No description available.

The Vascular system of the human spinal cord at birth has been investigated, and a report is submitted on the detailed pattern of the arterial and arteriolar vessels in 27 cadavers. In 21 instances, the anterior median spinal arterial trunk and in 9 instances the postero-lateral spinal arterial trunks have been recorded. Selection of cadavers has been on the basis of the absence of obvious congenital deformity or disease of the spine and spinal cord. Particular attention has been paid to the feeder arteries which contribute to the main longitudinal channels, both anteriorly and posteriorly. The number of feeder vessels, their ;.., sources of origin .and their approximate size~ have been determined. In 21 specimens the anterior vessels have been recorded and charted in detail. (Plates I - VII). In 9 specimens the posterior vessels have been recorded and the detailed charts of 3 of the latter are presented. (Plate X, p.46). Material and Methods Newborn cadavers, obtained on average 3-5 days after death from various causes such as prematurity, cerebral trauma, pneumonia and pulmonary hyaline membrane have been used. In each case the body was warmed to room temperature, before the introduction into the right femoral artery of a plastic tubular cannula of appropriate gauge. Dilute Ammonia, 2-3 ml., was introduced to promote the flow of the injection material and the specimens were injected with latex under pressures which varied from 5 lbs per square inch to 20 lbs per square inch. The manometric readings of intra-arterial pressure were between 300 mms. Hg and 1200 mms. Hg, and the optimal pressure of delivery was 15 lbs per square inch. Both the arterial and the venous sides of the circulation were well-filled by the injection material, which in all instances was administered via the femoral artery. Rupture of vessel walls with leakage of injection material was not excessive. The number of cadavers rejected on account of inadequate filling or excessive leakage was less than 10 out of approximately 50 cadavers. The injection material consisted of a prevulcanised latex, "Revultex", coloured red with an appropriate dye, and stained through fine muslin before use to ensure freedom from solid particles which could cause obstruction of vessels of fine calibre. The injection material was allowed to penetrate the vascular tree for periods varying from 5 to 15 minutes and the cadaver was then embalmed, injecting the body cavities and infiltrating the limbs as far as possible with a standard embalming fluid consisting of: White Industrial Spirits, 45%; Glycerine, 35%; Formaldethyde, 15%; Thymol, q.s. The cadaver was preserved in a 50% solution of the embalming fluid, and dissections were commenced not less than 14 - 21 days after preparation. Use was made in all instances of the binocular surgical microscope, and magnifications of 10 or of 16 were found to be optimal. Photographic reproductions were made in colour, and the dissected specimens have been preserved. The findings in respect of the anterior arterial system of supply of the cord have been consistent with those of a number of workers, in particular Woollam and Millen (1958) of Cambridge. Additional findings have been reported in respect of the smaller arteries (arteries of the 4. 4th order) including the perforating arteries of the median sulcus. The value of a computerised "average" for the vascular pattern of the cord is disputed. In the opinion of the author, it is likely to be misleading to the clinician and to the surgeon. Reliance upon an average picture in an individual case is liable to be harmful; in the present series of 21 specimens, the average picture as offered by Suh and Alexander (1939) was, in some respects only, applicable to 1 case. The presence of arterio-arterial anastomoses as a common feature in the spine is reported, and the possible significance discussed. Reference is made to a "critical narrow zone" which the author has determined by the radiological examination of 50 vertebral columns in people of all ages. When the region of the "narrow critical zone" is related to the regional blood supply of the spinal cord, then a significant factor in the post-operative development of paraplegia in scoliosis cases has been found to emerge. Vascular factors have been sought in the etiology of idiopathic scoliosis, but not found.

Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2012-07-20T21:20:40Z No. of bitstreams: 1 Kiyoshi Ferreira Fukutani Aplicação de técnicas sorológicas e moleculares....pdf: 8948929 bytes, checksum: 731ecff23760ac556b55cf07dd7c1cc5 (MD5) / Made available in DSpace on 2012-07-20T21:20:40Z (GMT). No. of bitstreams: 1 Kiyoshi Ferreira Fukutani Aplicação de técnicas sorológicas e moleculares....pdf: 8948929 bytes, checksum: 731ecff23760ac556b55cf07dd7c1cc5 (MD5) Previous issue date: 2011 / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil / Aplicação do Exame sorológico (ELISA) e do PCR na detecção de Leishmania chagasi em doadores de sangue na cidade de Salvador. A leishmaniose é causada por protozoários do gênero Leishmania e constitui um problema grave de saúde pública na Bahia. A transmissão do protozoário pela transfusão de sangue já foi relatada e existe a possibilidade dos hemoderivados serem um potencial risco para a manutenção da doença. O presente trabalho teve como objetivo avaliar positividade sorológica contra Leishmania e a presença deste parasita no sangue periférico de doadores, na cidade de Salvador, BA. Para estipulando a soroprevalência de leishmaniose em doadores de sangue, foram coletadas amostras de sangue periférico de 700 indivíduos, no Hemocentro da Bahia (HEMOBA/SESAB), de janeiro a setembro de 2010. As amostras foram processadas para a obtenção de plasma e de DNA. A sorologia anti-Leishmania foi feita por ELISA, empregando antígeno solúvel de Leishmania chagasi (SLA). A presença de parasitas foi determinada por PCR qualitativo e por PCR quantitativo (qPCR). A população amostral foi composta por 74.5% de indivíduos masculinos, com média de idade de 34 anos. A partir de uma curva ROC, empregando soros de pacientes com leishmaniose visceral e soros de pacientes residentes em área não endêmica, o ponto de corte para o teste sorológico foi estabelecido em 0,0167 (DO em 405nm). A sorologia anti-Leishmania foi positiva em 5.4% (38/700) das amostras. Destes indivíduos, 73% (28/38) apresentaram amplificação para uma região repetitiva do genoma de Leishmania, empregando-se o PCR qualitativo. Empregando o qPCR, foi possível determinar a presença de parasitas em 0.4% (3/700) amostras e, nestas, a quantificação foi inferior a 10 parasitas. Nossos resultados mostram a prevalência de sorologia anti-Leishmania é de 5.4%, em doadores do HEMOBA/SESAB, similar ao encontrado em outras área onde ocorre a leishmania. / Application of serological examination (ELISA) and PCR detection of Leishmania chagasi infection in blood donors in Salvador. Leishmaniasis is caused by protozoa of the genus Leishmania and is a serious public health problem in Bahia. The transmission of the parasite by blood transfusion has been reported and the possibility of blood products being a potential risk for disease transmission currently exists. This study aimed to evaluate seropositivity against Leishmania and the presence of parasites in peripheral blood from blood donors in Salvador, Bahia. To assess the prevalence of anti-Leishmania antibodies in blood donors, we collected peripheral blood samples from 700 individuals in the Blood Bank of Bahia (HEMOBA/SESAB), from January to September 2010. The samples were processed to obtain plasma and DNA. The anti-Leishmania serology was performed by ELISA employing Leishmania chagasi soluble antigen (SLA). The presence of parasites was determined by qualitative PCR and quantitative PCR (qPCR). The sample population comprised 74.5% of males with a mean age of 34 years. From a ROC curve, using sera from patients with visceral leishmaniasis and sera from patients residing in non-endemic areas, the cutoff for the serologic test was set at 0.0167 (OD at 405nm). The anti-Leishmania serology was positive in 5.4% (38/700) samples. Of these, 73% (28/38) showed amplification of a repetitive region of the genome of Leishmania, using the qualitative PCR. Using the qPCR, we determined the presence of parasites in 0.4% (3 / 700) samples, and in these, the amount was less than 10 parasites. Our results show the prevalence of anti-Leishmania serology is 5.4% in donors, similar to that found in other areas where Leishmania is.

A PC based waveform acquisition and analysis system has been developed for use in aorta-iliac arterial assessment. A Motorola DSP56001 based system containing dual Analog to Digital converters is used to sample phase quadrature demodulated signals from a commercially available continuous wave Doppler unit. The Power Spectral Density is calculated using an autoregressive model from which the mean velocity waveform is calculated. This waveform is used to calculate the damping factor, vessel compliance and runoff resistance of a simple electrical model of the lower limb arterial circulation using a non-linear regression technique of curve fitting in the time domain. A pilot study using the system shows a significant separation (p < 0.001 Mann Whitney U-test) between the damping factors of a normal control group (quartile range = 0. 15 - 0.25 ; median = 0. 19) and a patient group with angiographically determined aorta-iliac arterial disease (quartile range = 0.45 - 0.89 ; median= 0.49).

