30 results on '"Mueller RW"'
Search Results
2. Dysregulated liver lipid metabolism and innate immunity associated with hepatic steatosis in neonatal BBdp rats and NOD mice.
- Author
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Serrano D, Crookshank JA, Morgan BS, Mueller RW, Paré MF, Marandi L, Poussier P, and Scott FW
- Subjects
- Animals, Animals, Newborn, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Diabetes Mellitus, Type 1 immunology, Diabetes Mellitus, Type 1 physiopathology, Disease Models, Animal, Female, Gene Expression Profiling, Liver metabolism, Liver physiopathology, Male, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Phenotype, Phosphorylation, Polymerase Chain Reaction, Rats, Triglycerides metabolism, Fatty Liver immunology, Fatty Liver physiopathology, Immunity, Innate, Lipid Metabolism
- Abstract
In a previous study we reported that prediabetic rats have a unique gene signature that was apparent even in neonates. Several of the changes we observed, including enhanced expression of pro-inflammatory genes and dysregulated UPR and metabolism genes were first observed in the liver followed by the pancreas. In the present study we investigated further early changes in hepatic innate immunity and metabolism in two models of type 1 diabetes (T1D), the BBdp rat and NOD mouse. There was a striking increase in lipid deposits in liver, particularly in neonatal BBdp rats, with a less striking but significant increase in neonatal NOD mice in association with dysregulated expression of lipid metabolism genes. This was associated with a decreased number of extramedullary hematopoietic clusters as well as CD68
+ macrophages in the liver of both models. In addition, PPARɣ and phosphorylated AMPKα protein were decreased in neonatal BBdp rats. BBdp rats displayed decreased expression of antimicrobial genes in neonates and decreased M2 genes at 30 days. This suggests hepatic steatosis could be a common early feature in development of T1D that impacts metabolic homeostasis and tolerogenic phenotype in the prediabetic liver.- Published
- 2019
- Full Text
- View/download PDF
3. Cloning and characterization of glutamate receptors in Californian sea lions (Zalophus californianus).
- Author
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Gill S, Goldstein T, Situ D, Zabka TS, Gulland FM, and Mueller RW
- Subjects
- Animals, Base Sequence, Cardiomyopathies chemically induced, Cardiomyopathies metabolism, Cloning, Molecular, DNA Primers, Immunohistochemistry, Kainic Acid metabolism, Kainic Acid toxicity, Molecular Sequence Data, Neurotoxins toxicity, Polymerase Chain Reaction, Receptors, Glutamate genetics, Cardiomyopathies veterinary, Kainic Acid analogs & derivatives, Marine Toxins toxicity, Myocardium chemistry, Receptors, Glutamate chemistry, Receptors, Glutamate isolation & purification, Sea Lions physiology
- Abstract
Domoic acid produced by marine algae has been shown to cause acute and chronic neurologic sequelae in Californian sea lions following acute or low-dose exposure. Histological findings in affected animals included a degenerative cardiomyopathy that was hypothesized to be caused by over-excitation of the glutamate receptors (GluRs) speculated to be present in the sea lion heart. Thus tissues from five sea lions without lesions associated with domoic acid toxicity and one animal with domoic acid-induced chronic neurologic sequelae and degenerative cardiomyopathy were examined for the presence of GluRs. Immunohistochemistry localized mGluR 2/3, mGluR 5, GluR 2/3 and NMDAR 1 in structures of the conducting system and blood vessels. NMDAR 1 and GluR 2/3 were the most widespread as immunoreactivity was observed within sea lion conducting system structures. PCR analysis, cloning and subsequent sequencing of the seal lion GluRs showed only 80% homology to those from rats, but more than 95% homologous to those from dogs. The cellular distribution and expression of subtypes of GluRs in the sea lion hearts suggests that exposure to domoic acid may induce cardiac damage and functional disturbances.
