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. Kłosowska D., Kłosowski B., Nowak B. (1995). Histopathological changes in longissimus muscle of Pietrain pigs and its crosses. Proceedings of the 2nd Dummerstorf Muscle Workshop on Muscle Growth and Meat Quality, Rostock, 17-19 May 1995, pp. 84-91. Paciello O., Papparella S. (2009). Histochemical and immunohistochemical approach to comparative neuromuscular diseases. Folia Histochem. Cytobiol., 47: 143-152. Pospiech E., Borzuta K., Łyczyński A., Plókarz W. (1998). Meat defects and their economic importance. Pol. J. Food Nutr. Sci., 7/48, 4: 7-20. Rahelič S., Pauc S

pathogenesis associated with wood smoke exposure. Chest 2005;128:124-31. 4. Pandey MR, Regmi HN, Neupane RP, Gautam A, Bhandari DP. Domestic smoke pollution and respiratory function in rural Nepal. Tokai J Exp Clin Med 1985;10:471-81. 5. Boleij JSM, Ruigewaard P, Hoek F, Thairu H, Wafula E, Onyango F, de Koning H. Domestic air pollution from biomass burning in Kenya. Atmos Environ (1967) 1989;23:1677-81. 6. Ozbay B, Yener Z, Acar S, Kanter M. Histopathological changes in the lung of rat following long - term exposure to biomass smoke. Turkiye Klinikleri J Med Sci 2009

Abstract

The presence of metacercariae of Centrocestus formosanus was detected on the gills of goldfish (Carassius auratus L.) imported from Singapore and obtained from two pet shops. This is the first report of the parasite in Croatia. The histopathological changes observed lead to the conclusion that the infection could be one of the reasons for the death of goldfish.

note on related genera - J. Helminthol. 32: 1-16. Hayunga E. G. 1979 - Observation on the intestinal pathology caused by three caryophyllid tapeworms of the white sucker Catostomus commersoni Lacepede - J. Fish. Dis. 2: 239-248. Hoste H. 2001 - Adaptive physiological processes in the host during gastrointestinal parasitism - Int. J. Parasitol. 31: 231-244. Jara Z., Szerow D. 1981 - Histopathological changes and localization of the cestode Khawia sinensis in the intestine of carp ( Cyrinus carpio ) - Wiad. Parazytol. 27: 695-703 (in Polish) Kapustina N. I. 1978

Abstract

Butyl p-hydroxybenzoic acid, also known as butylparaben (BP), is one of the most common parabens absorbed by the skin and gastrointestinal tract and metabolised in the liver and kidney. Recent in vivo and in vitro studies have raised concern that BP causes reproductive, development, and teratogenic toxicity. However, BP-induced oxidative stress and its relation to tissue damage has not been widely investigated before. Therefore, we aimed to investigate the effects of butyl 4-hydroxybenzoate on enzyme activities related to the pentose phosphate pathway and on glutathione-dependent enzymes such as glucose 6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) in kidney, liver, brain, and testis tissues. Male rats were randomly divided into four groups to orally receive corn oil (control) or 200, 400, or 800 mg/kg/day of BP for 14 days. Then we measured G6PD, GR, GST, 6-PGD, and GPx enzyme activities in these tissues and studied histopathological changes. BP treatment caused imbalance in antioxidant enzyme activities and tissue damage in the liver, kidney, brain, and testis. These findings are the first to show the degenerative role of BP on the cellular level. The observed impairment of equivalent homeostasis and antioxidant defence points to oxidative stress as a mechanism behind tissue damage caused by BP.

