273 research outputs found
Clinicopathologic significance of sialyl Le xexpression in advanced gastric carcinoma
Sialyl Lewis xantigen (SLX) is a carbohydrate antigen that serves as a ligand for selectin, an adhesion molecule expressed on vascular endothelial cells. The expression of SLX in 245 patients with advanced gastric carcinoma was examined immunohistochemically, and its clinicopathologic significance was analysed. We classified the patients with advanced gastric carcinoma into 91 with differentiated type and 154 with undifferentiated type. SLX expressed in 135 of 245 patients (55%), comprising 68 (75%) patients with differentiated carcinoma and 67 (44%) with undifferentiated carcinoma. The positive rate for SLX expression was significantly higher among patients with differentiated carcinoma than among those in undifferentiated carcinoma (P < 0.0001). With differentiated carcinoma, the incidence of lymph node metastasis, advanced tumour stage (stage III and IV) and liver recurrence was significantly higher in SLX-positive patients than in SLX-negative ones (P < .0001, P = 0.0065 and P = 0.028, respectively). Moreover, the prognoses were better in patients with SLX-negative tumours than in those with SLX-positive tumours (P = 0.019). With undifferentiated carcinoma, there were no significant correlations between SLX expression and any clinicopathological features or prognoses. The clinicopathologic significance of SLX expression in gastric carcinoma patients depends on histologic type. SLX expression may be of great relevance in predicting liver metastases in patients with differentiated carcinoma. © 2000 Cancer Research Campaign http://www.bjcancer.co
ASCA and XMM-Newton Observations of A2029
The X-ray data of A2029 obtained with XMM-Newton show no evidence of an
embedded AGN in the central region of this cluster, which was suggested from
the analysis of restored ASCA image data, although some hot spots are seen
within or around the central cD galaxy. The absence of AGN at the cluster
center is consistentent with the result of Chandra observations. Radial
profiles of the iron abundance and the 2D (surface) temperature obtained from
the XMM-Newton data are in good agreement with the Chandra data as a whole.Comment: 8 pages, 13 figures, accepted for publication in Advances in Space
Researc
Cell Migration in the Immune System: the Evolving Inter-Related Roles of Adhesion Molecules and Proteinases
Leukocyte extravasation into perivascular tissue during inflammation and lymphocyte homing
to lymphoid organs involve transient adhesion to the vessel endothelium, followed by transmigration
through the endothelial cell (EC) layer and establishment of residency at the tissue site
for a period of time. In these processes, leukocytes undergo multiple attachments to, and detachments
from, the vessel-lining endothelial cells, prior to transendothelial cell migration. Transmigrating
leukocytes must traverse a subendothelial basement membrane en route to perivascular
tissues and utilize enzymes known as matrix metalloproteinases to make selective clips in the
extracellular matrix components of the basement membrane. This review will focus on the evidence
for a link between adhesion of leukocytes to endothelial cells, the induction of matrix
metalloproteinases mediated by engagement of adhesion receptors on leukocytes, and the ability
to utilize these matrix metalloproteinases to facilitate leukocyte invasion of tissues. Leukocytes
with invasive phenotypes express high levels of MMPs, and expression of MMPs
enhances the migratory and invasive properties of these cells. Furthermore, MMPs may be used
by lymphocytes to proteolytically cleave molecules such as adhesion receptors and membrane
bound cytokines, increasing their efficiency in the immune response. Engagement of leukocyte
adhesion receptors may modulate adhesive (modulation of integrin affinities and expression),
synthetic (proteinase induction and activation), and surface organization (clustering of proteolyric
complexes) behaviors of invasive leukocytes. Elucidation of these pathways will lead to
better understanding of controlling mechanisms in order to develop rational therapeutic
approaches in the areas of inflammation and autoimmunity
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Cannabidivarin is anticonvulsant in mouse and rat in vitro and in seizure models
Summary
Background and purpose: Phytocannabinoids in Cannabis sativa have diverse
pharmacological targets extending beyond cannabinoid receptors and several exert notable
anticonvulsant effects. For the first time, we investigated the anticonvulsant profile of the
phytocannabinoid cannabidivarin (CBDV) in vitro and in in vivo seizure models.
Experimental approach: The effect of CBDV (1-100μM) on epileptiform local field
potentials (LFPs) induced in rat hippocampal brain slices by 4-AP application or Mg2+-free
conditions was assessed by in vitro multi-electrode array recordings. Additionally, the
anticonvulsant profile of CBDV (50-200 mg kg-1) in vivo was investigated in four rodent
seizure models: maximal electroshock (mES) and audiogenic seizures in mice, and
pentylenetetrazole (PTZ) and pilocarpine-induced seizures in rat. CBDV effects in
combination with commonly-used antiepileptic drugs were investigated in rat seizures.
