The Experts below are selected from a list of 144 Experts worldwide ranked by ideXlab platform
Gary Gerfen - One of the best experts on this subject based on the ideXlab platform.
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Human 2-Oxoglutarate Dehydrogenase and 2-Oxoadipate Dehydrogenase Both Generate Superoxide/H_2O_2 in a Side Reaction and Each Could Contribute to Oxidative Stress in Mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H_2O_2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l -lysine, l -hydroxylysine and l -tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H_2O_2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H_2O_2 in mitochondria.
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human 2 oxoglutarate dehydrogenase and 2 oxoadipate dehydrogenase both generate superoxide h2o2 in a side reaction and each could contribute to oxidative stress in mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H2O2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l-lysine, l-hydroxylysine and l-tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H2O2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H2O2 in mitochondria.
Ronnie Fass - One of the best experts on this subject based on the ideXlab platform.
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Overlap Between GERD and Functional Esophageal Disorders-a Pivotal Mechanism for Treatment Failure.
Current treatment options in gastroenterology, 2019Co-Authors: Ofer Z. Fass, Ronnie FassAbstract:ᅟRefractory GERD is very common, and while many different underlying mechanisms have been identified, the main focus has remained on residual reflux (acidic or non-acidic). Recently, Rome IV introduced two new concepts with important impact on patients with refractory GERD. They include the introduction of the reflux hypersensitivity group and the proposal that GERD can overlap with a functional Esophageal Disorder. Recent studies have demonstrated that the latter affects approximately three quarters of the GERD patients who failed PPI once daily.
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Reflux Hypersensitivity: A New Functional Esophageal Disorder.
Journal of neurogastroenterology and motility, 2017Co-Authors: Takahisa Yamasaki, Ronnie FassAbstract:Reflux hypersensitivity, recently introduced by Rome IV as a new functional Esophageal Disorder, is currently considered as the presence of typical heartburn symptoms in patients with normal upper endoscopy and Esophageal biopsies, normal Esophageal pH test and with evidence of a close correlation between patients' heartburn and reflux events. Reflux hypersensitivity is very common and together with functional heartburn accounts for more than 90% of the heartburn patients who failed treatment with proton pump inhibitor twice daily. In addition, reflux hypersensitivity affects primarily young to middle aged women, commonly overlaps with another functional gastrointestinal Disorders, and is often associated with some type of psychological comorbidity. Diagnosis is made by using endoscopy with Esophageal biopsies, pH-impedance, and high-resolution Esophageal manometry. Reflux hypersensitivity is primarily treated with Esophageal neuromodulators, such as tricyclic anti-depressants and selective serotonin reuptake inhibitors among others. Surgical anti-reflux management may also play an important role in the treatment of reflux hypersensitivity.
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Current perspectives on the diagnosis and treatment of functional Esophageal Disorders.
Current gastroenterology reports, 2003Co-Authors: Roy Dekel, Ronnie FassAbstract:Among the functional gastrointestinal Disorders, functional Disorders of the esophagus are second in prevalence only to irritable bowel syndrome. Progress has been made in recent years in our understanding of the pathophysiology of functional Esophageal Disorders. In this review we focus on recent advances in their diagnosis and treatment. Additionally, we critically appraise the current understanding of the various clinical aspects of each Esophageal Disorder. Finally, we highlight unanswered questions and areas of controversy.
Frank Jordan - One of the best experts on this subject based on the ideXlab platform.
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Human 2-Oxoglutarate Dehydrogenase and 2-Oxoadipate Dehydrogenase Both Generate Superoxide/H_2O_2 in a Side Reaction and Each Could Contribute to Oxidative Stress in Mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H_2O_2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l -lysine, l -hydroxylysine and l -tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H_2O_2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H_2O_2 in mitochondria.
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human 2 oxoglutarate dehydrogenase and 2 oxoadipate dehydrogenase both generate superoxide h2o2 in a side reaction and each could contribute to oxidative stress in mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H2O2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l-lysine, l-hydroxylysine and l-tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H2O2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H2O2 in mitochondria.
Natalia Nemeria - One of the best experts on this subject based on the ideXlab platform.
