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Histochemical and electron microscope studies indicated there was amyloid in corpora amylacea in tumors, duct ectasias and lobular hyperplasias of rat mammary glands. Electron microscopy showed fibrils that closely resembled amyloid fibrils in human and bovine amyloid and in bovine corpora amylacea. Amyloid deposition may be more common in rats than is generally thought.

Age-related changes in phospholipid and free cholesterol contents of hindleg muscles from normal and dystrophic (C57BL/6J dy/dy) mice were investigated. Free cholesterol contents in liver, whole blood and brain of dystrophic mice at 3 weeks of age were also compared with the control. Free cholesterol content tended to increase in the liver of the dystrophic mouse. Free cholesterol content of dystrophic muscle was significantly higher than that of normal muscle at each age (2.1 to 30 weeks old), while phospholipid contents in dystrophic muscles were nearly equal to those of the normal in age from 4 to 20 weeks.

The components and variations of glycosaminoglycan (GAG) in the growth of transplantable tumors derived from a spontaneous mouse mammary tumor were investigated. A 45-week-old ddY female mouse, obtained from Shizuoka Laboratory Animal Center, was found to have a bean-sized mass at the third mammary gland of the left side. The tumor mass was surgically excised and used for transplantation in the present study. This mammary tumor was histologically found to be Type B-adenocarcinoma. Transplantable mammary tumors consisted of the fibrous or edematous interstitium contained a large amount of GAG components, which was mainly hyaluronic acid (HA), dermatan sulfate (DS) and chondroitin sulfate A/C (ChS). In the analysis of GAG components, HA content was present in a large amount in logarithmic growth phase of transplanted mammary tumors, but it was markedly decreased in stationary phase. On the other hand, the contents of DS and ChS increased in stationary phase of the tumor growth, and these increases corresponded, histologically, with the propagation of the fibrous interstitial tissues.

An experimental model of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was developed using continuous subcutaneous infusions of arginine vasopressin (AVP) or 1-desamino-8-D-arginine vasopressin (DDAVP) in conscious unrestrained rats drinking 5% dextrose solution. Retention of both ingested water and endogenously generated free water from tissue catabolism was the primary determinant of hyponatremia using either AVP or DDAVP infusions. Natriuresis occurred transiently following water expansion but only slightly further lowered plasma [Na+]. Cessation of antidiuretic infusion resulted in free water excretion with correction of plasma [Na+]. Erythrocyte cell volume was significantly increased in hyponatremic animals and intracellular [K+] and [Na+] both decreased equivalently, consistent with dilution of intracellular fluid by retained water. This model of SIADH differs significantly from those previously described, in that escape from the hydroosmotic effect of AVP and DDAVP does not occur in the absence of high urinary flow rates. The observed results using this model suggest that the retained water in SIADH primarily resides intracellularly following isotonic equilibration of extracellular fluid volume.

Gastric hyperplasia occurred more frequently among densely housed mice than mice housed singly, and crowding stress may have been implicated in this increased prevalence. Affected stomachs had striking increases in sulfomucin secretion when compared with unaffected gastric mucosa. The mucin changes suggested incomplete maturation of mucous cells in this condition and were similar to those reported in association with early neoplastic or pre-neoplastic lesions in the stomach of both man and rodents.

The jimpy mouse, an X-linked recessive dysmyelinating and demyelinating mutant, has been shown to contain abnormal myelin proteolipid protein (PLP) mRNA. To understand the molecular basis of the mutation, we analyzed the structure of PLP mRNA by an RNase-mapping procedure, using the probes specific to each exon of the mouse PLP gene. We found that the fifth exon of the PLP gene is not utilized in the jimpy.

The early phase of insulin secretion to an oral glucose load was blunted in spontaneous diabetic rats. The blunted insulin secretion was associated with markedly impaired glucose tolerance. A single injection of the islet activating protein (IAP), a protein derived from the culture medium of Bordetella pertussis, into the spontaneous diabetic rats normalised glucose tolerance. The increase in insulin response to glucose was an important contributing factor to the improvement of glucose tolerance. This curative effect of the IAP on the diabetic state was of long duration; glucose tolerance remained virtually normal over a period of one month in the diabetic rats. Perfusion of the isolated pancreas of the diabetic rats pretreated with IAP showed an increase in insulin response to glucose and loss of suppression of glucagon secretion by noradrenaline.

