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Metabolic Acidosis In Patients With Sepsis: Epiphenomenon Or Part Of The Pathophysiology?

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>

Metabolic Acidosis In Patients With Sepsis: Epiphenomenon Or Part Of The Pathophysiology?

Metabolic Acidosis In Patients With Sepsis: Epiphenomenon Or Part Of The Pathophysiology?

Metabolic acidosis in patients with sepsis: epiphenomenon or part of the pathophysiology? Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 1526, USA. To review the mechanisms of metabolic acidosis in sepsis. Articles and published reviews on metabolic acidosis in sepsis. Sepsis affects millions of patients each year and efforts to limit mortality have been limited. It is associated with many features one of which is acidosis which may be a result of the underlying pathophysiology (e.g. respiratory failure, shock, renal failure) or may also result from the way in which we manage critically ill patients. Lactic acidosis identifies septic patients at risk and aggressive fluid resuscitation (along with inotropes and blood in some patients) to reverse acidosis and improve venous oxygen saturation will improve mortality. However, most patients with severe sepsis or septic shock receive 0.9% saline and therefore may develop hyperchloraemic acidosis as a consequence of their resuscitation. Therefore alterations in acid-base balance are almost always in the background in the management of patients with sepsis. What is unknown is whether acidosis is in the causal pathway for organ dysfunction or whether it is simply an epiphenomenon. Changes in acid-base balance, of the type and magnitude commonly encountered in patients with sepsis, significantly alter the release of inflammatory mediators. Less significant changes in the immune response have already been implicated in influencing outcome for patients with sepsis and a reduction in acidosis in septic patients may have the same effect. Understanding the effects of acid-base on the inflammatory response is relevant as all forms of metabolic acidosis appear to be associated with pro Continue reading >>

High-anion-gap Metabolic Acidosis: Topics By Science.gov

High-anion-gap Metabolic Acidosis: Topics By Science.gov

Liss, D B; Paden, M S; Schwarz, E S; Mullins, M E Paracetamol (acetaminophen) ingestion is the most frequent pharmaceutical overdose in the developed world. Metabolic acidosis sometimes occurs, but the acidosis is infrequently persistent or severe. A growing number of case reports and case series describe high anion gap metabolic acidosis (HAGMA) following paracetamol exposure with subsequent detection or measurement of 5-oxoproline (also called pyroglutamic acid) in blood, urine, or both. Typically 5-oxoprolinuria or 5-oxoprolinemia occurs in the setting of inborn genetic errors in glutathione metabolism. It is unknown whether 5-oxoprolinemia in the setting of paracetamol exposure reflects an acquired or transient derangement of glutathione metabolism or previously unrecognized genetic defects. We reviewed the published cases of 5-oxoprolinemia or 5-oxoprolinuria among patients with HAGMA in the setting of paracetamol exposure. Our goal was to identify any consistent features that might increase our understanding of the pathophysiology, diagnosis, and treatment of similar cases. We searched the medical literature using PUBMED and EMBASE from inception to 28 August 2013 applying search terms ("oxoproline" OR "pyroglutamic acid" AND "paracetamol" OR "acetaminophen"). The intersection of these two searches returned 77 articles, of which 64 involved human subjects and were in English. Two articles, one each in Spanish and Dutch, were reviewed. An additional Google Scholar search was done with the same terms. We manually searched the reference lists of retrieved articles to identify additional four relevant articles. We focused on articles including measured 5-oxoproline concentrations in urine or blood. Twenty-two articles included quantified 5-oxoproline concentrations. Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Erythrocyte Gs Activity Reduced & Acidosis: Causes & Diagnoses | Symptoma.com

