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C T Hansen

Publications and source records attributed to C T Hansen.

At least 37 records · Page 2Linked to original sources
PubMed1991

Hemorrhagic cardiomyopathy and hemothorax in vitamin K deficient mice.

The cause of a fatal condition characterized by hemorrhagic cardiomyopathy, hemothorax, and coagulation defects in hysterectomy-derived male mice was investigated. Microscopic heart alterations included multifocal hemorrhage and necrosis with variable degrees of acute inflammation and fibroplasia that were most severe in the region of the atrioventricular junction. A spontaneous outbreak was arrested by increasing menadione Na-bisulfite (vitamin K) in the feed to 20 ppm. The complete syndrome including hemorrhagic cardiomyopathy was readily reproduced in germ-free male mice given a vitamin K-free diet, and in conventional male and female mice given Warfarin in the diet. We concluded that the cause of this condition was vitamin K deficiency.

Animals↗
PubMed1991

A difference in mortality between two strains of jaundiced rats.

Homozygous Gunn rats lack bilirubin glucuronyltransferase, become jaundiced, and often develop kernicterus, thus providing a model for neonatal hyperbilirubinemia. Two new, inbred rat strains that carry the Gunn mutation are described. These were developed by breeding the mutant Gunn gene (j) into the RHA/N and ACI/N strains, producing the new lines, which were designated RHA/N-j and ACI/N-j. Liver assay confirmed the absence of transferase activity in jaundiced rats from both of the new strains, but marked differences in mortality between the strains were observed. The mortality of jaundiced RHA/N-j rats through 8 weeks was the same as that of their nonjaundiced littermates (20%). In contrast, mortality of jaundiced ACI/N-j rats was distinctly greater than that of their nonjaundiced littermates (81% vs 34%, P less than .001). Signs of kernicterus such as ataxia were much more frequent in jaundiced ACI/N-j rats than in jaundiced RHA/N-j rats (73% vs 11%, P less than .001). Both strains had comparable albumin concentrations through 8 weeks of age. Serum bilirubin concentrations were also comparable, except for a small but significant difference at 20 days of age (ACI/N-j = 294 mumols/L, RHA/N-j = 248 mumols/L, P less than .01). Similarly, the bilirubin-to-albumin ratios were comparable except for a significantly higher ratio at 20 days of age in the ACI/N-j rats (ACI/N-j = 0.70, RHA/N-j = 0.51, P less than .01). Thus, the RHA/N-j strain is unusual in that the jaundiced animals remain healthy. Conversely, the ACI/N-j animals demonstrate a high incidence of kernicterus with mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of dietary carbohydrate on liver and kidney enzyme activities and plasma amino acids in the LA/N-cp rat.

Twenty obese and 20 lean LA/N-cp male rats and 20 male Sprague-Dawley rats were fed a diet containing either 54 percent sucrose or starch for six weeks. After a 14-16 hour fast, rats were killed. Liver and kidney enzyme activities were determined in the LA/N-cp rats while plasma urea and selected amino acids were determined in all rats. Liver glucose-6-phosphatase (G6PASE), fructose-1,6-bisphosphatase (FBPASE), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), glucokinase (GK), pyruvate kinase (PK), phosphofructokinase (PFK), glutamic-oxaloacetic-transaminase (GOT), glutamic-pyruvic transaminase (GPT), arginase (ARGASE), arginine-synthase (ARG-SYN) and ornithine transcarbamylase (OTC) levels were significantly affected by phenotype (obese greater than lean). All the above changes in enzyme levels were exaggerated by sucrose-feeding with the exception of PK, PFK, GOT, GPT, ARGASE and ARG-SYN. Kidney cortex G6PASE, PEPCK and ARGASE activities were higher in the obese rats as compared to the lean littermates. Sucrose feeding resulted in higher cortex G6PASE, FBPASE and PEPCK as compared to starch-fed rats. A phenotype effect was noted with plasma glutamate, urea, leucine, isoleucine and valine (obese greater than lean) and a diet effect was seen with aspartate, phenylalanine, leucine and valine (sucrose greater than starch) concentration. Sprague-Dawley rats had higher plasma urea and lower alanine than lean LA/N-cp males. Metabolic obesity in the LA/N-cp rat appears to involve an elevated capacity for pathways of glycolysis, gluconeogensis, lipogenesis and amino acid catabolism in the liver.

