Malignant lymphoma with tumor thrombus in the portal venous system.

We report a case of malignant lymphoma presenting with tumor thrombus of the portal venous system. Computed tomography showed a mass in the portal vein and mesenteric lymphadenopathy. Filling defects in the dilated portal vein also were identified by angiography. This type of the lymphoma is extremely rare, but it should be considered in the differential diagnosis of portal vein thrombus.

Brain dysgenesis in Cornelia de Lange syndrome.

The neuropathological findings in a neonatal case of Cornelia de Lange syndrome (CDLS) were described. Two different types of lesions were revealed in the affected brain. The first type was classified as perinatal hypoxic-ischemic brain damage, associated with cyanotic congenital heart anomalies: subarachnoideal, intraventricular, and parenchymal hemorrhage, and multiple necrosis in the cerebral white matter, basal ganglia, internal capsule, thalamus, mammillary bodies and dentate nucleus. This type may be non-specific and common in premature babies dying soon after birth. On the other hand, the second type was classified as congenital dysgenesis of the brain: microbrachycephaly, immature or simple convolution pattern of the cerebral gyri, thickened leptomeninges, persistent subpial granule cells, hypoplasia of the anterior thalamic nuclei, neurohypophysis, lateral geniculate body, cerebral peduncle, ventral pons and cerebellar internal granular layer, and heterotopic cell nests in the cerebellar white matter. This type may indicate that the maturation of the brain can be disturbed in the fetal period, particularly in the mid-gestational period. In conclusion, pathognomonic or specific changes of CDLS might be absent in the brain. However, congenital dysgenesis of the brain, especially that found in the diencephalon and the cortico-ponto-cerebellar system, may constitute morphologic evidence explaining the severe growth retardation and neurological abnormalities in CDLS.

Effects of dietary salt restriction on blood pressure and the renal vasoactive system in the congenitally bilateral hydronephrotic rat.

We examined the responses on blood pressure when the renal vasoactive system such as renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) was activated by dietary salt restriction in the congenitally bilateral hydronephrotic rat (BHN). In a low salt diet (LS)-normotensive and normal kidney control rats after 8 weeks from initiating dietary salt restriction, the plasma sodium concentration (PNa) was retained at a level similar to that in the normal diet (ND)-control rats, and plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein activity (UKA) were about 1.8-, 9.4-and 1.7-fold higher, respectively, than those in the ND-control rats. In addition, LS-control rats had a significantly (p < 0.001) high systolic blood pressure (163 +/- 2.0 mm Hg) compared with that (136 +/- 5.8) of ND-control rats. These results suggest that the activated renal vasoactive system acted for not only sodium retention but also for elevation of blood pressure in LS-control rats. In LS-BHN at week 8, PNa was also retained at a nearly normal level. However, the renal vasoactive system activation for sodium retention was higher than that of LS-control rats; that is, increase of PRA, PAC and UKA were about 3.8-, 24.7-and 10.0-fold, respectively, than in ND-BHN. The higher activation of RAAS, nevertheless, does not affect blood pressure in BHN; that is, both hypertension of BHN fed LS and ND developed similarly. These findings suggest that dietary salt restriction could markedly activate the renal vasoactive system for sodium retention without elevating blood pressure in BHN different from control rats.

[Protective effect of tetramethylpyrazine on ischemic neuronal damage in the gerbil hippocampus].

The effect of tetramethylpyrazine on ischemic neuronal damage was studied in gerbil hippocampus in the terms of histopathological change and cerebral tissue lipid peroxides. Fifteen-five Mongolian gerbils were randomly assigned to one of three groups: sham-operated as control, subjected to 12 min global cerebral ischemia followed by 7 day spontaneous circulatory reperfusion, in which animals were treated with either ip. physiological saline or 60 mg/kg of tetramethylpyrazine 30 min before ischemia and daily thereafter for 7 days. The number of survival pyramidal neurons in the CA1 was counted: 263 +/- 8 (cell/mm) in the sham-operated group, 20 +/- 6 in the ischemia group, and 189 +/- 56 in the group treated with tetramethylpyrazine. Changes in lipid peroxides, expressed as malondialdehyde (MDA), was 134.5 +/- 5.0 nmol/g tissue in the sham-operated group, 193.5 +/- 5.1 in the ischemia group, and 137.6 +/- 10.8 in the group treated with tetramethylpyrazine. These results indicate that tetramethylpyrazine has a protective effect on the ischemic neuronal damage in hippocampus. Free radicals and free calcium may play an important role in pyramidal neuron necrosis in hippocampus following cerebral ischemia.

