Home About us Contact
|
Home About us Contact | ||
|
|
||
End Stage (end + stage)
Terms modified by End Stage Selected AbstractsKarnofsky performance score in acute renal failure as a predictor of short-term survivalNEPHROLOGY, Issue 6 2007JOSE RAMON PEREZ VALDIVIESO SUMMARY: Background: Karnofsky Performance Scale Index (KPS) is a measure of functional status that allows patients to be classified according to their functional impairment. We aim to assess if the prior KPS may predict the risk of death among patients with acute renal failure (ARF). Methods: A cohort of 668 consecutive patients who had been admitted in an university-affiliated hospital between June 2000 and June 2006, and had been diagnosed with ARF, were studied. Three hundred and eighty-six patients with ARF who matched at least one of the RIFLE (Risk, Injury, Failure, Loss and End stage) criteria on increased serum creatinine were included for subsequent analysis. The group was divided into four categories, according to different Karnofsky scores measured by a nephrologist (,80, 70, 60 and ,50). We used an adjusted logistic regression model to assess the relationship between the Karnofky score and mortality. Results: A significant risk of in-hospital mortality within 90 days was observed when the other groups were compared with the ,80 Karnofsky group. Adjusted odds ratios were 8.87 (95% confidence interval (CI) 3.03,25.99), 6.78 (95% CI 2.61,17.58) and 2.83 (95% CI 1.04,7.68), for Karnofsky groups of ,50, 60 and 70, respectively. An adjusted odds ratio of 1.75 (95% CI 1.37,2.23) was observed for every 10 point decrease in KPS score. Conclusion: Functional status as indicated by the KPS is an independent predictor of death in this cohort of patients with ARF. Patients who presented lower scores had increased mortality rates. [source] The clinical syndrome of Alzheimer's disease: aspects particularly relevant to clinical trialsGENES, BRAIN AND BEHAVIOR, Issue 3 2005R. C. Mohs This paper describes the natural history of the clinical syndrome of Alzheimer's disease (AD) including the cognitive deficit, the neuropsychiatric symptoms, impact on daily functioning, risk factors, medical complications and impact on the use of health-care resources. The clinical presentation of the disease varies greatly from the prodrome through end stage; instruments used to quantify the severity of each aspect of the disease have been developed and are described along with their use in clinical drug trials. Drug treatments for AD are usually developed by first showing a positive effect on the cognitive deficit, with later studies investigating drug effects on other clinical aspects of the disease. [source] N-myc downstream-regulated gene 1 expression in injured sciatic nervesGLIA, Issue 4 2004Kazuho Hirata Abstract N-myc downstream-regulated gene 1 (NDRG1)/RTP/Drg1/Cap43/rit42/TDD5/Ndr1 is expressed ubiquitously and has been proposed to play a role in growth arrest and cell differentiation. A recent study showed that mutation of this gene is responsible for hereditary motor and sensory neuropathy-Lom. However, the role of this gene in the peripheral nervous system is not fully understood. In our study, rabbit polyclonal antibodies were raised against this gene product and were used to examine changes in its expression over the time course of Wallerian degeneration and ensuing regeneration after crush injury of mouse sciatic nerves. Fluorescent immunohistochemistry showed that NDRG1 was expressed over the intact nerve fibers. Double labeling with a Schwann cell (SC) marker, S-100 protein (S-100), revealed that NDRG1 was localized in the cytoplasm of S-100-positive Schwann cells (SCs). NDRG1 expression was maintained in the early stage of myelin degradation but was then markedly depleted at the end stage of myelin degradation when frequent occurrence of BrdU-labeled SCs was observed (at 7,9 days). The depletion of NDRG1 at this time point was also confirmed by Western blotting analysis. NDRG1 expression finally recovered at the stage of remyelination, with immunoreactivity stronger than that in intact nerves. These findings suggest that NDRG1 may play an important role in the terminal differentiation of SCs during nerve regeneration. © 2004 Wiley-Liss, Inc. [source] Immunoexpression of Bcl-x in squamous cell carcinoma and keratoacanthoma: differences in pattern and correlation with pathobiologyHISTOPATHOLOGY, Issue 3 2009Kong-Bing Tan Aims:, Bcl-x is an important anti-apoptotic member of the Bcl-2 family. The aim was to determine its immunoexpression in cutaneous squamous cell carcinoma (SCC) and keratoacanthoma (KA). Methods and results:, Sixteen SCCs and 39 KAs were investigated by Bcl-x immunohistochemistry. Bcl-x immunoreactivity was mostly diffuse in SCC (75% of cases), whereas that in KA was typically confined to the mid-to-upper spinous keratinocytes (95%) (P < 0.0001). There was a trend for SCC to have a higher likelihood of immunopositivity (weighted staining score ,6 of 12) compared with KA (88% versus 59%, P = 0.058). Twenty-nine per cent of regressing KA had