233 research outputs found

    Population III Wolf-Rayet Stars in the CAK Regime

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    Wolf-Rayet (WR) stars near solar metallicity are believed to be driven by radiation pressure on the UV spectral lines of metal ions. As the metallicity decreases so does the line opacity, therefore the mass-loss rate. However, since the composition of a WR atmosphere is determined by the burn products of the core, there is a lower limit on the line opacity -- and therefore the mass-loss rate -- of a WR star, even in a star with zero initial metallicity. This presentation is the result of attempt to calculate the mass-loss rate of a Population III-type WO star using a modified version of the CAK approximation. I find that n_e greater than or equal to 10^{13} cm^{-3} and Gamma between 0.5 and 0.7 give the most plausible results, with the resulting mass-loss rate between 2x10^{-9} M_sun yr^{-1} and 3x10^{-8} M_sun yr^{-1}.Comment: 3 pages, 2 figures, to be published in the proceedings of First Stars III, Santa Fe, NM, July 16-20, 200

    Pulsation-Initiated Mass Loss in Luminous Blue Variables: A Parameter Study

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    Luminous blue variables (LBVs) are characterized by semi-periodic episodes of enhanced mass-loss, or outburst. The cause of these outbursts has thus far been a mystery. One explanation is that they are initiated by kappa-effect pulsations in the atmosphere caused by an increase in luminosity at temperatures near the so-called ``iron bump'' (T ~ 200,000 K), where the Fe opacity suddenly increases. Due to a lag in the onset of convection, this luminosity can build until it exceeds the Eddington limit locally, seeding pulsations and possibly driving some mass from the star. We present some preliminary results from a parameter study focusing on the conditions necessary to trigger normal S-Dor type (as opposed to extreme eta-Car type) outbursts. We find that as Y increases or Z decreases, the pulsational amplitude decreases and outburst-like behavior, indicated by a large, sudden increase in photospheric velocity, becomes likes likely.Comment: 6 pages, 4 figures, to be published in the Proceedings of Massive Stars as Cosmic Engines, IAU Symp 250, ed. F. Bresolin, P. A. Crowther, & J. Puls (Cambridge Univ. Press

    Antinociceptive Effects of Spinal Manipulative Therapy on Nociceptive Behavior of Adult Rats during the Formalin Test

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    Optimizing pain relief resulting from spinal manipulative therapies, including low velocity variable amplitude spinal manipulation (LVVA-SM), requires determining their mechanisms. Pain models that incorporate simulated spinal manipulative therapy treatments are needed for these studies. The antinociceptive effects of a single LVVA-SM treatment on rat nociceptive behavior during the commonly used formalin test were investigated. Dilute formalin was injected subcutaneously into a plantar hindpaw. Licking behavior was video-recorded for 5 minutes. Ten minutes of LVVA-SM at 20° flexion was administered with a custom-made device at the lumbar (L5) vertebra of isoflurane-anesthetized experimental rats (n=12) beginning 10 minutes after formalin injection. Hindpaw licking was video-recorded for 60 minutes beginning 5 minutes after LVVA-SM. Control rats (n=12) underwent the same methods except for LVVA-SM. The mean times spent licking the formalin-injected hindpaw of both groups 1–5 minutes after injection were not different. The mean licking time during the first 20 minutes post-LVVA-SM of experimental rats was significantly less than that of control rats (P<0.001). The mean licking times of both groups during the second and third 20 minutes post-LVVA-SM were not different. Administration of LVVA-SM had a short-term, remote antinociceptive effect similar to clinical findings. Therefore, mechanistic investigations using this experimental approach are warranted

    Explaining semantic short-term memory deficits:evidence for the critical role of semantic control

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    Patients with apparently selective short-term memory (STM) deficits for semantic information have played an important role in developing multi-store theories of STM and challenge the idea that verbal STM is supported by maintaining activation in the language system. We propose that semantic STM deficits are not as selective as previously thought and can occur as a result of mild disruption to semantic control processes, i.e., mechanisms that bias semantic processing towards task-relevant aspects of knowledge and away from irrelevant information. We tested three semantic STM patients with tasks that tapped four aspects of semantic control: (i) resolving ambiguity between word meanings, (ii) sensitivity to cues, (iii) ignoring irrelevant information and (iv) detecting weak semantic associations. All were impaired in conditions requiring more semantic control, irrespective of the STM demands of the task, suggesting a mild, but task-general, deficit in regulating semantic knowledge. This mild deficit has a disproportionate effect on STM tasks because they have high intrinsic control demands: in STM tasks, control is required to keep information active when it is no longer available in the environment and to manage competition between items held in memory simultaneously. By re-interpreting the core deficit in semantic STM patients in this way, we are able to explain their apparently selective impairment without the need for a specialised STM store. Instead, we argue that semantic STM patients occupy the mildest end of spectrum of semantic control disorders

    Aberrant crossed corticospinal facilitation in muscles distant from a spinal cord injury.

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    Crossed facilitatory interactions in the corticospinal pathway are impaired in humans with chronic incomplete spinal cord injury (SCI). The extent to which crossed facilitation is affected in muscles above and below the injury remains unknown. To address this question we tested 51 patients with neurological injuries between C2-T12 and 17 age-matched healthy controls. Using transcranial magnetic stimulation we elicited motor evoked potentials (MEPs) in the resting first dorsal interosseous, biceps brachii, and tibialis anterior muscles when the contralateral side remained at rest or performed 70% of maximal voluntary contraction (MVC) into index finger abduction, elbow flexion, and ankle dorsiflexion, respectively. By testing MEPs in muscles with motoneurons located at different spinal cord segments we were able to relate the neurological level of injury to be above, at, or below the location of the motoneurons of the muscle tested. We demonstrate that in patients the size of MEPs was increased to a similar extent as in controls in muscles above the injury during 70% of MVC compared to rest. MEPs remained unchanged in muscles at and within 5 segments below the injury during 70% of MVC compared to rest. However, in muscles beyond 5 segments below the injury the size of MEPs increased similar to controls and was aberrantly high, 2-fold above controls, in muscles distant (>15 segments) from the injury. These aberrantly large MEPs were accompanied by larger F-wave amplitudes compared to controls. Thus, our findings support the view that corticospinal degeneration does not spread rostral to the lesion, and highlights the potential of caudal regions distant from an injury to facilitate residual corticospinal output after SCI
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