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PubMed1992

Dietary fat and the development of pancreatic cancer.

Pancreatic cancer is the fifth most common cause of death due to cancer. Except for an association with cigarette smoking, its etiology is poorly understood. Because of the dearth of epidemiological clues as to causation, studies with experimental animal models assume greater importance. Rodent models of pancreatic cancer indicate that while dietary fat per se does not cause pancreatic cancer, it does enhance or promote tumor development. Subsequent to treatment with a pancreatic carcinogen, high intakes of dietary unsaturated fats of the n-6 series, but not saturated fats, enhance or promote tumor development. A requisite level of linoleic acid is needed for this promotion. Fats of the n-3 series (e.g., certain fish oils) are inhibitory to tumor growth. Promotion by dietary fats appears only partly related to the high caloric content of fat. Mechanistically, certain dietary unsaturated fats appear to selectively enhance the growth rate of carcinogen-induced, pre-cancerous lesions. Irrespective of precise understanding of mechanisms of promotion, it appears possible to intervene in the process of cancer development and reduce the burden of cancer. Experimentally, this may be accomplished by decreasing total fat intake, decreasing caloric intake, increasing exercise or increasing the intake of n-3 fatty acids.

Animals↗
PubMed2004

Effects of piracetam alone and in combination with antiepileptic drugs in rodent seizure models.

The nootropic drug piracetam was investigated in various experimental models of epilepsy. Generally, piracetam exhibits no or only moderate anticonvulsant properties against generalized tonic or clonic seizures. However, in many cases it did increase the anticonvulsant effectiveness of conventional antiepileptics, as shown in the maximal electroshock seizure (MES) threshold test, the traditional MES test or in DBA/2 mice. A pharmacokinetic interaction does not seem to be responsible for this effect. In lethargic mice, a model of absence seizures, piracetam significantly decreased the incidence and duration of spike-wave discharges. Furthermore, in the cobalt-induced focal epilepsy model piracetam reduced the number of spikes/min and in the hippocampal stimulation model it increased the anticonvulsant potency of phenobarbital and phenytoin after single and repeated administration. In conclusion, the well tolerated piracetam itself did not show marked anticonvulsant effects in most screening tests, however, its co-medication with antiepileptic drugs improved seizure protection in various models which may bear potential clinical significance.

Action Potentials↗
PubMed1992

Role of platelet-activating factor in hemodynamic derangements in an acute rodent pancreatic model.

Systemic hemodynamics were assessed in a model of experimental pancreatitis induced in rats by the retrograde injection of sodium deoxycholate, 40%, 1 mL/kg, in the pancreatic duct, using the radioactive microsphere technique before and 25 minutes after pancreatitis induction while blood pressure was stable (n = 10). A 55% decrease in cardiac out-put, a 14% decrease in heart rate, and a 3.3-fold increase in total peripheral resistances, without significant changes in blood pressure, were observed. Renal blood flow decreased by 68%. When rats were given BN-52021, a blocker of platelet-activating factor receptors (5 mg/h, IV; n = 13) coinciding with pancreatitis induction, no significant hemodynamic changes were observed. Animals treated with BN-52021 survived 89 +/- 10 minutes, whereas death occurred 67 +/- 5 minutes after pancreatitis induction in untreated rats (P less than 0.001). A different group of rats with pancreatitis showed higher blood levels of platelet-activating factor (0.28 +/- 0.06 ng/mL; n = 11) than control rats (0.16 +/- 0.03; n = 15; P less than 0.05). Very high levels of platelet-activating factor were found in peritoneal exudate from rats with pancreatitis. These data show an effective protective effect of BN-52021 on the hemodynamic impairment that follows pancreatitis induction, as well as a role of platelet-activating factor in these alterations.

Acute Disease↗
PubMed1990

Effects of recombinant human alpha-interferon in a rodent cardiotoxicity model.

Recombinant human alpha-interferon infused intravenously into rats at doses of 10(6) (1st infusion) and 10(5) IU (2nd and 3rd infusion) produced marginal evidence of liver damage but no serious toxicity. During the 2nd and 3rd infusions an increased incidence of cardiac arrhythmias of various types was observed. In 2 rats electrocardiographic evidence of myocardial ischemia was noted. No changes in myocardial structure were demonstrated by light and electron microscopy. With the high dose the decrease in body temperature resulting from anesthesia was significantly reduced. Antibodies to interferon were demonstrated in the majority of the animals.

