Dietary fat, cholesterol, and cholic acid affect the histopathologic severity of nonalcoholic steatohepatitis in Sprague-Dawley rats.

Understanding of the pathogenesis of nonalcoholic steatohepatitis (NASH)-associated fibrosis has been hampered by the lack of a comprehensive and physiological small animal model of NASH with fibrosis. Feeding a high-fat and high-cholesterol (HFC) diet supplemented with cholic acid to rats is known to replicate human NASH pathology, and it induces fibrosis earlier than with an HFC diet alone. In the present study, physiological and histopathological observations from 65 Sprague-Dawley (SD) rats fed an HFC diet with or without cholic acid for 9 or 18 weeks in our laboratory between January 2013 and February 2018 were retrospectively reviewed.

Age-Related Alterations of Nonalcoholic Steatohepatitis in Sprague-Dawley Rats Fed a High-Fat and High-Cholesterol Diet.

Nonalcoholic steatohepatitis (NASH), a subtype of nonalcoholic fatty liver disease (NAFLD), has a potentially progressive course that can lead to liver cirrhosis. Age is strongly associated with the development and progression of NAFLD/NASH, but the natural history of pediatric NAFLD is still not fully understood. Here, we evaluated the age-related alterations of NASH in 5-, 9- and 13-wk-old male Sprague-Dawley rats that were fed a high-fat and high-cholesterol diet (30% fat, 1.

Volvulus of the gall bladder diagnosed by ultrasonography, computed tomography, coronal magnetic resonance imaging and magnetic resonance cholangio-pancreatography.

A 54-year-old woman was admitted to our hospital with the complaint of right upper quadrant pain. Upon physical examination the vital signs of the patient were within normal ranges. Ultrasonography and computed tomography (CT) examination of the abdomen was obtained, which demonstrated a large dilatated cystic structure, measuring approximately 68.

MRI of metanephric adenoma.

We report the imaging findings of metanephric adenoma. US examination showed a protruding hypoechoic mass at the right kidney. CT revealed a well defined isodense mass with calcifications.

[Mitral valve plasty for better long term results].

Between July 1991 and January 1995, 74 patients with pure mitral valve regurgitation (MR) underwent mitral valve plasty (MVP) at out institute. Our procedure includes chordal replacement of the anterior leaflet with PTFE sutures (42 patients). There were one hospital death (1.

Enhancement of rat liver cell foci development by combined treatment with heterocyclic amines at low doses.

Potential synergism between 5 or 10 carcinogenic heterocyclic amines (Trp-P-1, Trp-P-2, Glu-P-1, Glu-P-2, IQ, MeIQ, MeIQx, MeA alpha C, A alpha C and PhIP) acting at low doses was examined in a medium-term liver bioassay system for carcinogens. Immunohistochemically-demonstrated glutathione S-transferase placental form (GST-P) positive foci were assessed as the endpoint marker lesions. Male F344 rats were initially given diethylnitrosamine (DEN, 200mg/kg, ip) and beginning 2 weeks later received heterocyclic amines individually or in combination for 6 weeks.

Carcinogenicity of 4-methoxyphenol and 4-methylcatechol in F344 rats.

The carcinogenic potentials of 4-methoxyphenol (4-MP) and 4-methylcatechol (4-MC), phenolic compounds which are structurally similar to the known forestomach carcinogen BHA and the glandular stomach carcinogen catechol respectively, and cause considerably enhanced cell proliferation and cytotoxicities in rat forestomach and/or glandular stomach epithelium, were examined in male and female F344 rats. Groups of 30 male and female animals were administered diets containing 2% 4-MP or 2% 4-MC for 104 weeks. Histopathological findings in the 4-MP case included atypical hyperplasias (male, 67%, female, 37%), papillomas (50%, 23%) and squamous-cell carcinomas (77%, 20%) in the forestomach.

No enhancing effects of calcium/magnesium salts of L-glutamate and L-ascorbate on tumor development in a rat medium-term multiorgan carcinogenesis bioassay.

Calcium/magnesium salts of L-glutamate and L-ascorbate were tested for modification potential using a rat multiorgan carcinogenesis bioassay. Following sequential treatment with three different carcinogens (diethylnitrosamine, N-methylnitrosourea, and dihydroxydi-N-propylnitrosamine) over a 4-wk period, rats were given diet containing 5% monocalcium di-L-glutamate tetrahydrate (Ca-glutamate), 2.5% monomagnesium di-L-glutamate tetrahydrate (Mg-glutamate), 5% L-glutamic acid, 5% monocalcium di-L-ascorbate dihydrate (Ca-ascorbate), 2.

