The anatomy of the retina was studied and counts wore made of the retinal elements. It was found that the rods single and double cones decrease in number centrally and the triple and quadruple cones increase centrally. The visual acuity calculated from the counts do not agree with the acuity figures given by other workers. The dorsal or ventral parts of the retina were removed surgically or destroyed by high intensity light. The chromatic behaviour of these fish led to the conclusion that the whole of the retina is important for normal chromatic adaptation to white or black backgrounds. The anatomy of the optic tract, chiasma, geniculate complex, and optic tectum are described. The fibres from the optic tract were traced into the brain. The ability of the fish to adapt chromatically after cutting the optic tract and/or the ablation of the optic tectum indicated that the fibres which are important in background adaptation enter the geniculate complex from the retina and from there run to the tectum. In the tectum the final interpretation of the background occurs. The region where the fibres involved in chromatic adaptation pass out of the tectum was identified and the fibres were traced to the medullary centre. This is described. Encephalograms were recored from bipolar electrodes in the optic tectum. The surface ECG amplitude appears to be correlated with the retinal input. Recordings from electrodes implanted at different depths showed frequency changes associated with the tint of the background. A possible hypothesis for the mechanism of the central nervous control of colour change is proposed. The pattern of the locomotory behaviour of normal, blind, and tectal damaged fish in conditions of limited confinement are described and the role of the optic tectum in the control of general and motor behaviour are discussed. It is experimentally demostrated that the optic tectum plays an important role in the control of the Mauthner cells of the medulla, and the relationship between the tectum and the Mauthner cells is discussed.

Intact and chromatically spinal sectioned minnows of known background histories; were exposed to illuminated white and black backgrounds for 2 months. A definite skin area was photographed and the melanophores lost and formed in it were recorded. Loss and formation of melanophores occurred simultaneously in intact minnows whether placed on a white or on a black background although their relative numbers were very different in the two situations and depended largely on previous background histories. After chromatic spinal section, the loss of melanophores was reduced and formation increased in minnows on a white background, whereas the reverse was observed in minnows on a black background, these results followed irrespective of difference in background histories. two conclusions are drawn from the results. Firstly, that the chromatic nerve fibres play a significant part in 'morphological' colour changes of the minnow. Secondly, that a dineuroic control is involved. It is suggested that the pigment-aggregated transmitter substance promotes loss of melanophores and limits their formation and that the pigment-dispersing transmitter promotes their formation and limits their loss. In the second set of experiments minnows were exposed on a black background for varying periods to allow melanophore formation, the ages and time of appearance of melanophores were photographically determined. The background responses of the newly formed melanophores were assessed microscopically in fixed preparations of animals killed in at different time-intervals. The results were interpreted according to the generally accepted belief that slow and rapid colour changes indicate hormonal and nervous mediation respectively. The age of the melanophores was: found to be a significant factor in determining their background responses, the older melanophores being more responsive. It is suggested that the sensitivity to hormonal control develops first in the life of a pigment cell, to be followed later by sensitivity to nervous control, nervous control, however, does act appear simultaneously for w/B and B/w adaptations. It develops first for B/w colour change. This differential development is considered to provide evidence for double innervation of melanophores.

Kleine Levin Syndrome (KLS) is a hypersomniac disease of episodic nature that affects only 1-5 per million individuals globally. In addition to extensive periods of sleep (> 20 hours) patients experience a wide range of symptoms during an episode, which occur approximately 1-12 times a year with a median of 10 days. The etiology and pathophysiology of the disease is unknown. Diagnostic criteria (The International Classification of Sleep disorders, third addition) rely solemnly on symptomatic characteristics. Misdiagnosis is unfortunately common. The potential of using hypocretin-1, amyloid-beta/tau and the IgG index in the CSF as potential disease biomarkers was investigated. Measurements were taken during the asymptomatic and/or symptomatic phase of the disease. All values were within the normal range. Lower hypocretin-1 values were observed in the asymptomatic phase compared to the symptomatic phase in two of the three patients, although not statistically significant.