- Published
- 2010
- Full Text
- View/download PDF
4. Characterization of a degenerative cardiomyopathy associated with domoic acid toxicity in California sea lions (Zalophus californianus).
- Author
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Zabka TS, Goldstein T, Cross C, Mueller RW, Kreuder-Johnson C, Gill S, and Gulland FM
- Subjects
- Animals, Caspase 3 metabolism, Dissection methods, Dissection veterinary, Female, Immunohistochemistry, Kainic Acid toxicity, Male, Myocardium pathology, Cardiomyopathies chemically induced, Cardiomyopathies pathology, Cardiomyopathies veterinary, Kainic Acid analogs & derivatives, Marine Toxins toxicity, Neurotoxins toxicity, Sea Lions
- Abstract
Domoic acid, produced by marine algae, can cause acute and chronic neurologic sequela in California sea lions (Zalophus californianus) from acute toxicity or sublethal exposure. Eight sea lions, representing acute and chronic cases, both sexes, and all age classes, were selected to demonstrate a concurrent degenerative cardiomyopathy. Critical aspects of characterizing the cardiomyopathy by lesion distribution and morphology were the development of a heart dissection and tissue-trimming protocol and the delineation of the cardiac conducting system by histomorphology and immunohistochemistry for neuron-specific protein gene product 9.5. Histopathologic features and progression of the cardiomyopathy are described, varying from acute to chronic active and mild to severe. The cardiomyopathy is distinguished from other heart lesions in pinnipeds. Based on histopathologic features, immunopositive staining for cleaved caspase-3, and comparison with known, similar-appearing cardiomyopathies, the proposed pathogenesis for the degenerative cardiomyopathy is the primary or at least initial direct interaction of domoic acid with receptors that are suspected to exist in the heart. l-Carnitine, measured in the heart and skeletal muscle, and troponin-I, measured in serum collected at the time of death from additional animals (n = 58), were not predictive of the domoic acid-associated cardiomyopathy. This degenerative cardiomyopathy in California sea lions represents another syndrome beyond central neurologic disease associated with exposure to domoic acid and may contribute to morbidity and mortality.
- Published
- 2009
- Full Text
- View/download PDF
5. The monkey (Macaca fascicularis) heart neural structures and conducting system: an immunochemical study of selected neural biomarkers and glutamate receptors.
- Author
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Mueller RW, Gill SS, and Pulido OM
- Subjects
- Animals, Biomarkers analysis, Heart Conduction System metabolism, Immunohistochemistry, Nerve Fibers metabolism, Ubiquitin Thiolesterase, Heart innervation, Heart Conduction System anatomy & histology, Macaca fascicularis, Neurofilament Proteins metabolism, Receptors, Glutamate metabolism, Thiolester Hydrolases metabolism
- Abstract
The neural markers, protein gene product 9.5 (PGP 9.5), neurofilaments (NF) and glutamate receptors (GluRs) were visualized by immunohistochemistry in the monkey heart. PGP 9.5 showed the greatest affinity for intramural ganglia cells and nerve fibres. Structural components of the conducting system were also stained, particularly the bundle of His, AV node and Purkinje fibres. Anti-NF 200 and NF 160 showed strong, preferential affinity to nerve fibres and ganglia throughout the heart. Further studies concentrated on the presence and the distribution of glutamate receptors: NMDAR 1, GluR 1, GluR 2/3, GluR 5/6/7, mGluR 2/3, and mGluR 5. Positive immunoreactivity of GluRs was evident in nerve terminals within the atrium, myocardium, intramural ganglia and elements of the conducting system. The intensity of the stain varied for each antibody according to the anatomical distribution within neural structures and conducting system. The specificity of immunolabelling was confirmed by absorption studies with each corresponding peptide. There is preferential affinity to and differential distribution of staining with PGP 9.5, NFs and several subtypes of GluRs in the various components of the cardiac conducting system in adult monkeys. The expression of specific neural markers and glutamate receptors common to nerve fibers and ganglia cells is consistent to our previous report in rodents. These expressions suggests that such structures in the heart share common characteristics with a variety of neural tissues and hence are potential targets for neurotoxins. Furthermore, the strong affinity and specific distribution of several subtypes of GluRs in the monkey heart fosters our view that these receptors may be able to influence the physiology and pathophysiology of cardiac rhythm and excitation. Hence as in the brain, the GluRs may be involved in the mediation of excitatory effects in the heart.
