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Li-na Zhang - One of the best experts on this subject based on the ideXlab platform.
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The clinical significance of transcranial Doppler in early diagnosis of Sepsis-Associated Encephalopathy
Zhonghua nei ke za zhi, 2019Co-Authors: Li Huang, Qiong Feng, Q Y Peng, Li-na ZhangAbstract:Objective: To investigate the clinical significance of transcranial Doppler (TCD) in early diagnosis of Sepsis-Associated Encephalopathy(SAE). Methods: Septic patients admitted to the intensive care unit(ICU) were recruited at Xiangya Hospital, Central South University from July 2015 to March 2016. Clinical data and TCD parameters during 24 hours after admission were collected. All patients were screened for delirium using the confusion assessment method for the intensive care unit (CAM-ICU) twice a day. The gold standard of the diagnosis of SAE was positive CAM-ICU evaluation. Patients were divided into SAE group and the non-SAE group. TCD data including systolic velocity (Vs), diastolic velocity (Vd), mean velocity (Vm), pulsatility index (PI) and resistant index (RI) were analyzed to determine the optimal diagnostic cut-off value. Results: A total of 43 patients were enrolled including 12 in SAE group and 31 in non-SAE group. Vm and Vd were lower in SAE group [Vm: (53.50±12.22) cm/s vs. (61.68±9.63) cm/s, P
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Serum glial fibrillary acidic protein and ubiquitin C-terminal hydrolase-L1 for diagnosis of Sepsis-Associated Encephalopathy and outcome prognostication
Journal of Critical Care, 2019Co-Authors: Long Wu, Songyun Deng, Mei-lin Ai, Li-na Zhang, Qing Feng, Yu-hang AiAbstract:Abstract Purpose We investigated the role of serum Glial Fibrillary Acidic Protein (GFAP) and Ubiquitin C-Terminal Hydrolase-L1 (UCH-L1) in diagnosis of Sepsis-Associated Encephalopathy(SAE), predicting prognosis and long-term quality of life with patients of Sepsis. Materials and methods This is a prospective single center study entailed 105 patients whosuffered from Sepsis from Jan 2015 to Aug 2016. Serum concentrations of GFAP and UCH-L1 for diagnosis of SAE and predicting prognosis and long-term quality of life with patients of Sepsis were analyzed. Results The serum concentrations of GFAP and UCH-L1 were higher in SAE group than in no-SAE group (p Conclusions Serum concentrations GFAP and UCH-L1 early elevated and Associated with Sepsis-Associated Encephalopathy, poor prognosis and quality of life.
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the diagnostic value of neuron specific enolase central nervous system specific protein and interleukin 6 in Sepsis Associated Encephalopathy
Chinese Journal of Internal Medicine, 2017Co-Authors: Qiong Feng, Songyun Deng, Li Huang, Z Y Liu, Li-na ZhangAbstract:Objective To investigate the diagnostic value of neuron-specific enolase(NSE), central nervous system specific protein(S100β), interleukin-6(IL-6) in Sepsis-Associated Encephalopathy(SAE). Methods Clinical data of patients admitted to ICU and diagnosed with Sepsis were collected from January 2015 to June 2016 in Xiangya Hospital, Central South University. SAE was defined as cerebral dysfunction in the presence of Sepsis that also fulfilled the exclusion criteria. The acute physiology and chronic health score (APACHE Ⅱ), sequential organ failure assessment (SOFA), NSE, S100β, IL-6, ICU stay time and 28-day mortality were compared between the two groups. NSE, S100β and IL-6 were measured on the 1st and 3rd day in ICU to determine the optimal cut-off value of SAE. Results Among 59 enrolled patients, 36 were assigned to SAE group while 23 were non-SAE group. The SAE group had a significantly higher APACHE Ⅱ and SOFA scores, as well as the length of ICU stay (P 0.05). The diagnostic values for SAE of NSE, S100β and IL-6 were 14.36 μg/L, 0.14 μg/L and 91.305 mg/L with sensitivity 61.1%, 61.1%, 72.2% and specificity 73.9%, 69.6%, 69.6%, respectively. The diagnostic AUC of NSE and IL-6 combination was 0.774, 95%CI 0.651-0.896. Conclusion All Sepsis patients have different degrees of brain injury. NSE combined with IL-6 on the 3rd day in ICU demonstrates the diagnostic significance of SAE. Key words: Sepsis; Sepsis-Associated Encephalopathy; Neuron-specific enolase; Central nervous system specific protein; Interleukin-6
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Characterization of Sepsis and Sepsis-Associated Encephalopathy:
Journal of intensive care medicine, 2017Co-Authors: Qing Feng, Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Li-na ZhangAbstract:Background:Sepsis and Sepsis-Associated Encephalopathy (SAE) are common intensive care unit (ICU) diseases; the morbidity and mortality are high. The present study analyzed the sensitivity of diffe...
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Neuroglobin Protects Rats from Sepsis-Associated Encephalopathy via a PI3K/Akt/Bax-Dependent Mechanism.
