4,469 research outputs found

    Franklin M. Wright to Professor Silver, 15 November 1960

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    Professional correspondenc

    Chinoiserie in the novels of Robert Hans van Gulik

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    This thesis considers the cultural transactions that occur in Robert Hans van Gulik\u27s Judge Dee stories, a set of Chinese investigative fiction works written by a Dutchman in English. These works are investigated through the interpretive lens of chinoiserie --an extension of Edward Said\u27s Orientalism, named for a design aesthetic that featured the creation of Chinese goods by European artisans who were less interested in closely emulating Chinese styles than in creating fashionable exotica for the domestic market. Chinoiserie investigates the alterations done to foreign cultural products as they are changed to meet the domestic culture\u27s preferences and expectations. The object of this thesis is to explore the ways in which van Gulik\u27s Chinese investigative fiction was adapted to his Western audience by focusing on his presentation of the ideological domains of rationality versus the supernatural and the religious traditions of Buddhism and Daoism. Using his authority as a scholar of Chinese culture, van Gulik wrote these works in opposition to the popular misconception of China. The study demonstrates that van Gulik catered to Western preferences by positioning Judge Dee as a far more rational investigator than was the norm for Chinese investigative fiction, and that van Gulik wrote with Western expectations in mind, replicating in his works the position held on Chinese religions by the Western scholars of his day. In so doing, he disseminated his own conception of China and also demonstrated how removed a work can be from its origins and still be called Chinese

    Phonological output errors in conduction aphasia

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    Reproduction conduction aphasia is a phonological output impairment where all phonological output modalities are impaired, errors are phonologically related and longer words are harder than short. An understanding of the way in which phonological errors are generated should therefore give us information about phonological encoding, as well suggesting appropriate remediation. 5 individuals with conduction aphasia are given a list of words for repetition on two separate occasions. Errors are transcribed and the data is analysed according to a range of theories, namely interactive accounts predicting lexical mediation, phonological processing theories and phonological encoding constraints

    Redistribution Of Air Within The Lungs May Potentiate "Fright" Bradycardia In Submerged Crocodiles (Crocodylus porosus)

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    1. Voluntary undisturbed dives by Crocodylus porosus were short in duration (3.08 + 1.87 min, mean + SD) and accompanied by a small but significant bradycardia (14.3 + 5.9% drop). 2. When crocodiles were disturbed underwater there was a rapid onset of "fright" bradycardia, to 65 + 6.0% of surface heart rates and dive durations were prolonged to 19.6 + 1.8 min. 3. The development of "fright" bradycardia was not accompanied by any increase in intratracheal pressure or expulsion of lung gas. However, sustained contraction of the abdomen and expansion of the thorax revealed a redistribution of air anteriorly within the lungs. 4. We propose that the redistribution of air within the lungs may generate an afferent signal which potentiates the initiation of a severe, dive-prolonging bradycardia

    Using Action-congruent Language Facilitates the Motor Response during Action Observation: A Combined Transcranial Magnetic Stimulation and Eye-tracking Study.

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    There is evidence that action observation (AO) and the processing of action-related words are associated with increased activity in cortical motor regions. Research has examined the effects of AO and action verb processing on activity in the motor system independently. The aim of this experiment was to investigate, for the first time, the modulation of corticospinal excitability and visual attention during the concurrent processing of action verbs and AO stimuli. Twenty participants took part in an integrated transcranial magnetic stimulation and eye-tracking protocol. Single-pulse transcranial magnetic stimulation was delivered to the hand representation of the left motor cortex during (i) observation of a static hand, (ii) AO of a hand squeezing a sponge, (iii) AO of the same action with an audio recording of the word "squeeze," and (iv) AO of the same action with an audio recording of the word "green". Motor evoked potentials were recorded from the abductor pollicis brevis and abductor digiti minimi muscles of the right hand. Eye gaze was recorded throughout the four conditions as a proxy for visual attention. Interviews were conducted to discuss participants' preferences and imagery use for each condition. The AO and action verb condition resulted in significantly increased motor evoked potential amplitudes in the abductor pollicis brevis; participants also made significantly more fixations on the sponge and reported wanting to move their hand. The inclusion of auditory action verbs, alongside AO stimuli, in movement simulation interventions could have implications for the delivery of AO interventions for motor (re)learning

    Full gait cycle analysis of lower limb and trunk kinematics and muscle activations during walking in participants with and without ankle instability

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    This document is the Accepted Manuscript version of the following article: Lynsey Northeast, Charlotte N. Gautrey, Lindsay Bottoms, Gerwyn Hughes, Andrew C. S. Mitchell, and Andrew Greenhalgh, ‘Full gait cycle analysis of lower limb and trunk kinematics and muscle activations during walking in participants with and without ankle instability’, Gait & Posture, Vol. 64: 114-118, July 2018. Under embargo until 7 June 2019. The final, definitive version is available online at doi: https://doi.org/10.1016/j.gaitpost.2018.06.001Background Chronic ankle instability (CAI) has previously been linked to altered lower limb kinematics and muscle activation characteristics during walking, though little research has been performed analysing the full time-series across the stance and swing phases of gait. Research Question The aim of this study was to compare trunk and lower limb kinematics and muscle activity between those with chronic ankle instability and healthy controls. Methods Kinematics and muscle activity were measured in 18 (14 males, 4 females) healthy controls (age 22.4 ± 3.6 years, height 177.8 ± 7.6 cm, mass 70.4 ± 11.9 kg, UK shoe size 8.4 ± 1.6), and 18 (13 males, 5 females) participants with chronic ankle instability (age 22.0 ± 2.7 years, height 176.8 ± 7.9 cm, mass 74.1 ± 9.6 kg, UK shoe size 8.1 ± 1.9) during barefoot walking trials, using a combined Helen Hayes and Oxford foot model. Surface electromyography (sEMG) was recorded for the tibialis anterior and gluteus medius. Full curve statistical parametric mapping was performed using independent and paired-samples T-tests. Results No significant differences were observed in kinematic or sEMG variables between or within groups for the duration of the swing phase of gait. A significantly increased forefoot-tibia inversion was seen in the CAI affected limb when compared to the CAI unaffected limb at 4–16% stance (p = 0.039). No other significant differences were observed. Significance There appears to be no differences in muscle activation and movement between CAI and healthy control groups. However, participants with CAI exhibited increased inversion patterns during the stance phase of gait in their affected limb compared to their unaffected limb. This may predispose those with CAI to episodes of giving way and further ankle sprains.Peer reviewedFinal Accepted Versio

