The exact pathophysiology of hemorrhoidal development is poorly understood. For years the theory of varicose veins, which postulated that hemorrhoids were caused by varicose veins in the anal canal, had been popular but now it is obsolete because hemorrhoids and anorectal varices are proven to be distinct entities. In fact, patients with portal hypertension and varices do not have an increased incidence of hemorrhoids.Today, the theory of sliding anal canal lining is widely accepted. This proposes that hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate. Hemorrhoids are therefore the pathological term to describe the abnormal downward displacement of the anal cushions causing venous dilatation. There are typically three major anal cushions, located in the right anterior, right posterior and left lateral aspect of the anal canal, and various numbers of minor cushions lying between them. The anal cushions of patients with hemorrhoids show significant pathological changes. These changes include abnormal venous dilatation, vascular thrombosis, degenerative process in the collagen fibers and fibroelastic tissues, distortion and rupture of the anal subepithelial muscle. In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia, and thrombosis.Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. Among these, matrix metalloproteinase (MMP), a zinc-dependent proteinase, is one of the most potent enzymes, being capable of degrading extracellular proteins such as elastin, fibronectin, and collagen. MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. Activation of MMP-2 and MMP-9 by thrombin, plasmin, or other proteinases resulted in the di 1. Language: English. Narrator: Trevor Clinger. Audio sample: http://samples.audible.de/bk/acx0/189889/bk_acx0_189889_sample.mp3. Digital audiobook in aax.
Mullerian duct anomalies are generally rare clinical conditions that results from disruption during the development of the female internal duct system which include the fallopian tubes, uterus ,cervix and the upper portion of the vagina. In most cases most of the anomalies involve the uterus , cervix and upper vaginal. Uterine malformations result from failure in organogenesis or from fusion or reabsorption of the Müllerian ducts. Failures in organogenesis are related to incomplete development of one or both Müllerian ducts, thereby leading to agenesis, uterine hypoplasia or a unicornuate uterus. The causes of Müllerian anomalies have yet to be fully identified and clarified. The karyotypes are normal in most cases though in few patients abnormal karyptype has been described. Fusion defects result from incomplete merging of the caudal portion with the Müllerian ducts (lateral fusion) or incomplete merging of the structures of the urogenital sinus with the Müllerian tubercle (vertical fusion). Failures in lateral fusion may result in uterus didelphys, bicornuate uterus or arcuate uterus. When the defect occurs in vertical fusion, anomalies such as imperforate hymen.
High Quality Content by WIKIPEDIA articles! Wallis Zieff Goldblatt syndrome is a rare condition characterized by inherited skeletal disorders manifested mainly as rhizomelic short stature and lateral clavicular defects. It is also known as Cleidorhizomelic Syndrome.An initial clinical report of this syndrome describes a 6-month-old boy with rhizomelic shortening, particularly in the arms, and protuberances over the lateral aspects of the clavicles. On radiographs the lateral third of the clavicles had a bifid appearance resulting from an abnormal process or protuberance arising from the fusion center. His 22-year-old mother also had a height of 142 cm with an arm span of 136 cm and rhizomelic shortness of the limbs, maximal in the arms, and abnormalities of the acromioclavicular joints. Both the mother and the son had marked bilateral clinodactyly of the fifth fingers associated with hypoplastic middle phalanx.
In this book, two lateral load patterns existing in the FEMA-365 code (the uniform and triangular lateral load patterns) are evaluated.Afterwards, lateral load patterns, high-rise, mid-rise and low-rise structures are considered, load patterns of other structures such as bridges are referred to and other load patterns which have been previously proposed by other researchers are studied. Effects of these load patterns on the results are also discussed in detail. Moreover, a new lateral load pattern is offered for nonlinear static analysis of structural models.This book consists of six chapters: Chapter One: Introduction, Chapter Two: Materials, modeling samples, Chapter Three: Analysis methods and earthquake records, Chapter Four: Types of lateral load distribution patterns, Chapter Five: Evaluation and interpretation of results, Chapter Six: Conclusion
This book delineates the state of the art of the diagnosis and treatment of J wave syndromes, as well as where future research needs to be directed. It covers basic science, translational and clinical aspects of these syndromes. The authors are leading experts in their respective fields, who have contributed prominently to the literature concerning these topics.J wave syndromes are one of the hottest topics in cardiology today. Cardiac arrhythmias associated with Brugada syndrome (BrS) or an early repolarization (ER) pattern in the inferior or infero-lateral ECG leads are thought to be mechanistically linked to accentuation of transient outward current (Ito)-mediated J waves. Although BrS and ER syndrome (ERS) differ with respect to magnitude and lead location of abnormal J waves, they are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. ERS is divided into three subtypes with the most severe, Type 3, displaying an ER pattern globally in the inferior, lateral and right precordial leads. BrS has been linked to mutations in 19 different genes, whereas ERS has been associated with mutations in 7 different genes.There is a great deal of confusion as to how to properly diagnose and treat the J wave syndromes as well as confusion about the underlying mechanisms. The demonstration of successful epicardial ablation of BrS has provided new therapeutic options for the management of this syndrome for which treatment alternatives are currently very limited, particularly in the case of electrical storms caused by otherwise uncontrollable recurrent VT/VF. An early repolarization pattern is observed in 2-5% of the US population. While it is clear that the vast majority of individuals exhibiting an ER pattern are not at risk for sudden cardiac death, the challenge moving forward is to identify those individuals who truly are at risk and to design safe and effective treatments.