- Published
- 2003
- Full Text
- View/download PDF
6. Potential target sites in peripheral tissues for excitatory neurotransmission and excitotoxicity.
- Author
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Gill SS, Mueller RW, McGuire PF, and Pulido OM
- Subjects
- Animals, Immunoenzyme Techniques, Male, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Receptors, Glutamate genetics, Reverse Transcriptase Polymerase Chain Reaction, Tissue Distribution, Glutamic Acid metabolism, Kidney metabolism, Liver metabolism, Lung metabolism, Receptors, Glutamate metabolism, Spleen metabolism, Synaptic Transmission physiology, Testis metabolism
- Abstract
Glutamate receptors (GluRs) are ubiquitously present in the central nervous system (CNS) as the major mediators of excitatory neurotransmission and excitotoxicity. Neural injury associated with trauma, stroke, epilepsy, and many neurodegenerative diseases such as Alzheimer's, Huntington's, and Parkinson's diseases and amyotrophic lateral sclerosis may be mediated by excessive activation of GluRs. Neurotoxicity associated with excitatory amino acids encountered in food, such as domoic acid and monosodium glutamate, has also been linked to GluRs. Less is known about GluRs outside the CNS. Recent observations suggest that several subtypes of GluRs are widely distributed in peripheral tissues. Using immunochemical and molecular techniques, the presence of GluR subtypes was demonstrated in the rat and monkey heart, with preferential distribution within the conducting system, nerve terminals, and cardiac ganglia. GluR subtypes NMDAR 1, GluR 2/3, and mGluR 2/3 are also present in kidney, liver, lung, spleen, and testis. Further investigations are needed to assess the role of these receptors in peripheral tissues and their importance in the toxicity of excitatory compounds. Therefore, food safety assessment and neurobiotechnology focusing on drugs designed to interact with GluRs should consider these tissues as potential target/effector sites.
- Published
- 2000
- Full Text
- View/download PDF
7. Immunochemical localization of the metabotropic glutamate receptors in the rat heart.
- Author
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Gill SS, Pulido OM, Mueller RW, and McGuire PF
- Subjects
- Animals, Antibody Specificity, Immunohistochemistry, Male, Rats, Rats, Sprague-Dawley, Heart anatomy & histology, Myocardium metabolism, Receptors, Metabotropic Glutamate metabolism
- Abstract
The localization of the glutamate receptor outside of the central nervous system is becoming more evident. These receptors have been implicated in brain function and pathology. It can also be envisioned that they play a vital role in the physiology of other organs and systems. We recently reported the presence of ionotropic glutamate receptors in the rat heart. These were distributed differentially in specific cardiac structures, including nerve terminals, ganglion cells, and the conducting system. In this study, we investigated the presence and localization of the metabotropic glutamate receptors (mGluRs) in the rat heart by immunohistochemistry. The experimental data show that the mGluR 1alpha, mGLuR 2/3, and mGluR 5 are present in the rat heart. Their preferential localization includes nerve terminals, ganglion cells, and elements of the conducting system. The mGluR 5 was the only receptor located in the intercalated disks of the cardiac muscle and in the endothelial lining of the blood vessels. This preferential localization to the different components of the conducting system and cardiac neural structures suggest that they play a role in the physiology of the heart.
