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

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*

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

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*

As measurement of glomerular size in the assessment of several renal diseases becomes increasingly important, it has become necessary to devise rapid simple methods for the assessment of glomerular size and to have on hand reference ranges. A few reports on glomerular size have been published in Western literature, but their body builds are different from Koreans. In this study, 100 glomeruli(50 glomeruli each from the outer cortical and the juxtamedullary area) were measured in sections taken from 74 kidneys(ages 3 days~73 years) obtained from autopsy utilizing the semi-automatic image analyser. The percentage of glomerular sclerosis was measured based on its location. The sphere diameter, maximum diameter, area and sphere volume of non-sclerotic glomeruli were measured and evaluated with respect to age, sex and the location of the glomeruli. The results were as follows; 1) Mean glomerular dimensions including sphere and maximum diameter, area and sphere volume increased until 40 years of age, then reached a plateau. The percentage of sclerotic glomeruli then increased slowly with age but without statistical significance. 2) The glomerular dimensions and sclerosis showed no significant differences according to sex. 3) Juxtamedullary glomeruli were larger than the outer cortical ones which was statistically significant in age groups of 0~10, 11~20 and 41~50 years. The percentage of sclerotic glomeruli was generally greater in the outer cortex. 4) Differences in the values of glomerular dimensions between outer cortical and juxtamedullary area were similar in all age groups. 5) All parameters of measurement showed consistent and similar trends between the different groups. 6) The measurements of the largest 12 glomeruli out of randomly-selected 50 glomeruli gave similar results when compared with those of 50 glomeruli. It was evident from our results that glomerular size is influenced by age and glomerular location, but not by sex. The method of assessing glomerular size used in this study will not necessarily give the true, absolute value of size but it may be a simple, practical and useful method of comparing glomerular size in different groups of patients.

To know the correlation between glomerular and tubulointerstitial lesion and to define the characteristics of interstitial inflammatory cell in IgA nephropathy and classified according to WHO classification and graded tubulointerstitial lesion as mild, moderate and severe. Paraffin-embedded 5u sections were stained with UCHL-l, L26 and CD68 antibodies. More than 20 fields were examined in each case under the high power microscopy and the number of positive cells were counted. There was positive correlation between the severity of glomerular and that of tubulointerstitial lesion. The mostcommoninflammatory cells in the interstitiuin were UCHL-l positive cells followed by CD68 and L26 positive cells. As the WHO grade or tubulointerstitial lesion increased, the numbers of positive cells were increased in all three groups. The proportion of UCHL-1 Positive cells were increased in cases with high WHO grade whereas that of L26 positive cells incases with severe tubulointerstitial lesion Proteinuria was correlated with the degree of inflammatory cell infiltration, especially with that of L26 positive cells.