This book presents much of the exciting new information on mechanisms of neurodegenerative disorders that was presented at the XVth International Spring Symposium on Health Sciences at George Washington University in Washington, D.C. The organization of the symposium as weIl as the chapters within this book were based upon fundamental molecular and cellular mechanisms of neurodegeneration rather than upon different clinically defined disorders, in order to emphasize the commonality of cause rather than effect. The first part of the book is devoted to the relationships between selective vulnerability of different neuronal cell types to injury and their functional characteristics related to the transport, binding, and responses for excitatory amino acids, e.g., glutamate, as weIl as other neurotransmitters involved in toxicity. These relationships are studied in the context of neurodegeneration associated with several disorders including Parkinson's disease, amyotrophic lateral sclerosis (ALS), cerebral ischemia, and AIDS dementia. Part 11 emphasizes the role of amyloid proteins in neurodegeneration but also covers other molecular and genetic risk factors, e.g., expression of different apo lipoprotein isoforms and the involvement of abnormal superoxide dismutase in neuropathology. These topics are applied primarily to the aging brain, Alzheimer's disease, and ALS.
This book provides basic information about the relatively new and evolving technology -positron emission tomography- for its clinical applications and practical guidance for the referring physicians. Chapters cover application of PET in various clinical settings including oncology, cardiology, and neurology with a focus on role in various cancers. Because most of the new PET equipments come as hybrid machines with CT or MRI, two chapters have been included at the end of the book to provide basic and comprehensive information about these two technologies.Molecular imaging is going to revolutionize the way we practice medicine in the future. It will lead to more accurate diagnosis of diseases and its extent which will lead to better management and better outcomes. In the history of medicine no imaging modality has ever become so popular for use in such a short time as has the PET technology. PET imaging is mostly used in oncology, neurology and cardiology but also finds application in other situations such as infection imaging. The main focus, of course, is in management of cancer patients. PET (PET-CT) is not only very sensitive as it can detect changes in abnormal biochemical processes at cellular level but in one go all such areas can be detected in a whole body scan. It can show response to therapy, eradication of the disease or recurrence during the follow-up period. One of the main differences between a PET scan and other imaging tests like CT scan or MRI is that the PET scan reveals the cellular level metabolic changes occurring in an organ or tissue. This is important and unique because disease processes begin with functional changes at the cellular level. A PET scan can detect these very early changes whereas a CT or MRI detect changes much later as the disease begins to cause changes in the structure of organs or tissues. Some cancers, especially lymphoma or cancers of the head and neck, brain, lung, colon, or prostate, in very early stage may show up more clearly on a PET scan than on a CT scan or an MRI. A PET scan can measure such vital functions as blood flow, oxygen use, and glucose metabolism, which can help to evaluate the effectiveness of a patient's treatment plan, allowing the course of care to be adjusted if necessary.Apart from its vital role in oncology it can estimate brain's blood flow and metabolic activity. A PET scan can help finding nervous system problems, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, transient ischemic attack (TIA), amyotrophic lateral sclerosis (ALS), Huntington's disease, stroke, and schizophrenia. It can find changes in the brain that may cause epilepsy. PET scan is also increasingly being used to find poor blood flow to the heart, which may mean coronary artery disease. It can most accurately estimate the extent of damage to the heart tissue especially after a heart attack and help choose the best treatment, such as coronary artery bypass graft surgery, stenting or medical treatment. It can also contribute significantly in identifying areas exactly where radiotherapy is to be targeted avoiding unnecessary radiation exposure to surrounding tissue.