• Journal of Multimedia Information System
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• v.6 no.2
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• pp.81-86
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• 2019

Deep learning is emerging as one of the best tool in processing data related to medical imaging. In our research work, we have proposed a deep learning based framework CNN (Convolutional Neural Network) for the classification of dysplastic tissue images. The CNN has classified the given images into 4 different classes namely normal tissue, mild dysplastic tissue, moderate dysplastic tissue and severe dysplastic tissue. The dataset under taken for the study consists of 672 tissue images of epithelial squamous layer of oral cavity captured out of the biopsy samples of 52 patients. After applying the data pre-processing and augmentation on the given dataset, 2688 images were created. Further, these 2688 images were classified into 4 categories with the help of expert Oral Pathologist. The classified data was supplied to the convolutional neural network for training and testing of the proposed framework. It has been observed that training data shows 91.65% accuracy whereas the testing data achieves 89.3% accuracy. The results produced by our proposed framework are also tested and validated by comparing the manual results produced by the medical experts working in this area.

• Journal of Korean Dental Science
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• v.6 no.1
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• pp.34-40
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• 2013

Fibrous dysplasia is a benign fi bro-osseous lesion wherein normal bone is replaced with an excessive proliferation of cellular fibrous connective tissue intermixed with irregular bony trabeculae. Fibro-osseous lesions like fibrous dysplasia are often associated with non-epithelial cysts, such as simple bone cyst. The etiologic and pathogenic relationships between fi brous dysplasia and simple bone cyst have not been conclusively established. Nonetheless, the mechanism of cyst formation in fibro-osseous lesion associated with simple bone cyst can be said to differ from that of the typical simple bone cyst of the jaws. This article reports a case of bilateral lesions including fi brous dysplasia and simple bone cyst on each site and reviews the pathogenesis of cyst formation in the fibro-osseous lesion.

• Parasites, Hosts and Diseases
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• v.55 no.1
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• pp.21-29
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• 2017

Schistosoma haematobium is a biocarcinogen of human urinary bladder (UB). The present study investigated developing UB cancer mouse model by injecting S. haematobium eggs into the bladder wall and introduction of chemical carcinogens. Histopathological findings showed mild hyperplasia to epithelial vacuolar change, and high grade dysplasia. Squamous metaplasia was observed in the S. haematobium eggs+NDMA group at week 12 but not in other groups. Immunohistochemistry revealed significantly high expression of Ki-67 in urothelial epithelial cells of the S. haematobium eggs+BBN group at week 20. The qRT-PCR showed high expression of p53 gene in S. haematobium eggs group at week 4 and S. haematobium eggs+BBN group at week 20. E-cadherin and vimentin showed contrasting expression in S. haematobium eggs+BBN group. Such inverse expression of E-cadherin and vimentin may indicate epithelial mesenchymal transition in the UB tissue. In conclusion, S. haematobium eggs and nitrosamines may transform UB cells into squamous metaplasia and dysplasia in correlation with increased expression of Ki-67. Marked decrease in E-cadherin and increase in p53 and vimentin expressions may support the transformation. The present study introduces a promising modified animal model for UB cancer study using S. haematobium eggs.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1125-1131
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• 2014

Background: Schistosomiasis is a parasitic disease causing chronic ill health in humans with a serious consequences for socio-economic development in tropical and subtropical regions. There is also evidence linking Schistosoma mansoni to colonic carcinoma occurrence. The aim of this study was to evaluate some inflammatory and oxidative stress biomarkers, as well as L-fucose as linkers between intestinal schistosomiasis and colonic dysplasia development in mice. Materials and Methods: This study was conducted upon 80 mice that were divided the control group (10 non infected mice) and infected group which was subdivided into 7 sub-groups (10 mice each) according to the time of sacrifaction in the post infection (p.i.) period, 10 mice being sacrificed every two weeks from 6 weeks p.i. to 18 weeks p.i. Tumor necrosis factor alpha (TNF-${\alpha}$), inducible nitric oxide synthase (iNOS), and pentraxin 3 (PTX3) levels were estimated by immunoassay. The L-fucose level, and thioredoxin reductase (TrxR) and lactate dehydrogenase (LDH) activities were also evaluated in colonic tissue. Results: The current study revealed statistically significant elevation in the studied biochemical markers especially at 16 and 18 weeks p.i. The results were confirmed by histopathological examination that revealed atypical architectural and cytological changes in the form of epithelial surface serration and nuclear hyper-chromatizia at 14, 16 and 18 weeks p.i. Conclusions: inflammation, oxidative stress and L-fucose together may form an important link between Schistosomal mansoni infection and colonic dysplasia and they can be new tools for prediction of colonic dysplasia development in experimental schistosomiasis.

• Childhood Kidney Diseases
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• v.22 no.2
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• pp.64-66
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• 2018

Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent hereditary renal disease and causes terminal chronic renal failure. ADPKD is characterized by bilateral multiple renal cysts, which are produced by mutations of the PKD1 and PKD2 genes. PKD1 is located on chromosome 16 and encodes a protein that is involved in cell cycle regulation and intracellular calcium transport in epithelial cells and is responsible for 85% of ADPKD cases. Although nine cases of unilateral ADPKD with contralateral kidney agenesis have been reported, there have been no reports of early childhood ADPKD. Here, we report the only case of unilateral ADPKD with contralateral kidney dysplasia in the world in a four year-old girl who was intrauterinely diagnosed since she was 20 weeks old and followed for four years until present.