Thesis (Ph.D.)--University of the Witwatersrand, Faculty of Health Sciences, 2012 / Background and Purposes Suicide by hanging is a relatively common occurrence. The actual cause of death in suicidal hanging is, however, controversial, having been attributed variously to asphyxia, carotid artery compression and vagal nerve stimulation. The aim of this Ph.D thesis was to determine the possible neurovascular cause of death in suicides by hanging by careful study of the anatomy and physiology of the neck region in relation to the ensuing pathology. The study was, therefore, approached from an anatomical, physiological, histological and pathological pespective. It therefore comprised a detailed exploration of the anatomy and physiology of the neck structures to match these with the underlying traumatised neurovascular structures, the latter trauma being brought about by the suicidal hanging process. Methods The methods used in the study included an investigation of the ligature and position of the ligature in relation to the level of the neck and the physical effects of the ligature on the skin and underlying anatomical structures. A careful and detailed dissection of the neck was undertaken and samples of the vessels and nerves were processed for histological study. Fifty consecutive cases of suicidal hanging and five “non-hanging” cases which served as controls were used in the study. In addition, ten cases of suicidal hanging not included in the study were subjected to occlusion studies by means of probe exploration. This technique and procedure was not carried out or applied to the cases included in the study for fear that the probe itself might produce artefactual damage to the delicate endothelium lining the inner layer of the vessel wall. The study was classified into various components such as: 1. Examination of the type and structure of the ligature material; 2. The position of the ligature on the neck, i.e. whether involving upper, middle, or lower third of neck and to correlate this position with the underlying anatomical structures subjected to the accompanying tensile, compressive and haemodynamic forces; 3. The physical effects of the ligature upon the skin and the underlying deeper neurovascular structures of the neck; 4. Meticulous “bloodless” dissection of the neck structures to corroborate any pathology noted with the above three criteria. Currently, all putative causes of death remain speculative; 5. Particular attention was paid to those structures most vulnerable to the compressive forces, tensile forces and haemodynamic forces operative in hanging. These comprise the neurovascular structures contained within the fibrous carotid sheath and the phrenic nerves in the neck, in particular with regard to the anatomical relationship of these structures to the positioning of the ligature. As far as analysing the forces involved, the engineering principles pertaining to these were interpreted in consultation with the Faculty of Engineering at the University of the Witwatersrand. Results The main findings of the study showed damage to vascular, neural (including phrenic nerve), carotid bodies and accessory glomal bodies. The vascular findings emerged following an examination of the total number of arteries in the study, namely, 300, the figure derived as follows: six arteries in each of the fifty hanging subjects, viz., the left common carotid artery, the right common carotid artery, the left internal carotid artery, the right internal carotid artery, the left external carotid artery and the right external carotid artery (6 x 50 = 300). The damage shown was particularly the case with regard to the finding of tears in the various layers of the vessel wall. These extended from the intima through to the adventitia or outermost layer of the vessel wall and these were further subdivided into being either single or multiple. The tears found ranged from those involving the intima alone (single tears being found in 17 (5.6%) of the 300 arteries examined and multiple tears in 37 (12.3%) of the 300 arteries examined., the intima extending to the internal elastic lamina (single tears being found in 20 (6.6%) of the 300 arteries examined and multiple tears in 8 (2.6%) of the 300 arteries examined), tears involving the intima and extending through to involve the media, i.e. intimomedial tears and whether these latter tears involved the inner-, middle-, or outer-thirds of the media (single or multiple). Single intimo-medial tears extending through the intima to involve the inner-third of the media comprised 6 (2.0%) of the arteries examined, those extending from the intima to involve the middle-third of the media comprised 3 (1.0%) of the 300 arteries examined and single intimo-medial tears extending through the intima to involve the outeriv third