The field of biological acoustics has witnessed a steady increase in the research into overtone singing, or “throat-singing,” in which a singer utilizes resonance throughout the vocal tract to sing melodies with the overtones created by a vocal drone. Recent research has explored both how a singer vocalizes in order to obtain rich harmonics from a vocal drone, as well as how further manipulations of the vocal apparatus function to filter and amplify selected harmonics. In the field of phonetics, vowel production is quantified by measuring the frequencies of vocal tract resonances, or formants, which a speaker manipulates to voice a particular vowel. Thus, an investigation of throat singing is closely linked to human speech production. Formants are usually detected in vowel spectra obtained using Fast Fourier Transform algorithms (FFTs). An alternative method that provides much higher frequency resolution is external excitation of the vocal tract and measurement of the pressure response signal at the mouth’s opening, which can be used to calculate the acoustic impedance spectrum. We demonstrate the use of such an “acoustic impedance meter” to measure the formant frequencies of common vowels as well as the oscillatory modes of simple resonant pipe systems. The impedance meter accurately measures fundamental pipe modes and a variety of formant frequencies with an uncertainty of 1 Hz. Finally, we assess how the impedance meter may be used to measure the unique resonances achieved by qualified throat singers.

Respiratory conditions causing poor performance in horses are usually as result of upper respiratory tract diseases or are of pulmonary origin. The tracheal is rarely a cause of primary respiratory problems in the horse, but tracheal dimensions, particularly height, may be useful in evaluating upper repiratory tract conditions cranial to the trachea and lung pathology, due to resultant change in differential pressures between these areas. The normal radiological equine tracheal height along its length has as yet not been reported. Standing lateral radiographs of the cervical and thoracic trachea of 15 clinically normal sedated Thoroughbred horses, 3-6 years old, were made at peak inspiration and end expiration. Maximum height of the larynx, and trachea at the level of the third and fifth cervical vertebra, at the level of the first thoracic vertebra, carina and the left and right primary bronchi were measured. Ratios of laryngeal height relative to the third cervical vertebral body length and tracheal heights relative to the vertebral body lengths of adjacent third and fifth cervical vertebrae and first thoracic vertebra, and carina heights relative to a mid-thoracic vertebra, respectively were made, as well as tracheal height at the fist thoracic vertebra ratio with the thoracic inlet height. Known size metallic markers were used to determine magnification corrected tracheal heights in the sagittal plane and effect of body mass and height at the withers on tracheal height was determined. The magnification corrected radiological airway heights at end expiration and peak inspiration were measured and respectively the mean values were found to be: laryngeal height: 5.89 cm and 5.86 cm, tracheal height at the third cervical vertebra: 4.17 cm and 4.04 cm, tracheal height at the fifth cervical vertebra: 3.62 cm and 3.59 cm, tracheal height at the first thoracic vertebra: 3.4 cm and 3.23 cm and carina height: 3.85 cm and 4.12 cm. The ratios of these measurements to nearby vertebral body lengths were respectively: laryngeal height at the third cervical vertebra: 0.56 and 0.56, tracheal height at the third cervical vertebra: 0.4 and 0.39, tracheal height at the fifth cervical vertebra: 0.37 and 0.37, tracheal height at the first thoracic vertebra: 0.59 and 0.59, and carina height: 0.91 and 0.94. The ratio tracheal height at the first thoracic vertebra to the thoracic inlet respectively 0.15 and 0.15. Although there was no statistical difference in the data, there was a trend towards a higher tracheal height at expiration. No correlation was found between tracheal height and body mass or tracheal height and height at the withers, and measured tracheal height was generally lower than predicted tracheal height, possibly as result of sedation used. The small range of body mass and height in this study as well as the relatively small number of horses evaluated may account for the lack of correlation to predicted tracheal height. This study in normal horses may serve as a reference when radiologically evaluating cases of upper respiratory tract and lung pathology, where the tracheal dimensions may differ significantly due to differences in airway resistance and biomechanics. Radiographs to evaluate tracheal height can be made independent of respiratory phase in sedated horses, and it is recommended that ratios of tracheal height to an adjacent vertebral body length are more reliable values to compare within and between horses. It is recommended to take tracheal height measured at the fifth cervical vertebra since this measurement showed a slightly smaller standard deviation than at other sites measured as well as a medium amount of clinical effect. If only thoracic radiographs are made, measurements of tracheal height at the thoracic inlet is the alternative (the standard cranioventral view), but it is recommended to include the distal aspect of the first rib if the thoracic inlet is to be measured. / Dissertation (MMedVet)--University of Pretoria, 2008. / Companion Animal Clinical Studies / unrestricted