• Journal of Gastric Cancer
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• v.1 no.3
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• pp.129-135
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• 2001

Purpose: Dysplasia or flat adenoma of the stomach is regarded as a precancerous lesion. However, the frequency and the evolutionary process of malignant transformation of gastric dysplasia are still debated. In order to see whether the lesion was a monoclonal or a polyclonal proliferation, clonality was assayed by X-linked HUMARA polymorphism. Materials and Methods: DNA was extracted from the paraffin-embedded tissue of 16 consecutive cases of endoscopic biopsy, eight of which supplied both dysplastic and nondysplastic tissue for comparison. HUMARA was amplified by PCR with or without pretreatment with methylationsensitive restriction enzyme, HpaII. The amplification products were electrophoresed on polyacrylamide gel and silver-stained. Results: Among the 16 cases, 13 cases were informative and 3 cases noninformative. Of the 13 cases, one case showed skewed lyonization, rendering 12 cases to be analyzed further. A monoclonal band pattern was noted in 2 cases, and a polyclonal band pattern in 10 cases. A review of the histopathologies of the monoclonal and the polyclonal cases did not reveal features discriminating the two groups. Conclusion: These results suggest that gastric dysplasia is a disease entity heterogeneous in the genetic level, and many cases may be non-neoplastic.

• Anatomy and Cell Biology
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• v.51 no.4
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• pp.299-301
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• 2018

Killian-Jamieson diverticulum is a permanent protrusion of anterolateral proximal esophagus through anatomically weak muscular gap, known as Killian-Jamieson area, into adjacent area. During a routine educational dissection, we found a well-defined lateral diverticulum just inferior to the transverse fibers of the cricopharyngeus muscle in a Korean male cadaver. It had a dimension of $1.8{\times}1.4{\times}1.0cm$ with two types of epithelial cells, stratified squamous and simple cuboidal to low-columnar epithelium, and attenuated and haphazardly arranged muscle fibers. No epithelial dysplasia or malignant transformation was identified except ulcerative changes. Although Killian-Jamieson diverticulum is a very rare disease, clinicopathological aspects should be considered.

• The Korean Journal of Cytopathology
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• v.14 no.2
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• pp.91-95
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• 2003

Intraductal papillary mucinous tumor of the pancreas is characterized by intraductal papillary proliferation of mucin-producing epithelial cells with or without excessive mucin secretion. According to the degree of epithelial dysplasia, intraductal papillary mucinous tumor is classified into adenoma, borderline tumor, and carcinoma. We recently experienced a case of fine needle aspiration cytology of the intraductal papillary mucinous adenoma in a 69-year-old male. The fine needle aspiration cytology yielded flat sheets of columnar, mucin containing epithelial cells in the background of dense mucin containing degenerated cellular material and histiocytes.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.1
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• pp.147-151
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• 2016

Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity and some of these have been documented in association or preceded by oral epithelial dysplasia (OED). Aggressive cancers with fast growth have demonstrated overexpression of some glucose transporters (GLUTs). Thus, the aim of this study was to analyze the immunohistochemical expression of the glucose transporter, GLUT-1, in OEDs and OSCCs, seeking to better elucidate the biological behavior of neoplasias. Fifteen cases were selected this research of both lesions. Five areas were analyzed from each case by counting the percentage of positive cells at 400x magnification. Immunoreactivity of GLUT-1 was observed in 100% of the samples ranging from 54.2% to 86.2% for the OSCC and 73.9% to 97.4% for the OED. Statistical test revealed that there was greater overexpression of GLUT-1 in OED than the OSCC (p=0.01). It is believed the high expression of GLUT-1 may reflect the involvement of GLUT-1 in early stages of oral carcinogenesis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.25 no.6
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• pp.441-452
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• 2022

Congenital diarrheal disorders (CDDs) with genetic etiology are uncommon hereditary intestinal diseases characterized by chronic, life-threatening, intractable watery diarrhea that starts in infancy. CDDs can be mechanistically divided into osmotic and secretory diarrhea. Congenital tufting enteropathy (CTE), also known as intestinal epithelial dysplasia, is a type of secretory CDD. CTE is a rare autosomal recessive enteropathy that presents with intractable neonatal-onset diarrhea, intestinal failure, severe malnutrition, and parenteral nutrition dependence. Villous atrophy of the intestinal epithelium, crypt hyperplasia, and irregularity of surface enterocytes are the specific pathological findings of CTE. The small intestine and occasionally the colonic mucosa include focal epithelial tufts. In 2008, Sivagnanam et al. discovered that mutations in the epithelial cell adhesion molecule (EpCAM, MIM# 185535) were the genetic cause of CTE (MIM# 613217). More than a hundred mutations have been reported to date. Furthermore, mutations in the serine peptidase inhibitor Kunitz type 2 (SPINT2, MIM# 605124) have been linked to syndromic CTE. In this study, we report the case of a 17-month-old male infant with congenital diarrhea. Despite extensive etiological workup, no etiology could be established before admission to our center. The patient died 15 hours after being admitted to our center in a metabolically decompensated state, probably due to a delay in admission and diagnosis. Molecular autopsy with exome sequencing revealed a previously reported homozygous missense variant, c.757G>A, in EpCAM, which was confirmed by histopathological examination.