- Published
- 1999
- Full Text
- View/download PDF
8. Molecular and immunochemical characterization of the ionotropic glutamate receptors in the rat heart.
- Author
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Gill SS, Pulido OM, Mueller RW, and McGuire PF
- Subjects
- Animals, Blotting, Northern, Blotting, Western, Brain Chemistry physiology, Cloning, Molecular, Heart anatomy & histology, Immunohistochemistry, Male, Myocardium cytology, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Myocardium metabolism, Receptors, Glutamate metabolism
- Abstract
Excitatory amino acids (EAA) and glutamate receptors (GluRs) play a fundamental role in the central nervous system (CNS). Ionotropic glutamate receptors (iGluRs) are coupled to ion channels, which are classified according to their most selective agonists. These ligand-gated channels are permeable to Na+, K+, and Ca+. Interaction of EAA receptor is linked to Ca+2/Na+ influx. Influx changes lead to an action potential, which in the heart is transmitted along the cardiocyte membrane. Furthermore, the heart has a rich innervation and specialized conduction system for rapid conduction and regulation of cardiac rhythmicity. Availability of EAA receptors in the heart might be important for cardiac function. The following GluRs were cloned by isoform-specific RT-PCR from rat heart ribonucleic acid (RNA): GluR 1, GluR 3, GluR 4, GIuR 7, Ka 1, and Ka 2. Expression in cardiac tissue was confirmed by western (for anti-GluR 2/3) and northern blots (for GluR 3, NMDAR 1, and Ka 2). The anatomical distribution was investigated by immunohistochemistry. Antibodies to GluR 2/3, GluR 5/6/7, Ka 2, and NMDAR 1 showed the strongest signals. These signals were specifically localized to cardiac nerve terminals, ganglia, conducting fibers, and some to myocardiocytes particularly in the atrium. Each antibody had a specific pattern of distribution. This anatomical localization suggests that they might play a role in cardiac electrophysiology and pathology.
- Published
- 1998
- Full Text
- View/download PDF
9. Spiral fracture of the humerus in a ball thrower.
- Author
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Reed WJ and Mueller RW
- Subjects
- Adult, Diagnosis, Differential, Humans, Male, Radiography, Baseball injuries, First Aid, Humeral Fractures diagnostic imaging
- Abstract
Spiral fractures of the humerus in ball throwers are rare clinical entities that can be confused with pathologic fractures. These fractures have been reported in various throwing sports, arm wrestling, and hand grenade throwing. They most commonly occur in the distal third of the humerus in young, active individuals. They are often preceded by throwing arm pain. Neurologic sequelae are rare. Herein, a case is presented of spiral fracture of the humerus in a softball player, and the assessment and management of these fractures, as well as their etiologic contrast to stress and pathologic fractures, are reviewed.
- Published
- 1998
- Full Text
- View/download PDF
10. Gavage administration of the fungal toxin fumonisin B1 to female Sprague-Dawley rats.
- Author
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Bondy GS, Suzuki CA, Mueller RW, Fernie SM, Armstrong CL, Hierlihy SL, Savard ME, and Barker MG
- Subjects
- Administration, Oral, Adrenal Glands drug effects, Animals, Body Weight drug effects, Bone Marrow drug effects, Female, Intubation, Gastrointestinal, Kidney drug effects, Liver drug effects, Male, No-Observed-Adverse-Effect Level, Organ Size drug effects, Rats, Rats, Sprague-Dawley, Sex Characteristics, Thymus Gland drug effects, Urinalysis, Carboxylic Acids toxicity, Carcinogens, Environmental toxicity, Fumonisins
- Abstract
The fungal toxin fumonisin B1 (FB1) is a contaminant of corn-based foods and feeds produced by members of the genus Fusarium. Fumonisin B1 toxicity was examined using gavage administration of purified toxin to female Sprague-Dawley rats. For 11 consecutive days each rat received a single dose of FB1 at the following concentrations: control (saline), 1, 5, 15, 35, or 75 mg FB1/kg body weight/d. Significantly depressed body weight and food consumption occurred at 35 and 75 mg FB1/kg/d. By the end of the dosing period there were no significant changes in food consumption. Kidneys and bone marrow were most sensitive to FB1 exposure. Changes in renal morphology were observed from 5 to 75 mg FB1/kg/d, accompanied by transient changes in urine osmolality and urine enzyme levels. Increased cellular vacuolation was the primary change associated with bone-marrow toxicity, starting at doses of 5 mg FB1/kg/d. Hepatotoxicity was indicated by reduced liver weight, elevated serum alanine amonitransferase (ALT), and mild histopathological changes occurring at doses of 15 mg FB1/kg/d and higher. Increased cytoplasmic vacuolation of adrenal cortex cells occurred in rats treated with 15 mg FB1/kg/d and higher, indicating that the adrenals are also potential targets of FB1. Elevated serum cholesterol, which is a consistent response to FB1 was observed at 5 mg FB1/kg/d and higher. Based on responses in this study, gavage is an appropriate substitute for longer feeding studies. Compared to previous work with male rats, gender-related difference in FB1 responses lacked consistency but indicated that males may be marginally more sensitive than female Sprague-Dawley rats.