Amino Acids↗
PubMed1990

Organic mercury in Greenland birds and mammals.

Muscle, liver and kidney samples of 20 species of birds, seals, whales and polar bear were analyzed for total and organic mercury. Organic mercury concentrations varied considerably between individuals. A general tendency towards age accumulation was found, together with log-linear correlations between organic mercury concentrations in the three tissues. The major part of the muscle mercury was organic (maximum concentration found was 1235 micrograms kg-1 wet wt). This also applied to liver of birds, while in mammal liver organic mercury concentrations approached a level of 2000 micrograms kg-1 wet wt, which was not exceeded even when the total mercury concentration was greater than 100,000 micrograms kg-1 wet wt. The percentage of organic mercury in relation to total mercury in kidney of seals and whales was 10-20% (maximum 982 micrograms organic mercury kg-1 wet wt), while in polar bear it was less than 6% (maximum 217 micrograms kg-1 wet wt). For the monitoring of local food in the Arctic, the simpler and less expensive analysis of total mercury suffices when testing muscle, whereas liver and kidney should be tested for organic mercury as well.

Animals↗
PubMed1990

Influence of genetic obesity, dietary carbohydrate and age on parameters of glucose tolerance and kidney and adrenal gland histology in female SHR/N-corpulent rats.

Young female obese (cp/cp) and lean littermates (?/+) of the recently developed congenic strain, SHR/NIH-corpulent (SHR/N-cp), were fed for 6.5 months isocaloric diets containing 54 percent carbohydrate as either sucrose or starch. Glycemic, lipidemic and renal parameters were determined after 1, 3 and 6 months. Systolic blood pressure and plasma corticosterone levels were determined after 3 months. After 6.5 months rats were killed for histological examination. Obese rats were hyperglycemic following an oral glucose challenge (1 hour response greater than 11.1 mmol/l) (200 mg/dl), hyperinsulinemic, hypertriglyceridemic, and developed proteinuria and mild hypertension. Feeding sucrose, as compared to starch, further increased serum glucose, insulin and triglyceride levels and urinary protein excretion in obese rats and serum triglyceride levels in lean rats. An amelioration of glucose intolerance was observed in sucrose-fed obese rats by 6 months. In contrast to serum insulin levels, serum triglyceride levels increased with age in obese rats. Obese rats exhibited hypertrophy of the kidney and adrenal cortex with abnormal histology. The study demonstrates that obese female SHR/N-cp rats exhibit some of the metabolic and histopathological changes associated with NIDDM in humans and that feeding sucrose, as the source of dietary carbohydrate, further magnifies the expression of diabetes in this model.

Adrenal Cortex↗
PubMed1989

Effects of dietary carbohydrate and phenotype on thyroid hormones and brown adipose tissue locularity in adult LA/N-cp rats.

1. Groups of lean and corpulent LA/N-cp rats were fed isoenergetic diets containing, 54% carbohydrate as maize starch (MS) or sucrose (SU), 20% protein, 16% mixed fats, plus other essential nutrients and fiber from 1.5-9 months of age. Final body weights of corpulent rats were 2-3 times those of their lean littermates, and were greater with SU than MS diet in both phenotypes. 2. Interscapular brown adipose tissue (IBAT) mass was greater in corpulent than lean and was greater with SU than MS diet in lean but not corpulent rats. IBAT cell diameters and adipocyte volumes were generally similar in both phenotypes, and were not markedly affected by dietary carbohydrate type. 3. Brown adipocyte locularity profiles were qualitatively similar in both phenotypes, and were morphologically indicative of thermogenic activity in both phenotypes. Locule profiles of corpulent animals contained a greater proportion of thermogenically less active types IV and V brown adipocytes than similarly fed lean animals, however, and locule distribution profiles were not influenced by diet. 4. Serum T3 concentrations were similar in both phenotypes, were greater in SU than MS lean rats and were not influenced by diet in the corpulent phenotype. In contrast, serum thyroxine concentrations and percent thyroxine uptake were not influenced by diet or phenotype. 5. These results are consistent with a partial impairment in BAT-mediated thermogenic activity in the corpulent phenotype and suggest that obesity in this strain may be due to factors other than biochemically defective brown adipose tissue thermogenesis.