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Human 2-Oxoglutarate Dehydrogenase and 2-Oxoadipate Dehydrogenase Both Generate Superoxide/H_2O_2 in a Side Reaction and Each Could Contribute to Oxidative Stress in Mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H_2O_2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l -lysine, l -hydroxylysine and l -tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H_2O_2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H_2O_2 in mitochondria.
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human 2 oxoglutarate dehydrogenase and 2 oxoadipate dehydrogenase both generate superoxide h2o2 in a side reaction and each could contribute to oxidative stress in mitochondria
Neurochemical Research, 2019Co-Authors: Frank Jordan, Natalia Nemeria, Gary GerfenAbstract:According to recent findings, the human 2-oxoglutarate dehydrogenase complex (hOGDHc) could be an important source of the reactive oxygen species in the mitochondria and could contribute to mitochondrial abnormalities associated with multiple neurodegenerative diseases, including Alzheimer’s disease, Huntington disease, and Parkinson’s disease. The human 2-oxoadipate dehydrogenase (hE1a) is a novel protein, which is encoded by the DHTKD1 gene. Both missence and nonsense mutations were identified in the DHTKD1 that lead to alpha-aminoadipic and alpha-oxoadipic aciduria, a metabolic Disorder with a wide variety of the neurological abnormalities, and Charcot-Marie-Tooth disease type 2Q, an inherited neurological Disorder affecting the peripheral nervous system. Recently, the rare pathogenic mutations in DHTKD1 and an increased H2O2 production were linked to the genetic ethiology of Eosinophilic Esophagitis (EoE), a chronic allergic inflammatory Esophageal Disorder. In view of the importance of hOGDHc in the tricarboxylic acid cycle (TCA cycle) and hE1a on the l-lysine, l-hydroxylysine and l-tryptophan degradation pathway in mitochondria, and to enhance our current understanding of the mechanism of superoxide/H2O2 generation by hOGDHc, and by human 2-oxoadipate dehydrogenase complex (hOADHc), this review focuses on several novel and unanticipated recent findings in vitro that emerged from the Jordan group’s research. Most significantly, the hE1o and hE1a now join the hE3 as being able to generate the superoxide/H2O2 in mitochondria.
Claude Lenfant - One of the best experts on this subject based on the ideXlab platform.
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chest pain of cardiac and noncardiac origin
Metabolism-clinical and Experimental, 2010Co-Authors: Claude LenfantAbstract:Chest pain is one of the most common symptoms driving patients to a physician's office or the hospital's emergency department. In approximately half of the cases, chest pain is of cardiac origin, either ischemic cardiac or nonischemic cardiac disease. The other half is due to noncardiac causes, primarily Esophageal Disorder. Pain from either origin may occur in the same patient. In addition, psychological and psychiatric factors play a significant role in the perception and severity of the chest pain, irrespective of its cause. Chest pain of ischemic cardiac disease is called angina pectoris. Stable angina may be the prelude of ischemic cardiac disease; and for this reason, it is essential to ensure a correct diagnosis. In most cases, further testing, such as exercise testing and angiography, should be considered. The more severe form of chest pain, unstable angina, also requires a firm diagnosis because it indicates severe coronary disease and is the earliest manifestation of acute myocardial infarction. Once a diagnosis of stable or unstable angina is established, and if a decision is made not to use invasive therapy, such as coronary bypass, percutaneous transluminal coronary angioplasty, or stent insertion, effective medical treatment of associated cardiac risk factors is a must. Acute myocardial infarction occurring after a diagnosis of angina greatly increases the risk of subsequent death. Chest pain in women warrants added attention because women underestimate their likelihood to have coronary heart disease. A factor that complicates the clinical assessment of patients with chest pain (both cardiac and noncardiac in origin) is the relatively common presence of psychological and psychiatric conditions such as depression or panic Disorder. These factors have been found to cause or worsen chest pain; but unfortunately, they may not be easily detected. Noncardiac chest pain represents the remaining half of all cases of chest pain. Although there are a number of causes, gastroEsophageal Disorders are by far the most prevalent, especially gastroEsophageal reflux disease. Fortunately, this disease can be diagnosed and treated effectively by proton-pump inhibitors. The other types of non-gastroEsophageal reflux disease-related noncardiac chest pain are more difficult to diagnose and treat. In conclusion, the cause of chest pain must be accurately diagnosed; and treatment must be pursued according to the cause, especially if the cause is of cardiac origin.