- Published
- 1998
- Full Text
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11. Thoughts on the proper use and interpretation of clinical pathology data in preclinical safety testing: a Canadian perspective.
- Author
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Mueller RW
- Subjects
- Animals, Canada, Humans, Pathology, Clinical trends, Toxicology trends
- Published
- 1992
- Full Text
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12. Hepatic effects of ketoconazole in the male Swiss Webster mouse: temporal changes in drug metabolic parameters.
- Author
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Whitehouse LW, Pakuts AP, Paul CJ, Mueller RW, and Thomas BH
- Subjects
- Animals, Enzyme Induction drug effects, Ethylmorphine-N-Demethylase biosynthesis, Kinetics, Liver drug effects, Male, Mice, Microsomes, Liver drug effects, Microsomes, Liver enzymology, Mixed Function Oxygenases biosynthesis, Organ Size drug effects, Oxidoreductases, N-Demethylating biosynthesis, Testosterone metabolism, Time Factors, Cytochrome P-450 Enzyme System, Ketoconazole pharmacology, Liver metabolism, Pharmaceutical Preparations metabolism
- Abstract
There have been conflicting observations regarding the effects of ketoconazole on hepatic metabolism. The objectives of these studies were to determine whether ketoconazole was an enzyme inducer or inhibitor in the mouse and then to establish the time frame of these ketoconazole-induced enzyme changes. Ketoconazole was administered (150 mg/kg p.o. X 4 days) to male Swiss Webster mice. Biochemical observations over a period of 6 days following treatment indicated that ketoconazole had a temporal biphasic effect on the liver. Although liver weight and microsomal protein were elevated, all other parameters monitored were lower at 2 h following ketoconazole treatment. At 24 h after the last dose of ketoconazole, hepatic biochemical parameters (liver wt., % liver wt./body wt., microsomal protein, and cytochrome P-450) were statistically elevated, while enzyme activities (benzphetamine N-demethylation, 6 beta- and 7 alpha-hydroxylation of testosterone, formation of androstenedione and UDP-glucuronyltransferase) were inhibited. At 72 h the ketoconazole-induced changes in the hepatic biochemical parameters were comparable to those observed at 24 h, and enzymatic parameters generally appeared to be induced by ketoconazole, with the exception of benzphetamine N-demethylase and UDP-glucuronyltransferase, which exhibited lower enzyme activities. Ethoxyresorufin O-deethylase, 7 alpha-hydroxylation of testosterone and glutathione S-transferase, on the other hand, were unaltered by ketoconazole treatment. The opposing effects of ketoconazole on benzphetamine N-demethylase and ethylmorphine N-demethylase at 72 h were further examined. Enzyme kinetics studies indicated that ketoconazole did not effect the Michaelis constants (Km) of the two substrates, but the maximum velocity (Vmax) of the reactions was altered.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1990
- Full Text
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13. Ketoconazole-induced hepatic lysosomal phospholipidosis: the effect of concurrent barbiturate treatment.
