by Chan Pui Chung, Denise. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 119-135). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT --- p.iii / ABSTRACT (CHINESE VERSION) --- p.v / TABLE OF CONTENTS --- p.vi / LIST OF TABLES --- p.x / LIST OF FIGURES --- p.xii / LIST OF ABBREVIATIONS --- p.xiv / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Biology of Human Papillomaviruses --- p.2 / Chapter 1.1.1 --- Taxonomy --- p.2 / Chapter 1.1.2 --- Genomic organisation --- p.2 / Chapter 1.1.3 --- "Types, subtypes and variants" --- p.4 / Chapter 1.2 --- Epidemiology of cervical cancers --- p.6 / Chapter 1.2.1 --- Incidence --- p.8 / Chapter 1.2.2 --- Cervical cancers screening programme --- p.10 / Chapter 1.3 --- Association between human papillomavirus and cervical cancers --- p.11 / Chapter 1.3.1 --- Infection --- p.11 / Chapter 1.3.2 --- Multistep pathogenesis of cervical cancers --- p.13 / Chapter 1.3.3 --- Geographical distribution --- p.14 / Chapter 1.3.4 --- Age distribution of HPV infection --- p.15 / Chapter 1.3.5 --- Oncogenic property of HPV --- p.15 / Chapter 1.3.6 --- Sequence variation --- p.20 / Chapter 1.4 --- Project design --- p.23 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.25 / Chapter 2.1 --- Evaluation of HPV DNA extraction methods for paraffin-embedded tissues --- p.26 / Chapter 2.1.1 --- Study population --- p.26 / Chapter 2.1.2 --- Paraffin-embedded tissue collection --- p.26 / Chapter 2.1.3 --- DNA extraction --- p.26 / Chapter 2.1.3.1 --- Phenol-chloroform extraction --- p.27 / Chapter 2.1.3.2 --- Microwave extraction --- p.28 / Chapter 2.1.3.3 --- QIAGEN spin column extraction --- p.28 / Chapter 2.1.4 --- PCR amplification --- p.29 / Chapter 2.1.4.1 --- PCR amplification for human beta-globin gene --- p.29 / Chapter 2.1.4.2 --- PCR amplification for HPV DNA --- p.30 / Chapter 2.1.5 --- Optimisation of PCRs --- p.30 / Chapter 2.1.5.1 --- Optimisation of beta-globin PCRs --- p.30 / Chapter 2.1.5.2 --- Optimisation of HPV PCRs --- p.31 / Chapter 2.1.5.3 --- Analytical sensitivity of PCRs --- p.31 / Chapter 2.1.5.3.1 --- Analytical sensitivity of beta-globin PCRs --- p.31 / Chapter 2.1.5.3.2 --- Analytical sensitivity of HPV PCRs --- p.32 / Chapter 2.1.5.4 --- Detection of PCR products --- p.32 / Chapter 2.1.6 --- PCR evaluation of DNA extraction methods --- p.33 / Chapter 2.1.6.1 --- Beta-globin PCRs --- p.33 / Chapter 2.1.6.2 --- HPV PCRs --- p.33 / Chapter 2.1.6.2.1 --- MY09/MY11 PCR --- p.33 / Chapter 2.1.6.2.2 --- GP5+/GP6+ PCR --- p.34 / Chapter 2.1.6.3 --- Detection of PCR products --- p.34 / Chapter 2.2 --- Prevalence and genotype distribution of HPV --- p.35 / Chapter 2.2.1 --- Study populations --- p.35 / Chapter 2.2.1.1 --- Women with normal cervices --- p.35 / Chapter 2.2.1.2 --- Women with abnormal cervical cytologies --- p.35 / Chapter 2.2.1.3 --- Women with cervical cancer --- p.35 / Chapter 2.2.2 --- Disease classification --- p.36 / Chapter 2.2.3 --- Specimen collection and preparation --- p.36 / Chapter 2.2.3.1 --- Cervical scrape collection --- p.36 / Chapter 2.2.3.1.1 --- DNA extraction --- p.37 / Chapter 2.2.4 --- HPV DNA detection --- p.37 / Chapter 2.2.4.1 --- MY09/MY11 PCR --- p.38 / Chapter 2.2.4.2 --- GP5+/GP6+ PCR --- p.38 / Chapter 2.2.4.3 --- Detection of PCR products --- p.38 / Chapter 2.2.5 --- HPV genotyping --- p.39 / Chapter 2.3 --- Sequence variation of HPV 16 E7 gene --- p.39 / Chapter 2.3.1 --- Study population --- p.39 / Chapter 2.3.2 --- Optimisation of HPV 16 E7 nested PCR --- p.40 / Chapter 2.3.3 --- HPV 16 E7 nested PCR --- p.41 / Chapter 2.3.3.1 --- Detection of PCR products --- p.42 / Chapter 2.3.4 --- Purification of nested PCR products --- p.42 / Chapter 2.3.5 --- Direct cycle sequencing --- p.42 / Chapter 2.3.5.1 --- Cycle sequencing reaction --- p.42 / Chapter 2.3.5.2 --- Purification of cycle sequencing products --- p.43 / Chapter 2.3.5.3 --- Electrophoresis on DNA sequencer --- p.43 / Chapter 2.3.6 --- Data analysis --- p.44 / Chapter 2.4 --- Statistical methods --- p.44 / Chapter CHAPTER 3 --- RESULTS --- p.45 / Chapter 3.1 --- Evaluation of HPV DNA extraction methods for paraffin-embedded tissues --- p.46 / Chapter 3.1.1 --- Optimised conditions for beta-globin PCRs --- p.46 / Chapter 3.1.2 --- Optimised conditions for HPV PCRs --- p.47 / Chapter 