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At least 343 records · Page 19Linked to original sources
PubMed1992

[Experimental models of combined tuberculosis-opisthorchiasis pathology].

An experimental model of the combined course of tuberculosis and opisthorchiasis is presented in the following variants: pulmonary tuberculosis-chronic opisthorchiasis, acute and chronic opisthorchiasis in combination with tuberculosis contamination, BCG and opisthorchiasis. Specific changes in the combined pathology are shown which differ from those that accompany each of the nosological forma. Data obtained in bacteriologic, parasitologic, immunologic and pathomorphologic studies were used to describe characteristic features of the models. The results obtained allow a suggestion that parasitocenosis of mycobacteria and Opisthorchis organisms has an influence on the pathogenesis, clinical picture, diagnosis, treatment, epidemiology and prevention of tuberculosis-opisthorchiasis combined pathology.

Animals↗
PubMed1989

[Experimental models of osteo-arthrosis].

A number of experimental models that variably simulate human osteo-arthritis with respect to pathology, biochemistry, and pathogenesis are already available. They are reasonably consistent in reproducibility, and the exact time of induction of joint derangement leading to degenerative change can be accurately identified. The availability of such models has led to an increased understanding of pathology, biochemical changes, pathogenesis and therapeutic assessment of osteoarthritis.

Animals↗
PubMedDate not supplied

Proposal of an experimental model of fetal hydrocephalus.

There have been numerous experimental studies reported in literature that simulate congenital hydrocephalus. The various techniques that have been proposed present the obstacle of being difficult to reproduce and the results therefore, often do not match. We have proposed a new experimental model that is easily created, reproduced and that allows for precise monitoring of the hydrocephalic entity, in addiction to presenting itself as an example to follow in resolving the hydrocephalic pathology. The authors report the results relative to their case studies of 14 pregnant animals treated and they list and discuss the principal complications encountered.

Abortion, Veterinary↗
PubMed1985

[Cultivation of exo-erythrocytic schizonts of rodent Plasmodium in hepatocytes: a new experimental model for chemotherapy of malaria].

An in vitro experimental model using primary cultures of laboratory bred Thamnomys gazellae's hepatocytes and Plasmodium yoelii yoelii' sporozoites was set up for chemotherapeutic studies. The surface of the culture was reduced (0.5 cm) and allowed the rapid performance and analysis of schizonticide activity tests, with a reduced biological material (Rodents, Anopheles, sporozoites). Fifteen compounds were tested. When activity of molecules is known in vivo, both results in vivo and in vitro are parallel.

Animals↗
PubMed1979

Changes in transglutaminase activity in an experimental model of pulmonary fibrosis induced by paraquat.

An experimental model of pulmonary fibrosis has been developed by dosing rats with one-fifth the LD50 dose of the herbicide paraquat on 5 consecutive days. Approximately 50% of the rats died within 4 days of the completion of dosing, showing macroscopic changes and wet weight increases in the lung consistent with severe oedema. Those animals which died between Days 4 and 10 had markedly increased levels of hydroxyproline in the lung, maximum at Day 6, and increased prolyl hydroxylase activity, maximum at Day 4. These changes, together with an increase in thymidine incorporation into DNA, and increased lung DNA content, were consistent with the development of fibrosis. Measurement of transglutaminase activity in the lung showed marked increases at Days 4 and 10 after completion of dosing. This activity paralleled closely the changes in prolyl hydroxylase activity and became increasingly associated with particulate protein present in the "nuclear pellet" fraction. The presence of zymogen plasma transglutaminase trapped in lung homogenates could not be demonstrated but the contribution by the active plasma transglutaminase (Factor XIIIa) to increases shown at Day 4 cannot be ruled out.

Animals↗
PubMed2003

Poisoning of mice by Baccharis coridifolia: an experimental model.