Erythrocyte Gs Activity Reduced & Acidosis: Causes & Diagnoses | Symptoma.com

[] is accumulating that the tripeptide glutathione (-glutamyl-cysteinyL-glycine) participates in a variety of fundamental processes such as intracellular redox reactions, active [nejm.org] One of the rare (but potentially underdiagnosed) causes of anion gap metabolic acidosis is acquired 5-oxoprolinuria due to excessive Tylenol ingestion. [renalfellow.blogspot.com] Acta Paediatr Scand 63:18 Google Scholar Hopkins FJ, Morgan EJ (1938) The influence of thiol-groups in the activity of dehydrogenases. [link.springer.com] Genetic safety switches could help curb potential bioterror risks January 26, 2015 The potential threat of bioterrorism using man-made biological organisms could be reduced [phys.org] How is metabolic acidosis usually treated? [quizlet.com] Topiramate reduces energy and fat gains in lean ( Fa /?) [nature.com] (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis CAUSES [lifeinthefastlane.com] Lactate producers are skeletal muscle, the brain, the gut, and the erythrocytes. [emedicine.medscape.com] You may also be instructed to curb your activity level in the hours leading up to the test. [healthline.com] acidosis, galactosuria and glycosuria , albuminuria Abnormal carbohydrate metabolism- increased plasma galactose and RBC galactose-1-P concentration , increased blood and [pedclerk.bsd.uchicago.edu] Clinical Sensitivity DNA: Approaches 80 percent in Caucasians but reduced in other ethnic groups. [ltd.aruplab.com] In the homozygous state (D/D or N314D/N314D), erythrocyte GALT enzyme activity is reduced by only 50%. [en.wikibooks.org] JASN. 2002 The reabsorption of filtered bicarbonate in the proximal tubule depends on the activity of carbonic anhydras Continue reading >>

Temporal Trends In Acute Renal Dysfunction Among Critically Ill Patients According To I/d And -262a > T Ace Polymorphisms

Temporal Trends In Acute Renal Dysfunction Among Critically Ill Patients According To I/d And -262a > T Ace Polymorphisms

Multiple organ failure syndrome and acute renal dysfunction share many of physiologic factors involved in their development. Recent studies correlate the susceptibility to organ dysfunction in critically ill patients with genetic inheritance. Many of them consider ACE gene could be a possible candidate to elucidate a genetic predisposition or a genetic risk factor. We aimed to examine the effects of I/D and -262A > T ACE polymorphisms in the renal function in severely ill southern Brazilians patients. A multi-organic worldwide known failure score, the SOFA (sequential organ failure assessment), was used to determine the basal health state at first day (ICU admission). Considering admission SOFA score and trend of renal function (measured by daily renal SOFA scores, with daily measure of serum creatinine and diuresis), we hypothesize that ACE polymorphisms could influence in the trend of renal function in ICU patients. A total of 153 critically ill adult patients (79 men) were included in this study. We monitored the patients daily during their entire ICU and post-ICU (hospital) stay (measured from the ICU admission day to a maximum of 224 days). We observed progression to renal failure (SOFA scores 3 and 4) in first seven days of ICU stay and need for dialysis. The general genotypic frequencies in our sample were II=0.17; ID=0.46; DD=0.37 and AA=0.30; AT=0.55; TT=0.15, and the allelic frequencies were I=0.40; D=0.60 and A=0.56; T=0.44. This is the first study to verify the influence of I/D and -262A > T ACE polymorphisms in acute renal dysfunction among critically ill patients. No significant association was found between genotypes or allele frequencies and the trend of the renal function. The I/D and -262A > T ACE polymorphisms have no significant impact on the trend Continue reading >>

Critical Illness Myopathy And Polyneuropathy In Children Admitted To The Icu Mahmoud At, Tawfik Ma, Abd El-naby Abdella Sa, Said Nm - Menoufia Med J

Critical Illness Myopathy And Polyneuropathy In Children Admitted To The Icu Mahmoud At, Tawfik Ma, Abd El-naby Abdella Sa, Said Nm - Menoufia Med J

The aim of the present study was to detect critical illness polyneuropathy and myopathy in children admitted to the ICU in relation to clinical findings and therapeutic regimen. Critical illness polyneuropathy and myopathy is a frequent complication of critical illness, acutely and primarily affecting the motor and sensory axons. This disorder can cause severe limb weakness and prolonged weaning. This study included 75 patients with different diseases admitted to the pediatric ICU at Menoufia University and was conducted for the period of 2 years. The patients were divided into five groups. All patients underwent nerve conduction, and electromyography was carried out on the seventh day of admission to ICU. The mean age of the patients was 4.5 2.3 years. Twenty-four (24%) patients developed critical illness neuropathy and myopathy, among whom 21 (28%) patients developed axonal polyneuropathy, one (1.3%) had demyelinating polyneuropathy, and two (2.7%) cases were myopathic. In children with sepsis the prevalence of axonal polyneuropathy was five (33.3%) cases, one case had axonal polyneuropathy and one had myopathy. Among children with chest diseases, four cases of the ventilated ones had axonal polyneuropathy, six (40%) cases of the sepsis ventilated children developed axonal polyneuropathy, and one was myopathic. One child of the ventilated children due to chest disease had demyelinating polyneuropathy, whereas the other five cases had axonal polyneuropathy. Overall, 66.7% of the deaths were of those who developed axonal polyneuropathy, and 85.7, 47.6, and 90.5% of the deaths were of those who were hyperglycemic, ventilated, and acidotic, respectively. The incidence of critical illness axonal polyneuropathy was 28%, 1.3% for demyelinating polyneuropathy, and 2.7% for c Continue reading >>