Animals↗
PubMed2004

Are lethal audiogenic seizures a missing link to the sudden infant death syndrome?

The pathogenesis of human seizure disorders has largely been derived from rodent models. A number of rodent and chick strains exhibit a genetic predisposition for lethal audiogenic seizures (AGSs) in the first year of life. Consideration is warranted that this disorder may be linked to the sudden infant death syndrome (SIDS). Factors that carry a strong association with SIDS such as hyperthermia and the prone sleeping position would conceivably play a significant role in a human AGS syndrome. Importantly, there is data to support the likelihood that motor seizure activity may be absent in infants with an AGS syndrome. Rodent AGSs may hold important clues to unraveling the mystery of SIDS.

Animals↗
PubMed2004

Expression profiles of zinc transporters in rodent placental models.

Zinc is a vital metal that is a structural and functional component of many proteins. The precise mechanism of zinc transport in the placenta remains unclear. In this study, we investigated the expression of zinc transporters (ZnTs) in the mouse placenta and in two rat trophoblast cell lines, TR-TBT cells, which are syncytiotrophoblast cells of the labyrinth zone, and Rcho-1 cells, which retain trophoblast cell features and differentiate into trophoblast giant cells of the junctional zone. All of the ZnTs that have been identified in mice (ZnT1-7) were detected in the mouse placenta by RT-PCR. The expression profiles of ZnTs in the placenta during pregnancy were different. The mRNA levels of ZnTs, with the exception of ZnT7, did not change during pregnancy. The ZnT7 mRNA level in placenta was elevated during pregnancy. In TR-TBT cells, ZnT1, ZnT3 and ZnT4 were detected by RT-PCR analysis. In Rcho-1 cells, all of the ZnTs that have been identified in rats (ZnT1-4) were detected by RT-PCR analysis. There were no differences between the mRNA expression levels of ZnT family members in undifferentiated Rcho-1 cells and differentiated Rcho-1 cells. This is the first report of expression profiles of ZnTs during differentiation of the placenta in the mouse placenta and rat placental cell models.

Animals↗
PubMed2002

Ischemic preconditioning in a rodent hepatocyte model of liver hypothermic preservation injury.

Ischemic preconditioning (IPC) is a phenomenon of protection in various tissues from normothermic ischemic injury by previous exposure to short cycles of ischemia-reperfusion. The ability of IPC to protect hepatocytes from a model of hypothermic transplant preservation injury was tested in this study. Rat hepatocytes were subjected to 30min of warm ischemia (37 degrees C) followed by 24 or 48h of hypothermic (4 degrees C) storage in UW solution and subsequent re-oxygenation at normothermia for 1h. Studies were performed with untreated control cells and cells treated with IPC (10min anoxia followed by 10min re-oxygenation, 1 cycle). Hepatocytes exposed to IPC prior to warm ischemia released significantly less LDH and had higher ATP concentrations, relative to untreated ischemic hepatocytes. IPC significantly reduced LDH release after 24h of cold storage before reperfusion and after 48h of cold storage and after 60min of warm re-oxygenation, relative to the corresponding untreated hepatocytes. ATP levels were also significantly higher when IPC was used prior to the warm and cold ischemia-re-oxygenation protocols. In parallel studies, IPC increased new protein synthesis and lactate after cold storage and reperfusion compared to untreated cells but no differences in the patterns of protein banding were detected on electrophoresis between the groups. In conclusion, IPC significantly improves hepatocyte viability and energy metabolism in a model of hypothermic preservation injury preceded by normothermic ischemia. These protective effects on viability may be related to enhanced protein and ATP synthesis at reperfusion.

Adenosine↗
PubMed1996

A new rodent experimental model of esophageal atresia and tracheoesophageal fistula: preliminary report.