The poisonous plant Baccharis coridifolia causes necrosis in lymphoid tissues and the gastrointestinal tract of cattle, horses, sheep and rabbits. An experimental poisoning of mice was undertaken to establish an experimental model in a laboratory animal specie. A single 5 to 8-g/kg dose of a suspension of the plant was administered by gavage to 11 mice. To 3 other control mice, the same volume of water was administered. Plant-dosed mice manifested clinical effects after 12 h: tachipnea, trembles, dehydration and prostration. Most of the dosed mice died 14 to 33 h after plant administration--3 survived for 12 d. Six mice had remarkable necrosis of the germinative center of secondary follicles in lymph nodes and spleen; 3 mice had necrosis of lymphoid tissues in intestine and thymus. Mice reproduce most of the lesions observed in naturally poisoned cattle and the use of this specie as an experimental model is valid.

Administration, Oral↗
PubMed1997

Effect of policosanol on circulating endothelial cells in experimental models in Sprague-Dawley rats and in rabbits.

The effect of policosanol on circulating endothelial cells has been studied in different experimental models with endothelium damage. Oral administration of 25 mg kg-1 policosanol to Sprague-Dawley rats resulted in significant protection of the endothelial lining against the desquamating effect of citrate. Oral administration of 5 mg kg-1 policosanol to spontaneously hypertensive rats (SHR) resulted in a significant reduction of circulating endothelial cells compared with controls. Moreover, comparison between groups revealed a lower frequency of aortic lesions in policosanol-treated animals than in controls. On the other hand, administration of 5 mg kg-1 policosanol to rabbits with intimal hyperplasia induced by cuff placement in the carotid artery resulted in levels of circulating endothelial cells significantly lower than in controls. These results demonstrate the protective effect of policosanol in different experimental models and suggest its potential for endothelial protection.

Animals↗
PubMed2003

Experimental models of inflammatory bowel disease.

The etiology and pathogenesis of inflammatory bowel disease (IBD) remains unsolved, but improved experimental models of enterocolitis have led to progress. Intestinal inflammation and experimental IBD can be induced by chemical or dietary factors or by microbial products. Many animal models of IBD can be used to evaluate new anti-inflammatory drugs. These models, however, usually demonstrate acute, self-limiting colitis. The spontaneous colitis models developed in the cotton-top tamarin monkey and the C3H/HeJBir mouse mimic more features of human IBD. Inflammation is chronic and is under genetic control. The differential genetic susceptibility of inbred rat strains to chronic inflammation have been exploited. Lewis rats injected with bacterial products, peptidoglycan polysaccharide or indomethicin develop chronic relapsing enterocolitis, whereas closely related Buffalo or Fisher rat strains develop only transient inflammation. These models are also useful to test the specific inhibition of inflammatory mediators and target molecules. Over-expression (transgenic) or deletion (knockout) of specific genes have led to the development of rodent models of spontaneous colitis. Inflammation arises from a number of mutations of immunomodulatory molecules, supporting the concept of genetic heterogeneity for IBD. The results obtained from experimental models have generated new hypotheses, expanded human studies, and suggested novel forms of therapy for IBD patients.

Animals↗
PubMed2006

Hyperbaric oxygen therapy prevents coagulation disorders in an experimental model of multiple organ failure syndrome.