Academic Onefile - Document - The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Academic Onefile - Document - The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Listen Larger documents may require additional load time. The use of sodium bicarbonate in the treatment of acidosis in sepsis: a literature update on a long term debate Introduction. Sepsis and its consequences such as metabolicacidosis are resulting in increased mortality. Although correction ofmetabolic acidosis with sodium bicarbonate seems a reasonable approach, thereis ongoing debate regarding the role of bicarbonates as a therapeutic option.Methods. We conducted a PubMed literature search in order to identifypublished literature related to the effects of sodium bicarbonate treatmenton metabolic acidosis due to sepsis. The search included all articlespublished in English in the last 35 years. Results. There is ongoing debateregarding the use of bicarbonates for the treatment of acidosis in sepsis,but there is a trend towards not using bicarbonate in sepsis patients witharterial blood gas pH > 7.15. Conclusions. Routine use of bicarbonate fortreatment of severe acidemia and lactic acidosis due to sepsis is subject ofcontroversy, and current opinion does not favor routine use of bicarbonates.However, available evidence is inconclusive, and more studies are required todetermine the potential benefit, if any, of bicarbonate therapy in the sepsispatient with acidosis. Sepsis and septic shock constitute an important cause of morbidityand mortality in the critically ill patient. Metabolic acidosis, includinglactic acidosis, is part of the underlying pathophysiology in sepsis and isrelated to poor prognosis. The treatment of metabolic acidosis is based on control of theunderlying pathophysiologic process and reversal of organ dysfunction.Etiologic treatment is essential in metabolic acidosis, but optimization ofoxygen delivery to tissues and reduction of tissue oxygen de Continue reading >>

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting Ganesh K, Sharma R N, Varghese J, Pillai M - Int J Crit Illn Inj Sci

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting Ganesh K, Sharma R N, Varghese J, Pillai M - Int J Crit Illn Inj Sci

Metabolic acidosis is frequently found in patients with severe sepsis. Several studies have shown that the amount of metabolic acidosis and its evolution over hospital stay has an effect on the prognosis. However, the precise composition of metabolic acidosis in these patients is not well known. Metabolic acidosis in severe sepsis may be secondary to lactic acidosis, but studies have shown that there is an unidentified anion contributing to high anion gap metabolic acidosis in addition to lactate. [1] Alterations in acid-base balance occur both as part of the pathophysiology of the underlying disease and as part of therapeutic interventions. [2] Thus, an understanding of types of acidosis in sepsis and their evolution over the course of treatment may give us insight into the behavior of acid-base balance in these patients. To describe at Intensive Care Unit (ICU) admission and over the first 5 days the composition of metabolic acidosis in patients with sepsis and to evaluate and compare acidosis patterns in survivors and non survivors. It was a prospective study conducted at Amrita Institute of Medical Sciences, Kochi, Kerala, in the Department of Internal Medicine and done on patients with sepsis as defined by the standard criteria. ICU consecutive patients admitted in the medical ICU with sepsis and metabolic acidosis were assessed. This sample size had an allowable error of 28% on the estimate of mortality. Arterial blood gas and serum electrolytes were measured during the first 5 days of admission or until death, renal replacement, or discharge supervened. The arbitrary period of 5 days was decided based on previous studies conducted. [3] Hereafter, for the purpose of discussion, day 1 indicates the day of admission and last day indicates either day 5 after admissi Continue reading >>

Department Of Critical Care Medicine

Department Of Critical Care Medicine

MANTRA (Experimental and Mechanistic Research) Severe sepsis (acute onset organ failure in the setting of infection)1 is a major health problem that kills nearly 250,000 Americans each year and costs billions of dollars.2 Available therapies for sepsis, including those recently approved, are suboptimal and new therapies are urgently needed. While our understanding of the pathophysiology of sepsis remains incomplete, it is generally accepted that the inflammatory response to infection or injury includes the expression of numerous cell-associated and soluble molecules, and it is believed that this systemic inflammation is in large part responsible for the development of shock and the occurrence of organ injury.3 A class of these molecules, known as cytokines,4 includes species that are considered pro-inflammatory in the setting of sepsis (such as tumor necrosis factor [TNF] and interleukin [IL]-1) and other species considered anti-inflammatory (such as IL-10 and IL-4).5-7 Under normal conditions, cytokines appear to exert their effects on the local environment in an autocrine or paracrine fashion.4 However, numerous clinical conditions are associated with a systemic release of pro- and anti-inflammatory cytokines and these substances appear to produce systemic effects including fever, tachycardia, hypotension, tissue edema and leukocytosis in an endocrine fashion.8-10 These signs characterize the syndrome of sepsis. Sepsis also includes the diverse actions of multiple other systems including complement, coagulation, reactive oxygen and nitrogen species and multiple serum proteins and enzymes.11 Finally, supportive therapy including fluids, vasopressors and mechanic support all have the capacity to further affect systemic inflammation (figure 1).12-14 Figure 1. Pathophysi Continue reading >>