of the media similarly comprised 3 (1%) of the arteries examined. Multiple intimo-medial tears extending through from intima to inner-, middle-, and outerthirds of the media respectively, comprised 3 (1.0%), 5 (1.6%) and 1 (0.3%) of the arteries examined. Single tears involving the inner-third of the media alone comrised 6 (2.0%) of the 300 arteries examined, single tears involving the middle-third of the media comprised 9 (3.0%) of the arteries examined and single tears involving the outer-third of the media alone comprised 8 (2.6%) of the arteries examined. Multiple tears involving the inner-, middle and outer-thirds of the media respectively comprised 6 (2.0%), 13 (4.3%) and 16 (5.3%) of the arteries examined. Single tears involving both adventitia and media, i.e. adventitio-medial tears extending through the inner-, middle-, or outer-thirds of the media to involve the adventitia comprised 1 (0.3%), 2 (0.6%) and 6 (2.0%) respectively of the 300 arteries examined. Multiple adventitio-medial tears of the inner-, middle-, and outer-thirds of the media, respectively, comprised 0 (0.0%), 3 (1.0%) and 2 (0.6%) of the 300 arteries examined. Single tears of the adventitia alone comprised 21 (7.0%) of the arteries examined while multiple tears comprised 7 (2.3%). Complete circumferential transverse rupture of the vessel wall was found in 3 (1.0%) of the arteries examined while adventitial haemorrhage was found in 103 (34.3%) of the 300 arteries examined. The vascular findings were represented numerically in tabular form in the 50 hanging subjects in Table III and were further analysed and compared with regard to either unilateral or bilateral vessel involvement in the fifty (50) suicidal hanging subjects and the findings represented in Tables IIIa (unilateral involvement) and IIIb (bilateral involvement). Additional vascular findings comprised endothelial elevation/avulsion, internal elastic lamina dehiscence, subendothelial clefts, multiple medial fenestrations, adventitio-medial separation, vascular congestion and a vascular plane of cleavage. These were similarly represented in Table IV and analysed with regard to unilateral or bilateral involvement in Tables IVa and IVb. Endothelial elevation/avulsion was found in 295 (98.3%) of the 300 arteries examined, internal elastic lamina dehiscence in 290 (96.6%) of the arteries examined, subendothelial clefts in 289 (96.3%) of the arteries examined, multiple medial fenestrations in 17 (5.6%) of the arteries examined, adventitiomedial separation in 273 (91.0%) of the arteries examined, vascular congestion in 224 (74.6%) of the arteries examined and a vascular plane of cleavage in 98 (32.6%) of the arteries examined. These findings, unexpected, showed the extreme fragility and vulnerability of the intima and adventitia to the compressive and tensile forces acting on the vessel wall during hanging, being explicable not only on the basis of the various complex forces interacting simultaneously during hanging but on the magnitude of forces applied. A mathematical analysis, found at the end of the Discussion chapter, conducted in order to estimate the minimum peak pressure applied and exerted on the vessel wall during hanging, in collaboration with the School of Mechanical, Industrial and Aeronautical Engineering at the University of the Witwatersrand, confirmed the magnitude of these forces. The neural findings (Table V) were divided into neural congestion, neural haemorrhage, neural internal dehiscence, neural tearing and perineural separation and these were similarly analysed with regard to either unilateral or bilateral involvement in the fifty hanging subjects (Tables Va and Vb). Neural congestion was found in association with 20 (6.6%) of the 300 arteries examined, neural haemorrhage in14 (4.6%), neural internal dehiscence in 54 (18.0%), neural tearing in 35 (11.6%) and perineural separation in 112 (37.3%). Neural ganglionic findings were similarly divided into ganglionic congestion, ganglionic haemorrhage, ganglionic internal dehiscence and ganglionic tearing. Ganglionic congestion, in association with the 300 arteries examined, was found in 20 (6.6%), ganglionic haemorrhage in 8 (2.6%), ganglionic internal dehiscence in 15 (5.0%) and ganglionic tearing in 6 (2.0%). The findings in the carotid bodies were divided into carotid body congestion, carotid body haemorrhage, carotid body internal dehiscence and carotid body tearing. Carotid body congestion, in association with the 300 arteries examined, was found in 8 (2.6%), carotid body haemorrhage in 2 (0.6%), carotid body internal dehiscence in 4 (1.3%) and carotid body tearing in 2 (0.6%). Accessory glomal body findings were, once again, divided into accessory glomal congestion, accessory glomal haemorrhage, accessory glomal internal dehiscence and