- Author
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Pakuts AP, Parks RJ, Paul CJ, Bujaki SJ, and Mueller RW
- Subjects
- Animals, Body Weight drug effects, In Vitro Techniques, Liver anatomy & histology, Liver drug effects, Lysosomes drug effects, Mice, Microsomes, Liver drug effects, Microsomes, Liver enzymology, Microsomes, Liver metabolism, Mixed Function Oxygenases metabolism, Organ Size drug effects, Subcellular Fractions drug effects, Subcellular Fractions metabolism, Barbiturates pharmacology, Ketoconazole pharmacology, Liver metabolism, Lysosomes metabolism, Phospholipids metabolism
- Abstract
An unusual hepatic phospholipidosis produced by repeated high doses of ketoconazole in the mouse was investigated. This abnormal phospholipid accumulation was dose dependent after seven days of daily oral treatment over a 150-350 mg/kg ketoconazole dose range. The accumulation continued after 21 days at the 250 mg/kg dose level. Ultrastructural and biochemical studies revealed that ketoconazole produced a hepatic lysosomal accumulation of concentric lamellar bodies, as typically produced by many cationic amphiphilic drugs. Ketoconazole administered orally in mice at 250 mg/kg also induced total hepatic protein, microsomal protein, cytochrome p-450, and ethylmorphine N-demethylation. Concurrent phenobarbital and ketoconazole administration appeared to further increase hepatic drug metabolizing parameters and to reduce the extent of the hepatic phospholipid accumulation.
- Published
- 1990
14. Thyroxine 5'-deiodinase in brown adipose tissue of the cynomolgus monkey Macaca fascicularis.
- Author
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Kates AL, Park IR, Himms-Hagen J, and Mueller RW
- Subjects
- Animals, Electrophoresis, Polyacrylamide Gel, Female, Histocytochemistry, Immunoblotting, Macaca fascicularis, Male, Adipose Tissue, Brown enzymology, Iodide Peroxidase metabolism
- Abstract
Brown adipose tissue was identified in axillary, interscapular, subscapular, and cervical fat deposits of male and female cynomolgus monkeys (Macaca fascicularis) by histological and immunological techniques. Histology included staining of mitochondria with a Novelli stain and identification of mitochondria-rich multilocular cells. Immunological detection involved separation of homogenate proteins by sodium dodecyl sulphate--polyacrylamide gel chromatography, blotting on to nitrocellulose membranes, and identification of the specific uncoupling protein, unique to brown adipose tissue, with an antiserum to purified hamster uncoupling protein followed by detection with 125I-labelled protein A. The activity of thyroxine 5'-deiodinase in monkey brown adipose tissue homogenates was much higher than that seen previously in brown adipose tissue of rats, mice, and hamsters. This is the first demonstration of the presence of this enzyme in brown adipose tissue of a primate species.
- Published
- 1990
- Full Text
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15. Aortic changes in cynomolgus monkeys fed high-fat diets (long-term study).
- Author
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Mueller RW, Schiefer HB, Laxdal VA, and Ackman RG
- Subjects
- Animals, Hypercholesterolemia etiology, Lipoproteins blood, Macaca fascicularis, Species Specificity, Time Factors, Aorta pathology, Arteriosclerosis etiology, Dietary Fats adverse effects
- Abstract
Two diets containing either a lard-corn oil mixture (LCO) or partially hydrogenated herring oil (PHHO) were fed to cynomolgus monkeys (Macaca fascicularis) for up to 30 months. Serum cholesterol values rose to 180 mg/dl in the LCO-group and to 260 mg/dl in the PHHO-group. Serum lipoprotein concentrations were normal in the LCO-group, but PHHO-fed monkeys had lower HDL- and higher LDL- and VLDL-proportions. Only one animal on the LCO-diet for 24 months developed a pre-atherosclerotic lesion in the aorta. The general absence of true atherosclerotic lesions in the presence of high serum cholesterol levels and abnormal serum lipoprotein proportions may be interpreted as being indicative of the low atherogenicity of the fats used. This finding points toward a specific fat-animal species interaction.