OBJECTIVE: To evaluate the effects of hyperbaric oxygen (HBO) therapy on the coagulation cascade using an experimental model of multiple organ failure syndrome (MOFS). DESIGN: MOFS was induced by zymosan (500mg/kg i.p.) in rats. HBO therapy (2ATA) was administered in a cylindrical steel chamber 4 and 11h after zymosan administration. In a separate set of experiments animals were monitored for 72h, and systemic toxicity was scored. INTERVENTION: Eighteen hours after zymosan administration, rats were killed and blood samples were used for analysis of hemocoagulative parameters, hemodynamics, and arterial blood gas. MAIN RESULTS: Zymosan administration caused MOFS by affecting the coagulation cascade, as shown by a significant increase in plasma levels of fibrinogen, tissue plasminogen activator, inhibitor of tissue plasminogen activator of type 1, and plasma levels of fibrin degradation products vs. control rats. Zymosan-induced MOFS was also characterized by a significant increase in von Willebrand antigen plasma levels vs. controls. Moreover, zymosan administration induced a significant fall in mean arterial blood pressure and alteration in blood gas values. HBO therapy significantly reduced the derangements of coagulation cascade, the fall in mean blood pressure and alteration in blood gas induced by zymosan administration. CONCLUSIONS: The hypercoagulability induced by zymosan could be responsible for organ failure and death. Our data demonstrate that HBO therapy significantly prevents the alteration in the coagulation cascade and arterial blood gas in an experimental model of MOFS.

Animals↗
PubMedDate not supplied

Connexin 43 mRNA expression in two experimental models of epilepsy.

The expression of mRNA for connexin 43, a gap junction protein putatively found in astrocytes, is studied in two experimental models of epilepsy: the electrically kindled rat and the tetanus-toxin-injected rat. Rats were kindled by electrical stimulation of the amygdala to Racine class 5 seizures and divided into cohorts of three to undergo 3, 6, or 10 such events, respectively. Another two cohorts of rats received injections of tetanus toxin at strengths of 3 and 9 MLD50, respectively, into the amygdala. Features of epileptogenicity were identified electrographically in both cohorts during the first 4 wk following toxin injection with spontaneous ictal events recorded in the latter cohort. All rats were sacrificed 4 wk after electrode or cannula implantation, except for two toxin-injected cohorts that were sacrificed at wk 8 or 10. The epileptogeonic area in the region of the amygdala was harvested and pooled by cohort for Northern blot analysis. These were compared with control nonimplanted tissues. In the tetanus-toxin-injected animals, at time-points of 4, 8, and 10 wk, connexin 43 mRNA expression in epileptogenic tissues is found to be decreased or unchanged relative to control cases. Kindled rats demonstrated reductions of connexin mRNA with a trend toward normalizing levels with increasing numbers of stimulations when compared to control animals. Connexin 43 immunostained sections of the basolateral amygdala showed a similar trend in protein expression. Both experimental models of epilepsy show no connexin 43 mRNA upregulation despite varying degrees of epileptogenicity. This study therefore does not support the hypothesis that an increase in transcription is the basis for any proposed increase in gap junction communication involving connexin 43 in the context of epileptogenicity or as a reaction to increased neuronal excitability.

Animals↗
PubMed1991

Importance of experimental models for the development of clinical trials on thromboatherosclerosis.

Experimental models of vascular injury have enhanced our understanding of the pathophysiological process leading to vascular obstruction in both spontaneous and accelerated atherosclerosis. Based on experimental findings, we present and discuss a pathological classification of vascular injury or damage and its role in the pathogenesis of various vascular diseases. In addition, these animal models have provided insights into the roles of platelets and lipid metabolism in the evolution and progression of atherosclerosis and have suggested potential therapeutic applications. Thus, based on studies in the pig models, antiplatelet agents have been shown for the first time to have a beneficial effect in preventing the formation and progression of coronary atherosclerotic lesions in humans. Similarly, our findings in high density lipoprotein plasma fractions regarding inhibition and even reversal of the process of atherosclerosis in a hypercholesterolemic rabbit model have added new insights to an explosive field of lipoprotein research and provided new avenues of therapeutic strategies. our in vivo and ex vivo pig models of an extracorporeal perfusion chamber mimicking the various coronary conditions have aided in the understanding of the pathophysiology of the acute coronary syndromes and intensified our search for the ideal antithrombotic regimen in these high-risk patients. Finally, a carotid pig model of balloon angioplasty, a dog model of saphenous vein grafting, and a pig model of heart transplantation not only have provided insights into the pathophysiological process of accelerated atherosclerosis but also are allowing development of new antithrombotic and antiproliferative approaches for the prevention of these accelerated vascular diseases. In summary, we are entering an exciting era in vascular research. Significant advances in our understanding of vascular injury or damage as well as the interactions of blood cells and lipids with the vascular wall have allowed us to formulate new experimental strategies with subsequent clinical application in the prevention and progression of these vascular diseases.