3.1.3 --- Analytical sensitivity of beta-globin and HPV PCRs --- p.48 / Chapter 3.1.4 --- PCR evaluation of DNA extraction methods --- p.48 / Chapter 3.1.4.1 --- PC03/PC07 PCRs --- p.48 / Chapter 3.1.4.2 --- Beta-GPl/Beta-GP2 PCRs --- p.49 / Chapter 3.1.4.3 --- HPV PCRs --- p.49 / Chapter 3.2 --- Prevalence and genotype distribution of HPV --- p.50 / Chapter 3.2.1 --- HPV detection --- p.50 / Chapter 3.2.2 --- HPV typing --- p.50 / Chapter 3.2.3 --- Women with normal cervices --- p.51 / Chapter 3.2.4 --- Women with abnormal cervical cytologies --- p.51 / Chapter 3.2.5 --- Women with cervical cancer --- p.53 / Chapter 3.3 --- Sequence variation of HPV 16 E7 gene --- p.54 / Chapter 3.3.1 --- Optimised conditions for HPV 16 E7 nested PCR --- p.54 / Chapter 3.3.2 --- HPV 16 E7 sequencing --- p.55 / Chapter 3.3.3 --- HPV 16 E7 variants --- p.55 / Chapter 3.3.4 --- Distribution of HPV 16 E7 variants --- p.56 / Chapter CHAPTER 4 --- DISCUSSION --- p.58 / Chapter 4.1 --- Evaluation of HPV DNA extraction methods for paraffin-embedded tissues --- p.59 / Chapter 4.1.1 --- PCR evaluation of DNA extraction methods --- p.59 / Chapter 4.2 --- Prevalence and genotype distribution of HPV --- p.61 / Chapter 4.2.1 --- Women with normal cervices --- p.61 / Chapter 4.2.2 --- Women with abnormal cervical cytologies --- p.62 / Chapter 4.2.3 --- Women with cervical cancer --- p.64 / Chapter 4.3 --- Sequence variation of HPV 16 E7 gene --- p.64 / Chapter CHAPTER 5 --- CONCLUSION --- p.69 / REFERENCES --- p.119

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L’infection congénitale à CMV est la première cause de retard psychomoteur et de surdité, toutes causes confondues. En France, la prévalence de l’infection congénitale à CMV en France est estimée entre 0,6 et 0,7%. Parmi les enfants présentant une infection symptomatique, 10-20% des nourrissons font une forme sévère et décèdent, et 50 à 60% développent des lésions cérébrales avec un handicap neurologique parfois lourd consécutif à une microcéphalie, des calcifications intracrâniennes, des dilatations ventriculaires ou des convulsions. Certains parmi ceux-ci développeront aussi des séquelles neurosensorielles consécutives à une atteinte visuelle, auditive ou vestibulaire. La première partie de ce travail permet de décrire l’histoire et la physiopathologie des lésions de l’oreille interne chez l’homme. Les lésions de l’oreille interne sont évaluées chez 6 fœtus ayant une infection congénitale à CMV, âgés de 21 à 35 semaines d’aménorrhée, et corrélées aux atteintes centrales et viscérales. Dans la cochlée, les lésions prédominent au niveau de la strie vasculaire alors que l’infection est moins fréquente au niveau des cellules de l’organe de Corti. Les lésions vestibulaires sont plus florides que les lésions cochléaires et prédominent au sein de l’épithélium non sensoriel, en particulier des cellules sombres du saccule et de l’utricule, et de l’épithélium des canaux semi-circulaires. Ces lésions du compartiment endolymphatique de l’oreille interne pourraient être responsables d’une altération de la sécrétion du potassium et ainsi d’une modification de l’homéostasie de la cochlée et du vestibule par atteinte de la strie vasculaire et des cellules sombres. Secondairement, cela pourrait être responsable d’une dégénérescence de l’organe de Corti et des organes sensoriels vestibulaires. La survenue de la surdité neurosensorielle et de l’atteinte vestibulaire dépend très certainement de la durée et de l’intensité de l’infection virale et de l’inflammation. La deuxième partie de ce travail analyse les atteintes du système nerveux central qui n'ont pas fait l'objet d'étude détaillée. Nous avons sélectionné 9 fœtus de 23 SA à 38 SA dont la gestation a été interrompue devant une suspicion d’infection congénitale par le CMV. Ils ont été étudiés sur le plan foetopathologique standard, neuropathologiques, immunohistochimiques et morphométriques. La réplication virale productive prédomine dans le cortex et dans la région périventriculaire. Le virus infecte préférentiellement les cellules GFAP-positive et nestine-positive, mais aussi à un moindre degré les neurones, les cellules endothéliales et la microglie. La réaction immune microgliale et cellulaire cytotoxique semble insuffisante pour contrer l’importance de la