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This study investigated the changes in cerebral near-infrared spectroscopy (NIRS) signals, cerebrovascular and ventilatory responses to hypoxia and CO2 during altitude exposure. At sea level (SL), after 24 hours and 5 days at 4,350 m, 11 healthy subjects were exposed to normoxia, isocapnic hypoxia, hypercapnia, and hypocapnia. The following parameters were measured: prefrontal tissue oxygenation index (TOI), oxy- (HbO2), deoxy- and total hemoglobin (HbTot) concentrations with NIRS, blood velocity in the middle cerebral artery (MCAv) with transcranial Doppler and ventilation. Smaller prefrontal deoxygenation and larger ΔHbTot in response to hypoxia were observed at altitude compared with SL (day 5: ΔHbO2−0.6±1.1 versus −1.8±1.3 μmol/cmper mm Hg and ΔHbTot 1.4±1.3 versus 0.7±1.1 μmol/cm per mm Hg). The hypoxic MCAv and ventilatory responses were enhanced at altitude. Prefrontal oxygenation increased less in response to hypercapnia at altitude compared with SL (day 5: ΔTOI 0.3±0.2 versus 0.5±0.3% mm Hg). The hypercapnic MCAv and ventilatory responses were decreased and increased, respectively, at altitude. Hemodynamic responses to hypocapnia did not change at altitude. Short-term altitude exposure improves cerebral oxygenation in response to hypoxia but decreases it during hypercapnia. Although these changes may be relevant for conditions such as exercise or sleep at altitude, they were not associated with symptoms of acute mountain sickness.

International audience; Acute mountain sickness (AMS) can occur during climbs to high altitudes and may seriously disturb the behavioral and intellectual capacities of susceptible subjects. During a Himalayan expedition 32 mountaineers were examined with electroencephalography (EEG) and transcranial doppler sonography (TCD) to assess relative changes of middle cerebral artery velocity in relation to end-expiratory CO2 (EtCO2), peripheral saturation (SaO2), and symptoms of AMS. We tested the hypothesis that O2 desaturation and EtCO2 changes precede the development of AMS and result in brain dysfunction and compensatory mechanisms which can be measured by EEG and TCD, respectively. Contrary to our hypothesis, we found that subjects who later developed symptoms of AMS between 3,440 m and 5,050 m altitude exhibited an increase of slow cerebral activity in the right temporal region already at 3,440 m. Cerebral blood flow increased in these mountaineers in the right middle cerebral artery at 5,050 m. These findings indicate that regional brain dysfunction, which can be documented by EEG, heralds the appearance of clinical symptoms of AMS.

This study questioned the effect of living and training at moderate altitude on cardiac morphological and functional adaptations and tested the incidences of potential specific adaptations compared with aerobic sea level training on maximal left ventricular performance. Sea level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Cardiac adaptations were evaluated throughout the study period by Doppler echocardiography. Maximal stroke volume (LVSVmax) was measured during volume overloading before and after the study period. Finally, at the end of the study period, passive pressure-volume relationships on isolated heart and cardiac weighing were obtained. Altitude training resulted in a specific left ventricular (LV) remodeling compared with NT, characterized by an increase in wall thicknesses without any alteration in internal dimensions. These morphological adaptations associated with hypoxia-induced alterations in pulmonary outflow and preload conditions led to a decrease in LV filling and subsequently no improvement in LV performance during resting physiological conditions in CHT compared with NT. Such a lack of improvement was confirmed during volume overloading that simulated maximal effort (LVSVmax pretest: NT = 0.58 ± 0.05, CHT = 0.57 ± 0.08 ml; posttest: NT = 0.72 ± 0.06, CHT = 0.58 ± 0.07 ml; NT vs. CHT in posttest session, P < 0.05). Maximal aerobic velocities increased to the same extent in NT and CHT rats despite marked polycythemia in the latter. The lack of LVSVmax improvement resulting from altitude training-induced cardiac morphological and functional adaptations could be responsible for this phenomenon.

