bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mitochondrial Dysfunction and Ultrastructural Damage in the Hippocampus during Kainic Acid–induced Status Epilepticus in the Rat
Authors: Chuang Yao‐Chung , Chang Alice Y. W. , Lin Jui‐Wei , Hsu Shih‐Pin , Chan Samuel H. H. 
Published: September 2004

Summary:  Purpose: Prolonged and continuous epileptic seizure (status epilepticus) results in cellular changes that lead to neuronal damage. We investigated whether these cellular changes entail mitochondrial dysfunction and ultrastructural damage in the hippocampus, by using a kainic acid (KA)‐induced experimental status epilepticus model. Methods: In Sprague–Dawley rats maintained under chloral hydrate anesthesia, KA (0.5 nmol) was microinjected unilaterally into the CA3 subfield of the hippocampus to induce seizure‐like hippocampal EEG activity. The activity of key mitochondrial respiratory chain enzymes in the dentate gyrus (DG), or CA1 or CA3 subfield of the hippocampus was measured 30 or 180 min after application of KA. Ultrastructure of mitochondria in those three hippocampal subfields during KA‐induced status epilepticus also was examined with electron microscopy. Results: Microinjection of KA into the CA3 subfield of the hippocampus elicited progressive build‐up of seizure‐like hippocampal EEG activity. Enzyme assay revealed significant depression of the activity of nicotinamide adenine dinucleotide cytochrome c reductase (marker for Complexes I+III) in the DG, or CA1 or CA3 subfields 180 min after KA‐elicited temporal lobe status epilepticus. Conversely, the activities of succinate cytochrome c reductase (marker for Complexes II+III) and cytochrome c oxidase (marker for Complex IV) remained unaltered. Discernible mitochondrial ultrastructural damage, varying from swelling to disruption of membrane integrity, also was observed in the hippocampus 180 min after hippocampal application of KA. Conclusions: Our results demonstrated that dysfunction of Complex I respiratory chain enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental temporal lobe status epilepticus.
Epilepsy and Synaptic Reorganization in a Perinatal Rat Model of Hypoxia–Ischemia
Authors: Williams Philip A. , Dou Ping , Dudek F. Edward 
Published: September 2004

Summary:  Purpose: One of the potential consequences of perinatal hypoxia–ischemia (H‐I) is the development of epilepsy, and synaptic reorganization in the hippocampus has been associated with epilepsy after an injury. We tested the hypothesis that perinatal H‐I will induce spontaneous motor seizures, hippocampal lesions, and synaptic reorganization in the dentate gyrus. Methods: The right common carotid artery of 7‐day‐old rats was permanently ligated, and the rats were placed for 120 min into a chamber filled with 8% oxygen (37°C). Animals were directly observed for chronic motor seizures for 7 to 24 months after the H‐I insult. Results: Nearly half of the rats (i.e., eight of 20) were seen to have spontaneous motor seizures after the H‐I injury. The ipsilateral hippocampi from both the rats with seizures and the rats not seen to have seizures had hippocampal lesions and increased amounts of Timm stain in the inner molecular layer (IML) compared with controls. The contralateral hippocampi from the rats with seizures, but not the hippocampi from the rats not seen to have seizures, had significantly increased amounts of Timm stain in the IML. Conclusions: These results suggest that perinatal H‐I can induce epilepsy, ipsilateral hippocampal lesions, and mossy fiber sprouting in the lesioned and contralateral hippocampus.
Aging Alters Electroencephalographic and Clinical Manifestations of Kainate‐induced Status Epilepticus
Authors: Darbin Olivier , Naritoku Dean , Patrylo Peter R. 
Published: September 2004

