<Emphasis Type="Italic">GPC5</Emphasis> is a possible target for the 13q31-q32 amplification detected in lymphoma cell lines

Comparative genomic hybridization (CGH) analyses have detected gains of copy number on 13q, especially at 13q31-q32, in cell lines and primary cases of various types of lymphoma. Since amplification of chromosomal DNA is one of the mechanisms that can activate tumor-associated genes, and because 13q amplification had been reported in various other types of tumors as well, we attempted to define by fluorescence in situ hybridization (FISH) a common region at 13q31-q32 in which to explore genes that might be targets for the amplification events. Although the commonly amplified region we defined was relatively large (approximately 4 Mb), only one true gene, GPC5, was found there. GPC5 was over-expressed in lymphoma cell lines that had shown amplification, in comparison with those that had not. Our findings suggest that GPC5 is a likely target for amplification, and that over-expression of this gene may contribute to development and/or progression of lymphomas and other tumors.     

Osteoclast-type giant cell tumor of the endometrium. An immunohistochemical study

We present a rare case of a 55 year old female with an osteoclast-type giant cell tumor of the endometrium associated with leiomyoma and adenomyosis. Multinucleated giant cells and mononuclear stromal cells reacted with vimentin and alpha-1-antichymotrypsin (AACT) using the immunoperoxidase method. Epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), and keratin exhibited negative immunoreaction in these tumor cells. Our immunohistochemical results do not support the epithelial origin of an osteoclast-type giant cell tumor and mesenchymal derivation appeared more likely, suggesting histiocytic origin.     

A CASE OF MYCOSIS FUNGOIDES

The clinical history and pathological findings of a 68-year-old female with mycosis fungoides were described.
Clinically she developed cutaneous eruptions, and plaques to nodules appearlng within the next 4 months. Histopathological examination at biopsy revealed mycosis fungoides. At autopsy, extensive visceral involvement was disclosed (lungs, liver, kidneys, spleen, esophagus, left adrenal gland, lumbar vertebral bone marrow, and lymph nodes). Acute exacerbation of pulmonary tuberculosis was thought to be a terminal event.     

Spinal projections to the cerebellar nuclei in the cat

Summary Projections from the spinal gray matter to the cerebellar nuclei in the cat have been studied using Nauta's silver technique. Following unilateral section of the ventrolateral cord at the cervical level, heavy degeneration is seen in the nucleus medialis on both sides. Scanty degeneration is present bilaterally in the nucleus interpositus. The degeneration is most intense on the contralateral side. Scanty degeneration is also present bilaterally in subnucleus medialis parvicellularis (SMP) (Flood and Jansen, 1961). No degeneration is seen in nucleus lateralis. Following unilateral section of the dorsolateral cord at the cervical level, scanty degeneration is present bilaterally in nucleus medialis and nucleus interpositus anterior. The degeneration is more pronounced ipsilaterally and is also seen in SMP on both sides. No degeneration is present in nucleus lateralis. Fibers from the ventral and dorsal spinocerebellar tracts (VSCT and DSCT) terminate bilaterally in nuclei medialis and interpositus, with the VSCT as the most important connection.     

Oscillation of electrical current in water-swollen polyelectrolyte gels

An artificial oscillating system consisting of water-swollen polyelectrolyte gels, to which a constant electric potential was applied, is described. It was found that repetitive oscillations occurred in three-dimensional crosslinked gels made of synthetic polyelectrolytes, proteins and of polysaccharides. The repetitive oscillations were rather stable regardless of the “stimulating” current density, and the frequency was of the order 0,01 to 0,2 Hz which gradually decreased with time. Power spectra and Lorentz plots were obtained and a semi-quantitative analysis of the oscillation was carried out.     

SIGN-R1, a novel C-type lectin expressed by marginal zone macrophages in spleen,mediates uptake of the polysaccharide dextran

The marginal zone macrophages of the spleen are implicated in the clearance of polysaccharides, but underlying mechanisms need to be pinpointed. SIGN-R1 is one of five recently identified mouse genes that are homologous to human DC-SIGN and encode a single, external, C-terminal C-type lectin domain. We find that a polyclonal antibody to a specific SIGN-R1 peptide reacts primarily and strongly with a subset of macrophages in the marginal zone of spleen and lymph node medulla. In both sites, SIGN-R1 exists primarily in an aggregated form, resistant to dissociation into monomers upon boiling in SDS under reducing conditions. Upon transfection into three different cell lines, high-mol.-wt forms bearing SIGN-R1 are expressed, as well as reactivity with ER-TR9, a mAb previously described to react selectively with marginal zone macrophages. SIGN-R1-expressing macrophages preferentially sequester dextrans following i.v. injection. Likewise, when phagocytic cells are enriched from spleen and tested in culture, dextran is selectively endocytosed by a subset of very large SIGN-R1(+) cells representing approximately 5% of total released macrophages. Uptake of FITC-dextran by these macrophages in vivo and in vitro is blocked by ER-TR9 and polyclonal anti-SIGN-R1 antibodies. Following transfection with SIGN-R1, cell lines become competent to endocytose dextrans. The dextran localizes primarily to compartments lacking transferrin receptor and the LAMP-1 CD107a panlysosomal antigen. Therefore, SIGN-R1 mediates the uptake of dextran polysaccharides, and it is predominantly expressed in the macrophages of the splenic marginal zone and lymph node medulla.     

