scholarly journals Splenohepatomegaly in Protein-Malourished Mice Infected with Plasmodium Vinckei

2019 ◽  
Vol 3 (1) ◽  
Keyword(s):  
Deleterious Effect ◽  
Fatty Infiltration ◽  
Inflammatory Cells ◽  
White Pulp ◽  
Casein Diet ◽  
Aminobenzoic Acid ◽  
Deficient Diet ◽  
Hepatic Cells ◽  
Uninfected Liver ◽  
Plasmodium Vinckei

Cellular and histopathological observations were made with light microscopy during the Plasmodium vinckeiinfection in protein-malnourished mice (fed on 2% casein diet and para-aminobenzoic acid deficient diet (PABA-DD).In the infected spleen, hyperplasia of the red as well as the white pulp was evident; active erythropoiesis and lymphopoiesis. Hyperemia and deposition of malarial pigments inside the macrophages. Cloudy swelling was noticed in the swollen hepatic cells of the uninfected liver due to protein deficiency. This lesion had developed to fatty infiltration in the infected protein-malnourished mice. These new and interesting changes represent the combined deleterious effect upon the host of infection and protein-malnutrition. Hypertrophy of the kupffer cells due to progressive phagocytosis of malarial pigments. In addition, focal necrosis surrounded by inflammatory cells was seen.

Hepatic function in rats with dietary-induced fatty liver, as measured by the uptake of indocyanine green

1982 ◽  
Vol 47 (3) ◽  
pp. 391-397 ◽  
Author(s):  
F. Jahoor ◽  
Alan A. Jackson
Keyword(s):  
Indocyanine Green ◽  
Fatty Liver ◽  
G Protein ◽  
Fatty Infiltration ◽  
Hepatic Function ◽  
Hepatic Uptake ◽  
Deficient Diet ◽  
Liver Lobule ◽  
Periportal Zone ◽  
Predominant Effect

1. The hepatic uptake of indocyanine green (ICG) has been measured in rats receiving a 50 g protein/kg diet for 6, 12 or 20 d or a choline-deficient diet for 2 or 6 d.2. There was no effect on ICG uptake on the choline-deficient diet, although all the rats developed an intense fatty infiltration of the liver by 6 d.3. The rats on the 50 g protein/kg diet showed impaired uptake of ICG at 6, 12 and 20 d, which appeared to be related to the extent of fatty infiltration.4. It is concluded that ICG uptake is predominantly a function of the periportal zone of the liver lobule, and therefore likely to be sensitive to insults that exert their predominant effect in this zone.

Abstract 17106: Transition From Adipose to Fibrotic Tissue in the Atrial Subepicardium in Humans and in a Sheep Model of Atrial Fibrillation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Peter Haemers ◽  
Hadhami Hamdi ◽  
Piet Claus ◽  
Patrick Farahmand ◽  
Patrick Bruneval ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Histological Study ◽  
Artery Bypass ◽  
Fatty Infiltration ◽  
Inflammatory Cells ◽  
Multiple Regression Model ◽  
Right Atrial ◽  
Human Right ◽  
Sheep Model

Epicardial adipose tissue (EAT) is recognized as potentially involved in the pathophysiology of atrial fibrillation (AF). In addition to EAT fatty infiltration commonly observed in myocardium might be also associated with the substrate for AF. We conducted a histological study in 93 human right atrial samples obtained during cardiac surgery and in a sheep model of long-term persistent AF (PAF) induced by atrial tachypacing (24±8 weeks) (15 PAF, 11 SR). Upon Sirius Red and Harris Haematoxylin staining, human atria showed various degree of fatty infiltration starting from the epicardium (rarely from vessels), which could be associated with various degree of subepicardial fibrosis realizing in some cases a true fibro-fatty infiltration. The extent of remodeled epicardium was assessed as % of infiltrating and fibrotic epicardium±adipose tissue to total epicardial length; 44±26 % of the epicardium was remodeled. A multiple regression model (including history of AF, % adipose tissue, age, BodyMassIndex, coronary artery bypass, ejection fraction) significantly predicted the percentage of epicardial remodeling (R=0.501, p=0.003). Only AF and the % adipose tissue were significant predictors (respectively β=0.27;p=0.016 and β=-0.267;p=0.016). To further analyze the relationship between fibro-fatty infiltration and AF, a histological study was performed in LA specimen of a sheep PAF model which revealed 4 grades of subepicardial infiltrates from pure fatty to dense fibro-fatty infiltration (fig A). EAT infiltrates (316) were graded, demonstrating a shift towards more severe grades in the AF group p<0.0001) (fig B). Inflammatory cells were detected in 14 fatty infiltrations (grade 2 and 3) of 6 AF sheep (and only in 1 fatty infiltration of SR sheep). Conclusion: , AF is associated with the transformation of fat into fibro-fatty infiltrations suggesting that the subepicardial adipose tissue plays a role in the atrial fibrotic remodeling.