<p> The purpose of this prospective, observational study was to determine if a technique used to detect early signs of small-fiber neuropathy (local skin heating) could detect signs of small-fiber taxane-induced peripheral neuropathy (TIPN) in breast cancer survivors (BCS) during the first 6 weeks of Taxol^&reg;. Aims of the study were to compare the mean size of (1) axon reflexes and (2) axon flares (both markers of small-fiber nerve function) in BCS receiving Taxol^&reg; to the size of reflexes/flares in healthy female controls (HCs). A third aim was to determine whether the size of axon reflexes/flares correlated with (a) overall TIPN severity and (b) severity of individual signs/symptoms of TIPN during early Taxol^&reg;. </p><p> Data for the study was collected from nine BCS and 20 HCs (<i>N </i> = 29). All BCS had first-time, non-metastatic cancer and received weekly or bi-weekly Taxol^&reg;. Data was collected at 3 time-points: Time 1 (day 0, before Taxol^&reg;), Time 2 (day 14), and Time 3 (day 42). Axon reflexes and flares were generated using a validated 40-minute skin heating protocol. Axon reflexes were measured using laser Doppler Flowmetry. Axon flares were measured using full-field laser perfusion imaging. TIPN was measured using the 5-item Short Form of the Total Neuropathy Score (Reduced Version). </p><p> Results identified potential signs of small-fiber TIPN in BCS after 6 weeks of Taxol^&reg;. Contrary to expectation, axon reflexes were larger for BCS at Time 3 than HCs, suggesting that Taxol^&reg; may be associated with an increase in small-fiber nerve function like that seen in pre-clinical studies. Clinical signs/symptoms of TIPN were not significantly correlated with axon reflexes or axon flares at the same time point. Analyses of axon flare size were confounded by issues with the data. </p><p> These results add to the growing body of evidence showing that Taxol^&reg; affects small-diameter sensory nerves and provides the first evidence in humans that changes in small-fiber nerve function may be detectable after just 6 weeks of Taxol^&reg; therapy. Studies in larger samples are needed to validate these findings.</p><p>

Mild Cognitive Impairment (MCI) refers to a transitional stage between normal aging and dementia. The purpose of this study was to predict the development of MCI patients based on cognitive function. 222 MCI patients were studied at baseline and at a follow-up of 2 years. Using discriminant analysis, they were predicted into four diagnostic groups: Improved, Stable MCI, Dementia of the Alzheimer’s Type (AD) and Other Dementia. Using four tests - Rey-Osterrieth Complex Figure Test recall, Auditory-Verbal Learning Test recall, TMTB time and Digit Symbol – overall 62.6% of cases were correctly classified after cross-validation. The rate of prediction in this study was 1.8 times better than chance, which is better than reported in most other studies. The model did best for the AD group with 80% of cases correctly classified. However, most cases in the Other Dementia group were also classified as AD.