Inhibition by dehydroepiandrosterone of butylated hydroxyanisole (BHA) promotion of rat-bladder carcinogenesis and enhancement of BHA-induced forestomach hyperplasia.

The effects of dehydroepiandrosterone (DHEA) with/without ribonucleoside (RNs) supplementation on butylated hydroxyanisole (BHA) bladder-tumor promotion and forestomach carcinogenesis were investigated. Male F344 rats were given N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in their drinking water for 4 weeks and then received basal diet or diet containing BHA, DHEA, a mixture of RNs, BHA + DHEA or BHA + DHEA + RNs for 32 weeks. The occurrences of papillomas and carcinomas in the urinary bladder were increased in the groups given BHA or BHA + DHEA + RNs, as compared with control group values.

Carcinogenicity of catechol in F344 rats and B6C3F1 mice.

Carcinogenicity of catechol, a naturally occurring and industrial chemical which has been shown to have strong cell proliferating potential on rat glandular stomach epithelium, was investigated in male and female F344 rats and B6C3F1 mice. Groups of 30 male and female F344 rats and B6C3F1 mice were treated with 0.8% catechol in powdered diet continuously for 104 weeks (rats) or 96 weeks (mice).

Lack of promotion of N-butyl-N-(4-hydroxybutyl)nitrosamine-initiated urinary bladder carcinogenesis in mice by rat cancer promoters.

The effects of dietary exposure to sodium L-ascorbate (Na-AsA), butylated hydroxyanisole (BHA), and diphenyl on the development of urinary bladder tumors in a mouse two-stage carcinogenesis model were examined. Male B6C3F1 mice received 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in the drinking water for 4 weeks and were then treated with 5% Na-AsA, 1% BHA, or 1% diphenyl for 32 weeks.

Forestomach neoplasm induction in F344/DuCrj rats and B6C3F1 mice exposed to sesamol.

Sesamol was administered at a dietary level of 2% to groups of 30 male and female F344/DuCrj rats and B6C3F1 mice for 104 and 96 weeks, respectively. Squamous cell carcinomas in the forestomach were induced in nine of 29 (31%) effective male rats, three of 30 (10%) female rats, eleven of 29 (38%) male mice and five of 30 (17%) female mice treated with sesamol. Papillomas developed in ten of 29 (34%) male rats and fourteen of 30 (47%) female rats, but not in any of the mice.

Enhancing effects of harman and norharman on induction of preneoplastic and neoplastic kidney lesions in rats initiated with N-ethyl-N-hydroxyethylnitrosamine.

The modifying potential of two nephrotoxic agents, harman and norharman, on N-ethyl-N-hydroxyethylnitrosamine (EHEN)-induced renal and hepatic carcinogenesis was investigated in male F344/DuCrj rats. Animals were given 0.1% EHEN in their drinking water for the first 2 weeks as an initiator.

Carcinogenicity of uracil, a nongenotoxic chemical, in rats and mice and its rationale.

In Experiment 1, groups of thirty 6-wk-old male and female F344 rats were given diets containing 0 (control) or 3% uracil for 104 wk. In the uracil-treated groups, carcinomas, in particular transitional cell carcinomas, developed in the urinary bladder of 90% of the males and 19% of the females. Squamous cell carcinomas also developed in 10% of the males, but not in females.

The modifying effects of indomethacin or ascorbic acid on cell proliferation induced by different types of bladder tumor promoters in rat urinary bladder and forestomach mucosal epithelium.

The effects of indomethacin (IM) or L-ascorbic acid (AsA) on cell proliferation induced by bladder tumor promoters such as butylated hydroxyanisole (BHA), sodium L-ascorbate (Na-AsA), sodium citrate (Na-Cit), and diphenyl (DP) in rat bladder and forestomach epithelium were investigated. Treatment with IM in combination with BHA or Na-AsA diminished DNA synthesis levels of bladder epithelium as compared to the BHA or Na-AsA alone values. On the other hand, AsA further amplified the increase of bladder epithelial DNA synthesis caused by Na-Cit treatment.

Dose-dependent renal tubular toxicity of harman and norharman in male F344 rats.