immunopositivity, whereas 47% and 82% of its stable and proliferating counterparts, respectively, had equivalent positivity (P = 0.024). Conclusions:, These results provide some insight into the pathobiology of SCC and KA. The generally diffuse and stronger Bcl-x immunoreactivity in SCC suggests that the protein contributes to the survival advantage and aggressiveness of the tumour. In KA, the preferential reactivity of the mid-to-upper neoplastic keratinocytes can plausibly be explained by such differentiated cells attempting to prolong their existence under rapidly evolving circumstances, whereas the reduced reactivity in regressing KA is consistent with the end stage of the tumour. [source] Gene and Cell Therapy for Heart DiseaseIUBMB LIFE, Issue 2 2002Regina M. Graham Abstract Heart disease is the most common cause of morbidity and mortality in Western society and the incidence is projected to increase significantly over the next few decades as our population ages. Heart failure occurs when the heart is unable to pump blood at a rate to commensurate with tissue metabolic requirements and represents the end stage of a variety of pathological conditions. Causes of heart failure include ischemia, hypertension, coronary artery disease, and idiopathic dilated cardiomyopathy. Hypertension and ischemia both cause infarction with loss of function and a consequent contractile deficit that promotes ventricular remodeling. Remodeling results in dramatic alterations in the size, shape, and composition of the walls and chambers of the heart and can have both positive and negative effects on function. In 30-40% of patients with heart failure, left ventricular systolic function is relatively unaffected while diastolic dysfunction predominates. Recent progress in our understanding of the molecular and cellular bases of heart disease has provided new therapeutic targets and led to novel approaches including the delivery of proteins, genes, and cells to replace defective or deficient components and restore function to the diseased heart. This review focuses on three such strategies that are currently under development: (a) gene transfer to modulate contractility, (b) therapeutic angiogenesis for the treatment of ischemia, and (c) embryonic and adult stem cell transfer to replace damaged myocardium. [source] An Internalist View on the Value of Life and Some Tricky Cases Relevant to itJOURNAL OF APPLIED PHILOSOPHY, Issue 1 2001Theo van Willigenburg If we understand death as the irreversible loss of the good of life, we can give meaning to the idea that for suffering patients in the end stage of their illness, life may become an evil and death no longer a threat. Life may lose its good already in the living person. But what does the good of life consist in, then? I defend an internalist view according to which the goodness of life is intrinsically related to the attitudes, concerns, interests and experiences of the person who is leading the life. This results in the contention that the core of what we understand as the value of a person's life is to be identified with what makes life go well for the person living the particular life. This internalist view does not presuppose (or imply) hedonism or mentalism, nor does it pose an experience requirement. Something may be good for you, because it is valuable as seen from your authentic viewpoint, even if you do not actually experience this goodness, or think otherwise because you are mistaken about your own well-being. To test this position, and the authenticity-requirement it includes, I discuss three cases of patients who are persistent in denying that in their life any value is left and who contend that death is no worse than further living. Internalism acknowledges that in the life of these patients there may be 'functionings' and 'beings' that are worthwhile, where the test of value is at least partially independent of subjective assessment. Still, internalism claims that something truly valuable can only contribute to the good of one's life of it has positive meaning as seen from the attitudinal viewpoint that identifies oneself. [source] Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 7 2003P. J. Watson Chronic pancreatitis is a common cause of exocrine pancreatic insufficiency (EPI) in humans and cats but is rarely recognised in dogs in which pancreatic acinar atrophy (PAA) is reportedly more common. This paper describes four dogs which developed EPI secondary to pancreatitis. Two of the dogs also had diabetes mellitus which developed before EPI. One diabetic dog had concurrent hyperadrenocorticism and was euthanased five months after presentation; the other diabetic dog died 48 months after diagnosis. The remaining dogs were alive 78 and 57 months after diagnosis. The number of affected dogs was comparable to the number of cases of presumed PAA seen over the same time period in the same institution. Chronic pancreatitis may be a more common cause of EPI in dogs than previously assumed and may be under-recognised because of difficulties in diagnosis. The relative importance