[Histopathological changes produced in organs by platelet activating factor].

This experiment was conducted to investigate the effect of platelet activating factor (PAF) on the pathological changes in organs using 10 mice (C3H/HeN). Ten mice were divided into two groups of acute and chronic experiment groups. In acute experiment, each mice received iv bolus injection of PAF 2.5 micrograms.kg-1 and in chronic experiment daily ip injection of PAF 7.5 micrograms.kg-1 for 7 days. Histopathology was observed with light microscopy after one hour or after 7 days by haematoxylin and eosin stain. In acute experiment, congestion of the lung, liver, kidney and spleen in all cases, right ventricular dilation in 2 cases and villous necrosis in the small intestine in 4 cases were observed. In chronic experiment, hyaline thrombus with congestion of the lung in 3 cases and congestion of the liver and kidney in all cases were observed. Splenomegaly with increased macrophage was observed, but no necrosis in the small intestine was observed. Marked findings were villous necrosis in the small intestine in acute experiment and hyaline thrombus in the lung as well as splenomegaly in chronic experiment.

Time course study of the extracellular matrix in puromycin-aminonucleoside-induced glomerulosclerosis.

The purpose of this study was to investigate the mechanism of glomerulosclerosis, which is an important histopathological feature of various renal diseases. Puromycin aminonucleoside (PAN) was administered to rats to produce glomerular lesions, and the kidneys were examined by repeated renal biopsy with light microscopy and immunohistochemical detection of glomerular extracellular matrix (ECM) components (laminin, fibronectin, type I, III, and IV collagen). Immunohistochemical studies utilizing the streptavidin-biotin method showed marked accumulation of laminin and type IV collagen in the adhesions between the glomerular epithelium and Bowman's capsule, as well as in the mesangial matrix. Fibronectin was detected in the normal mesangium and the basement membrane of Bowman's capsule, while adhesions and the matrix accumulations were also positive. The sclerotic lesions of the glomeruli were also stained for type I and III collagen, which exist in normal interstitial tissue, but never in healthy glomeruli. Type I collagen appeared in the lesions after type III collagen. All of the ECM components examined in this study were present in advanced glomerulosclerosis and showed distinctive patterns of progression. These finding suggest that abnormal accumulation and production of ECM components in the glomeruli may have a role in the development of glomerulosclerosis.

Morphometric analysis of the glomerular capillary area--a comparison of minimal change nephrotic syndrome, focal glomerular sclerosis, and pre-eclampsia.

A morphometric analysis was performed to compare the capillary area in non-sclerotic glomeruli in focal glomerular sclerosis (FGS), pre-eclampsia with focal sclerotic change of the glomeruli, and minimal change nephrotic syndrome (MCNS). The mean and standard deviation of the capillary area was greater in FGS than in pre-eclampsia and MCNS. Tubulo-interstitial lesions, such as tubular atrophy, interstitial fibrosis, and lymphocytic infiltration, were more severe in FGS than in pre-eclampsia. The presence of tubulo-interstitial changes including tubular atrophy and interstitial fibrosis with lymphocytic infiltration is thought to be an important prognostic factor in pre-eclampsia as well as in FGS. Unequal dilatation of the glomerular capillaries in non-sclerotic glomeruli may be harmful to the glomeruli and may lead to the development of glomerular sclerosis.

Focal segmental glomerular hyalinosis and/or sclerosis in rats with congenital unilateral hydronephrosis.