The renal toxicity of harman and norharman, administered for 2 or 4 weeks at dietary levels of 1,000, 500, or 0 parts per million (ppm), was investigated in 6-week-old male F344/DuCrj rats. Although rats fed 1,000 ppm harman or norharman, but not the 500 ppm level, demonstrated marked body weight retardation from 1 week to termination, no mortalities occurred. Marked elevation of water consumption was evident in rats given harman or norharman at 1,000 ppm, but not at 500 ppm, together with large increases in urine of low specific gravity.

Induction of renal cell tumors in rats and mice, and enhancement of hepatocellular tumor development in mice after long-term hydroquinone treatment.

Hydroquinone (HQ) was administered to F344 rats and B6C3F1 mice of both sexes at a level of 0.8% in the diet for two years. This treatment induced renal tubular hyperplasia as well as adenomas, predominantly in males of both species, and was associated with chronic nephropathy in rats.

DNA synthesis and scanning electron microscopic lesions in renal pelvic epithelium of rats treated with bladder cancer promoters.

The proliferation response of rat renal pelvic epithelium, lined by transitional epithelium, to administration of various bladder cancer promoters was investigated. In addition, prostaglandin E2 (PGE2), lipid peroxide (LPO), malondialdehyde (MDA) and cyclic adenosine 3':5'-monophosphate (cyclic AMP) levels were assessed in urine of rats given the non-promoter L-ascorbic acid (AsA) and the promoters sodium L-ascorbate (AsA-Na) or sodium bicarbonate (NaHCO3) for 4 or 8 weeks. DNA synthesis in the renal pelvic epithelium, as assessed by 5-bromo-2'-deoxyuridine (BrdU) incorporation, was increased in the groups given AsA-Na, an extremely high dose of sodium chloride (NaCl), tert-butylhydroquinone (TBHQ) or ethoxyquin (EQ).

Promoting effect of the peroxisome proliferator, clofibrate, but not di(2-ethylhexyl)phthalate, on urinary bladder carcinogenesis in F344 rats initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine.

The modifying potential of clofibrate and di(2-ethylhexyl)phthalate (DEHP) on second stage, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-initiated urinary bladder carcinogenesis was investigated in male F344 rats, using a uracil-accelerated transitional cell proliferation model. Six-week-old animals received 0.05% BBN in their drinking water for 4 weeks and then clofibrate (1.

Early proliferative responses of forestomach and glandular stomach of rats treated with five different phenolic antioxidants.

The effects of 8 weeks of oral administration of five different phenolic antioxidants, e.g. catechol (CC), resorcinol, hydroquinone (HQ), 2-tert-butyl-4-methylphenol (TBMP) and propylparabene (PP), on forestomach and glandular stomach epithelium of male F344 rats were evaluated using a combined immunohistochemical and histopathological approach.

Stomach carcinogenicity of caffeic acid, sesamol and catechol in rats and mice.

The carcinogenic potential of caffeic acid, sesamol and catechol was examined in male and female F344 rats and B6C3F1 mice, groups of 30 animals being treated with diets containing 2% caffeic acid, 2% sesamol or 0.8% catechol for 104 weeks (rats) or 96 weeks (mice). Histological examination revealed that caffeic acid induced forestomach squamous cell carcinoma in 57% (P less than 0.

Responses of rat urine and urothelium to bladder tumor promoters: possible roles of prostaglandin E2 and ascorbic acid synthesis in bladder carcinogenesis.

An investigation of sequential changes in urine composition, levels of DNA synthesis and morphology of bladder epithelium following administration of the tumor promoters sodium ascorbate (AsA-Na) or butylated hydroxyanisole (BHA) and the non-promoter ascorbic acid (AsA) for 36 weeks was performed. In addition, prostaglandin E2 (PGE2), cAMP and AsA content were assessed in bladder tissue after 16 weeks. While AsA-Na caused increase in pH, sodium content and volume, and a decrease in osmolality of the urine throughout the study, these changes were not observed with AsA administration which resulted in a decrease in urinary pH.

Pyloric gland phenotypic expression of gastric cancers developing in the rat fundic glandular stomach.

Mucin histochemistry of experimental gastric cancers induced in rats by N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline 1-oxide was analysed by labelled lectin staining for concanavalin A (Con A) after prior periodate oxidation (paradoxical Con A staining) or Arachis hypogarea agglutinin (peanut lectin, PNA) with or without prior periodate oxidation. In the digestive tracts of control-group rats the mucins were classified into class II or III by paradoxical Con A staining. Class II mucins were found in surface mucous cells, goblet cells and the surface coat of intestinal absorptive cells, while class III mucins were present in mucous neck cells, pyloric gland cells and Brunner's gland cells.