Dynamic cerebral autoregulation during cognitive task:Effect of hypoxia

Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA Vmean) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA Vmean increased during the cognitive activity ( P &lt; 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P &lt; 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA Vmean relationship. NEW &amp; NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship. </jats:p

Pathophysiology of unilateral asterixis due to thalamic lesion.

[Objective]:Unilateral asterixis has been reported in patients with thalamic lesion. This study aims at elucidating the pathophysiology of the thalamic asterixis. [Methods]:Two cases with unilateral asterixis caused by an infarction in the lateral thalamus were studied by analysing the asterixis-related cortical activities, transcranial magnetic stimulation (TMS) for motor cortex excitability and probabilistic diffusion tractography for the thalamo-cortical connectivity. [Results]:Averaging of electroencephalogram (EEG) time-locked to the asterixis revealed rhythmic oscillations of a beta band at the central area contralateral to the affected hand. TMS revealed a decrease in the motor evoked potential (MEP) amplitude and a prolongation of the silent period (SP). The anatomical mapping of connections between the thalamus and cortical areas using a diffusion-weighted image (DWI) showed that the lateral thalamus involved by the infarction was connected to the premotor cortex, the primary motor cortex (M1) and the primary somatosensory cortex (S1) of the corresponding hemisphere. [Conclusions]:The thalamic asterixis is mediated by the sensorimotor cortex, which is subjected to excessive inhibition as a result of the thalamic lesion involving the ventral lateral nucleus. [Significance]:This is the first demonstration of participation of the sensorimotor cortex in the generation of asterixis due to the lateral thalamic lesion

A comparison of static and dynamic cerebral autoregulation during mild whole-body cold stress in individuals with and without cervical spinal cord injury: a pilot study

Study design: Experimental study. Objectives: To characterize static and dynamic cerebral autoregulation (CA) of individuals with cervical spinal cord injury (SCI) compared to able-bodied controls in response to moderate increases in mean arterial pressure (MAP) caused by mild whole-body cold stress. Setting: Japan Methods: Five men with complete autonomic cervical SCI (sustained>5y) and six age-matched able-bodied men participated in hemodynamic, temperature, catecholamine and respiratory measurements for 60 min during three consecutive stages: baseline (10 min; 330C water through a thin-tubed whole-body suit), mild cold stress (20 min; 250C water) and post-cold recovery (30 min; 330C water). Static CA was determined as the ratio between mean changes in middle cerebral artery blood velocity and MAP, dynamic CA as transfer function coherence, gain and phase between spontaneous changes in MAP to middle cerebral artery blood velocity. Results: MAP increased in both groups during cold and post-cold recovery (mean differences: 5 to 10 mm Hg; main effect of time: p=0.001). Static CA was not different between the able-bodied vs the cervical SCI group (mean [95% CI] of between-group difference: -4 [-11 to 3] and -2 [-5 to 1] cm/s/mmHg for cold (p=0.22) and post-cold (p=0.24), respectively). At baseline, transfer function phase was shorter in the cervical SCI group (mean [95% CI] of between-group difference: 0.6 [0.2 to 1.0] rad; p=0.006), while between-group differences in changes in phase were not different in response to the cold stress (interaction term: p=0.06). Conclusions: This pilot study suggests that static CA is similar between individuals with cervical SCI and able-bodied controls in response to moderate increases in MAP, while dynamic CA may be impaired in cervical SCI due to disturbed sympathetic control

Differences in serum IL-6 response after 1°C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress

Objectives: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6. Setting: A cross-sectional study. Methods: The study subjects were 9 with CSCI, 10 with thoracic and lumbar spinal cord injury (TLSCI) and 8 able-bodied (AB) subjects. Time since injury was 16.4±4.1 years in TLSCI and 16.1±3.4 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1°C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumor necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH. Results: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups. Conclusion: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline

Pitavastatin Reduces Inflammation in Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice with Late Stage Renal Disease