Adipose Tissue, Brown↗
PubMed1989

Effect of dietary carbohydrates on insulin and glucagon receptors in a new model of noninsulin-dependent diabetes-SHR/N-corpulent rat.

A new congenic strain of rat, the SHR/N-corpulent, provides a good model for noninsulin-dependent diabetes and was used in the present study. Corpulent rats as compared to their lean littermates are obese, hyperlipidemic, and severely hyperinsulinemic, and show an age-dependent loss of glucose tolerance. Mild fasting hyperglycemia is seen only in corpulent rats fed sucrose. Since dietary sucrose is more lipogenic than starch and since insulin and glucagon are involved in lipid and carbohydrate metabolism, we studied the effect of the type of dietary carbohydrate on insulin and glucagon levels and their receptors in lean and corpulent SHR/N rats. A significant phenotypic effect was observed (corpulent greater than lean) on plasma levels of triglyceride, cholesterol, and insulin. Dietary sucrose increased these parameters in corpulent rats but not in lean rats. Insulin and glucagon binding to liver plasma membranes was lower in corpulent rats than in lean; decreases were due to fewer receptors without a significant change in affinity. Thus, in corpulent rats, in addition to hyperinsulinemia, fewer glucagon receptors and their failure to be regulated by plasma glucagon levels appear to contribute to the hyperlipidemia. Furthermore, the hyperglycemia observed in sucrose-fed corpulent rats may be due to extreme resistance to insulin despite lower plasma glucagon and fewer glucagon receptors.

Animals↗
PubMed1988

Cecocolitis in immunodeficient mice associated with an enteroinvasive lactose negative E. coli.

Infection with an atypical (lactose-negative) E. coli was associated with increased mortality rates in a colony of triple immune deficient N:NIH(S) III mice. Affected mice were lethargic and exhibited perianal fecal staining. Slight-to-moderate thickening of the wall of the cecum and colon was found on necropsy examination. Microscopic examination revealed segmental hyperplasia of the cecal and colonic mucosa with clusters of gram negative bacteria on the surface and within the cytoplasm of mucosal epithelial cells. Scattered foci of epithelial invasion and hyperplasia were observed in the colons of C57B1/6N-nunu mice after per os inoculation with the atypical E. coli. Immunocompetant mice housed in the same room as the N:NIH(S) III's remained healthy and exhibited no gross or microscopic lesions in spite of infection.

Animals↗
PubMed1987

The interaction of the xid and me genes.

The murine "motheaten" (me) mutation has been bred onto the NFS background and combined with the X-linked immunodeficiency (xid) mutation to investigate the effect of the xid-induced B cell maturational block on the widespread immune dysfunction, high levels of autoantibodies, and early mortality found in the motheaten mice. The xid markedly reduced spontaneous IgM secretion by spleen cells, serum IgM, anti-ssDNA antibodies, anti-bromelain-treated-erythrocyte antibodies, and T cell binding (but not thymocytotoxic) antibodies; however, neither phenotype nor mortality was affected, suggesting that other factors are responsible for early death. Marked expansion of the Ly-1+ B cell pool was prevented by xid in the motheaten mouse leaving only a very small population of sIgM-positive B cells. This failure of non-Ly-1+ B cell development in me/me X xid mice suggests that me/me leads to inhibition of non-Ly-1+ B cells and preferential expansion of Ly-1+ B cells in motheaten mice, perhaps as a result of their high levels of maturation and activation factors.