- Published
- 1982
16. Effects of milrinone treatment in cardiomyopathic hamsters (CHF 147) with severe congestive heart failure.
- Author
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Desjardins S, Mueller RW, Hubert RS, and Cauchy MJ
- Subjects
- Animals, Body Weight drug effects, Calcium analysis, Cardiomyopathy, Dilated genetics, Cricetinae, Disease Models, Animal, Heart Failure genetics, Heart Failure pathology, Magnesium analysis, Male, Mesocricetus genetics, Milrinone, Pulmonary Edema etiology, Pulmonary Edema prevention & control, Cardiomyopathy, Dilated complications, Cardiotonic Agents therapeutic use, Heart Failure drug therapy, Pyridones therapeutic use
- Abstract
The effects of oral milrinone treatment in cardiomyopathic hamsters with severe congestive heart failure (CHF) were evaluated. Strict criteria based on increase in body weight were established to define day no 1 of treatment. Survival rate of non-treated hamsters (group 1) ranged between 9 and 16 d, mean 12.9 (SEM 0.8) d, after entering the study. Hamsters treated with milrinone in drinking water (group 2a: 0.3 mg.ml-1, or group 2b: 0.6 mg.ml-1) survived between 6 and 36 d, mean 15.0(2.1) d, NS, for group 2a, and between 6 and 47 d, mean 19.6(4.0) d, NS, for group 2b. There was a significant difference between the number of hamsters that survived longer than 16 d between untreated hamsters (group 1, n = 0/12) and hamsters treated with milrinone (groups 2a, b, n = 7/24). There was no significant correlation between survival duration and milrinone daily dose nor between survival and milrinone plasma concentration at death. Milrinone treatment also significantly decreased pulmonary congestion as measured by the number of pigment containing macrophages per alveolus. No other pathological findings were modified by milrinone. It was concluded that, in addition to exerting a beneficial effect on pulmonary congestion, milrinone improved survival in some CHF hamsters. However, more studies are needed to evaluate the possibility of an arrythmogenic potential that might explain why some treated hamsters died earlier than non-treated hamsters.
- Published
- 1989
- Full Text
- View/download PDF
17. A pressure overload model of congestive heart failure in rats.
- Author
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Desjardins S, Mueller RW, and Cauchy MJ
- Subjects
- Animals, Aorta, Abdominal, Body Weight, Constriction, Electrocardiography, Heart Failure etiology, Heart Failure physiopathology, Hemodynamics, Male, Organ Size, Rats, Rats, Inbred Strains, Disease Models, Animal, Heart Failure pathology, Myocardium pathology
- Abstract
Approximately 32% of the rats used as animal models showed an elevated heart weight/body weight ratio (0.432[SEM 0.022] g.100 g-1 compared to 0.293[0.009] g.100 g-1 for sham-operated rats), a hydrothorax, pulmonary and liver congestion, and specific histological changes 82-93 weeks after surgically induced aortic constriction. The histological changes were comparable to those observed in hearts of people suffering from long term hypertension. Cardiac failure was also confirmed by depressed contractility as measured by maximum and minimum dP/dt (first derivative of left ventricular pressure), which were 4604(346) and 3627(526) mm Hg.sec-1, respectively, compared with 9165(745) and 5835(268) mm Hg.sec-1 respectively in rats that did not develop left ventricular hypertrophy and failure (CLIP rats). Systolic and left ventricular blood pressures measured under anaesthesia were also decreased: 71.6(5.0) and 88.1(6.3) mm Hg respectively in rats with congestive heart failure, compared with 83.6(2.4) and 109.5(3.6) mm Hg in CLIP rats. Except for a prolonged mean PQ interval associated with a lower heart rate and for a slightly shorter QRS interval in the conscious state, the electrocardiograms of rats with congestive heart failure did not show any major abnormalities specific to ventricular hypertrophy and/or failure. This model could be useful for studying the pathology and adaptative mechanisms in compensated pressure overload induced congestive heart failure as well as in studies comparing pathological changes and means of treatment of congestive heart failure with different aetiologies encountered in the human population.