Cn101511820a - Double Benzimidazole Derivative With Ppar Gamma Excitomotor Activity And Application Thereof - Google Patents

Cn101511820a - Double Benzimidazole Derivative With Ppar Gamma Excitomotor Activity And Application Thereof - Google Patents

CN101511820A - Double benzimidazole derivative with PPAR gamma excitomotor activity and application thereof - Google Patents Double benzimidazole derivative with PPAR gamma excitomotor activity and application thereof CN101511820A CN 200780033467 CN200780033467A CN101511820A CN 101511820 A CN101511820 A CN 101511820A CN 200780033467 CN200780033467 CN 200780033467 CN 200780033467 A CN200780033467 A CN 200780033467A CN 101511820 A CN101511820 A CN 101511820A Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.) C07D235/00Heterocyclic compounds containing 1,3-diazole or hydrogenated 1,3-diazole rings, condensed with other rings C07D235/02Heterocyclic compounds containing 1,3-diazole or hydrogenated 1,3-diazole rings, condensed with other rings condensed with carbocyclic rings or ring systems C07D235/04Benzimidazoles; Hydrogenated benzimidazoles C07D235/20Two benzimidazolyl-2 radicals linked together directly or via a hydrocarbon or substituted hydrocarbon radical Bibenzimidazole derivatives having PPARgama agonist activity or its salts, their manufacturing methods, and their uses in treating PPARgama receptor-related diseases. The compounds is selective PPARgama agonist and have specific PPARgama-activated activity, and thus can be used to treat PPARgama receptor-related diseases, abnormal increased blood sugar-related diseases, in particularly, diabetes mellitus, or metabolic syndrome, etc. CN 200780033467 2006-07-07 2007-07-06 Double benzimidazole derivative with PPAR gamma excitomotor activity and application thereof CN101511820A (en)

Lactic Acidosis Secondary To Metformin Overdose: A Case Report

Lactic Acidosis Secondary To Metformin Overdose: A Case Report

Timbrell et al.; licensee BioMed Central Ltd.2012 Metformin is a commonly used treatment modality in type 2 diabetes mellitus, with a well documented side effect of lactic acidosis. In the intensive care setting lactate and pH levels are regularly used as a useful predictor of poor prognosis. In this article we highlight how high lactate levels are not an accurate predictor of mortality in deliberate metformin overdose. We present the case of a 70-year-old Caucasian man who took a deliberate metformin overdose of unknown quantity. He had a profound lactic acidosis at presentation with a pH of 6.93 and a lactate level of more than 20mmol/L. These figures would normally correspond with a mortality of more than 80%; however, with appropriate management this patients condition improved. We provide evidence that the decision to treat severe lactic acidosis in deliberate metformin overdose should not be based on arterial lactate and pH levels, as would be the case in other overdoses. We also demonstrate that appropriate treatment with hemodiafiltration and 8.4% sodium bicarbonate, even in patients with a very high lactate and low pH, can be successful. MetforminLactate LevelLactic AcidosisArterial LactateCritical Care Patient Metformin is a biguanide typically used as a first line drug for the treatment of type 2 diabetes mellitus. Its chief modes of action are reduced absorption of glucose from the gastrointestinal tract, decreased hepatic gluconeogenesis and increased peripheral utilization of glucose[ 1 ]. All of these actions lower plasma levels of glucose. Commonly reported side effects are predominantly gastrointestinal and include: nausea, vomiting and abdominal pain. Lactic acidosis is a well-recognized consequence of toxicity and is often associated with concurrent Continue reading >>

Endocrine Disorders In The Critically Ill (section 3) - Core Topics In Endocrinology In Anaesthesia And Critical Care

Endocrine Disorders In The Critically Ill (section 3) - Core Topics In Endocrinology In Anaesthesia And Critical Care