The adaptive responses to sucrose and fat diets were investigated in two species of spiny mice, Acomys russatus and Acomys cahirinus, in relation to their propensity to develop diabetic-like symptoms. A russatus gained weight pronouncedly, both on regular and fat-rich seed diet, did not exhibit hyperglycemia or hyperlipidemia but had highly increased hepatic triglyceride content in association with high levels of circulating free fatty acids and incidence of ketonuria in 10 of 41 animals. On the other hand, A. cahirinus exhibited a moderate weight gain on the fat diet which was accompanied by hyperglycemia but no hyperlipidemia or ketonuria. Neither weight gain nor ketonuria were evident in A. russatus and A. cahirinus on the sucrose-rich diet, but there was hyperlipidemia in the latter species. A. cahirinus, in particular, showed many-fold induction of liver enzymes, of regulatory importance in the pathways of glycolysis and lipogenesis, which could be linked to the hyperlipidemia in this species. On the fat diet there was a smaller increase in activity in enzymes related to gluconeogenesis in A. russatus compared with A. cahirinus, as well as a smaller suppression of glycolytic and lipogenic enzymes. Adipose tissue lipoprotein lipase activity rose in response to the fat-rich diet, more markedly in A. russatus than A. cahirinus in correlation to the more marked weight gain and hyperinsulinemia in this species. The affluent diets, especially sucrose, elicited an increase in circulating triiodothyronine levels which was more pronounced in A. cahirinus than in A. russatus.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of zinc deficiency on trace metals in the liver, spleen, kidney, pancreas and duodenum was investigated in the control and zinc-deficient rats at 17 days and 20 days of pregnancy. Zinc-deficient rats fell into limosis after 5 days of pregnancy. The contents of zinc, iron, copper and manganese in the maternal tissues were measured by colorimetry with 5NPPF. The morphological changes of the liver were observed by light and electron microscopy. The contents of zinc in the pancreas and duodenum were less in the zinc-deficient group than in the control at both 17 days and 20 days of pregnancy. The contents of the copper and manganese in the liver, kidney, pancreas, duodenum and spleen, however, were not significantly different from the control. The contents of iron in the liver, spleen and kidney in the deficient group increased greatly at 17 days and 20 days of pregnancy compared with the control group. The combination rate of transferrin with iron also increased significantly in the deficient group. Staining with Berlin blue or Turnbull's blue showed intense reaction to iron around the interlobular connective tissue of the liver in the zinc deficient group at 20 days of pregnancy. Ultrastructurally, the liver of the zinc-deficient rats showed the decrease of glycogen granules and increase of lipid-like granules and lysosomes with various sizes and electron densities. These findings suggest that zinc deficiency causes the increase of iron contents in the various organs during pregnancy, and that there is an intimate interrelationship between zinc and iron in the metabolism of iron during pregnancy.

At different extracellular pH values fractional extracellular space (calculated from the distribution of 3H inulin) and fractional water content showed no significant differences. 72 h after nephrectomy both variables increased significantly. An exception to this was brain, where fractional extracellular space decreased and total intracellular water increased as a sign of brain oedema.

A genetically hypercholesterolemic strain of rats was selectively bred, starting from an ordinary albino mutant of Rattus norvegicus. The new strain was given the designation RICO, standing for rats with increased cholesterol. In these animals, hypercholesterolemia is established, in both sexes, one day after weaning, and it increases progressively thereafter. It is due to elevated concentrations of LDL- and HDL-cholesterol. As in the ordinary rat, the HDL fraction makes up the main part of the serum cholesterol in the RICO rat. Metabolic studies revealed that in the RICO strain the overall rate of hepatic cholesterol synthesis is accelerated, as a result of higher than normal activity of 3-hydroxy-3-methylglutaryl-CoA reductase. The activity of cholesterol-7 alpha-hydroxylase is decreased in RICO rats, indicating a lower than normal rate of cholesterol catabolism. No difference was found between RICO and ordinary rats with respect to fecal excretion of bile acids and cholesterol.