Summary:  Purpose: The elderly exhibit an increased risk for developing status epilepticus and status‐related morbidity and mortality. However, it is unclear how aging alters the progression of electroencephalographic (EEG) activity and behavioral manifestations during status epilepticus. Methods: A repetitive low‐dose kainate treatment protocol (2.5 mg/kg/h; i.p.) was used in this study in conjunction with EEG and behavioral monitoring from freely behaving adult (7–8 months) and aged (22–25 months) Fischer 344 rats to assess the effects of aging on status epilepticus. Results: During kainate treatment, both groups exhibited an increase in EEG power that corresponded with the time course of kainate treatment. However, visual inspection and spectral analysis revealed a reduction of the faster frequencies (12.5–35 Hz) in the EEGs of aged rodents. A similar progression of behavioral manifestations was observed in adult and aged rodents during kainate treatment, although the frequency of preseizure manifestations (e.g., wet‐dog shakes; aged rats, 110 events/h vs. adults, 25 events/h; median values) was greater, and latency to onset for any given behavioral manifestation (e.g., class V seizures; aged median, 60 min, vs. adult median, 145 min) was consistently shorter within the aged group. Conclusions: These data reveal that aged Fischer 344 rats exhibit altered EEG activity (reduction of higher frequencies) and clinical manifestations during kainate‐induced status epilepticus. Taken together, these data indicate an age‐related change in seizure onset and spread after exposure to glutamate analogues.
Reviews: Use of Insulin and Oral Hypoglycemic Medications in Patients with Diabetes Mellitus and Advanced Kidney Disease
Authors: Snyder Richard W. , Berns Jeffrey S. 
Published: September 2004

ABSTRACTDiabetes mellitus is recognized as a leading cause of chronic kidney disease (CKD) and end‐stage renal disease (ESRD) in the United States. There is a vast array of medications used to treat diabetes, including insulin and the sulfonylureas, as well as newer classes of drugs such as the thiazolidinediones and biguanides. In patients with reduced glomerular filtration rate (GFR), it is necessary to decrease the dosage of some of these drugs, while others are best avoided altogether. Accumulation of either the parent compound or its metabolites can result in symptomatic hypoglycemia, or in the case of metformin, significant lactic acidosis. In this article we will review the use of insulin and the various classes of oral medications used to treat type 2 diabetes mellitus, focusing on their pharmacokinetic properties and dosing in patients with advanced kidney disease.
K/DOQI Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease Patients: Some Therapeutic Implications
Authors: Uribarri Jaime 
Published: September 2004

ABSTRACTThe National Kidney Foundation (NKF) has recently published clinical practice guidelines for bone metabolism and disease in chronic kidney disease (CKD) patients (the Kidney Disease Outcomes Quality Initiative [K/DOQI]). Data from the literature show that the majority of dialysis patients treated with traditional calcium‐containing phosphorus binders and vitamin D or vitamin D analogue preparations have serum parathyroid hormone (PTH), calcium, and phosphorus levels outside these strict K/DOQI target ranges. In fact, it appears that achieving and maintaining the targets values set by these guidelines is virtually impossible without the simultaneous use of the new calcimimetic agents and non‐calcium‐containing binders, agents that have significant cost barriers to their use in many patients. These guidelines are welcome, but they may be impractical for the majority of dialysis patients. The impact of these guidelines in improving the parameters of bone metabolism and disease among dialysis patients remains to be determined.
American Society of Diagnostic and Interventional Nephrology Section Editor: Stephen Ash: Percutaneous Technique of Presternal Peritoneal Dialysis Catheter Placement
Authors: Sreenarasimhaiah Vijay P. , Margassery Suresh K. , Martin Kevin J. , Bander Steven J. 
Published: September 2004

ABSTRACTPresternally exiting peritoneal dialysis (PD) catheters have been described as advantageous compared to abdominally exiting catheters with regard to infection, wound healing, and other complications. Placement of such catheters has only been described with open surgical techniques and not by percutaneous means. In this article we describe 15 patients who received percutaneously placed PD catheters with a presternal exit site. These patients received their procedures in an outpatient procedure room performed by an interventional nephrologist. In all but one case, immediate technical success was achieved. In only one case was peritonitis documented. All catheters are still functional, including some with follow‐up as long as 15 months. Percutaneous placement of presternally exiting PD catheters is technically straightforward and can avoid an open surgical procedure.
Editorials: Antioxidant Therapy in Uremia: Evidence‐Based Medicine?
Authors: Gordon Carrie A. , Himmelfarb Jonathan 
Published: September 2004