Animals↗
PubMedDate not supplied

[An experimental model of the vertical transmission of the Coxsackie-group enteroviruses and its use in developing methods to prevent congenital coxsackievirus infection].

An experimental model of vertical transmission of Coxsackie group enteroviruses was developed in BALB/c mice the first generation of which was infected with Coxsackie A18 virus in the neonatal period. Persistence of the virus was demonstrated in all females of the first generation tested and in 90.9% to 100% of the animals of the next two generations. Cytochemical analysis of the enzyme status of lymphocytes revealed reliable relationship between the depression of energetic metabolism enzymes and the activity of virus amplification in the animals under study. The correction of aerobic respiration in pregnant females by administration of a complex of energy metabolism substrates and cofactors was accompanied by a significant reduction of the virus infection activity in the females and their offsprings as well as by prevention of transplacental infection in some litters. The experimental model of vertical transmission of enteroviruses is proposed for use in the development of methods for prevention of congenital Coxsackie virus infection. The authors express their deep gratitude to the sponsor of the publication--NOVRUZ Co., Turkmenistan.

Animals↗
PubMed2001

An experimental model of gastroschisis using fetoendoscopy: preliminary results and technical considerations.

BACKGROUND: The aim of this study was to show the feasibility of an experimental model of gastroschisis using fetoendoscopic surgery on sheep fetuses, and also to perform amnioinfusion until delivery using an in-dwelling intraamniotic catheter. METHODS: We analyzed the data from 18 pregnant ewes having 26 fetuses, which underwent surgery at 80 days of gestation (full term, 145 days). The fetendo technique was used to create a gastroschisis in 15 fetuses. The fetal abdominal wall was opened on the left side of the cord using scissors. The omentum and the intestinal loops were eviscerated using atraumatic forceps. Eleven fetuses were used as a control group. Twenty-one fetuses underwent amnioinfusion; a simple exteriorized catheter was used in seven cases and an intraamniotic catheter with an implantable port was used in the other 14. All ewes and fetuses were killed at the end of the experiment by an intravenous injection of pentotal; thereafter, the fetuses underwent necropsy. RESULTS: Twelve fetuses died and 14 survived (53.8%); seven of the 15 that underwent gastroschisis survived (46.7%). An amniotic infection occurred in nine fetuses (34.6%); of these, six died and three that were administered antibiotics survived. CONCLUSIONS: Our experience shows that this experimental model of gastroschisis is feasible and reproducible, and that a repeated amnioinfusion can be performed with an in-dwelling catheter in pregnant ewes. The use of an implantable port is safer than a simple exteriorized catheter.

Animals↗
PubMed2004

An in-vivo experimental model for studying wound-healing after laser irradiation in the mouse foetus.

OBJECTIVE: The purpose of this study was to develop an experimental model to study wound-healing in the mouse foetus by inducing an injury with an argon laser. MATERIAL AND METHODS: ICR strain mouse dams were used in this study at day 14 of gestation. Laparotomy was performed on the dams under sodium pentobarbital anaesthesia, and foetuses were exposed from the uterus while wrapped in the amnion. Laser radiation was conducted through the amniotic membrane, and the beam was focused on to the naso-labial region. After laser irradiation, the foetus was returned to the abdominal cavity of the dam. Then the abdominal wall was closed, and an extrauterine pregnancy was maintained. Foetuses were sacrificed at intervals and wound healing was examined histologically. RESULTS: Immediately after laser irradiation, the foetal epithelium was detached and degeneration of the epithelium and subepithelial mesenchymal tissue were observed. Twenty-four hours after laser irradiation, normal epithelial cells surrounding the wound began to migrate along the margin of the degenerate tissue mass. By seventy-two hours after laser irradiation, the laser-induced wound had recovered, and scar formation was not observed. CONCLUSION: The application of an argon laser allowed to inflict a wound on a mouse foetus without damaging the amnion, and this experimental model appeared to be useful for studying the mechanism of foetal wound-healing.