    Strength in Numbers

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    A timely NSF grant helps women scientists discover the value of networking and mentoring to their careers -- and their lives

    Caveolin-1 and Altered Neuregulin Signaling Contribute to the Pathophysiological Progression of Diabetic Peripheral Neuropathy

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    Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.OBJECTIVE Evaluate if Erb B2 activation and the loss of caveolin-1 (Cav1) contribute to the pathophysiological progression of diabetic peripheral neuropathy (DPN). RESEARCH DESIGN AND METHODS Cav1 knockout and wild-type C57BL/6 mice were rendered diabetic with streptozotocin, and changes in motor nerve conduction velocity (MNCV), mechanical and thermal hypoalgesia, Erb B2 phosphorylation (pErb B2), and epidermal nerve fiber density were assessed. The contribution of Erb B2 to DPN was assessed using the Erb B2 inhibitors PKI 166 and erlotinib and a conditional bitransgenic mouse that expressed a constitutively active form of Erb B2 in myelinated Schwann cells (SCs). RESULTS Diabetic mice exhibited decreased MNCV and mechanical and thermal sensitivity, but the extent of these deficits was more severe in diabetic Cav1 knockout mice. Diabetes increased pErb B2 levels in both genotypes, but the absence of Cav1 correlated with a greater increase in pErb B2. Erb B2 activation contributed to the mechanical hypoalgesia and MNCV deficits in both diabetic genotypes because treatment with erlotinib or PKI 166 improved these indexes of DPN. Similarly, induction of a constitutively active Erb B2 in myelinated SCs was sufficient to decrease MNCV and induce a mechanical hypoalgesia in the absence of diabetes. CONCLUSIONS Increased Erb B2 activity contributes to specific indexes of DPN, and Cav1 may be an endogenous regulator of Erb B2 signaling. Altered Erb B2 signaling is a novel mechanism that contributes to SC dysfunction in diabetes, and inhibiting Erb B2 may ameliorate deficits of tactile sensitivity in DPN. Diabetic peripheral neuropathy (DPN) is a common complication of diabetes (1). Although hyperglycemia is the definitive cause of DPN (2), the vascular, glial, and neuronal damage that underlies the progressive axonopathy in DPN has a complex biochemical etiology involving oxidative stress (3,4), protein glycation (5), protein kinase C activation (6), polyol synthesis (7), and the hexosamine pathway (8). Altered neurotrophic support also contributes to sensory neuron dysfunction in DPN (9), but whether diabetes may alter growth factor signaling in Schwann cells (SCs), which also undergo substantial degeneration in diabetes, is poorly defined. Neuregulins are growth factors that control SC growth, survival, and differentiation via their interaction with Erb B receptors (10). Although Erb B2 signaling promotes developmental myelination and is clearly trophic for SCs, pharmacological evidence supports that pathologic activation of Erb B2 after axotomy (11) or infection with leprosy bacilli (12) is sufficient to induce SC dedifferentiation and demyelination. Additionally, genetic evidence supports that Erb B2 can promote the development of sensory neuropathies independent of diabetes because expression of a dominant-negative Erb B4 in nonmyelinating (13) or myelinating (14) SCs induced a temperature or mechanical sensory neuropathy, respectively. Given the contribution of Erb B2 to the degeneration of SCs, endogenous proteins that regulate Erb B2 activity may influence the development of certain aspects of sensory neuropathies. The interaction of Erb B2 with the protein caveolin-1 (Cav1) inhibits the intrinsic tyrosine kinase activity of the receptor (15). Cav1 is highly expressed in mature, myelinated SCs (16), and we have shown that prolonged hyperglycemia promoted the downregulation of Cav1 in SCs of sciatic nerve (17). Cav1 may regulate Erb B2 signaling in SCs because its forced downregulation was sufficient to enhance neuregulin-induced demyelination of SC–dorsal root ganglion (DRG) neuron cocultures (18). However, it is unknown whether an increase in Erb B2 activity may contribute to the pathophysiological development of DPN and if changes in Cav1 expression may alter Erb B2 activation in diabetic nerve. In the current study, we demonstrate that diabetic Cav1 knockout mice showed an increased activation of Erb B2 and developed greater motor nerve conduction velocity (MNCV) deficits relative to their wild-type counterparts. Inhibition of Erb B2 with two structurally diverse inhibitors corrected the MNCV deficits and mechanical hypoalgesia evident after 6 or 15 weeks of diabetes. Also, induction of a constitutively active Erb B2 in myelinated SCs of adult mice was sufficient to recapitulate the MNCV and mechanical sensitivity deficits observed in the diabetic mice. These studies provide the first evidence that activation of Erb B2 contributes to deficits associated with myelinated fiber function in diabetic nerve and suggest that Cav1 may serve as an endogenous regulator of Erb B2.This work was supported by grants from the Juvenile Diabetes Research Foundation and the National Institutes of Health (NS-054847 and DK-073594)
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