dissémination virale suggérant son immaturité. Les malformations corticales sont de mécanismes variés et il existe une atteinte préalablement méconnue des bulbes olfactifs. Une troisième partie est consacrée au développement d’un modèle murin d’infection congénitale par le CMV visant à mieux comprendre les mécanismes physiopathologiques d'atteintes auditives et vestibulaires et à définir les modalités thérapeutiques. Les souriceaux infectés par injection intra-amniotique de virus MCMV développent une surdité dont le profil évolutif s’apparente à la clinique humaine. Les lésions histologiques se caractérisent par des atteintes de la strie vasculaire, de l’organe de Corti et du ganglion spiral. Ces différents axes de recherche complémentaires permettent de comprendre les mécanismes centraux et périphériques participant aux handicaps neurosensoriels chez les enfants atteints d’infection congénitale par le CMV. Les études cliniques et physiopathologiques complémentaires qui en découlent permettront d'affiner les cascades lésionnelles mis en jeu et d'optimiser la prise en charge de ces enfants / Congenital CMV infection is the leading cause of mental retardation and neurosensory-hearing loss. In France, the prevalence of congenital CMV infection is estimated between 0.6 and 0.7%. Amongst the children presenting with a symptomatic infection,10-20% of newborns will have a severe manifestation and die and 50-60% will develop cerebral lesions with a neurological handicap due to microcephaly, intracranial calcifications, ventricular dilations or convulsions. Some amongst these will also develop neurosensory sequelae such as visual, auditory or vestibular lesions. The first part of this work describes the history and the physiopathology of the inner ear lesions in human. The lesions were evaluated in 6 fetuses presenting with a congenital CMV infection, aged 21 to 35 gestational weeks and correlated to central and visceral lesions. In the cochlea, the lesions predominated in the stria vascularis whereas the lesions were les frequent in the organ of Corti. The vestibular lesions were more florid than cochlear lesions and predominated in the non-sensory epithelium in particular the dark cells of the saccula and the utricule and the epithelium of the semi-circular canals. These lesions of the endolymphatic compartment may be responsible of the alteration of the potassium secretion in the inner ear and therefore a modification of the homeostasis of the cochlea and the vestibule by lesion of the stria vascularis and the dark cells. With time, this could be responsible of the degeneration of the organ of Corti and of the vestibular sensory organs. The onset of neurosensory hearing loss and vestibular disorder probably depend upon the duration and the intensity of viral infection and inflammation. The second part of this work analyses the central nervous system lesions that have seldom been detailed. We have selected 9 fetuses aged 23-28 gestational weeks whose pregnancy has been interrupted due to congenital CMV infection. Standard fetopathological examination was completed with neuropathological, immunohistochemical and morphometric assessment. Viral replication predominated in the cortex and in the periventricular zone. The virus infects preferentially GFAP positive and nestin positive cells, but also, to a lesser degree, neurons, endothelial cells and microglia. Immune microglial and cytotoxic cellular responses seem insufficient to counter the importance of the viral dissemination suggesting immaturity. Cortical malformations are due to several mechanisms and olfactory bulbs are frequently infected. The third part describes the development of a murine model for congenital CMV infection in order to better understand the physiopathological mechanisms of the auditory and vestibular lesions and to define the guidelines for management. Infected newborn mice developed neurosensory-hearing loss with characteristics similar to human deafness. Histological lesions were mainly observed in the stria vascularis, the organ of Corti and the spiral ganglia. These different complementary research axes led to a better understanding of the central and peripheral mechanisms participating in the neurosensory handicaps of children with congenital CMV infection. Further clinical and physipathogical studies will allow a more precise comprehension of the lesional cascades and a optimization of the medical management of these children

