Studies on the number of fat cells and connective tissue cells in white adipose tissue in chronic starvation and after refeeding. II. Investigations on obese and lean C 57 BL/6 J-mice (author's transl)]

Former investigations (Rakow et al., 1970, 1971a, b 1974) have demonstrated a constancy of the adipocyte number in white adipose tissue (parepididymal fat pads) of lean NMRI-albino-mice and aurothioglucose-obese NMRI-albino-mice during starvation and subsequent refeeding. In contrast the number of cells of connective tissue showed great variations under the experimental conditions mentioned above. The present paper describes which changes of the different cell populations within the adipose tissue could be demonstrated in lean and obese C57BL/6 J-mice. Material and Methods: The investigations were performed with obese and lean male C57BL/6 J-mice. The control animal groups were fed for six weeks 2.5 g (lean mice) and 2 g (obese mice), respectively, Altromin 1115R daily (starvation phase). After this time some of these animalwere killed (exp. groups H). The remaining animals now were fed Altromin 1115R and additional oat falkes ad libitum. Three (exp. groups HW3) and seven (exp. groups HW 7) days, respectively, after the beginning of the refeeding phase the animals were killed. After sacrifice the epididymal fat pads were weighed and treated with either (fat extraction). The dry mass was hydrolized with PCA (0.5 m, 90 degrees C, 40 min). In the supernatant the DNA (Burton, 1956), RNA (Ceriotti, 1955) and polysaccharide content (Seifter et al., 1950) were measured. The sediment was hydrolized with NaOH (0.5 n, 37 degrees C, 24 hrs). In this solution the protein content (Lowry et al., 1951) was determined. In addition fat cells were isolated according to Rodbell (1964). The fat cell diameters were determined microscopically and the average masses of the fat cells were estimated. From the wet weight of the fat pads and the average fat cell mass and number of fat cells were calculated. The remaining suspension of fat cells and cells of connective tissue were utilized for cell smears. These cell smears were stained with Schiff's reagent (Feulgen et al., 1924; Graumann, 1953). With an integrating microdensitometer (Deeley, 1955) the average relative DNA-content of single cell nuclei was measured and the ploidy patterns were estimated. The DNA-content was measured chemically according to Burton (1956). From the whole DNA-content of the fat pads and the DNA-content of the fat cell population the number of cells of the connective tissue was calculated...     

Influence of acetylsalicylic acid on aListeria monocytogenes infection

The influence of acetylsalicylic acid (ASA, CAS 50-78-2) on theListeria monocytogenes infection in balb/c mice was investigated. One day prior to lethal or sublethal infection, balb/c mice were treated intravenously with therapeutic concentrations of ASA alone or ASA in combination with murine recombinant interferon , a lymphokine produced by T-helper cells. Three days post-infection, parasite burdens of spleen and liver were determined by the colony-forming unit assay. It was shown that the prophylactic application of ASA in a concentration of 5 mg/kg body weight resulted in a more than 10-fold reduction of viableListeria monocytogenes in spleen and liver of balb/c mice. In addition, the combination of a suboptimal dosage of interferon with ASA resulted in a significantly higher survival rate compared to the untreated controls.     

Hydroxylation of testosterone and induction of steroid hydroxylases by phenobarbital in genetically obese mice (author's transl)

In spite of the profound alterations in lipid metabolism in the liver of genetically obese mice (strain C57 BL/6J) the activity of the hepatic hydroxylases with testosterone as substrate does not differ from that of their litter mates of normal weight. However, when the increased liver weight of the obese animals is taken into account their total capacity for steroid hydroxylation exceeds that of their litter mates by a factor of more than 2. Moreover, the inducibility of the membrane-bound enzyme system is not affected: application of phenobarbital (20 or 40 mg/kg body weight twice daily for 4 days) leads to a 2--3fold increase of the activity.     

Intestinal structural changes in African green monkeys after long term psyllium or cellulose feeding

Intestinal structure of male adult African Green monkeys (Cercopithecus aethiops ssp vervets) was studied after 3 1/2 yr of consuming diets containing 10% psyllium husk or cellulose. Scanning electron microscopy (SEM) identified mild damage (cellular swelling and disarray, and microvillar denudation and disarray) at villous tips throughout the small intestine in the psyllium-fed monkeys. The cellulose group had similar duodenal damage. Differences were not found in colons by SEM. By light microscopy, jejunum had shorter villi with psyllium feeding, based upon villous height (P less than 0.05), and length around a sectioned villus (P less than 0.1), but not based upon the number of enterocytes per villus. Jejunal and ileal circular and longitudinal muscle layer thicknesses were increased in psyllium-fed monkeys. Colonic mucosal height was significantly (P less than 0.05) reduced and muscle layer thickness was mildly reduced in the psyllium-fed monkeys. Group differences were not found in intestinal weight or length or in the weight of small intestinal mucosal scrapings. Psyllium husk may cause epithelial cell loss and muscle layer hypertrophy in the jejunum and ileum and thinning of the colonic wall after prolonged feeding.     

