Can erosions on MRI of the sacroiliac joints be reliably detected in patients with ankylosing spondylitis? - A cross-sectional study

Introduction

Erosions of the sacroiliac joints (SIJ) on pelvic radiographs of patients with ankylosing spondylitis (AS) are an important feature of the modified New York classification criteria. However, radiographic SIJ erosions are often difficult to identify. Recent studies have shown that erosions can be detected also on magnetic resonance imaging (MRI) of the SIJ early in the disease course before they can be seen on radiography. The goals of this study were to assess the reproducibility of erosion and related features, namely, extended erosion (EE) and backfill (BF) of excavated erosion, in the SIJ using a standardized MRI methodology.

Methods

Four readers independently assessed T1-weighted and short tau inversion recovery sequence (STIR) images of the SIJ from 30 AS patients and 30 controls (15 patients with non-specific back pain and 15 healthy volunteers) ≤45 years old. Erosions, EE, and BF were recorded according to standardized definitions. Reproducibility was assessed by percentage concordance among six possible reader pairs, kappa statistics (erosion as binary variable) and intraclass correlation coefficient (ICC) (erosion as sum score) for all readers jointly.

Results

SIJ erosions were detected in all AS patients and six controls by ≥2 readers. The median number of SIJ quadrants affected by erosion recorded by four readers in 30 AS patients was 8.6 in the iliac and 2.1 in the sacral joint portion (P < 0.0001). For all 60 subjects and for all four readers, the kappa value for erosion was 0.72, 0.73 for EE, and 0.63 for BF. ICC for erosion was 0.79, 0.72 for EE, and 0.55 for BF, respectively. For comparison, the kappa and ICC values for bone marrow edema were 0.61 and 0.93, respectively.

Conclusions

Erosions can be detected on MRI to a comparable degree of reliability as bone marrow edema despite the significant heterogeneity of their appearance on MRI.     

Isocitrate dehydrogenase 1 R132C mutation occurs exclusively in microsatellite stable colorectal cancers with the CpG island methylator phenotype

The CpG Island Methylator Phenotype (CIMP) is fundamental to an important subset of colorectal cancer; however, its cause is unknown. CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. The entire coding sequence was examined in 81 CIMP-positive colorectal cancers. Forty-seven cancers varying by CIMP-status and IDH1 mutation status were examined using Illumina 450K DNA methylation microarrays. The R132C IDH1 mutation was detected in 4/166 cancers. All IDH1 mutations were in CIMP cancers that were BRAF mutant and microsatellite stable (4/45, 8.9%). Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. This study provides a precedent that a single gene mutation may cause CIMP in colorectal cancer, and that this will be associated with a specific epigenetic signature and clinicopathological features.     

DiSUMO-LIKE Interacts with RNA-Binding Proteins and Affects Cell-Cycle Progression during Maize Embryogenesis

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Production and characterization of polyclonal and monoclonal antibodies against Aflatoxin B1 oxime-BSA in an enzyme-linked immunosorbent assay

From a single aflatoxin B₁ oxime — bovine serum albumin conjugate, polyclonal and monoclonal antibody preparations were produced. The four rabbit polyclonal antisera were specific for aflatoxin Bi in a microtitration plate enzyme — linked immunosorbent assay. The monoclonal antibodies showed a wide range of differing specificities, recognizing, for example, aflatoxins B₁, B₂, G₁ and G₂; B₁ and B₂; B₁ and G₁; and G₁ alone. No antibody preparations reacted with aflatoxin M₁. The significance of these results to the strategy of anti-aflatoxin antibody production for use in quantitative enzyme immunoassays is discussed.     

Morphologie, Ökologie und Zonierung von Korallenriffen bei Aqaba, (Golf von Aqaba,Rotes Meer)

The coral reefs of the Gulf of Aqaba are among the most northern ones of the world. This study, the first concerning the east coast of this topographically and hydrographically peculiar sea, considers relationships of biophysiographical and structural reef zones to fundamental abiotic environmental factors. An introduction to paleogeography, geology, petrography, topography, climate and hydrography is followed by terminological definitions used to describe the different reef areas. The investigations were carried out on two transects crossing fringing reefs of different shape. Each transect was 20 m wide and run from the shore over nearly 200 m to the fore reef in about 30 m depth. One reef, a “coastal-fringing reef”, represents an unaltered straight reef flat from shore to the reef edge 60 m away; two large pinnacles reach the surface some 125 m off the shore. The other reef, a “lagoon-fringing reef”, is divided into a 100 m wide lagoon of 0.5–2.3 m depth and a reef crest separated from the former by a rear reef. The reef platform of the lagoon-fringing reef is cut by a system of channels and tunnels; the reef edge is about 135 m off shore. Such water depth, substrate, temperature, illumination and water movement were recorded, about 200 common or dominant species (plants and animals) were collected, their distribution plotted and, together with other data and structural items, charted. Indicator species characterize the biophysiographical zones. Their variation as well as that of the structural and substrate zones depend on different zones of water movement. This basic factor also controls other ecological parameters such as food and oxygen supply as well as temperature and salinity gradients between fore reef and shore. From this point of view the ecological requirements of some indicator and other species and conversely the ecological settings of different reef areas are discussed. The different shapes of both reefs are explained on the basis of a “reef development cycle” — a hypothesis applicable to fringing reefs at unchanging sea level and based on the fact that only a small surf-influenced area of “living reef” is able to compensate for reef destruction: While a young coastal fringing reef is growing outwards, its back reef is gradually altered to a reef lagoon by erosion. After stillstand of seaward expansion the reef crest, too, is cut by a channel system eroded by rip currents. This stage is represented by the lagoon-fringing reef. Isolated pinnacles remain as remnants of the former reef crest; young coastal-fringing reefs develop from the shore. This stage is examplified by the first reef studied. Extension, growth intensity, dominant frame building corals, and the number of species of the Aqaba reefs are compared with those of Eilat and with reefs of the middle Red Sea, South India, Southwest-Pacific and Jamaica.     