Lacunar stroke accounts for one quarter of all ischaemic stroke and in the long term carries a greater risk of death and disability than was previously realised. Much of our current knowledge originated from neuropathological studies in the 1950s and 1960s. In the last thirty years, brain computed tomography (CT) and magnetic resonance imaging (MRI) have revolutionised our understanding of lacunar stroke and associated features of cerebral small vessel disease (SVD), namely white matter lesions (WML), enlarged perivascular spaces (EPVS) and brain microbleeds (BMB). The purpose of the projects which led to the writing of this thesis was to improve understanding of imaging characteristics of cerebral SVD. We aimed to assess (i) clinical and imaging features which might explain misclassification of lacunar infarcts as cortical infarcts and vice versa, (ii) the proportion of symptomatic lacunar infarcts progressing to lacunar cavities and associations of cavitation, (iii) completeness of reporting of lacunar lesions in the lacunar stroke literature, (iv) definitions and detection of lacunar lesions amongst SVD researchers, (v) the relationship between WML and carotid stenosis, (vi) clinical and imaging associations of EPVS and, (vii) observer variability in the assessment of EPVS and BMB, in order to develop visual rating scales. Section one describes neuroimaging of lacunar stroke. To investigate features which might explain clinical stroke subtype misclassification (‘clinical-imaging dissociation’), I used data from a stroke study. The main factor associated with clinical-imaging dissociation was diabetes, and in patients with acute lacunar infarction, proximity of the lacunar infarct to the cortex, age, diabetes and left hemisphere location. To investigate the proportion of symptomatic lacunar infarcts progressing to cavities, I used data from two stroke studies. A fifth of patients with acute lacunar ischaemic stroke showed definite cavitation on follow-up imaging at a median of 227 days; cavitation was associated with increasing time to follow-up. To assess completeness of reporting of lacunar lesions in the lacunar stroke literature, I reviewed 50 articles from three journals with a stroke focus. There was marked variation in terminology and descriptions of imaging definitions of lacunar lesions. To assess lacunar lesion definitions and detection amongst SVD researchers, I used an online survey consisting of case-based and non-case-based questions. There was marked variation in definitions and descriptions. Cavitated lesions were detected with the highest degree of confidence. Section two describes neuroimaging of associated features of cerebral SVD. Using data from two stroke studies, I examined the relationship between WML and ipsilateral carotid artery stenosis. There was no association between carotid stenosis and WML. I tested the association of EPVS with WML and lacunar stroke subtype using data from a stroke study. Total EPVS were associated with age and deep WML; basal ganglia (BG) EPVS were associated with age, centrum semiovale (CS) EPVS, cerebral atrophy and lacunar stroke subtype. Quantification of observer variability in EPVS rating was assessed on 60 MRI scans selected from a stroke study and an ageing cohort. Intrarater agreement was good and interrater agreement was moderate. Main reasons for interrater disagreement included the visualisation of very small EPVS and the presence of concomitant WML and lacunar lesions. Observer variability in BMB rating was quantified using MRI scans from a stroke study. Interrater agreement was moderate but improved following modification of the pilot rating scale (BOMBS; Brain Observer MicroBleed Scale), which had its main effect by differentiating ‘certain’ BMB from ‘uncertain’ BMB and BMB ‘mimics’. In conclusion, neuroimaging, particularly MRI, is a valuable tool for the investigation of lacunar stroke and associated features of cerebral SVD. With recent technological advances in both CT and MRI, neuroimaging will remain central to future SVD studies, hopefully leading to a much improved understanding of this important disease.