Journal of molecular neuroscience : MN, 2017Co-Authors: Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Cai-xia Chen, Lemeng Zhang, Li-na ZhangAbstract:Sepsis-Associated Encephalopathy (SAE) is a common complication of Sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.
Li Huang - One of the best experts on this subject based on the ideXlab platform.
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The clinical significance of transcranial Doppler in early diagnosis of Sepsis-Associated Encephalopathy
Zhonghua nei ke za zhi, 2019Co-Authors: Li Huang, Qiong Feng, Q Y Peng, Li-na ZhangAbstract:Objective: To investigate the clinical significance of transcranial Doppler (TCD) in early diagnosis of Sepsis-Associated Encephalopathy(SAE). Methods: Septic patients admitted to the intensive care unit(ICU) were recruited at Xiangya Hospital, Central South University from July 2015 to March 2016. Clinical data and TCD parameters during 24 hours after admission were collected. All patients were screened for delirium using the confusion assessment method for the intensive care unit (CAM-ICU) twice a day. The gold standard of the diagnosis of SAE was positive CAM-ICU evaluation. Patients were divided into SAE group and the non-SAE group. TCD data including systolic velocity (Vs), diastolic velocity (Vd), mean velocity (Vm), pulsatility index (PI) and resistant index (RI) were analyzed to determine the optimal diagnostic cut-off value. Results: A total of 43 patients were enrolled including 12 in SAE group and 31 in non-SAE group. Vm and Vd were lower in SAE group [Vm: (53.50±12.22) cm/s vs. (61.68±9.63) cm/s, P
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the diagnostic value of neuron specific enolase central nervous system specific protein and interleukin 6 in Sepsis Associated Encephalopathy
Chinese Journal of Internal Medicine, 2017Co-Authors: Qiong Feng, Songyun Deng, Li Huang, Z Y Liu, Li-na ZhangAbstract:Objective To investigate the diagnostic value of neuron-specific enolase(NSE), central nervous system specific protein(S100β), interleukin-6(IL-6) in Sepsis-Associated Encephalopathy(SAE). Methods Clinical data of patients admitted to ICU and diagnosed with Sepsis were collected from January 2015 to June 2016 in Xiangya Hospital, Central South University. SAE was defined as cerebral dysfunction in the presence of Sepsis that also fulfilled the exclusion criteria. The acute physiology and chronic health score (APACHE Ⅱ), sequential organ failure assessment (SOFA), NSE, S100β, IL-6, ICU stay time and 28-day mortality were compared between the two groups. NSE, S100β and IL-6 were measured on the 1st and 3rd day in ICU to determine the optimal cut-off value of SAE. Results Among 59 enrolled patients, 36 were assigned to SAE group while 23 were non-SAE group. The SAE group had a significantly higher APACHE Ⅱ and SOFA scores, as well as the length of ICU stay (P 0.05). The diagnostic values for SAE of NSE, S100β and IL-6 were 14.36 μg/L, 0.14 μg/L and 91.305 mg/L with sensitivity 61.1%, 61.1%, 72.2% and specificity 73.9%, 69.6%, 69.6%, respectively. The diagnostic AUC of NSE and IL-6 combination was 0.774, 95%CI 0.651-0.896. Conclusion All Sepsis patients have different degrees of brain injury. NSE combined with IL-6 on the 3rd day in ICU demonstrates the diagnostic significance of SAE. Key words: Sepsis; Sepsis-Associated Encephalopathy; Neuron-specific enolase; Central nervous system specific protein; Interleukin-6
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Characterization of Sepsis and Sepsis-Associated Encephalopathy:
Journal of intensive care medicine, 2017Co-Authors: Qing Feng, Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Li-na ZhangAbstract:Background:Sepsis and Sepsis-Associated Encephalopathy (SAE) are common intensive care unit (ICU) diseases; the morbidity and mortality are high. The present study analyzed the sensitivity of diffe...
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Neuroglobin Protects Rats from Sepsis-Associated Encephalopathy via a PI3K/Akt/Bax-Dependent Mechanism.
Journal of molecular neuroscience : MN, 2017Co-Authors: Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Cai-xia Chen, Lemeng Zhang, Li-na ZhangAbstract:Sepsis-Associated Encephalopathy (SAE) is a common complication of Sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.
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neuroglobin protects rats from Sepsis Associated Encephalopathy via a pi3k akt bax dependent mechanism
Journal of Molecular Neuroscience, 2017Co-Authors: Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Cai-xia Chen, Lemeng Zhang, Li-na ZhangAbstract:Sepsis-Associated Encephalopathy (SAE) is a common complication of Sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.
Béla Fülesdi - One of the best experts on this subject based on the ideXlab platform.
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Sepsis-Associated Encephalopathy: A review of literature
Neurology India, 2018Co-Authors: Levente Molnár, Béla Fülesdi, Norbert Nemeth, Csilla MolnárAbstract:Sepsis is a leading cause of death in medical and surgical intensive care units (ICUs). Disturbance of consciousness of varying severity is an early warning sign of developing Sepsis in the majority of cases. Sepsis-Associated Encephalopathy (SAE) is the most frequent type of Encephalopathy in the ICU and is defined as a state of diffuse cerebral dysfunction caused by the inflammatory response of the body to various infections, where the inflammatory process does not affect the central nervous system (CNS) directly and the primary symptom is a disturbed level of consciousness. The aim of this comprehensive review was to collect the latest scientific knowledge regarding the epidemiology, clinical aspects, pathogenesis, diagnosis, and possible prevention strategies related to SAE.
