[Management of behavioral risk factors for cardiovascular disease (CVD)]. / Lifestyle in den Guidelines.

Changes in many patterns of individual risk behaviors (unhealthy diet, smoking, sedentary lifestyle) are necessary in a large majority of patients with established CVD or at high risk of CVD. Make healthy food choices. Energy intake must be adjusted to maintain ideal body weight. Eating from each major food group will ensure dietary balance. The consumption of fruits and vegetables, whole grain cereals and bread, low fat dairy products, fish and lean meat should be encouraged. Oily fish and omega-3-fatty acids are specially recommended. Saturated and trans fatty acids should be replaced with MUFA's or PUFA's of vegetable and seafood origins. Totalfat intake should account for no more than 30% of energy intake, and intake of saturated fats should not exceed a third of total fat intake. The intake of cholesterol should be less than 300 mg/day. Stop smoking tobacco. All smokers should be professionally encouraged to permanently stop smoking all forms of tobacco. Increase physical activity. A lack of regular physical activity may contribute to the early onset and progression of Cardiovascular Disease. Regular physical activity and the maintenance of physical fitness is beneficial in all age groups and should be promoted as an integral part of cardiovascular prevention. Healthy people should be advised to choose enjoyable activities, which fit into their daily routine, preferably 30-40 min, 4-5 times weekly at Borg 13 or at 60-75% of the average maximum heart rate. For patients with established CVD, advice must be based on a comprehensive clinical judgement including the results of an exercise test.

[Alimentary intake of opioid alkaloids by horses. Hazards due to poppy-containing feeds]. / Alimentäre Aufnahme von Opioid-Alkaloiden durch Pferde. Gefahren durch mohnhaltige Futtermittel.

Opioid alkaloids were identified in the urine of horses during an anti-doping control and in a case of intoxication. In both cases, it was suspected that the horses had ingested poppy-contaminated feed. To verify this suspicion, possible opioid alkaloid sources in Germany were identified through a literature research. Additionally, the contaminated feed was botanically and chemically analysed. The results indicated that both cases were most probably caused by the poppy in the feed. This highlights the previously underestimated risk of an intake of poppy-contaminated feed in horses. Recommendations are formulated for the prevention of positive doping-test results and intoxications by poppy-contaminated feeds in horses. Furthermore, a threshold for morphine in urine samples in competing horses is proposed.

Chemotherapeutic studies on N-nitrosoacetoxymethyl-methylamine-and 1,2-dimethylhydrazine-induced colonic tumors in rats: monotherapy with 5-fluorouracil, ftorafur, CGP 6809, and CGP 15'720A.

Colonic tumors were induced in male Sprague-Dawley rats by ten applications of 2 mg/kg/week N-nitrosoacetoxymethyl-methylamine (AMMN) or by three applications of 100 mg/kg/month 1,2-dimethylhydrazine (1,2-DMH). Application of AMMN and 1,2-DMH induced selective colonic tumors in 97% and 29-42% of the initial animals, respectively. Colonic-tumor-bearing animals were subjected to monotherapy with 5-fluorouracil, ftorafur, CGP 6809, and CGP 15'720A. No cures were achieved. The different therapies did not exert any clear influence on the survival time of animals, except for animals pretreated with AMMN and then subjected to ftorafur therapy.

Optimization of contrast dosage for gadolinium-enhanced 3D MRA of the pulmonary and renal arteries.

To determine the minimal contrast dosage required for diagnostic contrast-enhanced three-dimensional (3D) magnetic resonance angiography (MRA) image quality of the pulmonary (PAs) or renal arteries (RAs). In 12 volunteers (10 females, 2 males; mean age 24 years) imaging was performed with 4 different dosages: 0.05, 0.1, 0.2 and 0.3 mmol/kg of body weight (BW) 0.5 M gadolinium (Gd) contrast agent. The PAs and RAs were evaluated separately each in groups of six volunteers. Qualitative and quantitative signal-to-noise ratio (SNR) image analysis was performed. For the PAs, the increases in signal-to-noise ratio were paralleled by increases in image quality ratings. For the PAs, with the use of 0.05 mmol/kg, only 50.3% of all segments were rated diagnostic, whereas with higher dosages the percentage rose to 89.2% for 0.1 mmol/kg, 98.2% for 0.2 mmol/kg. and 99.1% for 0.3 mmol/kg. For the RAs, 0.3 mmol/kg provided no significant increase in singal-to-noise ratio compared to 0.2 mmol/kg (p = 0.4). Only by a dosage of 0.2 and 0.3 mmol/kg, all evaluated segments were diagnostic evaluable. A dose of 0.2 mmol/kg is required for proper assessment of the RAs or PAs.