Background: Feeding alfalfa hay is often recommended for its buffering components, like protein and calcium, to prevent lesions of the gastric mucosa in horses. Until now, there has been no information regarding the influence of alfalfa particle size on the gastric mucosa. The aim of this study was to investigate the effects of feeding two alfalfa preparations with different particle sizes (alfalfa chaff vs alfalfa pellets) in comparison with grass hay on the gastric mucosa in weanling horses. We hypothesized that feeding a high proportion of fine alfalfa particles would negatively impact gastric mucosa and that feeding long alfalfa chaff would improve gastric mucosal health in weanlings. Results: Before weaning, the prevalence of gastric mucosa lesions (one or more lesions considering all locations in the stomach) was 84.3 %; at 14 days after weaning, it was almost 100 %. Before and after weaning, most of the lesions were found at the greater curvature of the squamous mucosa and at the lesser curvature. After weaning, gastric mucosal lesions at the pylorus were significantly more severe in the group fed alfalfa chaff (p = 0.002). In the other regions, no differences related to the feeding regimes were observed. Conclusions: Feeding alfalfa failed to improve gastric mucosal lesion scores in weanlings. Furthermore, foals fed alfalfa chaff had higher lesion scores at the pylorus. Alfalfa leaves contain a superior protein source and high amounts of calcium and magnesium, providing extra nutritional advantages in growing horses. At this time, either traditional grass hay rations or grass hay with alfalfa pellets can be recommended.

Bone bruise lesions (BBL) are documented on MRIs diagnosing acute knee ligament injury (AKLI). Recent evidence has indicated that a majority of patients that sustain an AKLI, especially anterior cruciate ligament (ACL) knee injury, will develop post-traumatic osteoarthritis (PTOA) 10-20 years following injury. It has been proposed that the initial damage sustained to the articular cartilage overlying BBL causes a cascade of events that may result in PTOA. Researchers have proposed a modification to treatment protocols for more severe BBL, or have stressed the need for the development of protective therapies to protect the articular cartilage. However, there are limited tools available to evaluate the clinical outcome of articular cartilage overlying BBL. Furthermore, damage to the cartilage overlying BBL may be different according to differing BBL severities. Therefore, the use of a cartilage degradation biomarker, serum cartilage oligomeric matrix protein (sCOMP) and the use of a BBL severity classification system may be useful to determine if differences exist between patients with and without BBL, and with differing BBL severities. The purpose of this dissertation was to investigate the utility of sCOMP as a biomarker for acute articular cartilage damage. The purposes of these studies were to determine the inter and intraday reliability of this marker, to document sCOMP longitudinally in collegiate athletes and following AKLI, and to determine if differences in sCOMP and self-reported pain and function exist for patients with and without BBL, and differing BBL following AKLI. The results of these studies indicated sCOMP measures had strong inter and intraday reliability. Additionally, exercise does seem to influence sCOMP levels; however, these elevations may not be clinically meaningful. Furthermore, sCOMP levels were not different between patients with BBL and without, and between differing BBL severities. The results of these studies support the use of a BBL severity classification for future research studies in order to further elucidate the outcomes of these lesions.

Nucleotide excision repair (NER) is one of the major repair systems for removal of DNA lesions. The NER pathway has evolved mainly to repair UV-induced DNA damage and is also active against a broad range of endogenously generated oxidative lesions. Defects in NER result in the human inherited disorder xeroderma pigmentosum (XP), which is characterised by UV hypersensitivity and a 1000-fold increased risk of skin cancer. ERCC1 is essential for the NER pathway where it acts in a complex with the XPF protein to make the incision 5' to the DNA lesion. The normal 1.1kb Ercc1 transcript is expressed in all tissues. Our group has discovered a second larger 1.5 kb transcript, which initiates from an alternative promoter, and is the most abundant Ercc1 transcript in mouse skin. The aims of this project were: 1, To investigate the role of ERCC1 and of the 1.5kb skin specific Ercc1 transcript in protecting the skin against UV-induced DNA damage. 