scholarly journals CIRRHOSIS OF THE LIVER CAUSED BY EXCESS DIETARY CYSTINE

1941 ◽  
Vol 73 (2) ◽  
pp. 161-172 ◽  
Author(s):  
David P. Earle ◽  
Joseph Victor
Keyword(s):  
Fatty Infiltration ◽  
Cirrhosis Of The Liver ◽  
Cellular Damage ◽  
Albino Rats ◽  
Renal Lesion ◽  
Stock Diet ◽  
Hepatic Cells ◽  
Acute Lesion ◽  
Hemorrhagic Necrosis ◽  
Mitotic Figures

1. Cystine fed to young albino rats as 10 per cent of the diet resulted in: (a) Portal hemorrhagic necrosis, resembling eclampsia, within 3 or 4 days. (b) A high mortality rate. (c) Fatty infiltration of hepatic cells in all rats surviving the initial acute lesion. (d) Cirrhosis of the liver in rats surviving more than 2 weeks. 2. 5 per cent dietary cystine produced marked fatty infiltration of the liver, followed by portal hemorrhagic necrosis. Cirrhosis was present in one of the two rats on the diet for 6 weeks. 3. The livers of rats fed 5 or 10 per cent cystine diets followed by the McCollum stock diet, showed evidence of residual cellular damage, and of regeneration as shown by mitotic figures. 4. In this series of 30 rats on excess dietary cystine, a renal lesion was found in only one case.

Gastroenteritis of Basenji Dogs

1988 ◽  
Vol 25 (1) ◽  
pp. 36-41 ◽  
Author(s):  
N. J. MacLachlan ◽  
E. B. Breitschwerdt ◽  
J. M. Chambers ◽  
R. A. Argenzio ◽  
E. V. De Buysscher
Keyword(s):  
Chronic Diarrhea ◽  
Inflammatory Cells ◽  
Aminobenzoic Acid ◽  
Intestinal Function ◽  
Diffuse Infiltration ◽  
Mucosal Atrophy ◽  
Intestinal Lesions ◽  
Healthy Control ◽  
Small Intestinal ◽  
And Control

Intestinal digestive and absorptive function and the gross and histologic appearance of the gastrointestinal tract were evaluated in Basenji dogs with chronic diarrhea, asymptomatic Basenji dogs, and healthy control dogs. Gastric rugal hypertrophy, lymphocytic gastritis, and gastric mucosal atrophy occurred in asymptomatic and affected Basenji dogs. All affected dogs had moderate or severe intestinal lesions characterized by villous clubbing and fusion, increased tortuousity of intestinal crypts, and diffuse infiltration of mononuclear inflammatory cells. Intestinal lesions in asymptomatic Basenji dogs invariably were less severe than those in affected dogs, but the small intestinal lamina propria of asymptomatic Basenji dogs consistently contained greater numbers of mononuclear inflammatory cells than did that of control dogs. The proportion of cells containing each immunoglobulin isotype (IgG, IgM, IgA) was similar among affected Basenji dogs, asymptomatic Basenji dogs, and control dogs. As compared to healthy beagle controls, intestinal function was abnormal in both affected and asymptomatic Basenji dogs evaluated by combined N-benozoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test, but malabsorption and maldigestion were most pronounced in affected Basenji dogs.

scholarly journals Effect of experimental folate deficiency on lipid metabolism in liver and brain

1982 ◽  
Vol 47 (3) ◽  
pp. 505-520 ◽  
Author(s):  
B. Åkesson ◽  
C. Fehling ◽  
M. Jägerstad ◽  
U. Stenram
Keyword(s):  
Morphological Changes ◽  
Fatty Infiltration ◽  
Light And Electron Microscopy ◽  
Intraperitoneal Administration ◽  
Folate Deficiency ◽  
Neurological Dysfunction ◽  
Liver Phospholipid ◽  
Deficient Diet ◽  
Low Concentrations ◽  
Parenchymal Cells