ABSTRACTBecause of correlations between cardiovascular disease, inflammation, and renal failure, many investigators are pursuing nontraditional risk factors and therapies in order to reduce cardiovascular morbidity and mortality in the end‐stage renal disease (ESRD) population. Despite the disappointing lack of clinical effects with antioxidative therapies seen in large studies of the general population, some studies suggest a diminished cardiovascular risk in individuals with renal failure. This expanding new line of evidence is promising as a method to help alleviate the more than 20‐fold increase in risk of cardiovascular events in the ESRD population. Most of the current available studies have evaluated laboratory or physiologic endpoints, such as endothelial function and measures of oxidative burden, and have evaluated relatively small numbers of patients. However, it is currently premature to initiate widespread clinical therapy with antioxidants. Further investigation in this area should be supported to see if reported benefits can be duplicated in more widespread study populations, and to more accurately define the most appropriate choice of therapy, mode of therapy, and dose.
Serum Ferritin in Chronic Kidney Disease: Reconsidering the Upper Limit for Iron Treatment
Authors: Fishbane Steven , Kalantar‐Zadeh Kamyar , Nissenson Allen R. 
Published: September 2004

ABSTRACTIntravenous iron treatment in hemodialysis patients improves the response to recombinant human erythropoietin (rHuEPO) and facilitates achievement of targets for hemoglobin and hematocrit. Excessive treatment, however, could expose patients to risks related to iron overload and oxidative stress. Therefore international treatment guidelines generally recommend that intravenous iron be discontinued when serum ferritin is greater than 500–1000 ng/ml. In this article we explore the relevant issues that inform the decisions as to what levels of serum ferritin are used as the upper limit for treatment. We conclude that the current published literature is inadequate for developing evidence‐based guidelines. Clinical judgment is critical to properly weigh the risks and benefits of intravenous iron treatment in the context of the individual patient.
Peritoneal Dialysis International: Its Origins and Impact
Authors: Oreopoulos Dimitrios G. 
Published: September 2004

ABSTRACT Peritoneal Dialysis International (PDI) started in 1988 as a four‐page document (Peritoneal Dialysis Bulletin) intended to inform all those who visited the Toronto Western Hospital peritoneal dialysis unit about advances in peritoneal dialysis. Soon it became a journal distributed free of charge to 13,000 individuals. Subsequently it became the official publication of the International Society for Peritoneal Dialysis. For many years it was the main forum for publication of the best articles in peritoneal dialysis. As a result, in 1997, its “impact factor” increased to 2.129, putting it in fourth position among the nephrology journals. PDI greatly stimulated the expansion of peritoneal dialysis in the 1980s and 1990s, and remains the main source of knowledge on clinical and investigative aspects of peritoneal dialysis.
Phylogeny of the superfamily Gelechioidea (Lepidoptera: Ditrysia): an exemplar approach
Authors: Kaila Lauri 
Published: September 2004

AbstractPhylogenetic relationships within the megadiverse lepidopteran superfamily Gelechioidea have been poorly understood and consequently the family level classification has been problematic. An analysis of phylogeny using 193 characters, including 241 informative character states, derived from larval, pupal and adult morphology and larval ecology, was performed to resolve the phylogeny of the Gelechioidea. 143 species representing the diversity of the putative Gelechioidea were included, supplemented with 13 species representing 11 other Ditrysian families. The monophyly of the Gelechioidea was supported, although only with homoplastic characters. The putative position of the Gelechioidea as the sister group of the Apoditrysia was not supported, since the Gelechioidea was nested within this clade. The Gelechioidea was divided into two main lineages: (1) the gelechiid lineage constituting Deoclonidae, Syringopainae, a re‐composed Coleophoridae (including Coelopoetinae and Batrachedrinae as paraphyletic with Stathmopodinae, and Coleophorinae nested within it), Momphidae, Pterolonchidae, Scythrididae, Cosmopterigidae, and Gelechiidae, and (2) the oecophorid lineage constituting the “autostichid” family assemblage (including taxa formerly assigned to Autostichinae, Holcopogoninae, Symmocinae, Glyphidoceridae and Lecithoceridae), Xyloryctidae s.l. (including a paraphyletic Xyloryctidae of authors, some oecophorids of authors, Deuterogoniinae and Blastobasinae), Oecophoridae s.s., Amphisbatidae s.s., Carcinidae, Stenomati[n/d]ae, Chimabachidae and Elachistidae (including Depressariinae s.s., Telechrysis, Ethmiinae, Hypertrophinae s.l., miscellaneous “amphisbatids”sensu authors, Aeolanthinae, Parametriotinae, Agonoxeninae and Elachistinae). Detritivory/fungivory may have evolved only twice within Gelechioidea, though the evolution of larval food substrate use frequently reverses. To avoid an unnecessary further proliferation of names, it is recommended that no further family group names are introduced within the Gelechioidea, unless based on a rigorous analysis of inter‐relationships.
Escaping the matrix: a new algorithm for phylogenetic comparative studies of co‐evolution
Authors: Wojcicki Maggie , Brooks Daniel R. 
Published: September 2004

