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THE MODERN ASPECTS OF ETIOLOGY, PATHOGENESIS AND CLINICAL PRESENTATIONS OF PYODERMA
Pilugin S.M.
Annals of Mechnikov's Institute , 2013,
Abstract: The necessity of study of pyogenic skin infection is pre-sented in the article. The modern aspects of etiology,pathogenesis and clinical presentations of different formsof pyoderma (deep and superficial) are described.
Disorders of cerebrovascular angioarchitectonics and microcirculation in the etiology and pathogenesis of Alzheimer’s disease  [PDF]
Ivan V. Maksimovich
Advances in Alzheimer's Disease (AAD) , 2013, DOI: 10.4236/aad.2013.24022
Abstract: There have recently appeared many reports dedicated to cerebral hemodynamics disorders in AD. However, certain specific aspects of cerebral blood flow and microcirculation during this disease are not fully understood. This research focuses on the identification of particular features of cerebral angioarchitectonics and microcirculation at preclinical and clinical AD stages and on the determination of their importance in AD etiology and pathogenesis. 164 patients participated in the research: Test Group—81 patients with different AD stages; Control Group— 83 patients with etiologically different neurodegenerative brain lesions with manifestations of dementia and cognitive impairment but without AD. All patients underwent: assessment of cognitive function (MMSE), severity of dementia (CDR) and AD stages (TDR), laboratory examination, computed tomography (CT), magnetic resonance imaging (MRI), brain scintigraphy (SG), rheoencephalography (REG) and cerebral multigated angiography (MUGA). All Test Group patients, irrespective of their AD stage, had abnormalities of the cerebral microcirculation manifested in dyscirculatory angiopathy of Alzheimer’s type (DAAT), namely: reduction of the capillary bed in the hippocampus and frontal-parietal regions; development of multiple arteriovenous shunts in the same regions; early venous dumping of arterial blood through these shunts with simultaneous filling of arteries and veins; development of abnormally enlarged lateral venous trunks that receive blood from the arterio-venous shunts; anomalous venous congestion at the border of frontal and parietal region; increased loop formation of distal intracranial arterial branches. Control group patients did not have combinations of such changes. These abnormalities are specific for AD and can affect amyloid beta metabolism contributing to its accumulation in the brain tissue and thereby stimulating AD progression.
Eosinophilic gastroenteritis: Current aspects on etiology,pathogenesis, diagnosis and treatment
Cheracakis P.,Sklavaina Maria,Triantafillidis J.,Aikaterini Parasi
Annals of Gastroenterology , 2007,
Abstract: SUMMARY Idiopathic eosinophilic gastroenteritis is a rare inflammatory disease of unknown origin, characterized by diffuse eosinophilic infiltration of the gastrointestinal tract, accompanied by varying abdominal symptoms related to the location, severity and depth of invasion. Any part of the gastrointestinal tract including the esophagus may be involved, although the stomach and small bowel are the most frequently affected areas. Other sites of involvement include the pancreas, liver and biliary tree and tissues outside gastrointestinal tract. Although the exact etiology is unknown, an allergic disorder is present in almost of the patients. Increased production of Interleukin-5 and activated eosinophils has been shown to be the rule in all cases. A large proportion of patients demonstrates peripheral eosinophilia. Eosinophil localization to the lamina propria at baseline is critically regulated by eotaxin, a chemokine expressed throughout the gastrointestinal tract. Diagnosis may sometimes be difficult but it can be achieved with the help of endoscopy plus mucosal biopsies, while peripheral and tissue eosinophilia supported by the findings of radiology, ultrasound and computed tomography can establish the diagnosis in the majority of cases. Eosinophilic gastrenteritis should be considered in the differential diagnosis of patients with unexplained gastrointestinal symptoms even in the absence of peripheral eosinophilia. Treatment with corticosteroids and the newer ones such as budezonide produces rapid relief of symptoms and clinical signs of the disease. Other valuable therapeutic modalities include administration of immunosuppressives, chromoglycate and dietary restrictions. Surgery is advocated only for obstructing forms of the disease. The course of the disease is characterized by frequent exacerbations and remissions. The long-term prognosis is relatively benign. Patients suffering from eosinophilic gastroenteritis require regular surveillance and prompt treatment in order to avoid possible complications. Key words: Eosinophils, Gastroenteritis, Eosinophilic gastroenteritis, Corticosteroids, Immunosupressives, Surgery, Hypereosinophilic syndrome
Etiology and pathogenesis of Parkinson’s disease: role of mitochondrial pathology  [cached]
Ottolini D,Cali T,Brini M
Research and Reports in Biochemistry , 2013,