Finally, the motor side effect profile of CBDV was investigated using static beam and gripstrength
assays.
Key results: CDBV significantly attenuated status epilepticus-like epileptiform LFPs
induced by 4-AP and Mg2+-free conditions. CBDV had significant anticonvulsant effects in
mES (≥100 mg kg-1), audiogenic (≥50 mg kg-1) and PTZ-induced seizures (≥100 mg kg-1).
CBDV alone had no effect against pilocarpine-induced seizures, but significantly attenuated
these seizures when administered with valproate or phenobarbital at 200 mg kg-1 CBDV.
CBDV had no effect on motor function.
Conclusions and Implications: These results indicate that CBDV is an effective
anticonvulsant across a broad range of seizure models, does not significantly affect normal
motor function and therefore merits further investigation in chronic epilepsy models to justify
human trials
Homeomorphic Embedding for Online Termination of Symbolic Methods
Well-quasi orders in general, and homeomorphic embedding in particular, have gained popularity to ensure the termination of techniques for program analysis, specialisation, transformation, and verification. In this paper we survey and discuss this use of homeomorphic embedding and clarify the advantages of such an approach over one using well-founded orders. We also discuss various extensions of the homeomorphic embedding relation. We conclude with a study of homeomorphic embedding in the context of metaprogramming, presenting some new (positive and negative) results and open problems
A Symmetric Approach to Compilation and Decompilation
Just as specializing a source interpreter can achieve compilation from a source language to a target language, we observe that specializing a target interpreter can achieve compilation from the target language to the source language. In both cases, the key issue is the choice of whether to perform an evaluation or to emit code that represents this evaluation. We substantiate this observation by specializing two source interpreters and two target interpreters. We first consider a source language of arithmetic expressions and a target language for a stack machine, and then the lambda-calculus and the SECD-machine language. In each case, we prove that the target-to-source compiler is a left inverse of the source-to-target compiler, i.e., it is a decompiler. In the context of partial evaluation, compilation by source-interpreter specialization is classically referred to as a Futamura projection. By symmetry, it seems logical to refer to decompilation by target-interpreter specialization as a Futamura embedding
Resistance to autosomal dominant Alzheimer's disease in an APOE3 Christchurch homozygote: a case report.
We identified a PSEN1 (presenilin 1) mutation carrier from the world's largest autosomal dominant Alzheimer's disease kindred, who did not develop mild cognitive impairment until her seventies, three decades after the expected age of clinical onset. The individual had two copies of the APOE3 Christchurch (R136S) mutation, unusually high brain amyloid levels and limited tau and neurodegenerative measurements. Our findings have implications for the role of APOE in the pathogenesis, treatment and prevention of Alzheimer's disease
Mieap, a p53-Inducible Protein, Controls Mitochondrial Quality by Repairing or Eliminating Unhealthy Mitochondria
Maintenance of healthy mitochondria prevents aging, cancer, and a variety of degenerative diseases that are due to the result of defective mitochondrial quality control (MQC). Recently, we discovered a novel mechanism for MQC, in which Mieap induces intramitochondrial lysosome-like organella that plays a critical role in the elimination of oxidized mitochondrial proteins (designated MALM for Mieap-induced accumulation of lysosome-like organelles within mitochondria). However, a large part of the mechanisms for MQC remains unknown. Here, we report additional mechanisms for Mieap-regulated MQC. Reactive oxygen species (ROS) scavengers completely inhibited MALM. A mitochondrial outer membrane protein NIX interacted with Mieap in a ROS-dependent manner via the BH3 domain of NIX and the coiled-coil domain of Mieap. Deficiency of NIX also completely impaired MALM. When MALM was inhibited, Mieap induced vacuole-like structures (designated as MIV for Mieap-induced vacuole), which engulfed and degraded the unhealthy mitochondria by accumulating lysosomes. The inactivation of p53 severely impaired both MALM and MIV generation, leading to accumulation of unhealthy mitochondria. These results suggest that (1) mitochondrial ROS and NIX are essential factors for MALM, (2) MIV is a novel mechanism for lysosomal degradation of mitochondria, and (3) the p53-Mieap pathway plays a pivotal role in MQC by repairing or eliminating unhealthy mitochondria via MALM or MIV generation, respectively
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