Left atrial impression due to lymphadenopathy in an HIV seropositive patient infected with tuberculosis.

We describe a unique case of a 37-year-old patient who was diagnosed with human immunodeficiency virus/tuberculosis co-infection due to a cardiac involvement that consisted in atrial fibrillation as a consequence of a compression of the left atrium by a giant necrotic lymphadenopathy and a pericardial effusion.

Rupture of papillary muscle during dobutamine stress echocardiography.

A 72-year-old man presented with an acute myocardial infarction, he did not receive any reperfusion therapy because he presented as a non-ST elevation myocardial infarction (MI). A dobutamine stress echocardiography was done five days after. A partial rupture of the posterior papillary muscle occurred during the stress test. The patient developed cardiogenic shock; he improved after medical management, and mitral repair was done a few days after.

[Estrogen replacement therapy: for whom, why and how?]. / L'oestrogénothérapie substitutive: pour qui, pourquoi, comment?

Symptoms may appear during the perimenopause, but it is often difficult to treat them at that time. Progestins are used to treat abnormal bleeding. Low dose hormone replacement therapy (HRT) or oral contraception are often used also. HRT can be used to maintain the bone density even in elderly women. Nevertheless, the treatment is often not taken for sufficient time. In order to improve compliance, a number of low dose HRT have been developed. For most patients these medications will preserve the bone mass, but data showing a fracture protection are missing. The exact role of HRT on cardiovascular pathologies is controversial. Observational data indicated a protective effect on atherosclerosis. But randomised studies contradicted these results: the latest randomised trial involving a continuous combined regimen of estrogen and progestin reported an increased risk in cardiovascular events as compared to placebo. It is still possible that estrogen decreases atheromatosis but that it increases the risk of thrombosis. SERM (Selective Estrogen Receptor Modulators) have agonistic and antagonistic proprieties to estrogens on selective tissues. They have a proven protective effect on bone and possibly also on cardiovascular system. Nevertheless, the risk of thrombosis seems to be similar to that of estrogens. The risk of breast cancer seems to be increased in long term HRT users but this subject is also controversial since discordant results have been reported. Furthermore, breast cancer mortality in HRT users seems to be lower than in non users.

Effects of sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity.

Rats consuming Coca-Cola and Purina chow ad libitum increased their total energy intake by 50% without excess weight gain. Their resistance to cold was markedly improved. These phenomena were characterized by significant increases in interscapular brown adipose tissue weight (IBAT) (91%), cellularity (59%), triglyceride content (52%), protein content (94%), and cytochrome oxidase activity (167%). In contrast, Coca-Cola consumption did not significantly affect the cellularity or triglyceride content of parametrial white adipose tissue (PWAT), although it slightly augmented PWAT weight. The effects of Coca-Cola on cold resistance, IBAT cellularity, and composition were entirely reproduced by sucrose, but not caffeine, consumption. Although caffeine also increased IBAT cellularity and composition, it significantly decreased the rate of body weight gain, PWAT weight, and adipocyte size. Moreover, it markedly inhibited adipocyte proliferation in PWAT thereby mimicking the effects of exercise training and food restriction (Bukowiecki et al., Am. J. Physiol. 239 (Endocrinol. Metab. 2): E422-E429, 1980). It is concluded a) that sucrose and Coca-Cola consumption improve the resistance of rats to cold, most probably by increasing brown adipose tissue cellularity, and b) that moderate caffeine intake might be useful for inhibiting proliferative activity in white adipose tissue, thereby preventing obesity.

Brown adipose tissue hyperplasia: a fundamental mechanism of adaptation to cold and hyperphagia.

Cold acclimation (4 degrees C) and "cafeteria diets" increased the thermic response of rats to catecholamines. This phenomenon was accompanied by six- to eightfold increases of interscapular brown adipose tissue (IBAT) weight, total tissue cytochrome oxidase activity, and total number of brown adipocytes. Quantitative radioautographic experiments using [3H]thymidine disclosed that cold exposure markedly enhanced the mitotic activity in blood capillaries and small-venule endothelial cells, adipose tissue interstitial cells, and preadipocytes rather than in fully differentiated brown adipocytes. IBAT mitotic index increased 70 times over control values after only 2 days of cold exposure. Thereafter, the proliferative activity progressively decreased. IBAT cell composition was modified during cold acclimation as the percentage of interstitial cells and preadipocytes increased over the other cellular types. Because brown adipose tissue is the principal site of norepinephrine-induced thermogenesis in homeothermal animals, it is suggested that brown adipocyte proliferation from precursor cells represents the fundamental phenomenon explaining the increased capacity of cold-acclimated animals to respond calorigenically to catecholamines.

Ephedrine, a potential slimming drug, directly stimulates thermogenesis in brown adipocytes via beta-adrenoreceptors.

Ephedrine is a potential slimming drug that stimulates thermogenesis in man and laboratory animals. Considering that brown adipose tissue is an important site of catecholamine-induced thermogenesis in homeotherms, we tested the thermogenic efficiency of several ephedrine stereoisomers on adipocytes isolated from rat interscapular brown adipose tissue. Addition of (-)-ephedrine (0.1 mM) to brown adipocyte suspensions rapidly stimulated cellular respiration eight times above basal values. A stable Vmax of 335 nmol O2/min/10(6) cells was reached less than 5 min after the onset of respiratory stimulation. This value represents 85 percent of the maximal respiration observed with norepinephrine, the physiological effector of thermogenesis. The (-)isomer of ephedrine (1/2 Vmax = 20 microM) was more potent that other stereoisomers (+)-psi-ephedrine, (-)-psi-ephedrine (racephedrine) in enhancing brown adipocyte respiration. Beta-Adrenergic antagonists (alprenolol and propranolol) were much more effective than alpha-adrenergic antagonists (phentolamine and phenoxybenzamine) in inhibiting the respiratory effects of ephedrine. It is concluded that (-)-ephedrine mimics the calorigenic action of norepinephrine by directly stimulating brown adipocyte respiration via beta-adrenoreceptors.