Research on the screening for and study of animal models of inherited metabolic disease is reviewed. It is emphasized that an animal model, to be of value, must be an inherited deficiency of the same enzyme as the one deficient in the human syndrome. If this criterion is adhered to there is a remarkable identity in aetiology between animal and man. Specific examples of inherited metabolic disease in laboratory animals are described for: amino acid metabolism; lysosomal storage diseases, carbohydrate metabolism, transport disorders and trace element metabolism; the mutants found in mice being the easiest to manipulate biochemically and genetically. There is still a lack of adequate screening programmes for animal homologues of the more serious human inborn errors (such as lysosomal storage diseases) where laboratory studies could provide significant advances in therapy.

Histochemical studies were performed on glycosaminoglycan (GAG) components in Wilms tumors of rats and rabbits and fetal kidneys of rats. 1. Wilms tumors. The interstitial components had an intense stainability with Alcian blue, and digestion test with hyaluronidase and chondroitinase was intensely positive. The epithelial tumor cells, showing a tubular pattern, were also stained with Alcian blue. The enzyme-digestion test was positive in the basal portion of the tumor cells, whereas it was negative in the free surface of the cells. 2. Rat kidneys. In fetal rats, the epithelial cells as well as the interstitial components were stained with Alcian blue, and the enzyme-digestion test was intensely positive. However, in adult rats, Alcian blue-stainability in the free surface of the tubular epithelium was not abolished by treatment with hyaluronidase and chondroitinase. The substance in the free surface seemed to be consisted mainly of heparan sulfate. Although the physiological significance of GAG in the cell surface cannot be deduced, it is quite conceivable that GAG, especially heparan sulfate, plays an important role in fluid absorption and transportation.

Neither analysis of the urinary catecholamine metabolites vanillymandelic acid and 4-hydroxy-3-methoxyphenylglycol nor blood pressure measurements allowed the detection of adrenal medullary tumors or hyperplasia in 115 aged male Wistar rats (70 rats, 24 months of age and 45 rats, 30 months of age). Histochemical examination of the adrenal glands demonstrated that the 55 hyperplastic and 25 neoplastic lesions of the medulla usually had little or no chromaffinity. Chromaffinity was found comparable to normal medulla in only three tumors examined histochemically. Of these tumors, two were partially and one completely chromaffin-positive, but all three were small and did not result in elevated blood pressure or catecholamine metabolite excretion values. These observations indicate that excessive catecholamine synthesis and release is not a feature of adrenomedullary tumors and hyperplasia occurring spontaneously in aged male Wistar rats.

X-linked hypophosphatemia is a human and mouse disease characterized by reduced renal tubular reabsorption of phosphate, hypophosphatemia, and dwarfism. The gene is X-linked and dominant. There have been conflicting reports in the literature regarding possible malabsorption of minerals by the intestine as well. In this study we examined the mineral status in adult X-linked hypophosphatemic (Hyp) mice by measuring trace minerals in blood, bone, muscle, liver and hair and by performing a balance study for Ca, P, Mg, Na and K. The results indicate that Hyp mice have higher than normal levels of plasma iron, bone manganese and zinc, liver iron, and muscle zinc. The trace minerals in hair were not significantly affected. The balance study showed that the content of Ca, P, Mg, Na and K of the urine and feces of normal and Hyp mice were nonsignificantly different. Hyp mice did consume more diet per gram body weight. We conclude that there is no deficiency in intestinal mineral absorption in adult Hyp mice. No tissues studied were found to have reduced trace mineral levels. In fact, where differences occurred, Hyp mice had elevated trace mineral levels in various tissues and blood. This was probably the result of the increased dietary intake per gram body weight in the Hyp mice.

The metabolic-endocrine state of diabetes mellitus affects the brain and behavior of diabetic animals. Feeding, paradoxical sleep, analgesia, submissive behavior, and avoidance behavior, are generally increased in diabetic compared with nondiabetic rodents. In contrast, sexual behavior, aggressive behavior and sensitivity to the behavioral effects of amphetamine are decreased in diabetic rodents. This review examines behavioral changes in diabetes mellitus within the context of known disease-linked alterations in hypothalamo-pituitary relationships and brain monoamine metabolism.