Respiratory failure accounts for a large, if not the largest, percentage of deaths during the first 48 hours of life. During the last ten years a great deal of research has been devoted to this early respiratory failure. The syndrome has been known by different names at different times; hyaline membrane disease (because pulmonary hyaline membrane is a frequent autopsy finding), congestive pulmonary failure, vernix membrane disease, pulmonary syndrome, and more recently the respiratory distress syndrome. A vast literature on the subject has accumulated. Many new and interesting facts have come to light and although many new theories have been put forth to explain the syndrome, the cause is still unknown.

The blood of man is rich in plasminogen, the inactive precursor of plasmin, a protease (Astrup, 1956a); the most characteristic action of plasmin is the digestion of fibrin, i.e. fibrinolysis. Many tissues, including the prostate (Rasmussen and Albrechtsen, 1960a), contain substances which can activate plasminogen, and thus initiate fibrinolysis, and it has been assumed that both the excessive fibrinolysis seen in the blood of some patients with prostatic disease (Tagnon, Whitmore, Schulman and Kravitz, 1953a), and in prostatic surgery (Lombardo, 1957), is due to the release of this activator into the blood stream (Fearnley, 1965). Human semen contains a substance which can activate the blood fibrinolytic system (von Kaulla and Shettles, 1953). Indeed, when human seminal fluid is ejaculated, it undergoes a process resembling the clotting and fibrinolysis of the blood, by coagulating then liquefying spontaneously. The coagulum is formed when a fibrinogenlike protein secreted by the seminal vesicles is acted upon by a clotting enzyme from the prostate (Mann, 1964). Coagulation is followed within about 20 minutes by liquefactionliquefaction of the clots by an enzyme assumed to come from the prostate (Huggins and Neal, 1942). This enzyme resembles plasmin in that it is a protease acting on a fibrin-like substrate, and that it is derived from an inactive precursor.

In the adult brain, the thalamocortical tract conveys sensory information from the external environment to the cortex. The cortex analyzes and integrates this information and sends neural responses back to the thalamus through the corticothalamic tract. To reach their final target both thalamocortical and corticothalamic axons have to cover long distances during embryogenesis, changing direction several times and passing through different brain territories. The ventral telencephalon plays a major role in the early development of these tracts. At least three main axon guidance mechanisms act in the ventral telencephalon. First, two different populations of pioneer neurons in the lateral ganglionic eminence (LGE) (LGE pioneer neurons) and medial ganglionic eminence (MGE) (MGE pioneer neurons) provide scaffolds which allow growing corticothalamic and thalamocortical axons to cross the pallium sub pallium boundary (PSPB) and the diencephalic telencephalic boundary (DTB), respectively. Second, the ventral telencephalon forms a permissive corridor for thalamic axons by tangential migration of Isl1 and Ebf1 expressing cells from the LGE into the MGE. Finally, thalamortical and corticothalamic axons guide each other once they have met in the ventral telencephalon (“handshake hypothesis”). The Gli3 transcription factor has been shown to be essential for normal early embryonic regionalization of the mammalian forebrain, although roles of Gli3 in later aspects of forebrain development, like the formation of axonal connections, have not been investigated previously. Here, I present the analysis of axonal tract development in the forebrain of the Gli3 hypomorphic mutant mouse Polydactyly Nagoja (Pdn). These animals lack the major axonal commissures of the forebrain: the corpus callosum, the hippocampal commissure, the anterior commissure and the fimbria. In addition, DiI injections and neurofilament (NF) staining showed defects in the formation of the corticothalamic and thalamocortical tracts. Although the Pdn/Pdn cortex forms early coticofugal neurons and their axons, these axons do not penetrate the LGE and instead run along the PSPB. Later in development, although a thick bundle of Pdn/Pdn cortical axons is still observed to project along the PSPB, some Pdn/Pdn cortical axons eventually enter the ventral telencephalon navigating along several abnormal routes until they reach thalamic regions. In contrast, Pdn/Pdn thalamic axons penetrate into the ventral telencephalon at early stages of thalamic tract development. However, rostrally they deviate from their normal trajectory, leaving the internal capsule prematurely and only few of them reach the developing cortex. Caudally, an ectopic Pdn/Pdn dorsal thalamic axon tract projects ventrally in the ventral telencephalon not entering the internal capsule at all. These defects are still observed in newborn Pdn/Pdn mutant mice. Next, I investigated the developmental mechanisms causing these pathfindings defects. No obvious defects are present in Pdn/Pdn cortical laminae formation and in the patterning of the Pdn/Pdn dorsal thalamus. In addition, Pdn/Pdn thalamocortical axons are able to respond to ventral telencephalic guidance cues when transplanted into wild type brain sections. However, these axonal pathfinding defects correlate with patterning defects of the Pdn/Pdn LGE. This region is partially ventralized and displays a reduction in the number of postmitotic neurons in the mantle zone due to an elongated cell cycle length of LGE progenitor cells. Finally, Pdn/Pdn mutant display an upregulation of Shh expression and Shh signalling in the ventral telencephalon. Interestingly, these patterning defects lead to the absence of DiI back-labelled LGE pioneer neurons, which correlates with the failure of corticothalamic axons to penetrate the ventral telencephalon. In addition, ventral telencephalic thalamocortical guidance mistakes happen at the same time of abnormal formation of the corridor cells. Taken together these data reveal a novel role for Gli3 in the formation of ventral telencephalic intermediate cues important for the development of the thalamocortical and corticothalamic connections. Indeed, Pdn animals are the first known mutants with defective development of the LGE pioneer neurons, and their study provides a link between early patterning defects and axon pathfinding in the developing telencephalon.