AbstractAn algorithm for generating host cladograms from parasite‐host cladograms derived from parasite phylogenies, Phylogenetic Analysis for Comparing Trees (PACT), is described. PACT satisfies Assumption 0, that all the information in each parasite‐host cladogram must be used in a co‐evolutionary analysis, and that the host relationships depicted in the final host cladogram must be logically consistent with the phylogenetic relationships depicted in every part of every parasite‐host cladogram used to construct the host cladogram. It accounts for cases of speciation by host switching and expansion of host range, and reticulated host relationships, in addition to co‐speciation, sympatric speciation, and extinction in all input parasite‐host cladograms, and does so withouta prioriweighting schemes and withouta posteriorimanipulation of the data.
Review article: trials on reflux disease — the role of acid secretion and inhibition
Authors: Sonnenberg A. 
Published: September 2004

SummaryThe importance of gastric acid in the pathophysiology of gastro‐oesophageal reflux disease is substantiated by the extraordinary therapeutic success of acid inhibition in the management of the disease. The influence of many risk factors for gastro‐oesophageal reflux disease is also mediated through their effect on gastric acid secretion and acid reflux.Helicobacter pylorireduces the risk of gastro‐oesophageal reflux disease by causing corpus gastritis and reducing gastric acid output. The geographical and temporal trends ofH. pyloriinfection in human populations and its influence on gastric acid secretion are responsible for much of the apparent epidemiology of gastro‐oesophageal reflux disease.On average, intra‐oesophageal exposure to acid is higher in patients who respond poorly to antisecretory medication. It also tends to increase with increasing severity of reflux disease. However, gastric acid secretion and intra‐oesophageal acid exposure vary markedly in reflux patients. The degrees of gastric or intra‐oesophageal acidity do not allow the prediction of the presence or severity of gastro‐oesophageal reflux disease in the individual subject. The many clinical trials on gastro‐oesophageal reflux disease indicate that the reflux of gastric acid constitutes an essential mechanism in the development of this disease, but that additional and partly unknown risk factors must contribute to its aetiology and promote its occurrence in the individual patient.
Review article: towards consistency in the endoscopic diagnosis of Barrett's oesophagus and columnar metaplasia
Authors: Armstrong D. 
Published: September 2004

SummaryBarrett's oesophagus is associated with severe reflux disease and is a risk factor for oesophageal adenocarcinoma. However, there is a lack of consensus on how to assess the presence and extent of Barrett's oesophagus in clinical practice. A diagnosis of Barrett's oesophagus is currently based on the recognition of an abnormal oesophageal mucosa at endoscopy. However, a diagnosis cannot be made solely on this basis, and a true diagnosis requires the identification of an area suspicious for columnar metaplasia at endoscopy, followed by histological confirmation.Currently, difficulties in the assessment of Barrett's oesophagus include a lack of consistent definitions of endoscopic landmarks (such as the gastro‐oesophageal and squamo‐columnar junctions), a lack of standardization of descriptions of the extent of Barrett's oesophagus, and limited communication between the endoscopist and the pathologist, which hampers accurate histological confirmation. It is therefore important to develop an endoscopic description of Barrett's oesophagus, with a clear definition of endoscopic landmarks, to determine, amongst other things, whether anti‐reflux therapy produces regression or a reduction in the length of Barrett's oesophagus.With this background, a subgroup of the International Working Group on the Classification of Oesophagitis was charged with developing a simple, practicable classification system, suitable for use with standard endoscopes, which would be easy to apply in clinical practice and in large clinical studies. Described in this review are a series of propositions and an overview of the ‘CM classification’, developed by the International Working Group on the Classification of Oesophagitis, to facilitate the endoscopic description of Barrett's oesophagus. It is hoped that these propositions will be the first step in the development of standard endoscopic diagnostic criteria for Barrett's oesophagus, relevant to clinical practice and clinical research.
Review article: emerging techniques for screening and surveillance in Barrett's oesophagus
Authors: Sharma P. 
Published: September 2004

