LONG‐TERM FOLLOW UP OF PATIENTS WITH SMALL GASTROINTESTINAL STROMAL TUMORS IN THE STOMACH USING ENDOSCOPIC ULTRASONOGRAPHY‐GUIDED FINE‐NEEDLE ASPIRATION BIOPSY

Background: Gastrointestinal stromal tumors (GIST) are one of the most common mesenchymal tumors of the gastrointestinal tract. GIST are defined by positive immunohistochemical staining for KIT or CD34 and thus are generally diagnosed after surgery. Because small GIST are rarely diagnosed before surgery, the clinical course of these small tumors is not clear. The aim of the present study was to follow changes in size and configuration of small GIST that were pathologically confirmed using endoscopic ultrasonography‐guided fine‐needle aspiration biopsy (EUS‐FNAB). Methods: Between July 1997 and December 2003, 16 tumors in 16 patients (10 men and 6 women) with an immunohistochemical diagnosis of GIST were regularly followed in our hospital. The median patient age when EUS‐FNAB was performed was 62 years (range 26–82 years) and the median follow‐up period was 4.9 years (range 0.5–9.6 years). Results: Fourteen tumors showed no remarkable changes in size and shape during follow up compared with the initial diagnosis. Two tumors enlarged: one tumor approximately doubled its diameter in 8 years and the other tumor increased from 1.8 cm at diagnosis to up to 10 cm after only 2 years. Doubling time of the latter tumor was calculated as 3.1 months. Conclusions: We conclude that EUS‐FNAB might be a good modality for final diagnosis of GIST without surgery, and that GIST without rapid growth on follow up can be endoscopically followed.     

Immunocytochemical study of ballooned neurons in cortical degeneration with neuronal achromasia.

We studied the immunocytochemical characteristics of the ballooned neurons (BN) in three patients with cortical degeneration with neuronal achromasia (CDNA) using antibodies to phosphorylated neurofilaments (PNF), tau, Alz-50, ubiquitin, beta (A4) amyloid, and glial fibrillary acidic protein. All BN exhibited intense perikaryal staining for PNF protein. Most BN and some normal-appearing neurons also stained for ubiquitin and Alz-50. The BN did not immunostain for tau protein, and none of the cases had tau-reactive neocortical neurofibrillary tangles or Pick bodies. One case had occasional senile plaques that stained for beta amyloid; no case had amyloid angiopathy. Our findings suggest that the pathophysiologic basis of the cortical degeneration in CDNA involves an alteration of neuronal cytoskeletal metabolism affecting neurofilament and possibly microtubular proteins in conjunction with activation of the ubiquitin proteolytic system.     

Evaluation of a new enzyme-linked immunosorbent assay test for rotavirus antigen in faeces

A new commercial test for the diagnosis of rotavirus gastroenteritis was assessed. With some modifications it compared favourably with electron microscopy and immunofluorescence.     

Competitive control of the self-renewing T cell repertoire

We develop a mathematical model for the self-renewing part of the T cell repertoire. Assuming that self-renewing T cells have to be stimulated by immunogenic MHC-peptide complexes presented on the surfaces of antigen-presenting cells, we derive a model of T cell growth in which competition for MHC-peptide complexes limits T cell clone sizes and regulates the total number of self-renewing T cells in the animal. We show that for a sufficient diversity and/or degree of cross-reactivity, the total T cell number hardly depends upon the diversity of the T cell repertoire or the diversity of the set of presented peptides. Conversely, for repertoires of lower diversity and/or cross-reactivity, steady-state total T cell numbers may be limited by the diversity of the T cells. This provides a possible explanation for the limited repertoire expansion in some, but not all, mouse T cell re-constitution experiments. We suggest that the competitive interactions described by our model underlie the normal T cells numbers observed in transgenic mice, germ-free mice and various knockout mice.      

TGF-beta receptors-I and -II immunoexpression in Alzheimer's disease: a comparison with aging and progressive supranuclear palsy

The transforming growth factor-betas (TGF-betas) influence cell survival, and TGF-beta2 shows increased immunoexpression in neurofibrillary tangle-bearing neurons and reactive glia in Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). We compared immunohistochemical expression of TGF-beta type I (RI) and type II (RII) receptors in eight patients with AD, eight controls and three cases of progressive supranuclear palsy. Mild intraneuronal immunoreactivity for the RI receptor was observed in all cases. Intraneuronal TGF-beta RII receptor immunoexpression was more common in all groups, and its frequency did not differ between groups. We observed increased immunoreactivity for both RI and RII subtypes in reactive glia in the AD frontal cortex (RI: U = 0.5, p = 0.002; and RII: U = 9.000, p = 0.006) and parahippocampal gyrus (RI: U = 9.500, p = 0.013; RII: U = 14.5, p = 0.05) compared to control cases. We conclude that TGF-beta RI and II immunoreactivity is increased in reactive glia in AD and progressive supranuclear palsy, and RI immunoreactivity may occasionally be increased in neurons in cases with advanced AD.