<p> Information from auditory feedback plays an important role in speech motor control. This has been shown in particular in experiments that make real-time changes to speakers&rsquo; own productions, which are fed back to them while speaking (e.g. Houde and Jordan 1998). In response, speakers change their articulations so that their own altered feedback sounds more like the target word. While such experiments have succeeded in showing the importance of the role of auditory feedback, they have focused on the <i>acoustic </i> output of the speech system, the fact that speakers did change their production in response to altered auditory feedback. The experiments presented here focus on <i>how</i> speakers change their motor plans using the novel addition of ultrasound imaging. Well-documented cases of articulatory variation in American English provided the test case to study this question. The articulatory strategies which speakers use to compensate for the altered feedback are evidence of how much knowledge they have about how their articulations map onto acoustics. These experiments consider how individual vocal tract anatomy might affect this knowledge. </p><p> Chapter 2 uses an articulatory synthesizer with three different palates to show that there is a more sensitive map between articulation and acoustics for flatter than more domed palates. This provided the motivation for Chapter 3, which tested whether these differences influenced variability in the production of normal, unperturbed speech. This ultrasound experiment found that people with flatter palates reduce their articulatory variability in comparison with people who have more domed palates. Reducing articulatory variability effectively constrains acoustic variability in /r/ production but not /s/ production. </p><p> Chapter 3 found significant differences in articulatory variability that correlated strongly with palate shape. Chapter 4 presents an experiment that uses ultrasound to capture the strategies that speakers use during adaptation to altered auditory feedback to test whether these production differences determined by palate shape carry over into how speakers make corrections to speech production on line. In one block, speakers said the target word &ldquo;head,&rdquo; and their F1 was gradually raised. In a second block, speakers said the target word &ldquo;hood,&rdquo; and their F2 was gradually raised. The ultrasound revealed how speakers search their articulatory-acoustic space and settle on a compensation strategy. A global effect of palate shape was not seen in compensation; degree of compensation did not correlate with palate shape. If palate shape does inform articulatory habits or the detail in a speaker&rsquo;s knowledge of how their articulation maps onto acoustics, this knowledge does not influence speakers&rsquo; compensation degree. Despite a lack of overall trend in amount of compensation, palate shape did correlate with secondary characteristics in compensation. </p><p> Finally, Chapter 5 describes a preliminary study where speakers said the target word &ldquo;heard,&rdquo; and their F3 was gradually raised. The modeling in Chapter 2 predicted that a generally effective way to lower F3 is to raise and retract the tongue to minimize constriction size, a strategy that every speaker used. </p><p> The results from this dissertation suggest that while palate shape influences articulatory and acoustic variability in normal, unaltered speech, this behavior is not predictive of how <i>much</i> speakers will compensate when presented with altered feedback, only of certain secondary characteristics of this compensation. Speakers&rsquo; overall compensation is likely impacted more by higher-level factors which may influence sensitivity to auditory and somatosensory feedback.</p><p>

Recurrent processing is the corticocortical activity that appears after the feedforward sweep of information processing in the brain. According to Victor Lamme, this process is directly connected to visual awareness. Our consciousness can be divided into phenomenal and reflective consciousness. The underlying process of phenomenal consciousness is suggested to be localized recurrent processing. Widespread recurrent processing to motor and frontal regions correlates with reflective consciousness. Recent electroencephalographic studies have shown visual awareness negativity correlating with localized recurrent processing in both a temporal and spatial aspect. If we accept that localized recurrent processing is consciousness, we get the controversial implications that we can be conscious of something without being able to introspect.

Sammanfattning Syfte Syftet med denna studie var att ta reda på om akut visuell biofeedback i form av EMG, från qudriceps och hamstrings kan öka knäextensorernas muskelaktivitet samt styrkeutvecklingen, vid en maximal viljemässig isokinetisk benspark (20o.s-1).   Metod Totalt deltog 19 aktiva och motiverade försökspersoner, 9 kvinnor och 10 män, i denna studie. Försökspersonerna rekryterades under förutsättningarna att de inte hade några knäskador samt att de inte bedrev någon typ av kontinuerlig styrketräning för benen. Testet bestod av två omgångar koncentriska och excentriska maximala viljemässiga isokinetiska muskelaktioner (MVC) för respektive ben. Knävinkelhastigheten var 20o.s-1 och rörelseomfånget var 60o, från120o till 180o där 180o motsvarar sträckt knä. EMG-feedback från knämuskulaturen visades endast i omgång två då försökspersonen utförde kontraktioner med höger ben. Styrkan i knäextensorerna, den viljemässiga aktiveringsgraden samt EMG från quadriceps och hamstrings mättes under hela rörelseomfånget (60o).   Resultat Biofeedback i form av EMG-rms ökade styrkeutvecklingen signifikant i knäextensorerna (10 %) från 144 ± 48 till 158 ± 53 Nm. Beträffande den viljemässiga aktiveringen av knäextensorerna så ökade den signifikant (9 %) från 75 ±15 % till 81 ± 15 % då feedback gavs. Biofeedback påverkade dock inte till en minskad EMG aktiviteten i hamstringsmuskulaturen.   Slutsats Sammanfattningsvis så visar denna studie att fullt friska aktiva personer kan öka sin styrkeutveckling vid maximala viljemässiga knäextensioner med hjälp av visuell realtidsfeedback i form av EMG-rms från quadriceps och hamstrings. Vidare så visade studien att den viljemässiga aktiveringsförmågan ökade signifikant då feedback tillfördes. Dock visade studien ingen minskad hamstringsaktivering då feedback gavs till försökspersonen och styrkeökningen beror således snarare på ökad quadricepsaktivering än minskad hamstringsaktivering. / Abstract Aim The aim of this study was to investigate whether or not EMG-feedback from quadriceps and hamstrings has any acute effects on muscle activation and strength during a voluntary maximal isokinetic knee extensor action (eccentric and concentric) (20o.s-1).   Method Nineteen healthy subjects, 9 female and 10 male, participated in the study. They reported no previous knee injuries and were not involved in strength training for the leg muscles. Subjects performed two sets of maximal voluntary unilateral knee extensor actions at a velocity of 20o.s-1 through a 60o range of motion of the knee joint 120o to 180o, with 180o representing a fully extended knee. EMG-feedback from the knee muscles was only given for the right leg during the second set. Knee extensor strength, level of activation and electromyographic activity of quadriceps and hamstrings were recorded during the whole range of motion (60o).   Results The results of this study showed that the knee extensor strength increased significantly (by 10 %) from 144 ± 48 with no feedback to 158 ± 53 Nm with feedback. With regard to the level of activation of the knee extensors it increased significantly (by 9%) from 75 ±15 % with no feedback to 81 ± 15 % with feedback. However, biofeedback did not contribute to decreased levels of hamstrings activity.   Conclusions The main findings of the study were that the EMG-rms feedback acutely increased the strength and voluntary activation of quadriceps during a maximal voluntary isokinetic knee extensor action. However, the study showed no reduction in hamstring activation when feedback was given during the knee extensor actions. Therefore, the increased strength output was likely related to the enhanced activation of quadriceps and not a result of decreased hamstrings activation.