1. Rats were given a purified folate-deficient diet containing 5 g succinylsulphathiazole/kg for 4–5 months in two experiments. Control rats were supplemented with folic acid in the drinking-water.2. Weight gain was much below normal in the folate-deprived rats after the first month. Very low folate levels were recorded in blood, liver and peripheral nerve (12–33% of control). In Ihe central nervous system, including the cerebrospinal fluid, the folate depletion was less conspicuous (50–80% of control). Only marginal signs of anaemia were found and no signs of neurological dysfunction were detected, using nerve conduction velocity measurement and co-ordination tests.3. Light and electron microscopy of the folate deficient liver revealed fatty infiltration, and enlargement of liver parenchymal cells, nuclei and nucleoli. There was often a considerable amount of bile ductular cells in the lobuli but no cirrhosis. The morphological changes resembled those observed in choline deficiency.4. Phospholipid N-methylation in liver was depressed in folate deficiency. This was probably due to a decreased availability of S-adenosylmethionine caused by the low concentrations of methylated folate in liver. Intraperitoneal administration of methionine did not normalize phospholipid methylation.5. In folate deficiency the proportion of ethanolamine phosphoglyceride in liver was increased at the expense of choline phosphoglyceride, which is consistent with a decreased phospholipid methylation. Also an increase in liver triacylglycerol was noted, in accordance with the morphological observations. Brain lipid composition was unchanged.6. After the injection of labelled ethanolamine, isotope accumulated in liver phosphoethanolamine in folate deficiency, probably due to an impairment of the CTP: ethanolaminephosphate cytidylyltransferase(EC2.7.7.14) reaction. The mechanism of this impairment is discussed.7. Although the low concentrations of folate was the main nutritional change in the deprived animals, changes with respect to vitamin B12and maybe also choline cannot be excluded. We conclude that some of the changes in folate deficiency, i.e. fatty liver and decreased biosynthesis of liver phospholipids may be due to a precipitated deficiency of lipotropic agents, whereas other differences may be specific for deficiency of folateper se, such as changes in liver phospholipid fatty acids and some of the morphological aberrations.

scholarly journals Early induction of hepatic deiodinase type 1 inhibits hepatosteatosis during NAFLD progression

2021 ◽  
Author(s):  
Eveline Bruinstroop ◽  
Jin Zhou ◽  
Madhulika Tripathi ◽  
Winifred Yau ◽  
Anita Boelen ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Treatment ◽  
Compensatory Mechanisms ◽  
Deficient Diet ◽  
Alcoholic Fatty Liver ◽  
Thyroid Hormone Metabolism ◽  
Hepatic Cells ◽  
Triglyceride Content

Objective - Non-alcoholic fatty liver disease (NAFLD) comprises a spectrum ranging from hepatosteatosis to progressive non-alcoholic steatohepatitis that can lead to cirrhosis. Humans with low levels of the prohormone thyroxine (T4) have a higher incidence of NAFLD and thyroid hormone treatment is very promising in all patients with NAFLD. Deiodinase 1 (Dio1) is a hepatic enzyme that converts T4 to the bioactive T3, and therefore regulates intracellular thyroid hormone availability in the liver. The role of this intracellular regulation was investigated during the progression of NAFLD. Methods - We investigated intracellular thyroid hormone metabolism in two NAFLD models: wild-type mice fed Western diet with fructose and Leprdb mice fed a methionine- and choline-deficient diet. AAV8-mediated liver-specific Dio1 knockdown was employed to investigate the role of Dio1 during the progression of NAFLD. Intrahepatic thyroid hormone levels, deiodinase activity and metabolic parameters were measured. Results - Dio1 expression and activity were increased in the early stages of NAFLD and were associated with an increased T3/T4 ratio. Prevention of this increase by AAV8-mediated liver-specific Dio1 knockdown increased hepatic triglycerides and cholesterol as well as decreased pACC/ACC ratio and acylcarnitine levels suggesting there was lower β-oxidation. Dio1 siRNA KD in hepatic cells treated with fatty acids showed increased lipid accumulation and decreased oxidative phosphorylation. Conclusion - Hepatic Dio1 gene expression was modulated by dietary conditions, increased during hepatosteatosis and early NASH, and regulated hepatic triglyceride content. These early adaptations likely represent compensatory mechanisms to reduce hepatosteatosis and prevent NASH progression.