Core Topics in Endocrinology in Anaesthesia and Critical Care Section 3 - Endocrine disorders in the critically ill Edited by George M. Hall , St George's Hospital, London, Jennifer M. Hunter , University of Liverpool, Mark S. Cooper , University of Birmingham Pancreatic islet cell tumours and carcinoids are rare, and patients with these tumours form a small part of the case-load of the anaesthetist who regularly undertakes anaesthesia for major abdominal surgery. Insulinoma is the commonest functioning pancreatic neuroendocrine tumour (NET). Gastrinoma is the second commonest functioning pancreatic neuroendocrine tumour, and contrasts with insulinoma in several respects. The absence of symptoms is characteristic of non-functioning tumours. VIPoma is a rare tumour. Secretion of Vasoactive Intestinal Polypeptide produces watery diarrhea. Major upper abdominal surgery involves a bilateral subcostal incision, may last for several hours, requires dissection of lymphatic tissue and causes fluid shifts. It occasionally results in severe blood loss. A. Holdcroft has described a pre-operative checklist for the additional problems of the patient with a NET. Pre-operative investigations include pulmonary function tests, ECG, full blood count, clotting screen, electrolytes and liver function tests. Email your librarian or administrator to recommend adding this book to your organisation's collection. Core Topics in Endocrinology in Anaesthesia and Critical Care You can enter one or more administrator email addresses Please enter a valid email addressEmail already added 1. CuthbertsonD. Observations on the disturbance of metabolism produced by injury to the limbs. Lancet 1942; 1: 4337. 2. VincentJL. Metabolic support in sepsis and multiple organ failure: more questions than answers Continue reading >>

Metabolic Theory Of Septic Shock

Metabolic Theory Of Septic Shock

Number of Hits and Downloads for This Article May 4, 2014 (publication date) through Apr 27, 2018 Baishideng Publishing Group Inc, 7901 Stoneridge Drive, Suite 501, Pleasanton, CA 94588, USA Copyright 2014 Baishideng Publishing Group Co., Limited. All rights reserved. World J Crit Care Med.May 4, 2014;3(2): 45-54 Published online May 4, 2014.doi: 10.5492/wjccm.v3.i2.45 Jay Pravda, Inflammatory Disease Research Centre, West Palm Beach, FL 33420, United States Author contributions: Pravda J is the sole author of this manuscript and solely responsible for its content; Pravda J performed all the research, collected, analyzed and interpreted all the data; Pravda J conceived of and developed the Metabolic Theory of Septic Shock; Pravda J prepared and wrote the manuscript and performed all critical revisions; Pravda J certifies that the Metabolic Theory of Septic Shock is the product of his original research and Pravda J has overall responsibility for this manuscript. Correspondence to: Jay Pravda, MD, MPH, Inflammatory Disease Research Centre, West Palm Beach, P.O. Box 32632, FL 33420, United States. Septic shock is a life threatening condition that can develop subsequent to infection. Mortality can reach as high as 80% with over 150000 deaths yearly in the United States alone. Septic shock causes progressive failure of vital homeostatic mechanisms culminating in immunosuppression, coagulopathy and microvascular dysfunction which can lead to refractory hypotension, organ failure and death. The hypermetabolic response that accompanies a systemic inflammatory reaction places high demands upon stored nutritional resources. A crucial element that can become depleted early during the progression to septic shock is glutathione. Glutathione is chiefly responsible for supplying redu Continue reading >>

Epiphenomenon | Sci-napse | Academic Search Engine For Paper

Epiphenomenon | Sci-napse | Academic Search Engine For Paper

SYNOPSIS. Neighboring males in rhythmically calling insects and anurans often chorus in a synchronizing or alternating fashion. Neuroethological investigations of chorusing species reveal that their rhythms are maintained by pacemakers and that a basic interactive algorithm, common to many species, yields the collective synchrony or alternation observed. Traditionally, synchrony has been viewed as a cooperative event. However, recent evidence suggests that a collective synchronous display can also be an incidental outcome of signal jamming activities between neighboring males competing to attract females. This arises when female phonotaxis is influenced by a precedence effect in which the first of two or more closely synchronized calls is preferred. Under such circumstances, males are selected to adopt a timing mechanism averting following calls. If males happen to call at comparable rates, the adopted mechanism can yield synchrony as a by-product. Alternation, too, may be produced by a similar mechanism and also represent an epiphenomenon. That alternation, as opposed to synchrony, results may be a mere artefact of the species' solo calling rate, but perceptual constraints may select specifically for alternation in some species. Continue reading >>

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