International audience; Concern is growing in Europe about alveolar echinococcosis (AE) with the increase in grassland rodent and red fox populations, intermediate and definitive hosts for Echinococcus multilocularis, respectively. The objective of this study was to assess the influence of rodent densities on human AE distribution. Spatial Poisson regression analyses were performed with geomorphologic features, landscape composition, climatic characteristics, and water vole density as independent variables. The outcome consisted of AE cases diagnosed over the period 1980-1992. High vole density yielded a 10-fold risk (relative risk [RR] = 10.34, 95% confidence interval [CI] = 2.78-38.39), and the first plateau (400-700 m altitude) compared with the plain (200-400 m) was associated with a large increase in risk (RR = 7.10, 95% CI = 1.30-38.63). These results confirm that human AE is strongly influenced by the densities of arvicolid species. Foxes feeding almost exclusively on grassland rodents when the latter expand could mediate this relation.

International audience; In Madagascar, Anopheles gambiae has been found below altitudes of 1,000 m. We sampled An. gambiae sensu lato (sl) between 2008 and 2010 in the Central Highlands of Madagascar at altitudes over 1,200 m. The study site consists of rainforest, rainforest edge, and an open savanna biotope. Anopheles gambiae and An. arabiensis, as well as molecular forms of An. gambiae, were identified molecularly. An. gambiae accounted for 26.7% at the edge of the rainforest and 2.3% in the open savanna biotope. One specimen of this species was caught in the forest. An. arabiensis accounted for 66.3% at the edge of the rainforest and 97.7 % in the open savanna biotope. All An. gambiae adults tested belonged to the S molecular form. An. gambiae is present at high altitudes in Madagascar, with a high prevalence at the rainforest edge. Several factors, including the appearance of new favorable biotopes, recolonization after a reduction of indoor vector control, and climate change, may contribute to its distribution. The changing distribution of An. gambiae may have consequences for the distribution and incidence of malaria in the Malagasy Highlands.

International audience; BACKGROUND: Malaria is influenced by a web of individual and ecological factors, i.e. factors relating to people and relating to environment. For a long time analysing these factors concurrently has raised statistical problems. Multilevel modelling provides a new attractive solution, which is still uncommon in tropical medicine. METHODS: Using an actual data set of 3864 individuals from 38 villages of the Highland Madagascar, a two-level modelling process is presented. Individual malaria parasitaemia is modelled step by step according to age (individual factor), altitude, and DDT indoor house-spraying status (village factors). RESULTS: The hierarchical organization of a data set in levels, fixed and random effects, and cross-level interactions are considered. Accurate estimations of standard errors, impact of unknown or unmeasured variables quantified and accounted for through random effects, are the highlighted advantages of multilevel modelling. CONCLUSION: While not denying the importance of understanding an aetiological chain, the authors recommend an increased use of multilevel modelling, mainly to identify accurately ecological targets for public health policy.

International audience; Carotid blood flow was measured in rats by implanted transit-time ultrasonic flowprobes during hyperbaric experiments at up to 70 bar (7 MPa) using an helium-oxygen hyperoxic (partial pressure of O2 = 400 mbar) mixture. Before the hyperbaric experiment, an intracerebroventricular injection of phosphate saline buffered solution (PBS) or aminophylline, an adenosine receptor blocker, in PBS was given. Throughout the hyperbaric experiment carotid blood flow increased with ambient pressure in both PBS, i.e. control, and aminophylline treated rats. The increase in carotid blood flow was significantly attenuated in aminophylline treated rats. Additional experiments showed that the increased carotid blood flow was independent of hyperoxia as well as of temperature. The hypothesis that the hyperbaric dependent increase in carotid blood flow was mediated by brain adenosine receptors and its implication regarding a cerebral vasodilatation are discussed.