The purpose of this study was to determine the prevalence of coprophagy in rats with differing iron status and its effect on the measurement of iron absorption from test meals with and without bran. Two experiments were performed using radioisotope-labelled microspheres added as a non-digestible marker for the ingested faeces and the diet and 59Fe added as a marker for the nonhaem iron in the test meal. In this study, coprophagy occurred at group mean rates of between 5 and 22% and was independent of the iron status of the rats or the presence or absence of bran in the diet. The relative absorption of iron, measured as the retention of 59Fe from a single meal, was affected to the same extent in groups with the same iron status, if it was affected at all. Thus comparisons of iron absorption from diets with and without bran should not be affected by coprophagy.

Melatonin was measured by radioimmunoassay in several genetic strains of Japanese quail. Plasma melatonin (PM), measured at the nighttime peak, was highest in wild type quail reared on a diurnal lighting schedule; this PM peak was suppressed in continuous light. Albino quail had low melatonin levels, whether reared under diurnal conditions or in continuous light. Ocular melatonin was also suppressed in albinos and in dilute mutants. At midday sampling, melatonin was only half as high in albinos as in wild types. Intraocular pressure (IOP, daytime readings) was uniformly low in diurnal birds and was elevated in all quail reared under continuous light. Thus in pigmented birds, a high melatonin level was associated with high IOP, but in albinos displaying high IOP, ocular melatonin was not elevated. Lithium chloride, mixed in the feed, brought about a pronounced reduction in plasma, pineal, and ocular melatonin, in wild-type quail reared on a diurnal schedule. This confirms earlier findings in lithium-fed rats. Golden hamsters displayed a characteristic diurnal cycle of pineal melatonin, with a sharp middark peak; in albino hamsters, also kept on a diurnal schedule, this peak occurred at the same time, but albinos had melatonin levels only about one-third as high as those of pigmented animals.

Elevated serum lipids are associated with infections of laboratory rodents with plerocercoids of Spirometra mansonoides. The effect of infection with these larval tapeworms on triglyceride degradation and hepatic de novo fatty acid synthesis was investigated in Syrian hamsters. Serum lipoprotein electrophoresis revealed a consistent elevation in very low density lipoproteins in the infected animals. Lipoprotein lipase activity was enhanced in the infected animals. After seven days of plerocercoid infection the activity of acetyl-CoA carboxylase (E.C. 6.4.1.2) was significantly elevated after 6, 12 and 18 hours of fasting. Fatty acid synthetase was significantly increased after 0, 6, 12, 18 and 24 hours of fasting. Therefore, a chronic insulin-like activity on lipid metabolism of hamsters is associated with plerocercoid infection.

The aim of this study was to examine the long-term effects of synthetic chow diet on the metabolic pattern of diabetic syndrome in a large group of sand rats. Few animals had a fulminating reaction with markedly decreased glucose tolerance, low plasma insulin levels and death within 3-4 weeks. But the most of sand rats developed obesity and elevated plasma insulin levels. From the third month, 40% of sand rats presented a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance and insulin resistance. Plasma lipids were increased; the lipid and glycogen accumulation in the liver was high. So this diabetic syndrome can be compared to maturity onset diabetes. If this synthetic chow diet lasted more than 6 months, the most of animals lost considerable weight with a strong lipid depletion of fat stores. Serum immunoreactive insulin levels fall and the blood glucose rose over 500 mg/100 ml with glycosuria and ketonuria . The elevated triglyceride content of plasma and the lipid deposits in the liver were exaggerated; glycogen had disappeared. Animals developed an overtly insulin- dependent diabetes, the latter phase of the disease. The sand rat appears to us as a potentially interesting model for investigation both maturity onset and ketotic-type diabetic syndrome.

Brain edema was produced by 6-aminonicotinamide (6-AN) in the rat with accompanying metabolic disturbance due to the accumulation of an antimetabolite of nicotinamide in the CNS. Twenty-four hours after intraperitoneal administration of 6-AN, significant (P less than 0.01) increases of sodium and water in the medulla oblongata were observed. By electron microscopy, the lesion was characterized by swelling of the perivascular neuroglial processes, producing disturbances of the active transport in the cell membrane and increased pinocytosis in the endothelial cells, especially of the arterioles and venules. The metabolic inhibitor was shown to produce not only an increased water and sodium uptake in neuroglias, which is characteristic of cytotoxic brain edema, but also produced protein-rich edema in the extracellular space, ie, vasogenic brain edema. The protein transport in the metabolic disturbance caused by 6-AN was traced, using horseradish peroxidase, revealing that it occurred from the vasculature into the extracellular spaces via pinocytotic vesicles due to the change in the cerebrovascular permeability.