Abstract: Denis Ottolini, Tito Calì, Marisa BriniDepartment of Comparative Biomedicine and Food Science, University of Padova, Padova, ItalyAbstract: Neurons critically rely on mitochondrial activity: they are characterized by high energy demand and they are totally dependent on the process of oxidative phosphorylation to produce adenosine triphosphate. Thus, any impairment in mitochondrial function results in neuronal damage and degeneration. Some particular neuronal populations are more susceptible to mitochondrial damage, as it has been recently proposed for the ventral midbrain dopaminergic neurons, the degeneration of which represents a clinical sign of Parkinson’s disease. Different cellular pathways are involved in the pathogenesis of this neurodegenerative disease, but intriguingly both sporadic and familial forms share common features that essentially recapitulate mitochondrial dysfunction. Mitochondrial biogenesis, bioenergetics, mitochondria dynamics, and quality-control process are the main affected pathways. General consensus agrees on the possibility that deficiency in these processes may represent the cause rather than the consequence of neurodegeneration. In this review, we will discuss these aspects and the substantial achievements that have been reached in recent years in identifying specific defects in precise biological processes, eg, mitochondrial quality control. The development of cell and animal genetic models has been an important tool to dissect numerous molecular details; for this reason, we will mainly refer to experiments performed on them.Keywords: mitochondria, Parkinson’s disease, α-synuclein, PINK1/parkin, DJ-1, LRRK2
Cognitive-based Study of Conceptual Metaphor of Etiology and Pathogenesis of "Stroke Disease"
基于认知的“中风病”病因病机概念隐喻研究

Xie Jing,Gu Haorong,Jia Chunhua,
谢菁
,谷浩荣,贾春华

世界科学技术-中医药现代化 , 2012,
Abstract: This paper was aimed to study the theory of etiology and pathogenesis of "stroke disease" in the context of cognitive science. By collection and analysis of theoretical literature of etiology and pathogenesis of "stroke disease," we have tried to discuss its metaphorical characteristics, and the cognitive root source of diverse origin domain of conceptual metaphor of etiology and pathogenesis of "stroke disease." It was concluded that the theory of etiology and pathogenesis of "stroke disease" is a kind of Chinese medicine constructed theory which is based on a series of "wind" conceptual metaphors. The uniqueness of the experience of physicians had formed differences of cognitive structure, which had eventually led to the diversity of metaphorical cognition of "stroke disease".
Pathogenesis, etiology and treatment of bronchiectasis  [cached]
AL-Shirawi Nehad,AL-Jahdali Hamdan,Al Shimemeri Abdullah
Annals of Thoracic Medicine , 2006,
Abstract: Bronchiectasis is a chronic lung disease, defined pathologically as irreversible dilatation of the bronchi. The clinical course of the disease is chronic and progressive and in most cases, causes lung damage over many years. There is usually an initial event, which causes impairment of mucociliary clearance of the bronchial tree. The respiratory tract becomes colonized by bacteria that inhibit the ciliary function and promote further lung damage. The hallmark of bronchiectasis, is a chronic cough with mucopurulent or purulent sputum, lasting for months to years and may progress to chronic respiratory failure. Diagnosis of bronchiectasis is suspected on the basis of clinical manifestations. In order to confirm the diagnosis and underlying causes, appropriate investigations must be performed. In this comprehensive review, we discuss the etiology, pathogenesis, clinical presentation, appropriate investigations and management of bronchiectasis.
Acute pancreatitis: Etiology and common pathogenesis  [cached]
Guo-Jun Wang, Chun-Fang Gao, Dong Wei, Cun Wang, Si-Qin Ding
World Journal of Gastroenterology , 2009,
Abstract: Acute pancreatitis is an inflammatory disease of the pancreas. The etiology and pathogenesis of acute pancreatitis have been intensively investigated for centuries worldwide. Many causes of acute pancreatitis have been discovered, but the pathogenetic theories are controversial. The most common cause of acute pancreatitis is gallstone impacting the distal common bile-pancreatic duct. The majority of investigators accept that the main factors for acute billiary pancreatitis are pancreatic hyperstimulation and bile-pancreatic duct obstruction which increase pancreatic duct pressure and active trypsin reflux. Acute pancreatitis occurs when intracellular protective mechanisms to prevent trypsinogen activation or reduce trypsin activity are overwhelmed. However, little is known about the other acute pancreatitis. We hypothesize that acute biliary pancreatitis and other causes of acute pancreatitis possess a common pathogenesis. Pancreatic hyperstimulation and pancreatic duct obstruction increase pancreatic duct pressure, active trypsin reflux, and subsequent unregulated activation of trypsin within pancreatic acinar cells. Enzyme activation within the pancreas leads to auto-digestion of the gland and local inflammation. Once the hypothesis is confirmed, traditional therapeutic strategies against acute pancreatitis may be improved. Decompression of pancreatic duct pressure should be advocated in the treatment of acute pancreatitits which may greatly improve its outcome.
