Most glomerular lesions are associated with qualitative and quantitative alterations of the extracellular matrix components, having relation to progressive glomerular sclerosis. We aimed to investigate the characteristic alteraltions in distribution of extracellular matrix components, such as fibronectin, laminin, collagen type III and IV in human glomerular diseases by immunohistochemical method. The materials included are 3 nephrectomy as normal control, 51 renal biopsies and I autopsy; 3 normal, 5 minimal change disease, 5 minimal change disease with minimal mesangial lgA deposit, 5 benign recurrent hematuria, 10 focal segmental glomerulosclerosis, 15 lgA nephropathy, 10 membranoproliferative glomerulonephritis, 2 diffuse mesangial sclerosis of infancy. Type IV collagen and laminin were present normally in the mesangium, GBM, TBM and interstitial vessels, and were increased at the portion of increased mesangial matrix, of sclerosis and thickened GBM in cases of lgA nephropathy, membranoproliferative glomerulonephritis, focal segmental glomrulosclerosis and diffuse mesangial sclerosis in the proportion to the glomerular damage. Type III collagen was absent in the normal glomeruli, but was detectable focally and segmentally in cases of membranoproliferative glomerulonephritis, IgA nephropathy and focal segmental glomerulosclerosis at the sclerotic portion. Fibronectin was normally detectable mainly in the mesangium, and partly and incompletely in GBM, and was increased at the portion of increased mesangial matrix, sclerosis and thickened GBM in cases of focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, IgA nephropathy and diffuse mesangial sclerosis, but was diminshed at the old slcerotic portion or global sclerosis. The expression of these antibodies in cases of minimal change disease, minimal change disease with minimal mesangial IgA deposit, benign recurrent hematuria was not different, quantitatively and qualitatively, from that of normal glomeruli. These findings suggest that progressive glomerular sclerosis was due to the increase of extraceuular matrix components such as type IV collagen, laminin, fibronectin and new appearance of type III collagen, and the expression was in proportion to the degree of sclerosis, but had no relation to the disease entity.
Humans ; Biopsy

This study was carried out to investigate the immunohistochemical expression of bcl-2 and p53 protein in the intestinal type and the diffuse type of gastric adenocarcinoma by Lauren's classification. A total of 100 cases, including 50 cases of the intestinal type and 50 cases of the diffuse type from paraffin embedded gastrectomy specimens, were immunohistochemically stained for bcl-2 and p53 protein. Bcl-2 protein was expressed in 38% (19/50) of intestinal type and 30% (15/50) of diffuse type. The incidence of bcl-2 protein expression was higher in the intestinal type than in the diffuse type, but no significant correlation was present (p>0.05). p53 protein was expressed in 68% (34/50) of the intestinal type and 60% (30/50) of the diffuse type. The incidence of p53 protein expression was higher in the intestinal type than in the diffuse type, but no significant correlation was present (p>0.05). And an expression of bcl-2 and p53 protein did not correlate with depth of invasion, lymph node meatastasis and TNM stage, respectively (p>0.05). These results suggest that bcl-2 and p53 gene alteration appear to play a more important role in the carcinogenesis of the intestinal type than the diffuse type. However, there is no significant difference between the intestinaPU: The Korean Society of Pathologistsl type and the diffuse type in bcl-2 and p53 protein expression.
Adenocarcinoma* ; Apoptosis ; Carcinogenesis ; Classification ; Gastrectomy ; Genes, p53 ; Incidence ; Lymph Nodes ; Paraffin

A forty-nine-year-old woman with polycystic disease had a right nephrectomy for what was preoperatively thought to be a polycystic disease, but at surgery turned out to be a tumor based on frozen section. Microscopic examination revealed papillary type, renal cell carcinoma with classical features of adult polycystic kidneys. Radiologic findings revealed multiple cysts in the liver. The clinical recognition of a carcinoma developing in polycystic kidneys is often difficult because of the presence of preexisting large renal masses and occasional hematuria. Renal cell carcinoma should be thought of when confronted with abdominal pain or back pain, severe hematuria, sudden dysuria or a new renal mass occurring in a patient with polycystic kidneys.
Adult ; Male ; Female ; Humans ; Cysts

The purpose of this study is to evaluate the change of mucosal immunity in gastric diseases. A quantative analysis of IgA and secretory component(SC) in gastric diseases by immunohistochemical method was performed in 110 specimens. The results are as follows: 1) In normal gastric mucosa, all of 10 cases revealed a negative reaction to antihuman SC but 4 cases were positive for IgA. 2) In chronic superficial gastritis and chronic atrophic gastritis with intestinal metaplasia, the metaplastic cells except for the goblet cells were positive for both IgA and SC. 3) The dysplastic cells were also positive for both IgA and SC, and the regenerating cells in ulcer as well. 4) All of the well differentiated or moderately well differentiated adenocarcinomas showed positive reactions to antihuman IgA and antihuman SC, and the intensity appeared to be stronger in the former. However, among 10 cases of poorly differentiated adenocarcinoma SC was not demonstrated in 5 cases, and no IgA was present in one case. In 10 cases of signet ring cell carcinoma, 6 cases revealed a negative reaction to antihuman IgA and 6 cases to antihuman SC. The above results suggest that the secretory immunity is not essential in normal gastric mucosa. The intestinal metaplasia in chronic gastritis is considered as an adaptive response to chronic inflammation. The degree of differentiation in adenocarcinoma may be related to the mucosal immunity.
Adenocarcinoma