In spite of the interest paid by pediatric surgeons to esophageal atresia (EA) with tracheoesophageal fistula (TEF), no animal experimental model has been available for investigation. This preliminary report describes a reproducible fetal model of these malformations. Time-mated pregnant rats were given 1.5, 1.75, or 2 mg/kg of Adriamycin intraperitoneally on days 6 to 9 of gestation, and the litters were recovered on day 21 (near full-term). The amount of amniotic fluid was measured, and the fetuses were dissected and studied histologically. The findings were compared with those of suitable control fetuses. Adriamycin-exposed fetuses weighed less than controls. EA with TEF (Gross' type C) was found in 28%, 45%, and 41% of animals in the three dose groups (respectively). The malformation was anatomically identical to that of the human neonate, and the amount of amniotic fluid in affected fetuses increased significantly. In one instance, an H-type fistula was observed. In addition to esophageal interruption, many other malformations fitting within the human VATER association were found: duodenal atresia (41%, 50%, and 47%, respectively), anorectal (28%, 50%, and 41%), renal (81%, 100%, and 100%), and limb malformations (0%, 2.3%, and 13.8%). This new, easily reproducible and relatively inexpensive experimental model of one of the most interesting pediatric surgical malformations permits new research into both its embryogenesis and the biology of the malformed fetus.

Abnormalities, Drug-Induced↗
PubMed1997

The vagus and recurrent laryngeal nerves in the rodent experimental model of esophageal atresia.

BACKGROUND: After surgical correction of their esophageal atresia and tracheoesophageal fistula (EA-TEF), many patients exhibit evidence of esophageal dysmotility. Controversy exists as to whether the esophageal motility disorders result from denervation caused by surgery or from an inherent abnormal innervation of the esophagus. METHODS: The present study used an Adriamycin-induced EA-TEF fetal rat model to trace the course and branching of both the vagus and recurrent laryngeal nerves. Abnormalities observed in EA-TEF rat fetuses include: (1) fewer branches from both recurrent laryngeal nerves; (2) deviation of the left vagus from its normal course below the aorta, passing behind the fistula to approach and join with the right vagus to form a single nerve trunk on the right side of the esophagus; (3) relatively few branches from the single vagal nerve trunk (composed of fibers of the left and the right vagus) on the surface of the lower esophagus. CONCLUSIONS: Fetuses affected by EA-TEF have inherent abnormalities in the course and branching pattern of the vagus nerves as they descend through the thorax, culminating in a deficient extrinsic nerve fiber plexus in the lower esophagus. These observations may account for the esophageal motility disorders seen in patients who have EA-TEF even before surgical intervention.

Animals↗
PubMed2000

Modulation of halofantrine resistance after coadministration of halofantrine with diverse pharmacological agents in a rodent malaria model.

The declining efficacy of antimalarial drugs against Plasmodium falciparum strains has been reported from several endemic regions of the world. Strategic evaluation of several pharmacological agents in combination with chloroquine to enhance the sensitivity of the latter against resistant parasites has been documented in several studies. However no attempts have been directed to monitor the efficacy of such biological response modifiers for reversing the resistance to halofantrine. In the present study the comparative efficacy of a total of 22 pharmacological agents representing diverse categories including antihistamines, antidepressants, calcium channel blockers, neuroleptics etc. has been determined in combination with halofantrine against halofantrine resistant Plasmodium yoelii nigeriensis. Results show significant potentiation of the efficacy of halofantrine when administered concurrently with histamine H1 receptor antagonists cyproheptadine and ketotifen. Combination with pheniramine, amitriptyline, verapamil and penfluridol also produced moderate degree of potentiation which was well marked during the early phase of progression of parasitaemia.

Animals↗
PubMed1997

Continuous, pulsed or single acute irradiation of a transplanted rodent tumour model.