accessory glomal tearing. However, in view of the close anatomical association between the accessory glomal bodies and the adventitia of the arterial walls, an additional pathological finding of accessory glomal adventitial separation emerged. Accessory glomal congestion, in association with the 300 arteries examined, was found in 20 (6.6%), accessory glomal haemorrhage in 7 (2.3%), accessory glomal internal dehiscence in 50 (16.6%), accessory glomal tearing in 18 (6.0%) and accessory glomal adventitial separation in 124 (41.3%). This latter finding once again demonstrated the vulnerability of the adventitial layer of the vessel wall to tensile forces, separating it from its associated structures. Damage to the phrenic nerves and surrounding muscles, underlying the site of ligature application, was similarly found, suggesting a role for phrenic nerve stimulation with consequent diaphragmatic paralysis in contributing to death in the hanging process. Discussion and Conclusion In this Ph.D thesis the principles of dimensional analysis i.e., the breaking down of a complex phenomenon into its component parts, have been applied. However, in view of the complexity and proximity of structures to one another in the neck, consisting not only of the rigid hyoid-larynx complex and vertebral column but also the integrated vascular and neural structures, it appears that not one single biological mechanism can be ascribed and attributed to the cause of death in suicidal hanging. Rather, it appears that unconsciousness and death causation appears to be multifactorial. Both the sympathetic and parasympathetic arms of the autonomic nervous system are involved, often with antagonistic and therefore paradoxical effects. In a ddition, pressure to the phrenic nerve, not previously considered in playing a role in death causation in hanging, may, it is suggested, be a major contributory factor in death causation. This nerve, the innervation to the major muscle of respiration, i.e. the diaphragm, in a neural response to the compressive and tensile forces in hanging, fixes the diaphragm in a state of inspiratory paralysis. This latter effect would be further augmented by neural stimulation of the accessory muscles of respiration, i.e. the sternocleidomastoid and scaleni muscles, similarly lying deep to the site of ligature application, contributing to the thoracic cage becoming fixed in a state of inspiratory paralysis. This latter effect, as described in that section of the Discussion chapter dealing with an analysis of the physiological functions at play, is brought about by initiation of the dynamic and static stretch reflexes occurring in these muscles on application of a compressive or tensile stimulus. Compression of the carotid arteries, on the other hand, results, as shown, not only in major damage to these vessels and their accompanying veins, but, in addition, must produce a dramatic element of cerebral ischaemia with ensuing loss of consciousness. It thus appears that loss of consciousness is the critical factor for it is the state when the victim is no longer able to save himself or herself. Without loss of consciousness survival may occur, but with it, death becomes inevitable. The question then arises :- what is the cause of unconsciousness? In physiological terms, carotid artery occlusion induces rapid unconsciousness, i.e. within 11 to 12 seconds, resulting ultimately in death. In other words, the sudden application and unremitting pressure of the ligature must inevitably result in death. On the other hand, the sudden application of a ligature with consequent vagal nerve compression may produce instantaneous cardiac arrest with cessation of blood flow to the brain and resultant loss of consciousness. This event would produce unconsciousness in less than the time period of 11 seconds of carotid artery occlusion (although the brain continues to survive for several minutes thereafter despite cessation of heart beat). If, however, unconsciousness is contributed to by phrenic nerve compression, it would not be instantaneous as shown by the fact that one can normally hold one’s breath for several minutes (as underwater swimmers do) and unconsciousness does not supervene either instantaneously or within 11 seconds. In short, unconsciousness would not occur within 11 seconds in the case of compression of the phrenic nerve unless a more critical factor supervenes.Thus, the rapidity of onset of unconsciousness appears to be the critical factor in determining the progression to ultimate (and inevitable) death. Moreover, as pointed out in the Materials and Methods chapter, the carotid arteries in several tested cases would not allow the passage of a probe through the obstructed arteries beneath a tightly applied ligature. This obstruction would, therefore, appear