96 research outputs found

    Low intense physical exercise in normobaric hypoxia leads to more weight loss in obese people than low intense physical exercise in normobaric sham hypoxia

    Get PDF
    Training in mild to moderate hypoxia (14–17% O2 in breathing air) and extended resting in moderate hypoxia (9–13% O2) have been shown to have effects in animals and humans on lipid and glucose metabolism, appetite loss, and, in part, on body weight. The causality for these effects is not yet known in detail, and the available data in humans from high-altitude and low-pressure chamber studies are scarce. New technical developments by German companies in the production of artificial climates with normobaric hypoxic conditions in larger rooms at reasonable energy costs allow now to perform hypoxia weight loss studies in obese humans with stable experimental conditions and protocols with a sham hypoxia control. Thirty-two obese people were recruited for a mild intense training study in normobaric hypoxia (15 vol.% O2) and normoxia/sham hypoxia (20.1 vol.% O2). Twenty of these [mean age 47.6 years, mean body mass index (BMI) 33.1, 16 m, 4 f) were willing to follow up on an 8-week, three times per week, 90-min low intense physical exercise in their individual fat burning mode, which has been determined by an exercise testing with spiro-ergometry upfront. The subjects were evenly randomized into a hypoxia and sham hypoxia group. The difference of the two groups in weight loss and changes in HBa1C values were analyzed before and after the training period. No nutritional diet was applied. Subjects in the hypoxia group in mean lost significantly more weight than in the sham hypoxia group (Δ1.14 kg vs Δ0.03 kg; p = 0.026). This resulted in a tendency to reduce the BMI more in the hypoxia group (p = 0.326). In the mean, there was no HbA1C exceeding normal values (mean 5.67 and 5.47%), and the HbA1C stayed basically unchanged after the 8-week training. Mild physical exercise three times per week for 90 min in normobaric hypoxia for 8 weeks led to significantly greater weight loss in obese persons than the exercise in sham hypoxia in this, to our knowledge, first sham hypoxia controlled study

    Angiogenic Activity of Sera from Pulmonary Tuberculosis Patients in Relation to IL-12p40 and TNFα Serum Levels

    Get PDF
    The role of angiogenesis in the pathogenesis of tuberculosis (TB) is not clear. The aim of this study was to examine the effect of sera from TB patients on angiogenesis induced by different subsets of normal human mononuclear cells (MNC) in relation to IL-12p40 and TNFα serum levels. Serum samples from 36 pulmonary TB patients and from 22 healthy volunteers were evaluated. To assess angiogenic reaction the leukocytes-induced angiogenesis test according to Sidky and Auerbach was performed. IL-12p40 and TNFα serum levels were evaluated by ELISA. Sera from TB patients significantly stimulated angiogenic activity of MNC compared to sera from healthy donors and PBS (p < 0.001). The number of microvessels formed after injection of lymphocytes preincubated with sera from TB patients was significantly lower compared to the number of microvessels created after injection of MNC preincubated with the same sera (p < 0.016). However, the number of microvessels created after the injection of lymphocytes preincubated with sera from healthy donors or with PBS alone was significantly higher (p < 0.017). The mean levels of IL-12p40 and TNFα were significantly elevated in sera from TB patients compared to healthy donors. We observed a correlation between angiogenic activity of sera from TB patients and IL-12p40 and TNFα serum levels (p < 0.01). Sera from TB patients constitute a source of mediators that participate in angiogenesis and prime monocytes for production of proangiogenic factors. The main proangiogenic effect of TB patients’ sera is mediated by macrophages/monocytes. TNFα and IL-12p40 may indirectly stimulate angiogenesis in TB

    Angiogenesis in Interstitial Lung Diseases: a pathogenetic hallmark or a bystander?

    Get PDF
    The past ten years parallels have been drawn between the biology of cancer and pulmonary fibrosis. The unremitting recruitment and maintenance of the altered fibroblast phenotype with generation and proliferation of immortal myofibroblasts is reminiscent with the transformation of cancer cells. A hallmark of tumorigenesis is the production of new blood vessels to facilitate tumor growth and mediate organ-specific metastases. On the other hand several chronic fibroproliferative disorders including fibrotic lung diseases are associated with aberrant angiogenesis. Angiogenesis, the process of new blood vessel formation is under strict regulation determined by a dual, yet opposing balance of angiogenic and angiostatic factors that promote or inhibit neovascularization, respectively. While numerous studies have examined so far the interplay between aberrant vascular and matrix remodeling the relative role of angiogenesis in the initiation and/or progression of the fibrotic cascade still remains elusive and controversial. The current article reviews data concerning the pathogenetic role of angiogenesis in the most prevalent and studied members of ILD disease-group such as IIPs and sarcoidosis, presents some of the future perspectives and formulates questions for potential further research

    CO reductive oligomerization by a divalent thulium complex and CO2-induced functionalization

    No full text
    International audienceThe divalent thulium complex [Tm(Cp-ttt)(2)] (Cp-ttt = 1,2,4-tris(tert-butyl)cyclopentadienyl) reacts with CO to afford selective CO reductive dimerization and trimerization into ethynediolate (C-2) and ketenecarboxylate (C-3) complexes, respectively. DFT calculations were performed to shed light on the elementary steps of CO homologation and support a stepwise chain growth. The attempted decoordination of the ethynediolate fragment by treatment with Me3SiI led to dimerization and rearrangement into a 3,4-dihydroxyfuran-2-one complex. Investigation of the reactivity of the C-2 and C-3 complexes towards other electrophiles led to unusual functionalization reactions: while the reaction of the ketenecarboxylate C-3 complex with electrophiles yielded new multicarbon oxygenated complexes, the addition of CO2 to the ethynediolate C-2 complex resulted in the formation of a very reactive intermediate, allowing C-H activation of aromatic solvents. This original intermolecular reactivity corresponds to an unprecedented functionalization of CO-derived ligands, which is induced by CO2

    CO Reductive Oligomerization by a Divalent Thulium Complex and CO2-Induced Functionalization

    No full text
    To date, only a very limited number of complexes based on low-valent main group or f-block elements have allowed the reductive coupling of CO molecules to afford multicarbon oxygenates. Herein, we described the reactivity of the divalent thulium complex [Tm(Cpttt)2] (Cpttt = 1,2,4-tris(tert-butyl)cyclopentadienyl) towards CO, leading to selective CO reductive dimerization and trimerization into ethynediolate (C2) and ketenecarboxylate (C3) complexes, respectively. Quantum chemical (DFT) calculations were performed to shed light on the elementary steps of CO homologation and support a stepwise chain growth from the C2 to the C3 product upon addition of extra CO. The attempted decoordination of the ethynediolate frag-ment by treatment with Me3SiI led to dimerization and rearrangement into a 3,4-dihydroxyfuran-2-one complex. Investiga-tion of the reactivity of the C2 and C3 complexes towards other electrophiles led to unusual functionalization reactions: while the reaction of the ketenecarboxylate C3 complex with electrophiles yielded new multicarbon oxygenated complexes, the addition of CO2 to the ethynediolate C2 complex resulted in the formation of a very reactive intermediate, allowing C–H activation of the toluene solvent. This original intermolecular reactivity corresponds to an unprecedented functionalization of CO-derived ligands, which is induced by CO2

    Place des lipides dans l'alimentation du sportif

    No full text
    Les acides gras, en tant que substrats énergétiques. Limites à la contribution des lipides dans la fourniture d'énergie. Comment augmenter l'utilisation des acides gras à l'exercice ? Apports lipidiques conseillés chez le sportif
    corecore