- Published
- 1988
- Full Text
- View/download PDF
18. Myocarditis in young dogs associated with a parvovirus-like agent.
- Author
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Hayes MA, Russel RG, Mueller RW, and Lewis RJ
- Subjects
- Animals, Dogs, Myocarditis microbiology, Dog Diseases microbiology, Myocarditis veterinary, Parvoviridae isolation & purification
- Published
- 1979
19. [TO THE DEATH OF GERHARD DOMAGK].
- Author
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MUELLER RW
- Subjects
- Germany, Germany, West, History, 20th Century, Sulfanilamide, Sulfanilamides, Antitubercular Agents, Death, History, 19th Century, Medicine, Sulfonamides
- Published
- 1964
20. [ON THE NOMENCLATURE OF CAVERN RESEARCH].
- Author
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MUELLER RW
- Subjects
- Humans, Caves, Names, Research, Terminology as Topic, Tuberculosis, Tuberculosis, Pulmonary
- Published
- 1963
21. [ON OUR PAST AND PRESENT THERAPEUTIC METHODS IN THE TREATMENT OF TUBERCULOSIS].
- Author
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MUELLER RW
- Subjects
- Antitubercular Agents, Surgical Procedures, Operative, Tuberculosis
- Published
- 1965
22. [The prevention of tuberculosis in China].
- Author
-
MUELLER RW
- Subjects
- China, Humans, Antibiotic Prophylaxis, Biomedical Research, Tuberculosis prevention & control
- Published
- 1960
23. [DOES THE CHILD REALLY HAVE TUBERCULOSIS?].
- Author
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MUELLER RW
- Subjects
- Child, Humans, Infant, Aminosalicylic Acid, Aminosalicylic Acids, BCG Vaccine, Diagnosis, Isoniazid, Mycobacterium bovis, Radiography, Thoracic, Tuberculin Test, Tuberculosis, Vaccination
- Published
- 1963
24. [Franz REDEKER on his 70th birthday on June 17, 1961].
- Author
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MUELLER RW
- Subjects
- History, 19th Century, History, 20th Century, Humans
- Published
- 1961
25. [What is and what does a positive tuberculin reaction signify?].
- Author
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MUELLER RW
- Subjects
- Humans, Immune System Phenomena, Tuberculin, Tuberculin Test
- Published
- 1961
26. [Tuberculosis in man caused by the bovine type and Mycobacterium avium].
- Author
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MUELLER RW
- Subjects
- Animals, Cattle, Birds, Mycobacterium avium, Tuberculosis, Tuberculosis, Avian, Tuberculosis, Bovine
- Published
- 1960
27. [On the death of a pathologist (Paul HUEB-SCHMANN)].
- Author
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MUELLER RW
- Subjects
- Death, History, Physicians
- Published
- 1960
28. [TUBERCULOSIS IN THE RURAL ENVIRONMENT OF EUROPE].
- Author
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MUELLER RW
- Subjects
- Europe, Communicable Disease Control, Rural Health, Social Environment, Tuberculosis
- Published
- 1964
29. Feeding tuberculosis.
- Author
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NAEGELI T and MUELLER RW
- Subjects
- Disease, Tuberculosis epidemiology, Tuberculosis etiology, Tuberculosis statistics & numerical data, Warfare
- Published
- 1947
30. [BRONCHIAL CARCINOMA--LUNG CARCINOMA].
- Author
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MUELLER RW
- Subjects
- Humans, Bronchial Neoplasms, Carcinoma, Bronchogenic, Cytodiagnosis, Lung Neoplasms, Neoplasms diagnosis, Radiography, Thoracic
- Published
- 1965
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