Perception relies on the integration of sensory information and prior expectations. Here we show that selective neurodegeneration of human frontal speech regions results in delayed reconciliation of predictions in temporal cortex. These temporal regions were not atrophic, displayed normal evoked magnetic and electrical power, and preserved neural sensitivity to manipulations of sensory detail. Frontal neurodegeneration does not prevent the perceptual effects of contextual information; instead, prior expectations are applied inflexibly. The precision of predictions correlates with beta power, in line with theoretical models of the neural instantiation of predictive coding. Fronto-temporal interactions are enhanced while participants reconcile prior predictions with degraded sensory signals. Excessively precise predictions can explain several challenging phenomena in frontal aphasias, including agrammatism and subjective difficulties with speech perception. This work demonstrates that higher-level frontal mechanisms for cognitive and behavioural flexibility make a causal functional contribution to the hierarchical generative models underlying speech perception.

4. The frequency characteristics of the excess noise could be analysed as the sum of I/f and 1/f2 components. While the 1/f component remained unaffected by the external application of 20 mM-tetraethylammonium (TEA) and either 2 mM-Mn2+ or 2 mM-Co2+, the 1/f2 component was suppressed by both Mn2+ and Co2+.5. The corner frequency, fc of the 1/f2 component depended on membrane potential, which was adjusted by adjusting the [K+]o jump. These results support the idea that f, in these experiments is a measure of the channel relaxation.6. Measurements of the input resistance in the frequency range from 0 to 25 Hz were used to obtain a rough estimate of the size of the channel conductance as 5 x 10-12 f-i

The effects of Zn2+ and CO2+ on glucose-induced beta-cell electrical activity and on insulin release from microdissected mouse pancreatic islets were studied. In 11 mM glucose the electrical activity is characterized by a burst pattern with a bimodal distribution of spike amplitudes along the plateau phase. Zn2+ at 0.05 mM induced a reduction in the number of spikes during the bursts and preferentially blocked the large action potentials. Zn2+ at 0.1 mM and CO2+ at 1.0 mM completely inhibited the electrical activity in response to glucose. Zn2+ inhibition of electrical activity was poorly reversible, whereas CO2+ inhibition was rapidly and completely reversible. Zn2+ and CO2+ inhibited the glucose-stimulated insulin release from microdissected perifused islets. Half-maximal inhibition occurred at about 0.3 mM for both metals. Zn2+ also inhibited K+-induced insulin release in the absence of glucose, indicating that Zn2+ inhibition does not involve glucose metabolism. It is proposed that Zn2+ blocks the voltage-gated Ca2+ channels in pancreatic beta-cells.

Objectives: To review the arterial carbon dioxide tensions (PaCO 2 ) in newborn infants ventilated using synchronized intermittent mandatory ventilation (SIMV) in volume guarantee mode (using the Dräger Babylog 8000+) with a unit policy targeting tidal volumes of approximately 4 mL/kg. Methods: Data on ventilator settings and arterial (PaCO 2 levels were collected on all arterial blood gases (ABG; n = 288) from 50 neonates (<33 weeks gestational age) ventilated using the Dräger Babylog 8000+ ventilator (Dräger Medizintechnik GmbH, Lübeck, Germany) in SIMV plus volume guarantee mode. Data were analysed for all blood gases done on the entire cohort in the first 48 h of life and a subanalysis was done on the first gas for each infant (n = 38) ventilated using volume guarantee from admission to the nursery. The number of ABG showing severe hypocapnoea ((PaCO 2 < 25 mmHg) and/or severe hypercapnoea ((PaCO 2 > 65 mmHg) were determined. Results: The mean (SD) (PaCO 2 during the first 48 h was 46.6 (9.0) mmHg. The mean (SD) (PaCO 2 on the first blood gas of those infants commenced on volume guarantee from admission was 45.1 (12.5) mmHg. Severe hypo-or hypercapnoea occurred in 8% of infants at the time of their first blood gas measurement, and in <4% of blood gas measurements in the first 48 h. Conclusions: Infants ventilated with volume guarantee ventilation targeting approximately 4 mL/kg (range: 2.9-5.1) have acceptable PaCO 2 levels at the first blood gas measurement and during the first 48 h of life; and avoid severe hypo-or hypercapnoea over 90% of the time.

Previous studies have shown that cholinergic blockade in normal subjects induces impairment of vigilance as well as memory deficits. In the present investigation we have examined the validity of this pharmacological model of dementia by administering a battery of cognitive tasks to patients with mild and moderate senile dementia of the Alzheimer type and to age-matched controls. In contrast to volunteers receiving scopolamine all the mildly demented patients, and half of those moderately affected, performed normally on tests of vigilance whilst exhibiting the expected memory deficits. These data suggest that the mechanism of memory loss in Alzheimer's disease may differ from that found in scopolamine-induced amnesia.