Mutations in the p53 gene occur during the development of colorectal carcinomas, and play an important role in the conversion of adenoma into carcinoma. To detect the p53 gene mutation and its pattern of expression in colorectal carcinomas, polymerase chain reaction for exons 5, 6, 7, and 8, recombinant gene cloning, and automated DNA sequencing were performed with 30 fresh colorectal carcinomas. Each tissue was also analyzed by immunohistochemical staining for p53 protein. p53 protein was detected in 25 of 30 (83.3%) colorectal carcinomas by immunohistochemical study. p53 mutation was detected in 4 of 30 (13.3%) colorectal carcinomas. The distribution of these mutations among these exons investigated was as follows: Three mutations in exon 5 (66.7%) and 1 mutation in exon 7 (33.3%). One case with mutation in exon 5 had mutations at three different codons. Mutations in exon 5 were found at codon 153 (GGG to AGG: Gly to Arg), 170 (TGC to GGC: Cys to Gly), 186 (CTA to TTA: silent mutation), 158 (GCG to ACG: Ala to Thr), and 176 (ACG to ATG: Thr to Met). Mutation in exon 7 was found at codon 248 (AGG to AGA: silent mutation). Four of them were missense mutations. Two of 6 mutations were silent mutations. Five transition mutations and 1 transversion mutation were also detected. All cases with mutations by automated DNA sequencing showed positive p53 protein immunohistochemical stainining. In conclusion, p53 gene mutation was detected in 4 of 30 (13.3%) colorectal carcinomas, located in codon 153, 158, 170, 176, and 186 of exon 5 and codon 248 of exon 7. Further studies are needed to evaluate the significance of the codon 153 mutation which was not recognized in other studies on colorectal carcinomas.
Adenoma ; Clone Cells ; Cloning, Organism ; Codon ; Colorectal Neoplasms* ; DNA* ; Exons ; Genes, p53* ; Mutation, Missense ; Polymerase Chain Reaction ; Sequence Analysis, DNA*

The aim of this study was to clarify the role of Kupffer cells in the mechanism of endotoxin-induced liver injury. The study on fine structure of Kupffer cells was performed after the injection of endotoxin. The endotoxin(Escherichia soli lipopolysaccharide 026: B6, 1.5mg/100 g of body weight) was intraperitoneally injected in Sprague-Dewley rats. Animals were sacrificed at 1/4, 1/2, 1, 2, 4, 8, 16, 24, 72 and 120 hours after the injection of endotoxin. Livers were extirpated and processed to be examined by light and electron microscopy. The results obtained were summerized as follows: Early changes observed in liver after endotoxin injection included the increased number and hypertrophy of Kupffer cells, infiltration of neutrophils and presence of fibrin thrombi within the sinusoids. The coritinuous increase of the Kupffer cells in number with hypertrophy, congestion and infiltration of inflammatory cells within the sinusoids were observed. Hepatocytes showed* fatty change and occasional necrosis. At 72 hours the congestion decreased. At 120 hours the number of Kupffer cells was increased, but the morphology of Kupffer cells became similar to that of the control group. The numbers and sizes of primary and secondary lysosomes and amount of euchromatin of Kupffer cells increased. Swellings and increase in number of mitochondria, Golgi complex, smooth endoplasmic reticulum, rough endoplasmic reticulum were evident. Microthrombi were present within the sinusoids. The swelling of rough endoplasmic reticulum and mitochondria, decrease of glycogen particles, fatty change, hypoxic vacuoles, pyknotic nuclei and occasional necrosis were observed in hepatocytes. At 72 hours the number of secondary lysosomes in Kupffer cells decreased. At 120 hours the morphology of Kupffer cells became similar to that of the control group. According to these results, it was postulated that the endotoxin was initially taken up by pinocytosis into Kupffer cells and degraded in secondary lysosomes of activated Kupffer cells. Kupffer cells may play an important role in the defense mechanism of liver during endotoxemia. The dysfunction of Kupffer cells and ischemia by sinusoidal microthrombi may cause liver injury.
Animals ; Endoplasmic Reticulum, Rough ; Endoplasmic Reticulum, Smooth ; Endotoxemia ; Estrogens, Conjugated (USP) ; Euchromatin ; Fibrin ; Glycogen ; Golgi Apparatus ; Hepatocytes ; Hypertrophy ; Ischemia ; Kinetics* ; Kupffer Cells* ; Liver ; Lysosomes ; Microscopy, Electron ; Mitochondria ; Necrosis ; Neutrophils ; Pinocytosis ; Rats* ; Vacuoles