Pathological Effects of Matebrnal Hypoglycemia on Fetal Development in Cats

The pathogenesis of fetal brain damage caused by acute maternal hypoglycemia was investigated experimentally in cats: profound hypoglycemia (blood glucose concentration:less than 30 mg/dl) was induced in 12 pregnant cats at various stages of gestation by intravenous bolus injections of insulin. Maximal hypoglycemia was attained within 2 3 h, although the grade and duration in individual cats varied. The EEGs of all of seven maternal cats examined showed an increased frequency of slow high-voltage waves as hypoglycemia progressed, eventually becoming flat in 3 for a maximum period of 20 min. Some fetuses showed severe neuropathological changes, such as infarction or intrauterine death. Subventricular soften ing, cortical hemorrhage and ischemic neuronal changes also occurred, being distributed symmetrically in the para-sagittal areas of the cerebrum, basal ganglia, thalamus and tegrnentum of the brainstem. In general, these patho logical changes were more marked in fetuses and neonates than in the maternal cats, in which only ischemic neuronal changes were present, and may have been due to fetal systemic hypotension and cerebral ischemia induced by hypoglycemia. In maternal cats, the distribution of neu rons showing ischemic changes was widest in the cerebral cortex, and some were also present in the dentate gyri of the hippocampus. Moreover, ultrastructural examination of the ischemic neurons in maternal cats, unlike those of the fetuses, showed no mitochondrial swelling. Therefore, the distribution and ultrastructural nature of the ischemic neurons found in the maternal cats were considered to be characteristic of hypoglycemia, as proposed by Agardh et al . (1980). Acta Pathol Jpn 42 : 316–324, 1992.     

Possible role of hepatocyte growth factor in regeneration of human peritoneal mesothelial cells

Human peritoneal mesothelial cells (HPMCs) play an important role in peritoneal functions. During long term peritoneal dialysis, it has been reported that HPMCs are damaged by high glucose solution via the signal of transforming growth factor (TGF)-beta1 produced by HPMCs. In this study, we focused on the effect of hepatocyte growth factor (HGF), known as an anti-fibrotic and anti-TGF-beta1 agent, on HPMCs damaged by high glucose solution. HPMCs were isolated from specimens of the omentum from nonuremic patients after informed consent had been obtained. After confirming adhesion for 6 hours, 100 microL of DMEM with 0.5%FCS were added at different concentrations (D-glucose; 6, 30 mM) with or without HGF (10, 30, 100 ng/mL) for 48 hours. We examined the effects of a high concentration of glucose and then focused on following four critical points: 1) the production of HGF from HPMCs exposed to a high concentration of glucose, 2) the expression of c-Met on HPMCs, 3) the viability of those cells, and 4) matrix metalloproteinase-2 (MMP-2) and tissue inhibitors of metalloproteinase-2 (TIMP-2). The following significant changes are described herein: high glucose solution and TGF-beta1 i) decreased HGF production from HPMCs and ii) up-regulated expression of c-Met on HPMCs, and addition of HGF iii) restored viability of HPMCs damaged by glucose, iv) suppressed TGF-beta1 production by HGF, and v) induced up-regulation of MMP-2 and decreased TIMP-2 production by HPMCs. Levels of HGF decreased by high concentrations of glucose in the peritoneal cavity may induce the loss of HPMCs and thereby result in peritoneal fibrosis. These results suggest that HGF is an effective agent in the regeneration of peritoneal membrane damaged by high glucose solution.     

Estrogen affects vascular tone differently according to vasoactive substances in ovariectomized Sprague-Dawley rat

The favorable effects of estrogen on cardiovascular diseases can be explained by several mechanisms such as changes in serum lipid profiles and thrombogenecity. Estrogen also affects the vascular tone, but there has been no report in which the effect of estrogen was tested comprehensively for several vasoactive substances, especially after long-term administration. Two weeks after bilateral ovariectomy in 8-week old female Sprague-Dawley rats, placebo or 17 beta-estradiol (E2) pellets (0.5 mg; released over 3 weeks) were implanted subcutaneously. Two weeks after pellet implantation, organ chamber experiments were performed using aortae. Compared with control, E2-treated vessels showed impaired endothelium-dependent relaxation to acetylcholine. E2 enhanced the contraction to norepinephrine and U46619 and had no effect on endothelin-1-induced contraction. In contrast, the contraction to angiotensin (AT)-II was inhibited by E2. Northern blot analysis for AT1 receptor expression using cultured aortic smooth muscle cells showed no difference between control and E2-treated cells, suggesting that AT1 receptor downregulation is not the likely mechanism. These results suggest that E2 affects the vascular tone variably according to vasoactive substances.