of chronic pancreatitis as a cause of canine diabetes mellitus remains to be ascertained. [source] Opioid Rotation in the Management of Chronic Pain: Where Is the Evidence?PAIN PRACTICE, Issue 2 2010K.C.P. Vissers MD Abstract The management of chronic pain remains a challenge because of its complexity and unpredictable response to pharmacological treatment. In addition, accurate pain management may be hindered by the prejudice of physicians and patients that strong opioids, classified as step 3 medications in the World Health Organization ladder for cancer pain management, are reserved for the end stage of life. Recent information indicates the potential value of strong opioids in the treatment of chronic nonmalignant pain. There are, up until now, insufficient data to provide indications about which opioid to use to initiate treatment or the dose to be used for any specific pain syndrome. The strong inter-patient variability in opioid receptor response and in the pharmacokinetic and pharmacodynamic behavior of strong opioids justifies an individual selection of the appropriate opioid and stepwise dose titration. Clinical experience shows that switching from one opioid to another may optimize pain control while maintaining an acceptable side effect profile or even improving the side effects. This treatment strategy, described as opioid rotation or switch, requires a dose calculation for the newly started opioid. Currently, conversion tables and equianalgesic doses are available. However, those recommendations are often based on data derived from studies designed to evaluate acute pain relief, and sometimes on single dose studies, which reduces this information to the level of an indication. In daily practice, the clinician needs to titrate the optimal dose during the opioid rotation from a reduced calculated dose, based on the clinical response of the patient. Further research and studies are needed to optimize the equianalgesic dosing tables. [source] 4411: Immunohistochemical methods to evaluate vitreoretinal scaringACTA OPHTHALMOLOGICA, Issue 2010ML BOCHATON-PIALLAT Purpose Formation of scarlike epiretinal membranes (ERMs) constitutes potentially the end stage of evolution of proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR) and idiopathic vitreoretinopathy. Among various cellular populations, ERMs contain cells with contractile features typical of myofibroblasts. Myofibroblasts have been described in granulation tissue during wound healing and in practically all fibrocontractive diseases, in which they participate in the generation of isometric tension and in the synthesis of extracellular matrix components; these phenomena are in turn responsible for granulation tissue remodeling and retraction. The main marker of the myofibroblastic phenotype is the expression of alpha-SMA. The transforming growth factor-beta1 and the ED-A splice variant of cellular fibronectin, an extracellular matrix component, are key players of the complex process of myofibroblast differentiation. Methods Proteins were detected by means of immunohistochemical staining on paraffin sections from formol fixed tissues and double immunofluorescence staining on whole tissues. Samples were observed by using classical light and confocal microscopes. Results The presence of alpha-SM actin-positive myofibroblasts was associated with the expression of TGF-beta1, TGF-beta receptor II, and ED-A FN in all types of ERMs studied. Conclusion The results furnish new data on the mechanism of alpha-SM actin stimulation in fibroblasts in a human pathologic setting. [source] Japanese familial amyotrophic lateral sclerosis family with a two-base deletion in the superoxide dismutase-1 geneNEUROPATHOLOGY, Issue 1 2001Yasuhiro Watanabe The clinical characteristics of members of a familial amyotrophic lateral sclerosis (FALS) family from Oki Island, whose members have a 2-bp deletion at codon 126 of Cu/Zn superoxide dismutase (SOD1) gene, are presented here. Mean age of the onset in the members was 42 years. Mean disease duration among the members who had not been placed on a respirator was approximately 2 years. Long-term survivors with respiratory support presented disturbances in eye movement and urination toward the end stages of the disease. They predominantly exhibited lower motor neuron symptoms. In addition, the authors focused on frameshift, nonsense and non-amino-acid-altering mutations. Frameshift and nonsense mutations were all found within exon 4, exon 5 and intron 4. These amyotrophic lateral sclerosis cases were likely to have shorter disease duration than the FALS patients with single substitution. Several hypotheses were presented on the pathogenesis of FALS with SOD1 mutation. [source] Identification and management of chronic kidney diseasePRESCRIBER, Issue 10 2008FRCGP, Simon de Lusignan MSc Chronic kidney disease, a common long-term condition, typically remains asymptomatic until the severe end stages are reached. Here, the authors describe its diagnosis and management. Copyright © 2008 Wiley Interface Ltd [source] | |||||||||||||