To investigate the immunohistochemical expression of mutated p53 protein and bcl-2 protein in the cutaneous melanocytic lesion, 15 cases of compound nevus, 10 cases of congenital melanocytic nevus, 15 cases of primary malignant melanoma(4 cases less than 1.5 mm thick and 11 cases more than 1.5 mm thick), and 10 cases of metastatic malignant melanoma(7 cases in lymph node and 3 cases in soft tissue) were examined. All cases of compound nevi and of congenital melanocytic nevi showed no immunoreactivity for p53 protein. p53 protein overexpression was observed in 75%(3/4) wth primary malignant melanoma less than 1.5 mm thick, 81%(9/11) with primary malignant melanoma more than 1.5 mm thick, and 100%(10/10) with metastatic malignant melanoma. The difference in p53 protein overexpression was statistically significant between benign nevi and malignant melanoma(p<0.01). Bcl-2 protein expression was observed in 73%(11/15) with compound nevus, 70%(7/10) with congenital melanocytic nevus, 75% (3/4) in primary malignant melanoma less than 1.5 mm thick, 54%(6/11) with primary malignant melanoma more than 1.5 mm thick, and 40%(4/10) with metastatic malignant melanoma. These findings suggested that mutation of p53 gene may be an important mechanism in the development of malignant melanoma. Although bcl-2 protein was expressed in cutaneous melanocytic lesion, no correlation was found between p53 protein and bcl-2 protein expression in malignant melanoma.
Genes, p53 ; Lymph Nodes ; Melanoma ; Nevus ; Nevus, Pigmented ; Skin*

To investigate the immunohistochemical expression of mutated p53 protein and bcl-2 protein in the cutaneous melanocytic lesion, 15 cases of compound nevus, 10 cases of congenital melanocytic nevus, 15 cases of primary malignant melanoma(4 cases less than 1.5 mm thick and 11 cases more than 1.5 mm thick), and 10 cases of metastatic malignant melanoma(7 cases in lymph node and 3 cases in soft tissue) were examined. All cases of compound nevi and of congenital melanocytic nevi showed no immunoreactivity for p53 protein. p53 protein overexpression was observed in 75%(3/4) wth primary malignant melanoma less than 1.5 mm thick, 81%(9/11) with primary malignant melanoma more than 1.5 mm thick, and 100%(10/10) with metastatic malignant melanoma. The difference in p53 protein overexpression was statistically significant between benign nevi and malignant melanoma(p<0.01). Bcl-2 protein expression was observed in 73%(11/15) with compound nevus, 70%(7/10) with congenital melanocytic nevus, 75% (3/4) in primary malignant melanoma less than 1.5 mm thick, 54%(6/11) with primary malignant melanoma more than 1.5 mm thick, and 40%(4/10) with metastatic malignant melanoma. These findings suggested that mutation of p53 gene may be an important mechanism in the development of malignant melanoma. Although bcl-2 protein was expressed in cutaneous melanocytic lesion, no correlation was found between p53 protein and bcl-2 protein expression in malignant melanoma.
Genes, p53 ; Lymph Nodes ; Melanoma ; Nevus ; Nevus, Pigmented ; Skin*

We observed 17 cases of cafe au lait spots histopathplogi ally. Out of 17 cases, 9 cases were neurofibromatosis with neurofibromas, 6 cases were neurofibromatosis without neurofibroma, and 2 cases were normal healthy persons. The results were as follows. l. In all 17 cases, melanin pigment was increased in melanocytes and keratinocytes. 2. Griant pigment granules were identified only in 3 cases of neurofibromatosis with neurofibromas.
Cafe-au-Lait Spots* ; Humans ; Keratinocytes ; Melanins ; Melanocytes ; Neurofibroma ; Neurofibromatoses

The immunoreactivities of surgically removed 16 cardiac myxomas were studies for factor VIII-related Ag (F VIII-RA), Ulex europaeus agglutinin I (UEA-I) and desmin alpha1-antichymotrypsin, and this study was accompained by a clinicopathologic review. More than 50% of the patients with cardiac myxomas were in their fourth and fifth decades, and cardiac myxomas were much more common in women than in men. All but on occurred in the left atrium, and the majority were attached to the atrial septum, usually in the region corresponding to the fossa ovalis. In one case, an atrial myxoma recurred 37 months after the initial excision. Microscopically, the myxomas contained a myxoid matrix composed of acid mucopolysaccharides within which were embedded polygonal cells. The cells forming both the surface and complicated vascular like channels throuhout the myxoid stroma tested positive for F VIII-RA and UEA-I. The outer cell layers of the complex vascular structures demonstrated variable staining for F VIII-RA, while isolated bundles of smooth muscle cells were present and stained for desmin. A small number of the so-called myxoma cells, immunoreactive for alpha1-antichymotrypsin which were not laden with hemosiderin pigment but were similar to histiocytes, were present particularly around the areas of hemorrhage. These findings support the current view that cellular and histologic heterogeneity arose from the divergent differentiation of multipotential mesenchymal cells. In particular, it remains to be confirmed by further study whether or not true histiocytic differentiation occurs.
Female ; Male ; Humans