scholarly journals Histopathological changes and immunosuppression induce by diazepam in mice

2014 ◽  
Vol 13 (1) ◽  
pp. 59
Author(s):  
A. H. Ali
Keyword(s):  
Immune Response ◽  
Mononuclear Cells ◽  
Inflammatory Cells ◽  
Brain Parenchyma ◽  
Pathological Examination ◽  
Central Vein ◽  
Cell Mediated Immunity ◽  
White Pulp ◽  
Histological Changes ◽  
Immunological Examination

In order to investigate the histological changes and immunosuppression effects of diazepam in mice, forty white mice of both sexes were divided into four groups equally. 1st group was immunized twice with pasturella multocida (bacterines) with two weeks intervals. 2nd group was immunized as in the 1st group and at same time administrated orally with 0.6 mg\kg b.w of diazepam daily for 8 weeks. 3rd group was administrated with diazepam as in the 2nd group while 4th group was served as control negative group. Immunological examination revealed that the diazepam inducing depresses of the both arms of immune response, the cell mediated immunity and humeral immunity as comparing with vaccinated non-treatment animals. The pathological examination revealed that the diazepam induced large multiple granulomatous liver lesions consist form aggregation mononuclear cells particularly macrophages and lymphocytes. In addition, section of kidney showed marked inflammatory cells infiltration particularly mononuclear cells and neutrophils in the interstitial tissues was seen. In spleen there was congestion of blood vessels with mononuclear cells in their lumen and depletion of white pulp as well as proliferation of megakaryocytes, in addition to gliosis in the brain parenchyma was seen. The immunized animals showed mild pathological changes characterized by aggregation mononuclear cells around central vein in addition to proliferation of kupffer cells, Spleen show proliferation of lymphocytes in the periartiriolar sheath as well as protein aqueous materials deposition around white pulp. We concluded that diazepam induced Histological changes in the internal organs of mice and stimulated the immune response diminished its toxic effects.

scholarly journals Histopathological Changes in the Liver and Spleen of Common Carp Cyprinus carpio L. Challenge with Pseudomonas aeruginosa (Schroeter, 1872) Fed with Dietary Chitosan and Ciprofloxacin

2019 ◽  
Vol 32 (2) ◽  
pp. 193-207
Author(s):  
Omeet F.M.H Al-Mossawai ◽  
Atheer H. Ali
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Post Infection ◽  
Inflammatory Cells ◽  
Positive Control ◽  
White Pulp ◽  
Standard Diet ◽  
Feeding Period ◽  
Histopathological Changes ◽  
Infection Period ◽  
Mortality Percentage

The current study was conducted for 90 days in order to study the efficacy of dietary chitosan and antibiotic ciprofloxacin supplement as a resistance and presentation of fishes against the bacteria (Pseudomonas aeruginosa) by effect on liver and spleen of fishes. The fishes were divided into four categories of groups at two periods; the former at infection (at 90th day of feeding period) and the latter at post infection (14 days after the challenge period). The first and second groups (T1 and T2) were considered as negative and positive controls (both fed on standard diet), respectively, while the third and fourth groups (T3 and T4) represent dietary chitosan and dietary antibiotic supplement, respectively. All groups, except T1, were challenged by bacteria at 90th day of feeding period. Liver of positive control revealed severe degeneration, especially around hepatic vein with congestion and fibrosis, while the spleen exhibited haemorrhage, lymphocytosis and lymphatic accumulation of white pulp with hemosiderin. The histopathological changes in liver of chitosan group at the infection period were characterized by vacuolation, inflammatory cells and hemorrhage, while necrosis and swelling of hepatocytes and infiltration with inflammatory cells at post infection period. The spleen at the infection period was suffered from leukocytosis, accumulation of inflammatory cells and macrophages, presence of focus from phagocytic macrophages. The liver in antibiotic group of infection period displayed narrowing of the sinusoid, swelling of hepatocytes and infiltration with inflammatory cells, hyperplasia in the bile duct, while the abnormal accumulation of lymphatic follicles. At postinfection period, the spleen showed thickness at the wall capsule, presence of homogeneous pinkish matter around arteriole in the red pulp and lymphocytosis in the white pulp. The supplemented chitosan groups showed a significant decrease in the mortality percentage . The supplemented chitosan groups showed a significant decrease in the mortality percentage.