Spatial intralobar correlation of spike and slow wave activity localisations in focal epilepsies: a MEG analysis

12 patients with focal epilepsy were examined by magnetoencephalography (MEG). Source localisations of interictal epileptiform activity (spikes) yielded clear results. Slow wave dipole density in the frequency range from 2 to 6 Hz, using time selections from an automatic principal component analysis (PCA), was calculated. Results of spike and slow wave dipole density localisations were superimposed on MR-images of each patient. Slow wave dipole densities were increased close to spike localisations. Distances between spike center of mass and slow wave maxima were calculated, average mean distance was 2.0 cm. Independant of the localisation in either TLE or ETLE a concordance of slow wave and spike localisations were found. Slow wave localisations were found in patients with lesions in MRI and patients with no abnormalities on the MRI. In comparison to healthy subjects, slow wave dipole density in patients with epilepsy was clearly increased. The localisation of slow wave dipole density yielded additional important information and may contribute to defining the irritative zone.     

The effect of complete Freund--adjuvant on chronic proliferating inflammation in an experimental granuloma model.

Histometric, biochemical, radiochemical and autoradiographic studies were undertaken to investigate the influence of complete Freund-adjuvant (CFA) on a defined chronic proliferating inflammation of a granuloma model in two different experimental situations. Where as the percentage fraction of the fibroblasts, 3H-thymidine marking index of the fibroblasts and the impulse rate of the fibroblasts and endothelial cells do not differ from the values found for the control animals, both the protein and DNA content of the implanted sponges, as well as the DNA content of the individual fibroblasts in the implants increased, independent of the stage of the chronic proliferating inflammation at which the CFA was administered. Surprisingly the quantity of the fibroblast specific synthetic product, collagen, did not increase in proportion to the absolute number of fibroblasts, but remained either constant or even significantly decreased. A possible inhibition of collagen synthesis after CFA administration during chronic proliferating inflammation is discussed.     

Exercise training associated with estrogen therapy induced cardiovascular benefits after ovarian hormones deprivation

Menopause is recognized as a period of increased risk for coronary heart disease. Although the benefits of exercise training in lowering cardiovascular risk factors are well established, the risks and benefits of hormone therapy have been questioned. The purpose of the present study was to investigate the effects of estrogen therapy (HT) associated or not with exercise training (ET) in autonomic cardiovascular control in ovariectomized (OVX) rats. Female rats were divided into: control, OVX, OVX + HT, OVX + ET and OVX + HT + ET. HT was performed using a 0.25 mg 8-weeks sustained release pellet. Trained groups were submitted to an 8-week exercise training protocol on treadmill. Baroreflex sensitivity (BRS) was evaluated by heart rate responses to arterial pressure (AP) changes, and vagal and sympathetic tonus by pharmacological blockade. Ovariectomy induced an AP increase (123 ± 2 mmHg vs. 108 ± 2 mmHg), BRS impairment (∼69%), sympathetic activation (∼100%) and vagal tonus reduction (∼77%) compared to controls. HT or ET normalized the changes in parasympathetic tonus. However, only the association HT + ET was able to promote normalization of AP, BRS and sympathetic tonus, as compared to controls. These results indicate that ET induces cardiovascular and autonomic benefits in OVX rats under HT, suggesting a positive role of this association in the management of cardiovascular risk factor in postmenopausal women.     

Mutagenicity testing of rutacridone epoxide and rutacridone, alkaloids in Ruta graveolens L., using the Salmonella/microsome assay

The mutagenicity of rutacridone and rutacridone epoxide wasinvestigated using Salmonella typhimurium without as well aswith different metabolic activation systems. Rutacridone epoxidewas found to be a direct acting mutagen in S. typhimurium strainsTA98, TA100 and TA1538; addition of rat liver preparations resultedin a marked decrease of mutagenicity. In contrast, rutacridonerequired metabolic conversion to exhibit mutagenic activity.Neither of the compounds had any effect on tester strain TA1978.S9 mixes as well as microsomal and cytosolic preparations fromuntreated, phenobarbital-treated and 3-methylcholanthrene-treatedrats were used to study the activation and deactivation capacitiesof the enzyme mixtures. In addition, the influence of enzymeinhibitors on the activation and deactivation of the furoacridoneswere tested. Evidence is presented that rutacridone is metabolizedby rat liver enzymes to the corresponding epoxide as the ultimatemutagen. ^*Dedicated to Professor Dr C.-G.Arnold on the occasion of his60th birthday.