Spontaneous hepatomas and hepatic preneoplastic changes were observed in sand rats (Psammomys obesus) from two colonies. Both colonies originated from 10 sand rats captured in the Judean desert in 1969. At the age of 6 months, and increasing in multiplicity with advancing age, histologic examination revealed nodules containing hepatocytes characterized by hyperbasophilia, accumulation of glycogen, eosinophilic cytoplasm, or a mixture of these cells. In animals over 25 months old hepatocellular carcinoma was diagnosed. The histologic changes described here were reported to be characteristic of chemical hepatomagenesis in rats. No external chemical carcinogen could be demonstrated in our animal colonies, and a hereditary predisposition to tumor formation is presumed. Identity of hepatic carcinogenesis, irrespective of etiology in distantly related rodents, ie, the laboratory rat and the sand rat, which in reality is a gerbil, supports the assumption of the existence of a general law governing hepatic carcinogenesis.

1. A specific dietary deficiency of potassium in young rats reduced the potassium concentration in thigh muscle by 48%, and in heart and kidney by 18%, but did not significantly affect the concentration in liver or brain. Conversely the sodium concentration rose in liver, heart and thigh muscle, and thigh muscle also accumulated increased amounts of magnesium. Apart from an increase in the water content of many tissues, no consistent changes in the composition of major cell constituents were observed. 2. The loss of potassium and accumulation of sodium and magnesium occurred predominantly in the supernatant fraction of the cell. The supernatant of all tissues studied contained about 80% of the total cellular potassium and sodium, and the potassium was present entirely in the ionic form. 3. Potassium and magnesium are the two most abundant intracellular metals, but their deficiencies have very different effects on the cell. The relationship between them is more complex than the inverse relationship between potassium and sodium.

Spontaneous diabetes mellitus has been documented in a colony of guinea pigs. The contagious nature of the disease has been verified, but the nature of the infectious agent is not known. Animals from the original colony or animals exposed to the colony with normal glucose tolerance tests (GTT) became diabetic, as evidenced by elevated one- and four-hour GTT values, and in most cases have significant glycosuria. The severity of pathologic changes in the pancreatic islets parallel, in general, the severity of the clinical symptoms (glycosuria and abnormal GTT). Those animals with severe glycosuria and elevated FBS as well as one- and four-hour GTT values had the most pronounced degranulation and most prominent cytoplasmic inclusions in islet B cells. The severity of scarring in the islets can be correlated with the duration of the overt diabetic state. The other clinical parameters of note were elevated serum triglycerides, normal serum but elevated aortic cholesterol, and absence of ketonemia or ketonuria. The reproductive capacity of diabetic females was compromised. While the clinical manifestations are mild or variable, the presence of significant islet pathology is reminiscent of human juvenile diabetes mellitus. These findings lend support to the concept that infectious and/or immune mechanisms could be operative in the etiology and pathogenesis of human diabetes mellitus.

Genetic and irradiation models of ovarian tumorigenesis were investigated for evidence that elevated gonadotropins have a role in tumorigenesis. Wx/Wv mice lack oocytes at birth, develop complex mesothelial adenomas by 6 mo, and additional ovarian tumor types later. Uptake of iodinated human chorionic gonadotropin (125I-hCG) was measured in mice aged 1 to 30 mo, and uptake iodinated human follicle-stimulating hormone (125I-hFSH) was measured in mice aged 1 to 12 mo. Gonadotropin uptake by Wx/Wv ovaries in vivo declined quickly and was undetectable by 6 mo. Irradiated ovaries rapidly lost oocytes and follicular structures, formed mesothelial adenomas by 5 mo, and later formed additional types of ovarian tumors. In the irradiation model, 125I-hCG uptake also declined quickly and was undetectable by 3 mo of age. Neither the surface nor the tubular epithelium of the mesothelial adenoma were consistently labeled by 125I-hCG in autoradiography studies with either model. Although these data do not exclude an acute role for gonadotropins in initiation of preneoplastic events, they do indicate that ovarian cells do not require chronic gonadotropin stimulation during subsequent tumorigenesis. These findings are discussed in relation to additional models of ovarian tumorigenesis.