Diss. (sammanfattning) Linköping : Univ., 2004. / Härtill 5 uppsatser.

Much of our understanding of the fascinating complexity of neuronal circuits comes from anatomical tracing studies that use dyes or fluorescent markers to highlight pathways that run through the brain and spinal cord. Viral vectors have been utilized by many previous groups as tools to highlight pathways or deliver transgenes to neuronal populations to stimulate growth after injury. In a series of studies, we explore anterograde and retrograde tracing with viral vectors to trace spinal pathways and explore their contribution to behavior in a rodent model. In a separate study, we explore the effect of stimulating intrinsic growth programs on regrowth of corticospinal tract (CST) axons after contusive injury. In the first study, we use self-complimentary adeno associated viral (scAAV) vectors to trace long descending tracts in the spinal cord. We demonstrate clear and bright labeling of cortico-, rubro- and reticulospinal pathways without the need for IH, and show that scAAV vectors transduce more efficiently than single stranded AAV (ssAAV) in neurons of both injured and uninjured animals. This study demonstrates the usefulness of these tracers in highlighting pathways descending from the brain. Retrograde tracing is also a key facet of neuroanatomical studies involving long distance projection neurons. In the next study, we highlight a lentivirus that permits highly efficient retrograde transport (HiRet) from synaptic terminals within the cervical and lumbar enlargements of the spinal cord. By injecting HiRet, we can clearly identify supraspinal and propriospinal circuits innervating MN pools relating to forelimb and hindlimb function. We observed robust labeling of propriospinal neurons, including high fidelity details of dendritic arbors and axon terminals seldom seen with chemical tracers. In addition, we examine changes in interneuronal circuits occurring after a thoracic contusion, highlighting populations that potentially contribute to spontaneous behavioral recovery in this lesion model. In a related study, we use a modified version of HiRet as part of a multi-vector system that synaptically silences neurons to explore the contribution of the rubrospinal tract (RST) and CST to forelimb motor behavior in an intact rat. This system employs Tetanus toxin at the neuronal synapse to prevent release of neurotransmitter via cleavage of vesicle docking proteins, effectively preventing the propagation of action potentials in those neurons. We find that shutdown of the RST has no effect on gross forelimb motor function in the intact state, and that shutdown of a small population of CST neurons in the FMC has a modest effect on grip strength. These studies demonstrate that the HiRet lentivirus is a unique tool for examining neuronal circuitry and its contribution to function. In the final study, we explore stimulation of the Phosphoinositide 3-kinase/Rac-alpha serine/threonine Protein Kinase (PI3K/AKT) growth pathway by antagonizing phosphatase and tensin homolog (PTEN), a major inhibitor, to encourage growth of CST axons after a contusive injury. We use systemic infusions of four distinct PTEN antagonist peptides (PAPs) targeted at different sites of the PTEN protein. We find robust axonal growth and sprouting caudal to a contusion in a subset of animals infused with PAPs targeted to the PTEN enzymatic pocket, including typical morphology of growing axons. Serotonergic fiber growth was unaffected by peptide infusion and did not correlate with CST fiber density. Though some variability was seen in the amount of growth within our animal groups, we find these PTEN antagonist peptides a promising and clinically relevant tool to encourage CST sprouting, and a potentially useful addition to therapies using combinatory strategies to enhance growth. These studies demonstrate that viral tracing is a powerful tool for mapping spinal pathways and elucidating their ability to reform spinal circuits after injury. Viral vectors can be used in both anterograde and retrograde tracing studies to highlight intricacies of neuronal cell bodies, axons and dendritic arbors with a high degree of fidelity. In the injured state, these tools can help identify pathways that contribute to spontaneous recovery of function by highlighting those that reform circuits past an injury site. In the uninjured state, these vectors can contain neuronal silencing methods that help define the contribution of specific pathways to behavior. / Neuroscience