Objectives: Chronic renal disease (CRD) accelerates atherosclerosis and cardiovascular calcification. Statins reduce low-density lipoprotein-cholesterol levels in patients with CRD, however, the benefits of statins on cardiovascular disease in CRD remain unclear. This study has determined the effects of pitavastatin, the newest statin, on arterial inflammation and calcification in atherogenic mice with CRD. Methods and Results: CRD was induced by 5/6 nephrectomy in cholesterol-fed apolipoprotein E-deficient mice. Mice were randomized into three groups: control mice, CRD mice, and CRD mice treated with pitavastatin. Ultrasonography showed that pitavastatin treatment significantly attenuated luminal stenosis in brachiocephalic arteries of CRD mice. Near-infrared molecular imaging and correlative Mac3 immunostaining demonstrated a significant reduction in macrophage accumulation in pitavastatin-treated CRD mice. Pitavastatin treatment reduced levels of osteopontin in plasma and atherosclerotic lesions in CRD mice, but did not produce a significant reduction in calcification in atherosclerotic plaques as assesses by histology. CRD mice had significantly higher levels of phosphate in plasma than did control mice, which did not change by pitavastatin. In vitro, pitavastatin suppressed the expression of osteopontin in peritoneal macrophages stimulated with phosphate or calcium/phosphate in concentrations similar to those found in human patients with CRD. Conclusion: Our study provides in vivo evidence that pitavastatin reduces inflammation within atherosclerotic lesions in CRD mice

TRPV4-dependent induction of a novel mammalian cold-inducible protein SRSF5 as well as CIRP and RBM3

Cold-inducible RNA-binding protein (CIRP) and RNA-binding motif protein 3 (RBM3) are two evolutionarily conserved RNA-binding proteins that are structurally related to hnRNPs and upregulated in response to moderately low temperatures in mammalian cells. Although contributions of splicing efficiency, the gene promoters activated upon mild hypothermia and the transcription factor Sp1 to induction of CIRP have been reported, precise mechanisms by which hypothermia and other stresses induce the expression of mammalian cold-inducible proteins (CIPs) are poorly understood. By screening the serine/arginine-rich splicing factors (SRSFs), we report that the transcript and protein levels of SRSF5 were increased in mammalian cells cultured at 32 °C. Expression of SRSF5 as well as CIRP and RBM3 were also induced by DNA damage, hypoxia, cycloheximide and hypotonicity. Immunohistochemical studies demonstrated that SRSF5 was constitutively expressed in male germ cells and the level was decreased in human testicular germ cell tumors. SRSF5 facilitated production of p19 H-RAS, and increased sensitivity to doxorubicin in human U-2 OS cells. Induction of CIPs was dependent on transient receptor potential vanilloid 4 (TRPV4) channel protein, but seemed independent of its ion channel activity. These findings indicate a previously unappreciated role for the TRP protein in linking environmental stress to splicing

Exploration of neural correlates of movement intention based on characterisation of temporal dependencies in electroencephalography

Brain computer interfaces (BCIs) provide a direct communication channel by using brain signals, enabling patients with motor impairments to interact with external devices. Motion intention detection is useful for intuitive movement-based BCI as movement is the fundamental mode of interaction with the environment. The aim of this paper is to investigate the temporal dynamics of brain processes using electroencephalography (EEG) to explore novel neural correlates of motion intention. We investigate the changes in temporal dependencies of the EEG by characterising the decay of autocorrelation during asynchronous voluntary finger tapping movement. The evolution of the autocorrelation function is characterised by its relaxation time, which is used as a robust marker for motion intention. We observed that there was reorganisation of temporal dependencies in EEG during motion intention. The autocorrelation decayed slower during movement intention and faster during the resting state. There was an increase in temporal dependence during movement intention. The relaxation time of the autocorrelation function showed significant (p < 0.05) discrimination between movement and resting state with the mean sensitivity of 78.37 ± 8.83%. The relaxation time provides movement related information that is complementary to the well-known event-related desynchronisation (ERD) by characterising the broad band EEG dynamics which is frequency independent in contrast to ERD. It can also detect motion intention on average 0.51s before the actual movement onset. We have thoroughly compared autocorrelation relaxation time features with ERD in four frequency bands. The relaxation time may therefore, complement the well-known features used in motion-based BCI leading to more robust and intuitive BCI solutions. The results obtained suggest that changes in autocorrelation decay may involve reorganisation of temporal dependencies of brain activity over longer duration during motion intention. This opens the possibilities of investigating further the temporal dynamics of fundamental neural processes underpinning motion intention

Effects of exercise intensity on the sweating response to a sustained static exercise

8 sujets masculins sont couchés pendant une heure dans une chambre climatique à une température de 35°C avec un taux d'humidité de 50%. Ils effectuent ensuite une série d'exercices de préhension isométrique à différents niveaux de contraction (15,30,45, 60%). Comparaison des taux de sudation selon l'intensité de contractio

Non thermoregulatory modulation of sweating in humans

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