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Characterisation of inflammatory responses in two models of experimental ischaemiaMarks, Louise January 2001 (has links)
No description available.
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The blood supply of the human spinal cord at birth: a report on a micro-dissection study of 27 foetal and neonate cadaversDommisse, George Frederick 06 April 2020 (has links)
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.
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Aplicação de técnicas sorológicas e moleculares na detecção de Leishmania em doadores de sangue na cidade de Salvador, Bahia. / Aplicação de técnicas sorológicas e moleculares na detecção de Leishmania em doadores de sangue na cidade de Salvador, BahiaFukutani, Kiyoshi Ferreira January 2011 (has links)
Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2012-07-20T21:20:40Z
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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.
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A system for the acquisition and digital analysis of lower limb flow waveformsSmith, Leonard January 1994 (has links)
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).
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Neurovascular lesions and mechanisms in suicidal hanging: an anatomical, physiological and pathological studyMoar, Jacob Joseph 25 April 2013 (has links)
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.
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Application of copper vapour laser in gastrointestinal tract-experimental studies in animal models.January 1994 (has links)
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
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Effects of somatostatin and glucagon on portal pressure, gastric mucosal blood flow and gastric mucosal injury in portal hypertension.January 1998 (has links)
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
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The role of prostaglandins, nitric oxide and neuropeptides in the regulation of synovial blood flow. / CUHK electronic theses & dissertations collectionJanuary 1998 (has links)
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.
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A study on the mechanisms of danshen-induced vasodilatation in the rat.January 2003 (has links)
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
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Klinische und radiologische Ergebnisse nach operativ versorgter Patellafraktur / Clinical and radiological results after surgical treatment of patella fracturesBehzadi, Cyrus 04 November 2013 (has links)
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.
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