Animals↗
PubMed1986

Nonshivering thermogenesis in the diabetic SHR/N-cp (corpulent) rat.

The effects of isoenergetic sucrose and starch-based diets on thermogenesis were investigated in young adult, male, lean and corpulent SHR/N-cp rats. Corpulent rats gained weight 1.5 times more rapidly than lean, and sucrose diets resulted in more rapid weight gains in both phenotypes. Rates of resting and of norepinephrine-stimulated oxygen consumption were similar in both groups of lean rats and in sucrose-fed corpulent rats, but were decreased in starch-fed corpulent rats. The thermic response to injected norepinephrine occurred normally in all groups. Colonic and rectal temperatures were greater in lean than in corpulent rats. Acute cold exposure (5 degrees C) resulted in decreases in rectal but not colonic temperature in lean rats fed both diets, but resulted in lower temperatures at both sites in corpulent rats, with the greatest decreases being observed in the starch fed corpulent rats. Fifty percent of the corpulent but none of the lean rats succumbed within 24-48 hours following cold exposure. Urinary vanilmandelic acid (VMA) excretion was greater in lean than in corpulent rats, and the sucrose diet induced a greater increment in urinary VMA excretion in lean rats than in corpulent rats. These results are consistent with an impaired activation of sympathetically-mediated thermogenesis via nutritional or environmental stimuli in the corpulent genotype of the SHR/N-cp rat in concert with an economy in energy expenditure which may be contributing factors in the causation of their obese state.

Animals↗
PubMed1986

Characterization of a new rodent model of diabetes insipidus: the Roman high avoidance rat homozygous for diabetes insipidus.

These experiments were designed to characterize the nature and extent of diabetes insipidus present in a new model of genetic vasopressin (VP) deficiency, the Roman high avoidance rat homozygous for diabetes insipidus (RHA: di/di strain). The new strain was developed from an initial cross between Long-Evans derived Brattleboro (LE:di/di) rats and normal Roman high avoidance (RHA: +/+) rats, and has been bred to be congenic with the parent RHA: +/+ strain. RHA: di/di rats exhibited polydipsia, excreted dilute urine, and exhibited elevated plasma osmolality. RHA: di/di rats shows a similar urinary response to dehydration as LE: di/di rats. VP was undetectable by radioimmunoassay in the serum, brain, and neurohypophysis of RHA: di/di rats. VP-neurophysin containing cells were not observed in the brains of RHA: di/di rats upon immunocytochemical analysis. Thus, the new RHA: di/di strain exhibits essentially the same profile of diabetes insipidus as the LE: di/di rat. The congenic relationship between RHA: di/di and RHA: +/+ rats makes the RHA: di/di rat a useful model under circumstances where genetic variables unrelated to VP deficiency may confound the interpretation of data.

Animals↗
PubMed1986

Rates of sterol synthesis in the liver and extrahepatic tissues of the SHR/N-corpulent rat, an animal with hyperlipidemia and insulin-independent diabetes.