scholarly journals Toxicological Pathologic Study of effect of various Insulin doses in mice

2006 ◽  
Vol 30 (2) ◽  
pp. 151-164
Author(s):  
Buthaina J. Jwaad
Keyword(s):  
Adipose Tissue ◽  
Fatty Infiltration ◽  
Normal Activity ◽  
Laboratory Animals ◽  
Control Group ◽  
High Dose ◽  
White Pulp ◽  
Splenic White Pulp ◽  
Extramedullary Haemopoiesis ◽  
Group B

This study concentrate on the effect of synthetic insulin in laboratory animals, 80 white mice, randomly divided into four main groups of males and females control –untreated, treated as low dose, intermediated dose and high dose, then every group also divided in two subgroups, the first subgroup was given Actrapid and second subgroup was given Monotrade , the tested material was given daily subcutaneously untreated control group . The injection was continued until animals were killed after 24 weeks of treatment .Clinical, macroscopical and microscopical studies of experimental mice in comparison with the control group and the result were as follows : 1- Injected mice showed normal activity, with increase body weight and low food consumption in comparison to controls. On several occasions, there were attacks of hypoglycaemia with coma in treated mice. 2- Macroscopic examination of treated mice showed presence of several layers of adipose tissue around visceral organs , in peri renal region , in the serosal areas of small intestine , in peri bronchial region, in subcutaneously , peri pancreatic region , splenic enlargement in scattered treated animals , 3- Histopathological changes were seen as fatty infiltration / degeneration in the liver, dilated cortical tubules in the kidney and enlarged zona fasciculate of the adrenals. In addition to atrophy and / or depletion of pancreatic islet of langerhans, also extramedullary haemopoiesis and / or atrophy of lymphoid tissue in the spleen, with peri follicular deposits of amyloid in Splenic white pulp and in glomeruli of kidneys of group B. Furthermore, there were evidence of steatitis (focal inflammation of adipose tissue) and enlargement of zona fasiculata in adrenals.    

Early interactions ofEntamoeba histolyticatrophozoites with parenchymal and inflammatory cells in the hamster liver: an immunocytochemical study

2002 ◽  
Vol 48 (2) ◽  
pp. 123-131 ◽  
Author(s):  
J Ventura-Juárez ◽  
R Campos-Rodríguez ◽  
V Tsutsumi
Keyword(s):  
Endothelial Cells ◽  
Entamoeba Histolytica ◽  
Close Contact ◽  
Inflammatory Cells ◽  
Ultrastructural Level ◽  
Target Cells ◽  
Nonparenchymal Cells ◽  
Hepatic Cells ◽  
Pmn Leukocytes ◽  
Parenchymal Cells

We studied the early in situ interactions of live and fixed Entamoeba histolytica trophozoites with hamster hepatic parenchymal and inflammatory cells using immunoperoxidase and immunoelectronmicroscopy. Close contact between trophozoites and endothelial cells and the diffusion of amoebic molecules from trophozoites towards nearby endothelial cells and distant hepatocytes were observed. The inflammatory cells around the amoebae and the remnants of parenchymal cells and hepatocytes located close to the lesion had a positive stain for amoebic molecules. In the amoebae, at the ultrastructural level, molecules were attached to the membranes and inside the vesicles. These molecules were apparently released into the space formed between the parasite and the endothelial cells. The endothelial cells and the nearby and distant hepatocytes captured amoebic molecules, and later they became necrotic. Contrarily, when fixed amoebae were inoculated, amoebic molecules were captured by endothelial cells and polymorphonuclear (PMN) leukocytes, but neither suffered any damage. In this work, we are presenting evidence clearly showing that some molecules of the amoeba can diffuse away long distances causing cytotoxic effects and even necrosis on hepatic cells of hamster liver without the need of the trophozoite being in close contact with the target cells. They also may promote lytic or proinflammatory effects by inducing the secretion of enzymes or cytokines in other nonparenchymal cells, like PMN leukocytes and endothelial cells. Our results suggest that the accepted mechanisms of cytotoxicity by amoebae are not exclusively restricted to the following sequence: adhesion, phagocytosis, and necrosis.Key words: amoebiasis, Entamoeba histolytica, liver, hamster, immunocytochemistry.

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