BACKGROUND: Recent advances in remote afterloading pulsed mode brachytherapy have provided a much needed tool for the radiation oncologist. It has the versatility of optimised physical dose distribution along with improved staff radiation protection and patient nursing. PURPOSE: This preliminary study was designed to explore the radiobiological equivalence between conventional continuous low dose rate tumour irradiation (CLDR) and the new technique of pulsed dose irradiation (PDR). MATERIALS AND METHODS: Subcutaneous isogenic sarcomas transplanted in female John's Strain Wistar rats were irradiated locally with acute, pulsed or continuous interstitial low dose-rate exposures at 9-11 mm mean diameter. RESULTS: As expected, single acute doses (5-40 Gy) were more effective (P < 0.01) in achieving tumour growth delay (1.4 days/Gy) than CLDR exposure (4-51 Gy) over 24-48 h (0.93 days/Gy). However, PDR treatment (8 hourly fractions/day) at high dose-rate (8-48Gy) over 8-72 h was significantly (P = 0.01) more effective (1.66 days/Gy) than CLDR but not acute exposures. CONCLUSIONS: These data suggest that, clinically a significantly improved therapeutic ratio may also be achievable with pulsed high dose rate brachytherapy, and that further radiobiological studies with in-vivo tumour models are needed.

Animals↗
PubMed2002

Effects of interleukin-15 (IL-15) on adipose tissue mass in rodent obesity models: evidence for direct IL-15 action on adipose tissue.

Interleukin-15 (IL-15) is a proinflammatory cytokine with multifunctional effects outside the immune system. Previous studies have indicated that treatment of normal rats with IL-15 reduces white adipose tissue (WAT) mass, but it was unclear if these effects were direct or indirect. In the present study, the effects of IL-15 on WAT mass and lipid metabolism were studied in two genetic models of obesity: the leptin receptor-negative fa/fa Zucker rat and the leptin-deficient ob/ob mouse. Lean Zucker rats, lean (+/+), and obese mice (ob/ob) responded to IL-15 with reductions in WAT mass and lipoprotein lipase activity (LPL), with no decreases in food intake. In contrast, fa/fa Zucker rats did not respond to IL-15 administration by any of the above measures of fat mass or lipid metabolism. In addition, ribonuclease protection assays (RPAs) were used to demonstrate that all three subunits (gamma(c), beta and alpha) of the IL-15 receptor complex are expressed by rat and mouse WAT, suggesting that the effects of IL-15 on adipose tissue metabolism could be direct. Additionally, the fa/fa rats expressed 84% lower levels of the gamma(c) signaling receptor subunit than lean Zucker rats, suggesting this decrease may play a role in the lack of adipose tissue response to IL-15 in the fa/fa genotype and lending further support for a direct action of IL-15 on adipose tissue.

Adipose Tissue↗
PubMed1998

Genetics of autoimmune diabetes in animal models.

Type I diabetes has resisted direct genetic analysis in humans but two excellent models of disease in rodents provide a more readily manipulated alternative for study. These rodent models are being used successfully to localize the genes that are involved in disease pathogenesis in preparation for positional cloning. In addition, mice carrying transgenes and null mutations related to T cell function have been used to demonstrate potential mechanisms for both MHC-dependence and specific effector functions, such as cytokine release and cytotoxicity.

Animals↗
PubMed1998

The photodynamic response of two rodent tumour models to four zinc (II)-substituted phthalocyanines.

Four novel zinc (II)-substituted phthalocyanines, varying in charge and hydrophobicity, were evaluated in vivo as new photosensitizers for photodynamic therapy. Two rat tumours with differing vascularity were used: a mammary carcinoma (LMC1) and a fibrosarcoma (LSBD1), with vascular components six times higher in the latter (10.8%+/-1.5) than in the former (1.8%+/-1.4). Each sensitizer was assessed for tumour response relative to normal tissue damage, and optimum doses were selected for further study, ranging from 0.5 to 20 mg kg(-1). Interstitial illumination of the tumours was carried out using a 200-microm-core optical fibre with a 0.5 cm length of diffusing tip, at either 680 or 692 nm, depending on the sensitizer. Light doses of between 200 and 600 J were delivered at a rate of 100 mW from the 0.5-cm diffusing section of the fibre. Maximum mean growth delays ranged from 9 to 13.5 days depending on sensitizer and type of tumour, with the most potent photosensitizer appearing to be the cationic compound. Histopathological changes were investigated after treatment to determine the mechanism by which tumour necrosis was effected. The tumours had the appearance of an infarct and, under the conditions used, the observed damage was shown to be mainly due to ischaemic processes, although some direct tumour cell damage could not be ruled out.

Animals↗