Parkinson’s disease-implicated kinases in the brain; insights into disease pathogenesis.  [PDF]
Nicolas Dzamko,Yue Huang,Glenda Halliday
Frontiers in Molecular Neuroscience , 2014, DOI: 10.3389/fnmol.2014.00057
Abstract: Substantial evidence implicates abnormal protein kinase function in various aspects of Parkinson’s disease (PD) etiology. Elevated phosphorylation of the PD-defining pathological protein, α-synuclein, correlates with its aggregation and toxic accumulation in neurons, whilst genetic missense mutations in the kinases PTEN-induced putative kinase 1 (PINK1) and leucine-rich repeat kinase 2 (LRRK2), increase susceptibility to PD. Experimental evidence also links kinases of the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways, amongst others, to PD. Understanding how the levels or activities of these enzymes or their substrates change in brain tissue in relation to pathological states can provide insight into disease pathogenesis. Moreover, understanding when and where kinase dysfunction occurs is important as modulation of some of these signaling pathways can potentially lead to PD therapeutics. This review will summarize what is currently known in regard to the expression of these PD-implicated kinases in pathological human postmortem brain tissue.
PEPTIC ULCER: A REVIEW ON ETIOLOGY AND PATHOGENESIS
Kaur Amandeep,Singh Robin,Sharma Ramica,Kumar Sunil
International Research Journal of Pharmacy , 2012,
Abstract: A peptic ulcer is a sore on the lining of the stomach or duodenum. The two most common types of peptic ulcer are called “gastric ulcers” and “duodenal ulcers”. Peptic ulcers are found to be due to an imbalance between aggressive factors such as hydrochloric acid (HCL), pepsin, refluxed bile, leukotrienes (LTs), reactive oxygen species (ROS) and defensive factors, which include the function of the mucus-bicarbonate barrier, prostaglandins (PGs), mucosal blood flow, cell renewal and migration, nonenzymatic and enzymatic antioxidants and some growth factors. H. pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant causes of peptic ulcer disease. Also, a numbers of factors are implicated in the pathogenesis of gastric ulcer, among which major factors involved are bacterial infection (Helicobacter pylori), certain medications (NSAID), chemicals (Hcl/ethanol) ,gastric cancer and minor factors are stress, smoking, spicy food and nutritional deficiencies. The idea behind treating ulcers is to lower the amount of acid that your stomach makes, to neutralize the acid that is made and to protect the injured area so it can have time to heal. The main aim of this review article has to summarize the ulcerogenic mechanisms of various mediators involved in Peptic ulcer disease.
Gastric Cancer: recent developments in its etiology and pathogenesis  [cached]
J.K. Triantafillidis, P. Cheracakis
Annals of Gastroenterology , 2007,
Abstract: SUMMARY During recent years significant progress has been made concerning our understanding the role of various factors involved in the etiology and pathogenesis of gastric carcinoma. Several factors are suspected to play a role in gastric carcinogenesis including environmental factors (diet, exogenous chemicals), intragastric synthesis of carcinogens, infectious factors (Helicobacter pylori) and genetic ones. Gastric tumorinogenesis is a multifactorial and multistep process, involving accumulation of genetic and epigenetic alterations in oncogenes, tumor-suppressor genes, cell-adhesion molecules, telomere and telomerase activity, as well as genetic instability at several microsatellite loci. These sequential alterations differ between the two histological types of gastric cancer (diffuse and intestinal). Genetic instability, chromosomal instability and immortality participate in the initial step of gastric carcinogenesis. According to the World Health Organization, Helicobacter pylori could be classified as a carcinogen of type I. It causes chronic gastritis leading to atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. The knowledge of these events, some of which appear in the early stage of gastric carcinogenesis, could be of value in relation to the prevention strategies and early diagnosis of this lethal condition. Key words: Gastric cancer, Carcinogenesis, Oncogenes, Helicobacter pylori, etiology
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