Effects of caffeine on sister-chromatid exchanges (SCE) in vivo.

Chinese hamsters were twice treated with caffeine via stomach tube. The single doses were either 20, 100, 200 or 400 mg per kg body weight. A dose-dependent increase was observed in the frequencies of SCE induced in vivo in bone-marrow cells. Two intraperitoneal injections of the chemical mutagens, cyclophosphamide or benzo[a]pyrene, led to a pronounced increase of the frequency of SCE. Simultaneous applications of the chemical mutagens and caffeine decreased the rate of SCE. The effect of caffeine per se to induce SCE, and the mechanisms by which caffeine reduces the level of SCE induced by chemical mutagens are discussed.

Endoscopic diagnosis of chemically induced autochthonous colonic tumors in rats.

The suitability of using coloscopy as a diagnostic method is investigated with respect to colonic carcinomas induced locally by the administration of N-nitrosoacetoxymethyl-methylamine, N-methyl-N-nitrosourea, and methylnitro-nitrosoguanidine, or systemically by subcutaneous injection of 1,2-dimethylhydrazine in Sprague-Dawley rats. The endoscopic diagnostic examination proved to be clearly superior to methods of animal inspection, palpation, investigation for occult blood and exploratory laparotomy which have so far been employed in animal experiments with small rodents. The relevance of this method is discussed for the early detection of chemically induced colonic tumors, and the observation of tumor development under experimental cytostatic therapy.

Activated astrocytes, but not pyramidal cells, increase glucose utilization in rat hippocampal CA1 subfield after ischemia.

The local cerebral glucose utilization (CMRglc) in the damaged rat hippocampal CA1 subfield increases 7 days after 10 min of cerebral ischemia. We have used the N-methyl-D-aspartate antagonist (NMDA antagonist) ketamine in rats 7 days after sham operation or cerebral ischemia to determine whether the elevated postischemic CMRglc of the CA1 subfield is due to long-lasting hyperexcitation of surviving or injured neurons, or, alternatively, to the metabolism of other cell types. The autoradiographic data were interpreted with the aid of histochemical analysis of the postischemic hippocampal cell changes. Anesthetic doses of ketamine significantly reduced the CMRglc in the CA1 strata oriens, pyramidale and radiatum of sham-operated rats, while the postischemic increases in CMRglc in these hippocampal CA1 strata were not affected by ketamine. In addition, there were ketamine-induced increases in the CMRglc of the CA1 stratum lacunosum moleculare of both sham-operated and postischemic rats. The immunoreactivity of the microtubule-associated protein 2 (MAP2), a postsynaptic protein marker, was decreased markedly in the CA1 subfield in postischemic rats, while the presynaptic protein marker, synaptophysin, remained the same in sham-operated and postischemic rats. The glial fibrillary acidic protein (GFAP) immunoreactivity of astrocytes raised markedly in the ischemically damaged CA1 subfield. Although it could be demonstrated that presynaptic terminals remain intact in the postischemic damaged CA1 subfield, the lacking ketamine effect on CA1 pyramidal neurons indicated that the increase in CMRglc in this brain area is not due to postsynaptic neural hyperexcitation, but probably has to be attributed to astrocytes activated by neuronal damage.

Impairment by interferon of mitogen-induced DNA synthesis in chick lymphocytes.

Chick interferon preparations inhibit mitogen-induced DNA synthesis of chicken peripheral and spleen lymphocytes. Mock interferon preparations showed also some inhibition of mitogen-induced DNA synthesis. The degree of inhibition is concentration dependent but varies also with the relative time of addition of homologous interferon and mitogen. Addition of the interferon preparations 6 h before mitogen resulted in a stronger inhibition of DNA synthesis than if the interferon preparations and mitogen were added at the same time. The interferon preparations seem to affect the metabolism of lymphocytes in a mroe general way and not only the trigger mechanism of the mitogenic response since addition of interferon even 24 h after the mitogen inhibits the induced DNA synthesis.