to be the initiator of the deadly unconsciousness factor, although respiratory arrest would be compounded by neural and muscular factors. While in this thesis the principles of dimensional analysis i.e., the breaking down of a complex phenomenon into its component parts have been applied, the principles of integrated analysis i.e., the combining and synthesis of separate parts into a whole have also been attempted. In essence, while it is suggested that the neural elements play a pivotal role in the hanging process due to the neural effect on both brain and heart as a result of autonomic nervous system stimulation and the function of the phrenic nerve in respiration, it appears that multiple factors, acting in concert, simultaneously or in rapid sequence to one another, all play a role in contributing to death causation in the hanging process.

by Ng Chung Ying Davy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 91-103). / ACKNOWLEDGMENT --- p.1 / ABSTRACT --- p.2 / Chapter CHAPTER 1 : --- INTRODUCTION --- p.3 / Chapter CHAPTER 2 : --- LITERATURE REVIEW --- p.5 / Chapter 2.1. --- The History of Laser --- p.5 / Chapter 2.1.1 --- Pre-Maser History (1917 - 1952) --- p.5 / Chapter 2.1.2. --- The Development of the Maser (1953 - 1959) --- p.6 / Chapter 2.1.3. --- The Development of the Laser (1960 - 1961) --- p.7 / Chapter 2.1.4. --- Expanding the Laser Concept (1962 - 1966) --- p.8 / Chapter 2.1.5. --- New Laser Development (1967 - at present) --- p.11 / Chapter 2.2. --- Basic Laser System --- p.11 / Chapter 2.2.1. --- The Active Laser Media --- p.12 / Chapter 2.2.2. --- The Source of Excitation Energy --- p.12 / Chapter 2.2.3. --- A Febry-Perot Interferometer --- p.13 / Chapter 2.3. --- Basic operational principles of laser --- p.13 / Chapter 2.4. --- Characteristics of Laser Radiation --- p.14 / Chapter 2.5. --- Laser Reactions in Living Tissue --- p.15 / Chapter 2.5.1. --- Laser Interactions with the Eye --- p.15 / Chapter 2.5.2. --- Laser Interaction with the Skin and its Appendages --- p.16 / Chapter 2.5.3. --- Laser Interaction with other tissues --- p.16 / Chapter 2.6. --- Thermal Effect of Laser Irradiation of Living Tissues --- p.20 / Chapter 2.7. --- Medical lasers and their applications --- p.21 / Chapter 2.7.1. --- Neodymium-doped yttrium-aluminium- garnet (Nd:YAG) laser --- p.21 / Chapter 2.7.2. --- Argon laser --- p.21 / Chapter 2.7.3. --- Carbon dioxide laser --- p.22 / Chapter 2.7.4. --- Tunable dye laser --- p.22 / Chapter 2.7.5. --- Gold Vapour Laser --- p.23 / Chapter 2.7.6. --- Copper Vapour Laser --- p.23 / Chapter 2.8. --- Port-wine stains --- p.24 / Chapter 2.8.1. --- Pathology of port-wine stains --- p.24 / Chapter 2.8.2. --- Treatment of port-wine stains by lasers --- p.24 / Chapter 2.9. --- Laser Therapy in the Gastrointestinal Tract --- p.28 / Chapter 2.10. --- Esophageal varices --- p.30 / Chapter 2.10.1. --- Etiology of oesophageal varices --- p.30 / Chapter 2.10.2. --- Pathology of oesophageal varices --- p.31 / Chapter 2.10.3. --- Diagnosis of esophageal varices --- p.31 / Chapter 2.10.4. --- Treatment of esophageal varices --- p.33 / Chapter CHAPTER 3 : --- ANIMAL EXPERIMENTS --- p.42 / Chapter 3.1. --- General Materials --- p.42 / Chapter 3.1.1. --- Equipment --- p.43 / Chapter 3.1.2. --- Drugs and chemical --- p.47 / Chapter 3.1.3. --- Laboratory Animals --- p.48 / Chapter 3.1.4. --- Surgical Instruments --- p.49 / Chapter 3.1.7. --- Disposable --- p.49 / Chapter 3.1.8. --- Sutures --- p.49 / Chapter 3.1.9. --- Histopathological Preparation --- p.50 / Chapter 3.2. --- Experiment 1 : Iatrogenic perforation of the rat's stomach by the continues application of the Copper Vapour Laser at different power level --- p.51 / Chapter 3.2.1. --- Introduction --- p.51 / Chapter 3.2.2. --- Methods --- p.52 / Chapter 3.2.3. --- Results --- p.55 / Chapter 3.2.4. --- Discussion --- p.60 / Chapter 3.3. --- Experiment 2 : Obliteration of the rats' mesenteric vein with the Copper Vapour Laser --- p.61 / Chapter 3.3.1. --- Introduction --- p.61 / Chapter 3.3.2. --- Method --- p.62 / Chapter 3.3.3. --- Results --- p.63 / Chapter 3.3.4. --- Discussion --- p.65 / Chapter CHAPTER 4 : --- CONCLUSION --- p.67 / REFERENCES --- p.91