Animals↗
PubMed1993

Is the Watanabe heritable hyperlipidemic rabbit a suitable experimental model for percutaneous transluminal coronary angioplasty in humans? A light microscopic, immunohistochemical and ultrastructural study.

OBJECTIVES: This study was designed to assess an experimental model for the study of mechanisms that underlie restenosis after percutaneous transluminal coronary angioplasty. BACKGROUND: The Watanabe heritable hyperlipidemic (WHHL) rabbit lacks the receptor for low density lipoproteins, produces atherosclerotic lesions very similar to those in humans and, therefore, could serve as a suitable model. METHODS: Percutaneous transluminal angioplasty was performed on the left subclavian artery of 10 homozygous rabbits. The animals were killed at a few hours or 3, 7, 14 or 28 days after the procedure. The artery was fixed by perfusion, and the site of angioplasty was examined by both light and electron microscopy with the use of conventional and immunohistochemical staining techniques. RESULTS: Angioplasty had caused a flap-like or dissecting tear into the media. At day 3, cells within the preexisting media adjacent to the injury had the ultrastructural characteristics of synthetic smooth muscle cells. At day 7, spindle cells at the site of injury stained either negative or very weakly positive with a marker for actin; ultrastructurally, these cells had the synthetic phenotype. At day 14, the spindle cells showed a mix of contractile and synthetic phenotypes. The surface was partially covered by endothelial cells. At day 28, the dominant cell type was the contractile smooth muscle cell and the surface was completely covered by endothelial cells. CONCLUSIONS: Both the injury and the response to injury after percutaneous transluminal angioplasty were almost identical to that seen in humans after coronary angioplasty. Thus, the WHHL rabbit appears to be an appropriate experimental model for use in further studies.

Angioplasty, Balloon, Coronary↗
PubMed1998

Changes in matrix metalloproteinases during the evolution of interstitial renal fibrosis in a rat experimental model.

The aim of the present study was to analyze the matrix metalloproteinase (MMP) activity during the evolution of interstitial renal fibrosis in a rat experimental model of unilateral ureteral obstruction. The interstitial type I collagenase and the gelatinolytic activities were analyzed by radiolabeled substrate degradation. Interstitial collagenase activity was low at all times while gelatinolytic activity increased on day 6 of evolution, with a decrease in activity from this point. The use of organomercurials revealed the presence of latent enzyme in all cases. Normal kidney samples contained MMP-9 in both active and proenzyme forms as revealed by zymography. On day 3 MMP-9 dimers appeared, and increased activity was observed until day 6. A decrease in the gelatinolytic activity was detected from days 9-15 of evolution. This observation was confirmed by Western blot analysis that revealed the presence of proMMP-9 mainly from days 6-12. Tissue inhibitor of metalloproteinase-1 (TIMP-1) was also detected alone and in combination with proMMP-1 and MMP-1, particularly from days 6-15 of evolution. The presence of MMP-9 and MMP-1 was detected in the cytoplasm of cortical tubular cells by immunohistochemistry, with no difference between the experimental and the normal kidneys. There was also an increase in collagen concentration from day 3 after surgery that increased during the entire evolution of the experimental model. This work reveals that the decrease in the MMP-9 and MMP-1 enzymatic activity, due to their interaction with TIMP-1 and to the lack of activation of the latent forms, may participate in the excessive collagen deposit during the evolution of experimental interstitial renal fibrosis.

Animals↗