The SHR/N-corpulent rat is a new genetically obese strain that exhibits both insulin-independent diabetes and hyperlipidemia. The present studies were undertaken to characterize various parameters of cholesterol metabolism in this model. At 11 weeks of age, the obese animals had markedly elevated plasma cholesterol, triglyceride, glucose, and insulin concentrations and elevated hepatic triglyceride concentrations compared to their lean littermates. The additional cholesterol in plasma was carried in the fractions of density less than 1.006, 1.020-1.055, 1.055-1.095, and 1.095-1.21 g/ml. In the obese rats the level of free cholesterol in the liver was decreased significantly while that of cholesteryl ester showed little change. Hepatic sterol synthesis was markedly suppressed in the obese animals. However, the rate of sterol synthesis in the small intestine and other extrahepatic tissues generally remained unchanged. Although hepatic synthesis was suppressed, whole animal sterol synthesis in the obese rats was similar to that in the lean controls. This resulted because, in the obese animals, not only was the reduced rate of hepatic synthesis partly balanced by a greater than 70% increase in liver mass, but the mass of the small intestine and adipose tissue was also increased more than 30% and 4-fold, respectively, thereby making these tissues quantitatively more important sites of sterol synthesis. When obese rats were pair-fed to the intake of their lean littermates for 10 weeks, there was only a modest reduction in body weight and plasma cholesterol concentration, and the rate of hepatic sterol synthesis remained very low. The suppression of synthesis in the liver also persisted when the obese rats were fed surfomer, a drug that specifically blocks cholesterol absorption. In contrast, feeding cholestyramine restored the rate of hepatic sterol synthesis to that found in lean animals. Bile acid pool size in the obese males and females was 2.5-fold greater than in their lean controls. The suppression of hepatic sterol synthesis in this model may be due to a change in the entero-hepatic circulation of bile acids arising from an expanded pool or, alternatively, it may represent a compensatory response to overproduction of sterol and its precursors in the intestinal and adipose compartments.

Adipose Tissue↗
PubMed1985

Viability of frozen-thawed mouse embryos is affected by genotype.

Embryos from mice of five different genotypes were evaluated for their ability to survive cryopreservation as measured by post-thaw in vitro development. In Study 1, ovulation was induced with a standardized pregnant mares' serum gonadotropin (PMSG)/human chorionic gonadotropin (hCG) regimen, after which females were mated with males of the same genotype to produce incrossed embryos. Four- to 8-cell embryos were frozen in 1.5 M dimethyl sulfoxide (DMSO) at a rate of 0.5 degrees C/min to -80 degrees C and stored in liquid nitrogen. Following thawing at room temperature, embryos were cultured and development was evaluated 24 h later. The mean (+/- SEM) number of 4- to 8-cell embryos/pregnant female by stock/strain were: N:NIH(S), 6.8 +/- 0.8; N:NIH(S)-B, 5.8 +/- 0.5; N:GP(S), 6.5 +/- 0.6; C57BL/6N, 9.7 +/- 1.0; C3H/HeN MTV-, 9.5 +/- 0.9 (P less than 0.05). Post-thaw in vitro development was related to genetic background; the proportion of embryos culturing after thawing was: N:NIH(S), 49%; N:NIH(S)-B, 61%; N:GP(S), 66%; C57BL/6N, 75%; C3H/HeN MTV-, 56% (P less than 0.05). Study 2 was conducted to evaluate the influence of mating various females to males of a genotype known to have a lower post-thaw embryo survival rate. N:NIH(S)-B, N:GP(S), C57BL/6N, and C3H/HeN MTV- female mice were mated with N:NIH(S) males to produce hybrid embryos. Post-thaw embryo survival was reduced (P less than 0.05) in three of the four hybrid groups. Fresh incrossed and hybrid embryos from each study were cultured for 24 h and yielded culture rates ranging from 95% to 99% (P greater than 0.05) among all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Motheaten mice--an animal model with an inherited form of interstitial lung disease.

The motheaten gene represents a single recessive mutation that occurs in mice and is associated with systemic immune abnormalities. Although they have abnormalities in several organs, homozygote animals (me/me) die by 8 wk of age from a diffuse, noninfectious lung disease. To evaluate this genetically determined model of interstitial lung disease, the lungs of these animals were studied by light and transmission electron microscopy and by bronchoalveolar lavage. Two control groups of mice were evaluated: (1) littermate normal mice, including mice without the motheaten gene (+/+) and mice heterozygous (me/+) the motheaten gene, and (2) nonlittermate normal mice (+/+). While the lungs of both control groups were normal morphologically, the lung disease in the homozygous motheaten mice progressed through 3 stages: (1) focal intra-alveolar hemorrhage with accumulations of alveolar macrophages and neutrophils in the lower respiratory tract; (2) persistent alveolitis and hemorrhage, and reparative processes including frequent mitoses of fibroblasts and type II alveolar epithelial cells; and (3) consolidation of the alveolar structures by massive accumulation of macrophages and marked derangement and fibrosis of the alveolar walls. Consistent with the morphologic findings, evaluation of mid-stage lung disease by lavage demonstrated that the alveolitis was characterized by a marked expansion of the total number of effector cells, an accumulation of neutrophils, and a marked expansion of the total numbers of T-lymphocytes and B-lymphocytes. Thus, the motheaten mouse can be regarded as a genetically determined model of interstitial lung disease characterized by alveolar hemorrhage, derangement of parenchymal cells, fibrosis, and an alveolitis with distinctive features.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Evidence that lymphokine-activated killer cells and natural killer cells are distinct based on an analysis of congenitally immunodeficient mice.