In keeping with studies of other desert rodents, the potentially diabetic spiny mouse has been demonstrated to have a very low basal metabolic rate, disproportionate to its body weight. The maintenance of a lower body temperature in response to high environmental temperatures and a lack of increase in metabolic rate in response to cooling have also been demonstrated. Assessments of "mechanical efficiency" have shown that spiny mice carry a potential selective advantage under fasting conditions. The findings, some of which are similar to those noted in other desert rodents, and in other species showing either spontaneous or induced hyperglycaemia, suggest that the low metabolic rate is at least partly based on ineffective glucose utilization. This phenomenon may be the common denominator of the survival advantage which has allowed both the successful evolution of species inhabiting warm, arid climes, and the persistence of the diabetic genotype in animal and human populations.

A remarkably severe spontaneous amyloidosis involving multiple organs has characterized the inbred PS mouse strain since the 25th generation. The amyloid substance was extracted with H2O and purified by successive gel filtrations on Sephadex G100, Sephadex G10 and Biogel P4. It was submitted to biochemical, immunochemical and histochemical analysis in order to determine its origin. Potassium permanganate resistance of the affinity for Congo Red dye, aminoacid composition, cross-reactivity with anti-mouse light chains antisera suggested an amyloidogenic process comparable to that described for the AL substance in man. However, even if abnormal lymphoid infiltrates were present in several organs, the presence of M component could not be demonstrated in serum or urine of these mice. This indicated either a limited tumoral mass or a tumor poorly secreting a precursor that would be strongly amyloidogenic. Alternatively, the existence of a so far unidentified precursor could not be excluded.

Sand rats (Psammomys obesus) developed in response to different food intake various states of hyperglycemia and hyperinsulinism. 12 normo- and 10 hyperglycemic animals were selected by means of a weekly control of plasma glucose and plasma insulin over a period of 12 weeks after separation from the mother. During this time also the development of body weight gain was checked. In both groups of rats the hormonal regulation of glycerol release by incubated adipose tissue was investigated. In any case, the fat tissue from hyperglycemic sand rats showed a lower lipolytic responsiveness to noradrenaline stimulation than that of their normoglycemic controls. This correlates well with previous results in hyperglycemic sand rats in which the catecholamine-stimulated cAMP production was disturbed (Knospe and Köhler 1981). Degradation of released adenosine by addition of adenosine deaminase significantly enhanced the noradrenaline action on glycerol release in both groups of sand rats. Even though the noradrenaline-stimulated lipolytic activity of adipose tissue from normo- and hyperglycemic animals was enhanced in the presence of adenosine deaminase, the hormone resistance of adipose tissue from hyperglycemic sand rats was nevertheless not abolished. The theophylline-mediated adenosine receptor blockade gave further evidence that particularly endogenous adenosine released during incubation of adipose tissue from sand rats inhibited the noradrenaline action on lipolysis. The antilipolytic action of insulin on glycerol release is negligibly low in normoglycemic as well as hyperglycemic sand rats. The degradation of adenosine by adenosine deaminase failed to improve the insulin action. Adenosine addition completely blocked the stimulating effects of noradrenaline on glycerol release.(ABSTRACT TRUNCATED AT 250 WORDS)

A high incidence (8/892) of urinary tract calculi was encountered during a study involving rats being fed diets supplemented with retinoids. When the incidence was compared to that observed in earlier studies without retinoid supplements and spanning several years (2/2998), the incidence in the current study was significantly higher. Possible causative factors such as age, sex, strain, diet and carcinogen or retinoid treatment have been analyzed without a clear explanation for the increased incidence. The data suggest that retinoid treatment increased the risk of stone formation, but that retinoids were less important than some other unidentified factor(s) that operated during the recent period.

Myocardial lesions were noticed in BALBc/Cr mice during experiments with Moloney sarcoma virus (MSV). A study was initiated using unifected BALBc/Cr mice to determine whether these lesions were the result of a viral infection. Sixty percent of the females and 30% of the males used were found to have macroscopic lesions (mainly white spots on the right ventricle). The reported lesions were studied both histologically and histochemically. The animals were also examined for parasites such as Toxoplasma and tapeworm larvae, and were found negative. The investigation, which is still in progress, demonstrates the spontaneity of myocardial lesions in BALBc/Cr mice.