Focal segmental glomerular hyalinosis and/or sclerosis (FSHS) was observed in five Wistar-Imamichi rats with congenital unilateral hydronephrosis (CUH rats). Marked proteinuria (164.9 +/- 138.4 mg/day) was observed in the CUH rats. Immunoperoxidase staining for IgM, C3 and IgG was positive in the glomeruli, showing in a focal, segmental pattern that corresponded to the areas of FSHS seen by light microscopy. These glomerular findings were extremely similar to those of human focal glomerular sclerosis (FGS). FSHS was found to be common to both the hydronephrotic kidney and the contralateral kidney without hydronephrosis. Morphometry revealed that the glomerular area of the juxtamedullary glomeruli was greater than that of superficial glomeruli in control rats (11,037 micron2 vs. 6,847 microns2). On the other hand, glomerular hypertrophy was observed in non-sclerotic glomeruli of CUH rats (superficial glomeruli; 12,477-16,123 microns2, juxtamedullary glomeruli; 14,635-18,418 microns2). Also, a decreased in the number of glomeruli within the range 1.8-4.1 per unit area (1 mm2) was seen in CUH rats compared with control rats (mean 4.4). These results suggest that the increased rate of development of FSHS is based on hyperfiltration in the remaining functional nephrons.

Changes of anionic sites in the mesangium with aging in rats: a comparison of the immersion and intravenous PEI methods.

We investigated the changes in anionic sites of the mesangial matrix related to aging in rats, employing polyethyleneimine (PEI) as a cationic probe. We compared the numbers of anionic sites detected by the immersion method and by the intravenous administration of PEI. Analysis of the mean numbers of PEI particles per 0.1 micron2 in the mesangial matrix revealed a significant decrease related to aging. Our results suggested that there was no significant difference in efficacy between the immersion and intravenous methods. Loss of negative charge of the mesangial matrix is believed to promote mesangial dysfunction and the entrapment of macromolecular substances, and so to play an important role in the onset of glomerular sclerosis.

[The effect of the elastase on aminonucleoside nephrosis].

In this paper, we studied the effect of elastase on aminonucleoside (AN) nephrosis which is considered a model of focal glomerular sclerosis (FGS). Elastase is an enzyme which disintegrates elastin, discovered by Balo, and used in the treatment of arteriosclerosis and hyperlipidemia. It has also been known to improve metabolism of acid mucopolysaccharides, so, this study focused on metabolic improvement. Three groups of male Sprague-Dawley rats were studied and observed at regular intervals; 30, 60, 90 days. The ANE group (AN + elastase) was administered one shot of AN (10 mg/100 g B.W.) during the test interval, while elastase (5 mg/kg B.W.) was injected 5 days/week for the entire test interval. The AN group was administered one shot of AN only. The third group was a control (C). The following results were observed: (1) Focal segmental hyalinosis and sclerosis (FSHS); ANE group was weaker than AN group. (2) Other significant qualifying glomerular changes (vacuolar change and hyaline droplets of the epithelial cells, adhesion, and foam cells); ANE group was weaker than AN group. (3) Anion loss in GBM was shown by a lack of colloidal iron staining under light microscopy, and by a lack of PEI particles under electron microscopy; there was significantly less anion loss with ANE group, than with AN group. The findings suggest that elastase has an affect on the metabolism of acid mucopolysaccharide and collagen in sclerotic lesion, and may restrain the progress of amino-nucleoside nephrosis.

[Pathomorphological studies on arterial cushion. 2. Aminonucleoside nephrotic rat].

The present study is an attempt to solve the problem of pathogenesis of focal glomerular sclerosis (FGS), especially in juxtamedullary cortex, we were investigated by measurement of luminal diameters of afferent arterioles (Aff), efferent arterioles (Eff) of numerous glomeruli, arterial cushion (AC), afferent arterioles (AC-aff) at a region of branching arteries from the interlobular arteries, using scanning electron micrographs of methyl methacrylate casts of intrarenal arteries of aminonucleoside nephrotic rats. As regards luminal diameters, Eff were nearly equal Aff in minor glomerular abnormalities (Minor). Nevertheless Eff of glomeruli with segmental sclerosis (FSHS) were smaller than Aff (t-test). AC with FSHS were smaller than ones of Minor, statistically (t-test). The results of these examination, the cushion may be important factor for the regulation of blood flow in sclerotic glomeruli.