The in vitro incubation of lymphoid cells in RIL 2 results in the generation of LAK cells that are broadly lytic to autologous, syngeneic, and allogeneic fresh tumor cells, but which do not lyse fresh, normal cells. Strains of mice with congenital immunodeficiencies were tested both for the presence of NK cells and for their capacity to generate LAK cells after in vitro incubation with IL 2. Splenocytes obtained from two immunodeficient mouse strains (NIH-Beige-Nude and NIH-Beige-Nude-XID) failed to generate LAK cells, but displayed significant activity. Splenocytes from another immunodeficient mouse strain (NIH-Beige-XID) generated LAK cells but did not display NK cell activity. This dissociation of activation of LAK cells from NK cells among the immunodeficient strains indicates that the LAK and NK cell lytic systems are distinct.

Animals↗
PubMed1984

Functional T cells in athymic nude mice.

After passage of spleen cells from nu/nu mice over a nylon wool column, concanavalin A-responsive cells can be detected in the presence of 2-mercaptoethanol, and specific cytotoxic T lymphocytes can be generated without exposure to interleukin 2 (IL-2). The spleen cells of the nu/nu mice born of nu/nu parents and nursed by nu/nu mothers had significantly fewer Thy-1+ T cells and a lesser capacity to generate cytotoxic T lymphocytes than did the conventionally bred nu/nu mice. Nonetheless, such cells were clearly present. IL-2 may act to cause these post-thymic T cells to proliferate. Therefore, it seems inappropriate to consider IL-2 as an inducer of the differentiation of T cells in the absence of thymic influence on the basis of the capacity of IL-2 to induce the appearance of a T-lymphocyte population in nu/nu mice.

Animals↗
PubMed1984

Effect of dietary sucrose on the SHR/N-corpulent rat: a new model for insulin-independent diabetes.

A new congenic strain of genetically obese rat, SHR/N-corpulent (cp), was studied. Young male corpulent (cp/cp) and lean (cp/+ or +/+) rats approximately 5 wk of age were fed a diet containing 54% carbohydrate as either sucrose or cooked cornstarch for 9 wk. A phenotype effect was observed with body weight, fasting levels of serum insulin, triglyceride and total cholesterol, levels of serum insulin and glucose after an oral glucose load, and level of urine glucose (corpulent greater than lean), and with systolic blood pressure (corpulent less than lean). Only lean rats were hypertensive. Corpulent rats were hyperinsulinemic, hyperlipidemic, exhibited glycosuria, and were hyperglycemic after an oral glucose load. Lean rats were hyperinsulinemic, but normoglycemic. A diet effect (sucrose greater than starch) was observed with body weight, level of serum glucose after an oral glucose load, and urine volume in both corpulent and lean rats, and with levels of serum insulin and total urine glucose in corpulent rats. Corpulent rats fed sucrose had 20 to 40% higher levels of serum glucose and insulin after an oral glucose load, and twice the amount of total urine glucose, than did corpulent rats fed starch. The data demonstrate that corpulent rats have metabolic characteristics associated with insulin-independent diabetes in humans and that sucrose is more diabetogenic than starch. Manifestation of hyperglycemia in this model may be the result of superimposing obesity on an insulin-resistant genetic background.

Animals↗