neutrophils with MPO defect were negative with sera from patients with MPO-ANCA, but uninactivated sera with aTPO and positive for pANCA on normal neutrophils showed a very high prevalence of positive results (90%). According to our data only few sera positive for aTPO recognize "normal" MPO, but the majority of sera from patients with autoimmune thyroiditis and positive for pANCA on normal neutrophils recognize also an "abnormal" MPO. On the other hand MPO-ANCA usually recognize epitopes presently only on the normal enzyme, a small proportion of these autoantibodies can react with TPO. Heat inactivated sera give false positive results for pANCA on ethanol fixed human neutrophils.

Antiphospholipid antibodies (aPL) increase the potential monocyte procoagulant activity in patients with systemic lupus erythematosus.

Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) are frequently detected in sera from patients affected by systemic lupus erythematosus (SLE). However, the role of antiphospholipid antibodies (aPL) in thrombus formation has not been defined as yet. Twenty-two patients affected by SLE, all fulfilling the 1982 ARA revised criteria, and twenty healthy subjects were investigated for the presence of LA, aCL and other aPLs. Monocyte procoagulant activity-PCA (Tissue Factor production) was evaluated by one stage plasma recalcification time. In all patients the plasma levels of F1 + 2 and of plasminogen activator inhibitor (PAI) were also determined. Monocyte PCA was significantly higher in SLE patients with LA and/or aCL in comparison to SLE patients without LA and/or aCL (p < 0.01) and to controls (p < 0.05). However, no connection was observed between PCA expression by mononuclear cells and LA or aCL levels. No differences in F1 + 2 and PAI plasma levels were found between SLE patients with or without aPL and controls. In our SLE patients LA and/or aCL positivity appears strictly related to an increased monocyte activation that could play an important role in the occurrence of thrombotic events.

Immunological abnormalities in a group of patients with limited cutaneous systemic sclerosis and prominent vascular disease.

Antinuclear antibodies, circulating immune complexes, rheumatoid factors and anticardiolipin antibodies were detected in the sera of 17 patients affected by the limited cutaneous subset of systemic sclerosis and marked clinical evidence of ischaemic cutaneous lesions (fingertip ulcerations). This study was designed to evaluate the possible role of anticardiolipin (aCL) antibodies and other immunological disorders in the endothelial damage characteristic of the disease. ACL antibodies were found in 41% of the patients. With the exception of a significant connection with positive rheumatoid factor tests (RIA), no notable associations between anticardiolipin antibodies and antinuclear antibodies, circulating immune complexes (CIC), and other serological abnormalities were found. ACL antibodies did not significantly correlate with the presence of vascular lesions in our patients. However, a role of these antibodies in endothelial damage cannot be excluded, possibly in association with other serum factors such as immune complexes and antinuclear antibodies. A positive connection between the incidence of CIC and the severity of lung perfusion impairment was observed, and the previously reported relationship between anticentromere antibodies and calcinosis was indirectly confirmed.