Histopathological Changes in Rat Liver After A Single High Dose of Aluminium

Aluminium (Al) exposure may affect the liver of experimental animals. This investigation aimed at evaluating morphological changes in rat liver after a single high dose of Al (as metallic powder suspension). A total of forty female Wistar rats were divided in one exposed and one control group, 20 rats each. The exposed rats received 0.5 mL of sterile physiological suspension of fine Al powder in the concentration of 100 mg mL-1 intraperitoneally (50 mg Al per rat). After 7 weeks all animals were killed (by exsanguination from the abdominal aorta in ether anaesthesia). Liver aluminium was analysed using electrothermal atomic absorption spectrometry. For light microscopy the liver tissue was stained with hematoxylin and eosin, and for histochemical analysis with aurin threecarbocsillic acid (aluminon).

Liver Al level was markedly higher in the exposed (37.1 μg g-1) than in control rats (0.71 μg g-1). The exposed rats showed crystalloid Al inclusions in the capsular, subcapsular, and portal liver tissue. The basic liver structure remained intact. Slightly multiplied bile ductuli were found in 16 of 20 exposed and in 8 of 20 control rats. Three exposed rats had mycrovesicular steatosis. The peritoneum and Glisson's capsule showed strong macrophage infiltration and a foreign-body-like reaction with multiple giant macrophages containing Al crystalloid inclusions. Although this reaction was a defense against the metal, some Al passed this barrier and entered the liver tissue, exerting toxic effects in bile ductuli and hepatocytes.

Summary

Until now studies in Brazil of the pathological action of Contracaecum sp. larvae in Hoplias malabaricus have been rare. The aim of the present study was to analyze and describe histopathological changes in the stomach of H. malabaricus caused by different intensities of infection by larvae of Contracaecum sp., and the hematological effects of such infection. The mean intensity of infection by L3 larvae of Contracaecum sp. correlated positively with Hematocrit percentage (Hct%) and correlated negatively with mean corpuscular volume (MCV). These findings are possibly related to the passage of larvae from the stomach to the mesentery, potentially due to hemorrhaging t. Fish with high infection intensity had larvae of Contracaecum sp in the submucosal of the stomach, which caused destruction of Type I and Type III collagen (finer and more delicate collagen fibers which do not form beams and are permeated by fundamental substances) around the parasite. Microscopic analysis showed that crypts were arranged regularly throughout the stomach mucosal, varying in number, size and depth, depending on the region of the stomach.

, India, Iran, and Jordan, have demonstrated the linear relationship and strong correlation between the serologic tests and histopathologic changes. [ 12 -13] CD disease has been underestimated throughout the world; however, data are not sufficient to support it strongly and most of the studies were on children. Besides, there are differences in genetics, race, and culture, and many countries depend on studies performed by other countries. Objectives of the study Aim of the study It is important to find more evidence to support or oppose the notion for confirming the

Liver, February 15–19, 2017, Shanghai, China (Rattanachaisit P, Susantitaphong P, Thanapirom K, Chaiteerakij R, Komolmit P, Tangkijvanich P, Treeprasertsuk P. Statin use and histopathological change in non-alcoholic fatty liver disease (NAFLD): meta-analysis [PP1555]. Hepatol Int. 2017; 11(Suppl 1):S929). This study was funded by the Liver Research Unit and an NAFLD research grant to the Division of Gastroenterology, and a research presentation grant from the Department of Medicine, Chulalongkorn University, Bangkok, Thailand. Author contributions ST proposed the

Abstract

The aim of the study was to find out the relationship between the progression of endometrosis and the appearance of the structural microscopic changes in mares’ ovaries. The investigation was performed on slaughtered mares of various age and breed. Four groups each received a portion of the specimens, and designation to group was according to the stage of endometrosis determined on the basis of Kenney’s classification. Uterine and ovarian sections were stained with haematoxylin and eosin. The results of the microscopic evaluation were compared between mares classified into specific Kenney’s categories. It was shown that an increase in ovarian follicular cysts was related to mares’ ages and correlated with significant progression of the endometrosis. These observations suggest that the same aetiological factors may take part both in triggering disorders of ovarian oo/folliculogenesis and in spurring uterine endometrosis. Further more detailed methods of investigation are needed to elucidate the mechanisms of both disease processes.