Unbuffered osmium staining of cell organelles: alterations induced by cell injury

We have studied the localization of osmium reduction products to investigate the functional state of organelles as well as organelle interrelationships during cell injury. In normal hepatocytes osmium deposits of variable intensity are seen in nuclear envelope, endoplasmic reticulum. Golgi cisternae and vesicles and lysosomes. Buffering of osmium with s- collidine (pH 7.4) prevents the deposition of osmium. Reversible (30 min) and irreversible (60 min) ischemia without reflow causes no change in the pattern of osmium deposition. Irreversible ischemia followed by reflow causes decreased staining of endoplasmic reticulum (ER) and redistribution of the osmium deposits through the cytoplasm. Reversibly injured pancreatic acinar cells in cultured explants manifest a similar loss of osmium staining in the endoplasmic reticulum cisternae. The administration of antimicrotubule drugs induces an accentuation of osmium staining in localized cisternal elements of hepatocytes. These heavily stained cisternae appear to give rise to the bounding membranes of drug-induced autophagic vacuoles. Cytoplasmic organelles sequestered inside the autophagic vacuoles acquire intense staining when they begin to undergo degradation. In homogenized liver tissue all the subcellular organelles show osmium deposits. The deposits are preferentially localized along the organelle membranes. In particular the dense deposits in the ER lumen are not seen in the subcellular fractions. Phospholipase A2 (3 units/mg protein) enhances the deposition of osmium in the lumen of microsomal vesicles, whereas the presence of detergent has no such effect. Addition of EDTA to the homogenizing medium enhances the ultrastructural preservation of the subcellular fractions but has little effect on the deposition of osmium. OsO4 deposition occurs at acid pH and the intensity and pattern of the stain can be modified in vivo and in vitro. Osmium tetroxide deposition is induced at sites of membrane transformation (autophagic vacuoles) and degradation (lysosomes). Calcium influx and phospholipase activation (ischemia, tissue homogenization, phospholipase addition) enhance osmium deposition and/or influence the localization of the staining pattern.     

Über die Induktion neuer Oscularrohre bieEphydatia fluviatilis

Ohne ZusammenfassungHerrn Prof. Dr. W. E.Ankel zum 65. Geburtstag am 7. August 1962 gewidmet.Habilitationsschrift der Naturwissenschaftlich-Philosophischen Fakultät der Justus Liebig-Universität Gießen.Ausgeführt mit Unterstützung der Deutschen Forschungsgemeinschaft, der ich sehr zu Dank verpflichtet bin.     

Meta level concept versus classic reflex concept for the control of posture and movement

Postural reflexes are replaced soon after birth by automatic reactions that allow for volition and cognition. It is still an enigma how this change in postural control is achieved. We suggest that the change involves the formation of a sensory processing level (meta level) that becomes interleaved in between the tight sensor-actuator coupling of the classic reflexes. We assume that the brain applies at this level intersensory interactions to reconstruct the physical stimuli which are causing the physiological stimuli and sensory signals. The thus derived estimates of the physical stimuli are then used as feedback signals in the posture control system. We present this concept on the background of the classic reflex concept and earlier attempts in the literature to overcome it. The earlier attempts were often motivated by the question how the brain prevents voluntary movements from being hampered by reflexive stabilisation of posture (so-called posture-movement problem). We compare our new concept with the classic reflex concept in a theoretical approach, by implementing both concepts into simple postural control models. In simulations of the two models we superimpose external perturbations (the physical stimuli) and a voluntary body lean movement. We show that it is possible to achieve successful stimulus compensation and unperturbed lean movement with both, the model derived from the new concept and the one of the classic reflex concept. With both approaches, the posture-movement problem does not arise. Based on preliminary considerations that include experimental findings from the literature, however, we conclude that the new concept provides more explanatory power than the classic reflex concept.