2, To study the importance of ERCC1 in melanoma skin cancer and investigate ERCC1as a possible target for therapy against melanoma. Using a panel of Ercc1 wild-type and deficient cells, we established a quantitative western blotting system to study the expression of ERCC1 in a range of mouse tissues and mouse and human cell types. Although the skin-specific Ercc1 transcript was found to be present at much higher levels in the skin of albino compared to pigmented mouse strains, this did not result in an elevated level of ERCC1 protein. We were also unable to demonstrate that UV-irradiation, or other stress-inducing treatments resulted in increased levels of ERCC1 protein in cultured mouse keratinocytes. We investigated the DNA methylation status of the normal Ercc1 promoter and that of two potential upstream promoter regions that were candidates for the source of the 1.5kb skin-specific Ercc1 transcript. We found no evidence that they were the source and, instead, used 5' RACE analysis to locate the skin-specific promoter to a polymorphic region 500bp upstream of the normal initiation site. In albino strains this region contains a SINE element, which we hypothesize could be involved in the production of the skin-specific Ercc1 transcript. We also investigated the protein level of ERCC1 and other DNA repair proteins, including XPF, MSH2, MSH6 and MLH1 in human melanoma cells and ovarian tumour cells. Significantly elevated protein levels of ERCC1 and XPF, as well as the mismatch repair protein MLH1 were found in melanoma cells. This could possibly contribute to the higher resistance to chemotherapy in melanoma, although the melanoma cell lines we tested did not show increased resistance to UV and cisplatin compared to the ovarian cancer cells tested. When Ercc1 proficient mouse melanoma cells were xenografted into nude mice the xenografts grew rapidly. Cisplatin treatment caused an initial shrinkage of the tumours, but re-growth rapidly followed. Cells re-isolated into culture from cisplatin treated xenografts had significantly higher levels of ERCC1 protein than either input cells, or cells re-isolated from untreated xenografts. An isogenic Ercc1 deficient derivative of the Ercc1 proficient mouse melanoma cell line grew as rapidly as the parent line in vitro, but grew much more slowly as xenografts. In addition, the xenografts shrank completely following cisplatin treatment and did not recover. This suggests that ERCC1 could be a drug target for melanoma therapy.

Studies on work-related skeletal lesions are a vital part of answering questions about how animals were used by prehistoric populations. In Sweden, this sort of research has mainly been done on cattle. Horse (equus) bones are simply to uncommon to find and the osteometric methods are severely lacking. This essay aims to use previous Swedish as well as foreign research on the subject, as a basis for a new study focusing on horse bones from different contexts. The aim is to find indications of whether or not the relationship between humans and horses has affected the way these animals were treated, and later disposed of after death. A new perspective of theory and methodology will be used to tackle the problems that have previously haunted osteological research on horse bones. By combining osteological analysis and microarchaeology the goal is to reach for information that in the past has been hard to come by.  Swedish osteology needs to step out of its comfort zone and start looking at animal bones as more than a statistic foundation.

OBJETIVO: presentar la experiencia en lesiones vasculares del tracto digestivo superior en los años 2007-2008 en el Hospital Daniel Alcides Carrion. METODOLOGÍA: Estudio descriptivo transversal. Se revisaron todas las endoscopias realizadas en el periodo señalado. Se consignaron las lesiones vasculares encontradas. Se utilizo la Clasificación de la OMED para lesiones vasculares. RESULTADOS: Se revisaron 1,979 exámenes. Se encontraron 26 lesiones vasculares (Prevalencia=13.13/1,000 endoscopias). La localización mas frecuente (65,4%) en estomago. El tipo de lesión más común fue la angiectasia vascular (57,7%). CONCLUSIÓN: Las lesiones vasculares del tracto digestivo superior son poco frecuentes, son mas comunes en estomago y las angiectasias vasculares son las mas frecuentemente reportadas. / To display the experience of vascular lesions in the upper digestive tract in 2007-2008 at Daniel Alcides Carrión Hospital. METHODOLOGY: Transverse study. All endoscopies performed in the indicated period were reviewed. Vascular lesions found were record. The OMED classification for vascular lesions was used in this research. RESULTS: 1.979 examinations were reviewed. 26 vascular injuries were found (prevalence = 13.13/1000 endoscopies). The most frequent location was in stomach (65.4%). The most common type of injury was vascular angiectasia(57.7%). CONCLUSION: Vascular lesions in the upper digestive tract were rare; these lesions were more common in the stomach. Vascular angiectasias were the most frequently reported

Serotonin has been implicated as a modulator of feeding behavior. This experiment was designed to alter brain serotonin levels through dietary means in hypothalamic ventromedial-lesioned and unlesioned rats. Daily food, water, and animal weights were measured. The purpose was to determine if VMH lesions altered the feeding pattern found in unlesioned rats. Although food intake for tryptophanenriched diets and tryptophan-deficient diets did not differ from their respective control groups, in some cases gross animal weights did differ significantly between experimental and control groups and between lesioned and unlesioned groups. A proposed model explains how a "low" energy signal and a "high" protein signal cycles amino acids through gluconeogenesis to comPensate for an energy deficit.