SummaryThe incidence of oesophageal adenocarcinoma continues to increase in the US and the Western world, with the 5‐year survival rate for this cancer still being very dismal.The diagnosis of Barrett's metaplasia and dysplasia (i.e. screening and surveillance) currently requires endoscopy with biopsy of the abnormally appearing distal oesophagus. Surveillance endoscopy in patients with Barrett's oesophagus relies on the performance of random biopsies from the metaplastic segment, with the aim of identifying dysplasia and/or cancer. However, intestinal metaplasia and dysplasia are not uniformly distributed within the columnar‐lined mucosa in the distal oesophagus, and the sensitivity of standard endoscopy with biopsy for the detection of these lesions is low.New techniques to improve the accuracy of endoscopic diagnosis, as well as to identify patients at high risk for neoplasia development, have recently been developed and most are currently being evaluated in clinical studies. The results with these techniques, although promising, are still preliminary. They hold promise for the improved detection of dysplasia and neoplasia at an early stage of development, with a greater chance for early treatment, and therefore a greater likelihood of either cure of adenocarcinoma or prevention of its development from dysplasia.
Review article: prevalence of Barrett's oesophagus and metaplasia at the gastro‐oesophageal junction
Authors: Sharma P. 
Published: September 2004

SummaryBarrett's oesophagus, a complication of chronic gastro‐oesophageal reflux disease, is the premalignant lesion for oesophageal and gastro‐oesophageal junction adenocarcinoma. Described in the 1950s by Norman Barrett, the diagnostic criterion for this lesion has evolved significantly over the last three decades. Endoscopic Barrett's oesophagus requires the recognition of columnar mucosa in the distal oesophagus; documentation of metaplastic tissue is confirmed by random biopsies. Given this changing definition of Barrett's metaplasia, the prevalence rates vary in the literature depending on the diagnostic criteria applied. However, it is generally accepted that approximately 10% of patients with chronic gastro‐oesophageal reflux disease will be diagnosed with this condition. There are no population‐based studies on the prevalence of Barrett's oesophagus, but emerging data indicate that it may be equally prevalent in asymptomatic individuals. These studies require confirmation. Although the incidence of oesophageal adenocarcinoma is increasing rapidly, it is unclear whether the true incidence of Barrett's oesophagus is increasing at the same time. On the other hand, metaplasia at the gastro‐oesophageal junction appears to be distinct from Barrett's oesophagus, is probably not related to chronic gastro‐oesophageal reflux disease and is a common finding if routine biopsies are obtained at the gastro‐oesophageal junction. This article reviews our current understanding of the diagnosis, definition and prevalence of both of these lesions.
Review article: what I do now to manage adenocarcinoma risk, and what I may be doing in 10 years' time
Authors: Spechler S. J. 
Published: September 2004

SummaryThis article summarizes the present recommendations for the screening, surveillance and treatment of Barrett's oesophagus, and identifies those areas in which change seems likely within the next decade. As a result of economic constraints and emerging data on ethnic variations in the frequency of Barrett's oesophagus, future screening programmes will probably focus on those individuals most likely to develop Barrett's adenocarcinomas: older white men whose gastro‐oesophageal reflux symptoms are of long duration. The present surveillance strategy for patients with Barrett's oesophagus relies heavily on random biopsy sampling of the oesophagus to find dysplasia. In the future, biomarkers other than dysplasia may be used to identify patients at high risk for carcinogenesis, and physicians may use endoscopic techniques, such as fluorescence spectroscopy, to identify areas of dysplasia for biopsy sampling. Indirect evidence suggests that super‐aggressive antisecretory therapy and treatment with non‐steroidal anti‐inflammatory drugs may reduce the risk of cancer in Barrett's oesophagus. Well‐designed prospective studies will be needed to determine whether these treatments have sufficient efficacy in cancer prophylaxis to justify the large numbers needed to treat. Finally, recent data are reviewed, which suggest that the gastro‐oesophageal junction is exposed repeatedly to concentrated acid and to potentially genotoxic concentrations of nitric oxide generated from dietary nitrate. Future studies on carcinogenesis in Barrett's oesophagus may well focus on the combined roles of nitric oxide and gastric acid.