Spina bifida myelomeningocele (SBM) is the most common and severe type of spina bifida which is a neural tube defect (NTD). Additionally to the defect of the spinal cord most cases of SBM develop an Arnold-Chiari-II malformation, which is the main reason behind the common development of hydrocephalus. Children with SBM have a rather different cognitive profile than typically developing children. Hence, this thesis reviews the neurological impact on the cognitive profile and its relation to the social impairments found for this population. The Arnold-Chiari-II malformation is a malformation of the hindbrain which affects structures of the hindbrain, midbrain, ventricular system and subcortical gray matter. These deficits lead to impairments in the cognitive domains of executive functioning, visual-spatial working memory, intelligence, language, and learning. The consequences of these cognitive deficits are often on the social aspects of life. Two aspects affected are education and work, projecting in less academic success and a higher rate of unemployment. By clarifying the relationship between all of these aspects there is hope to improve the life of these individuals, especially on an educational basis.

<p> My thesis work was to examine the hypothesis that during early development sexually dimorphic expression of the genes associated with RNA processing in the mouse cortex and hippocampus is regulated by perinatal testosterone to activate estrogen receptors (ERs) after its conversion to estradiol via aromatase within the brain, which might create differences in mRNA variants of their targets between the sexes, and then lead to sexual dimorphism in structure and function of these brain regions. To test this, I first used reverse transcriptase with quantitative PCR to measure relative mRNA levels of 14 selected candidate genes, encoding RNA binding proteins, in the cortex/hippocampus of male and female mice collected on the day of birth (PN0), and 7 (PN7), 14 (PN14), and 21 (PN21) days after birth. A significant sex difference in mRNA levels of <i>Khdrbs2, Nanos2, Rbm48</i>, and <i> Tdrd3</i> was observed, and females expressed more <i>Rbm48</i> and <i>Tdrd3</i> mRNA on PN0 and PN7 than males. Of these genes, the female-biased expression of <i>Rbm48</i> in neonates was abolished by prenatal exposure to testosterone propionate via down-regulation of <i> Rbm48</i> mRNA levels in females, but postnatal exposure to testosterone propionate during PN21-23 increased <i>Rbm48</i> expression in both sexes. Surprisingly, neonatal exposure to estradiol benzoate abolished the sex difference in <i>Rbm48</i> expression by up-regulating <i> Rbm48</i> mRNA levels in males. These results suggest that hormonally regulated expression of <i>Rbm48</i> presents a novel molecular mechanism underlying the development of sexual dimorphism in cortical and hippocampal structure and function.</p><p>