During development the nuclei of the thalamus form reciprocal connections with specific regions within the cortex. These connections give rise to the thalamocortical tract. The processes by which axons of the thalamocortical tract are guided to their target regions are poorly understood. It has been shown that diffusible or membrane bound factors can have a chemoattractive or chemorepulsive effect on the tip or growth cone of the axon. Thalamocortical axons may also be guided along ‘pioneer’ axon populations that form a scaffold along which axons may grow. The transcription factor Pax6 has been shown to have a role in a variety of developmental processes such as neuronal patterning, proliferation, migration and axon guidance. It is known that Pax6 is involved in the development of the thalamocortical tract but its exact role is unknown. To explore the role that Pax6 plays in the development of the thalamocortical tract I have used two different mouse models, the small eye (Pax6Sey/Sey) mouse which lacks functional Pax6, and a conditional Pax6 knock-out (Pax6cKO) mouse made using a Gsh2 Cre line that specifically reduces Pax6 expression in the ventral telencephalon and prethalamus. Using the Pax6Sey/Sey mouse I show that thalamocortical axons do not enter the ventral telencephalon in the absence of Pax6 and that a small number of axons incorrectly enter the hypothalamus. In addition axons found within the ventral telencephalon of the mutant do not originate from the thalamus but instead originate from cells within the ventral telencephalon itself. I have found that the expression of guidance molecule Robo2 is reduced in the Pax6Sey/Sey mouse, which may explain why thalamocortical axons enter the hypothalamus. When Pax6 expression is reduced at the prethalamus and ventral telencephalon using the Pax6cKO mouse I show that the majority of thalamocortical axons reach the cortex normally but some axons become disorganized within the thalamus. Pioneer axons which emanate from the prethalamus normally guide thalamocortical axons through the diencephalon but in the Pax6cKO I report that these axons are reduced which may explain the disorganization of thalamocortical axons within the thalamus. Taken together the data from these two models demonstrate that for the thalamocortical tract to form normally Pax6 expression is required in both the cells of the thalamus and in cells that lie along the route of the tract. In addition I provide evidence that Pax6 may influence axon guidance by controlling the expression of guidance molecules and the development of pioneer axon tracts.

Hyperspectral (HS) imaging combines spectral measurement of a pixel with 2D imaging technology. It is capable to provide a series of images containing both spectral and spatial information, and has been widely used in medical domain. However, most researches on medical HS imaging are regarding ex-vivo biopsy or skin and oral mucosa. The study on HS imaging regarding in-vivo disease lags far behind. In this thesis, we developed a novel flexible HS endoscope system. It is capable to obtain a series of HS images in vivo in a non-contact way among the wavelength range of 405 – 665 nm. After a lot of time-consuming modifying and debugging work, this new system has high stability and convenience to be applied in clinic now. We evaluated this system in clinic. First, we got ethics approval for clinical trials. Then, we obtained HS images regarding gastrointestinal (GI) diseases inside patients using this system. As far as we know, this type of in-vivo image data has not been reported in previous literatures. Thus using these HS images, we built a database for GI mucosa. Next, we analyzed some typical HS images tentatively. The method of Recursive Divergence is implemented to extract valuable and diagnostic information from these HS images. The results prove the effect and applicability of this new HS endoscope system, which has shown the great potential to be used as a platform and guidance for further medical studies. To further apply the analysis results in clinic, we propose a novel Adaptive Narrow-Band Imaging (ANBI) method based on band selection of HS images of a specific type of disease. It is expected that the new technique has higher accuracy, sensitivity, and specificity compared to conventional Narrow-Band Imaging (NBI) technique. In this thesis, we also discuss the future direction of the system improvement. Especially, to improve light intensity and signal-noise-ratio of HS images in wide-field view, we propose a new imaging method using broad- and overlapped-band filters. Although this method only performs greatly on the foundation of accurate image registration, we hope to apply it in our system in the future.

No description available.