by Tsui, Chi Ping. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 106-119). / Abstract also in Chinese. / ABSTRACT --- p.1 / INTRODUCTION --- p.4 / Chapter 1. --- Portal Hypertension --- p.5 / Chapter 1.1 --- Introduction --- p.5 / Chapter 1.2 --- Anatomy of Normal Portal System --- p.5 / Chapter 1.3 --- Classification and Causes of Portal Hypertension --- p.8 / Chapter 1.4 --- Pathophysiology of Portal Hypertension --- p.9 / Chapter 1.4.1 --- Vascular Change in Portal Hypertension --- p.9 / Chapter 1.4.2 --- Hemodynamic Changes in Portal Hypertension --- p.12 / Chapter 1.4.3 --- Gastric Abnormalities in Portal Hypertension --- p.17 / Chapter 2. --- Somatostatin --- p.22 / Chapter 2.1 --- Introduction --- p.22 / Chapter 2.2 --- Somatostatin Receptors --- p.23 / Chapter 2.3 --- Mechanism of Action --- p.26 / Chapter 2.4 --- Actions of Somatostatin in the Gastrointestinal Tract --- p.28 / Chapter 2.4.1 --- Somatostatin Action in the Stomach --- p.29 / Chapter 2.4.2 --- Somatostatin Action in the Intestine --- p.30 / Chapter 2.4.3 --- Somatostatin Action in the Pancreas --- p.30 / Chapter 2.5 --- Effects of SMT on Hemodynamics in Portal Hypertension --- p.31 / Chapter 2.5.1 --- Splanchnic Circulation --- p.31 / Chapter 2.5.2 --- Systemic Circulation --- p.33 / Chapter 2.5.3 --- Collateral Blood Flow --- p.33 / Chapter 2.5.4 --- Gastric Blood Flow --- p.33 / Chapter 2.6 --- Somatostatin and its analogues in management of acute variceal bleeding --- p.34 / Chapter 3. --- Glucagon --- p.35 / Chapter 3.1 --- Introduction --- p.35 / Chapter 3.2 --- Glucagon Receptor and Mechanism of Action --- p.35 / Chapter 3.3 --- Actions of Glucagon on Circulatory System --- p.38 / Chapter 3.3.1 --- Actions on the Heart --- p.38 / Chapter 3.3.2 --- Vascular Effects --- p.38 / Chapter 3.3.3 --- Hemodynamic Effects --- p.39 / Chapter 3.4 --- Glucagon in Portal Hypertension --- p.40 / Chapter 3.4.1 --- Hyperglucagonemia and portal hypertension --- p.40 / Chapter 3.4.2 --- Hyperglucagonemia and hemodynamic disturbance in portal hypertension --- p.40 / Chapter 4 --- Interaction of somatostatin and glucagon in portal hypertension --- p.41 / Chapter 5. --- Acute Gastric Mucosal Injury --- p.43 / Chapter 5.1 --- Introduction --- p.43 / Chapter 5.2 --- Acute Gastric Mucosal Injury due to Acid and/or Alcohol --- p.43 / Chapter 5.3 --- Gastric Mucosal Defense Mechanisms --- p.45 / Chapter 5.3.1 --- Pre-epithelial Protection --- p.46 / Chapter 5.3.2 --- Epithelial Protection --- p.46 / Chapter 5.3.3 --- Subepithelial Protection --- p.47 / Chapter 5.4 --- Portal Hypertension and Gastric Mucosal Injury --- p.48 / OBJECTIVES --- p.50 / EXPERIMENTAL DESIGN --- p.52 / Chapter 1. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Blood Flow in Portal Hypertension --- p.53 / Chapter 2. --- Effects of Somatostatin and Glucagon on Mucosal Injury Induced by Acid Alcohol in Portal Hypertension --- p.55 / MATERIALS AND METHODS --- p.57 / Chapter 1. --- Induction of portal hypertension --- p.58 / Chapter 2. --- Measurement of blood glucagon levels --- p.60 / Chapter 3. --- "Measurement of Gastric Mucosal Blood Flow, Systemic and Portal Blood Pressures" --- p.62 / Chapter 4. --- Induction of Gastric Mucosal Lesions by Acid Alcohol --- p.65 / Chapter 5. --- Assessment of the Gastric Mucosal Injury after Acid Alcohol Administration --- p.65 / Chapter 6. --- Effects of Somatostatin and Glucagon on Acid Alcohol-Induced Gastric Mucosal Injury --- p.66 / Chapter 7. --- Statistical Analysis --- p.68 / RESULTS --- p.69 / Chapter 1. --- Portal Hypertension Induction by Portal Vein Ligation --- p.70 / Chapter 2. --- Effect of Portal Vein Ligation on Glucagon Level --- p.74 / Chapter 3. --- Effect of Somatostatin and glucagon on Arterial Pressure --- p.77 / Chapter 4. --- Effect of Somatostatin and Glucagon on Portal Pressure --- p.80 / Chapter 5. --- Effect of Somatostatin and Glucagon on Gastric Mucosal Blood Flow --- p.85 / Chapter 8. --- Effect of Somatostatin and Glucagon on Acid Alcohol-induced Gastric Mucosal Injuryin Portal Hypertensive Rats --- p.92 / DISCUSSION --- p.95 / Chapter 1. --- Animal Model --- p.96 / Chapter 2. --- Glucagon Level in Portal Hypertension --- p.98 / Chapter 3. --- Effects of Somatostatin and Glucagon on Systemic and Portal Blood Pressure --- p.99 / Chapter 4. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Blood Flow --- p.102 / Chapter 5. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Injury --- p.103 / CONCLUSION --- p.104 / REFERENCES --- p.106

by Lo Ming Yip. / "July 1998." / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 208-247). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstract in Chinese.

Ng Chau Wah Stephen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 120-135). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.viii / Publications --- p.ix / Abbreviations --- p.x / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Traditional Chinese Medicine --- p.1 / Chapter 1.2 --- Danshen --- p.7 / Chapter 1.2.1 --- Chemical constituents of Danshen --- p.7 / Chapter 1.2.2 --- Pharmacology of Danshen --- p.10 / Chapter 1.3 --- Vascular system --- p.13 / Chapter 1.3.1 --- Physiology of blood vessels --- p.13 / Chapter 1.3.2 --- Vascular smooth muscle contraction --- p.14 / Chapter 1.3.3 --- Mechanism of vascular smooth muscle contraction --- p.15 / Chapter 1.3.3.1 --- Adrenoceptor in vascular system --- p.19 / Chapter 1.3.3.2 --- Muscarinic receptor in vascular system --- p.20 / Chapter 1.3.3.3 --- Synthesis and release of Nitric Oxide (NO)in vascular system --- p.22 / Chapter 1.3.3.4 --- Synthesis and release of postanoidsin vascular system --- p.25 / Chapter 1.3.3.5 --- Synthesis and release of histaminein vascular system --- p.28 / Chapter 1.3.3.6 --- Synthesis and release of Calcitonin gene-related peptide in vascular system --- p.29 / Chapter 1.4 --- Aims of the studies --- p.33 / Chapter Chapter 2 --- Materials and methods / Chapter 2.1 --- Materials --- p.35 / Chapter 2.2 --- Methods - General procedures --- p.35 / Chapter 2.2.1 --- Preparations of drug solutions --- p.35 / Chapter 2.2.2 --- Animals used and anaesthetization --- p.36 / Chapter 2.2.3 --- Cannulation of carotid artery and jugular vein --- p.37 / Chapter 2.2.4 --- Blood pressure measurement --- p.37 / Chapter 2.2.5 --- Knee joint denervation --- p.38 / Chapter 2.2.6 --- Knee joint blood flow measurement --- p.39 / Chapter 2.3 --- Methods - Specific procedures --- p.41 / Chapter 2.3.1 --- Validation of Laser Doppler Imaging (LDI) measurements --- p.41 / Chapter 2.3.2 --- Actions of topical administration of Danshen --- p.42 / Chapter 2.3.2.1 --- Studies of the mechanism(s) of action of Danshen --- p.43 / Chapter 2.3.2.2 --- Investigation for α-adrenoceptor antagonist activity --- p.44 / Chapter 2.3.2.3 --- Investigation for neural involvement --- p.44 / Chapter 2.3.3 --- Actions of intravenous administration of Danshen --- p.45 / Chapter 2.3.4 --- Data analysis --- p.45 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Validation of LDI measurement --- p.47 / Chapter 3.2 --- Actions of intravenous administration of Danshen --- p.53 / Chapter 3.3 --- Actions of topical administration of Danshen --- p.53 / Chapter 3.4 --- Muscarinic receptor antagonist on Danshen --- p.61 / Chapter 3.5 --- β-adrenoceptor antagonist on Danshen --- p.67 / Chapter 3.6 --- Danshen on α-adrenoceptor agonist-induced vasoconstriction --- p.74 / Chapter 3.7 --- Nitric oxide synthase inhibitor on Danshen --- p.79 / Chapter 3.8 --- Cyclo-oxygenase (COX) inhibitor on Danshen --- p.83 / Chapter 3.9 --- Histamine receptor antagonists on Danshen --- p.87 / Chapter 3.10 --- CGRP receptor antagonist on Danshen --- p.92 / Chapter 3.11 --- Effect of denervation on Danshen --- p.92 / Chapter Chapter 4 --- Discussion --- p.100 / Reference --- p.120

Die Durchblutung der Patella beruht auf 2 Zuflüssen. Einerseits Gefäße, welche im mittleren Drittel von ventral über Foramina in die Patella eintreten und außerdem Gefäße, welche am distalen Pol zwischen dem Lig. Patellae und der Gelenkfläche in die Patella eintreten und nach proximal verlaufen. Patellafrakturen können in Längs-, Quer- und Trümmerfrakturen unterteilt werden. Bei Frakturen der Patella kann im Bereich des proximalen Pols eine arterielle Minderversorgung resultieren, wohingegen der distale Pol doppelt versorgt ist und nicht affektiert erscheint. Die arterielle Hypoperfusion kann zu lokalisierten Osteonekrosen führen. Diese lokalen osteonekrotischen Areale können sich radiographisch als hyperdense Areale manifestieren. Im Rahmen dieser Studie sollte das klinische und radiologische Ergebnis nach operativ versorgter Patellafraktur untersucht werden. Dabei wurden 100 Patienten untersucht, die im Zeitraum von 1998 – 2008 operativ versorgt wurden. Davon konnten 60 Patienten im Mittel nach 60.61 ( ± 33.88) Monaten mit einem durchschnittlichen Alter 45.48 ( ± 18.51) Jahren im Rahmen eines Follow-Ups untersucht werden. Dabei wurden mehrere klinische Scores, die Patientenzufriedenheit und die visuelle Analogskala Schmerz erhoben und die vorher angefertigten radiologischen Aufnahmen ausgewertet. Diese wurden auf eventuelle Stufenbildungen, Defekte oder hyperdense Areale hin untersucht. Es zeigte sich bei 9 Patienten (9%) ein hyperdenses Areal im Bereich des proximalen Pols welches durchschnittlich 1 – 2 Monate nach der operativen Versorgung nachgewiesen wurde. Bei 7 Patienten war dieses Areal nach 6 Monaten nicht mehr nachweisbar. Bei 2 Patienten mit bestehenden hyperdensen Arealen konnten diese im Verlauf mittels MRT respektive einer histologischen Untersuchung gesichert werden. Es zeigte sich insgesamt kein signifikanter Unterschied zwischen Patienten ohne radiologische Auffälligkeiten und mit hyperdensen Arealen. Jedoch wurden für die Gruppe mit hyperdensen Arealen im Vergleich tendentiell schlechtere Werte notiert. Radiologisch hyperdense Areale im Bereich des proximalen Pols bei Zustand nach operativer Versorgung einer Patellafraktur können eine Osteonekrose repräsentieren. Eine frühere operative Versorgung bzw. schonendere Operationstechniken könnten die Entstehung von osteonekrotischen Arealen verhindern. Zur Bestätigung dieser Hypothese sind weitere Untersuchungen notwendig.