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Sepsis-Associated Encephalopathy
Orvosi hetilap, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, István Takács, Péter Siró, Béla FülesdiAbstract:Sepsis-Associated Encephalopathy is a common but neglected clinical symptom of systemic inflammatory reaction in the early phase. The clinical spectrum of diffuse cerebral dysfunction induced by systemic Sepsis--Sepsis-Associated Encephalopathy according to the new terms--varies from transient, reversible Encephalopathy, to severe irreversible brain damage. The aim of the present publication is to summarize the pathophysiology, frequent symptoms and possible treatments of the disease based on international and Hungarian articles on this topic. We want to emphasize the importance of monitoring the patient's mental status due to the fact that consciousness' disturbance of different severity is an early warning sign of Sepsis, so it has high clinical significance.
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impaired cerebrovascular reactivity in Sepsis Associated Encephalopathy studied by acetazolamide test
Critical Care, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, István Takács, Csilla Molnár, Akos Csomos, Judit Hallay, Béla FülesdiAbstract:Introduction The pathophysiology of Sepsis-Associated Encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.
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Acetazolamide-induced cerebrovascular reactivity is impaired in Sepsis-Associated Encephalopathy
Critical Care, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, Csilla Molnár, Béla FülesdiAbstract:The pathophysiology of Sepsis-Associated Encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with SAE.
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A szepszishez társuló encephalopathia = Sepsis-Associated Encephalopathy
2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, István Takács, Péter Siró, Béla FülesdiAbstract:A szepszishez tarsulo encephalopathia a szisztemas gyulladasos reakcio korai szakaszaban jelentkező, gyakori, de klinikai szempontbol elhanyagolt tunete. A szisztemas szepszis okozta diffuz agyi műkodeszavar, ujabb elnevezes szerint a szepszishez tarsulo encephalopathia (Sepsis-Associated Encephalopathy – SAE) valtozatos megjelenesű lehet: az atmeneti, reverzibilis encephalopathiaval jellemezhető formatol egeszen a visszafordithatatlan agyi karosodassal jaro sulyos formaig terjedhet a klinikai spektrum. A jelen kozlemenyben a hazai es a nemzetkozi szakirodalom attekintese alapjan ossze kivantuk foglalni a korkep korelettani hatteret, a leggyakrabban előfordulo klinikai tuneteket es a kezeles lehetseges modjait. Fel kivantuk hivni a figyelmet arra, hogy szepszisben a kulonboző sulyossagu tudatzavar az egyik legkorabbi figyelmeztető tunet, ezert a szepszis szempontjabol veszelyeztetett betegekben felismerese nagy klinikai jelentősegű. | Sepsis-Associated Encephalopathy is a common but neglected clinical symptom of systemic inflammatory reaction in the early phase. The clinical spectrum of diffuse cerebral dysfunction induced by systemic Sepsis – Sepsis-Associated Encephalopathy according to the new terms- varies from transient, reversible Encephalopathy, to severe irreversible brain damage. The aim of the present publication is to summarize the pathophysiology, frequent symptoms and possible treatments of the disease based on international and Hungarian articles on this topic. We want to emphasize the importance of monitoring the patient’s mental status due to the fact that consciousness’ disturbance of different severity is an early warning sign of Sepsis, so it has high clinical significance.
Hua Gong - One of the best experts on this subject based on the ideXlab platform.
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Characterization of Sepsis and Sepsis-Associated Encephalopathy:
Journal of intensive care medicine, 2017Co-Authors: Qing Feng, Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Li-na ZhangAbstract:Background:Sepsis and Sepsis-Associated Encephalopathy (SAE) are common intensive care unit (ICU) diseases; the morbidity and mortality are high. The present study analyzed the sensitivity of diffe...
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Neuroglobin Protects Rats from Sepsis-Associated Encephalopathy via a PI3K/Akt/Bax-Dependent Mechanism.
Journal of molecular neuroscience : MN, 2017Co-Authors: Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Cai-xia Chen, Lemeng Zhang, Li-na ZhangAbstract:Sepsis-Associated Encephalopathy (SAE) is a common complication of Sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.
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neuroglobin protects rats from Sepsis Associated Encephalopathy via a pi3k akt bax dependent mechanism
Journal of Molecular Neuroscience, 2017Co-Authors: Songyun Deng, Hua Gong, Li Huang, Qianyi Peng, Cai-xia Chen, Lemeng Zhang, Li-na ZhangAbstract:Sepsis-Associated Encephalopathy (SAE) is a common complication of Sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.
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Expression and role of neuroglobin in rats with Sepsis-Associated Encephalopathy.
Critical Care Medicine, 2014Co-Authors: Li-na Zhang, Yu-hang Ai, Hua Gong, Li HuangAbstract:To determine the role of neuroglobin in the pathology of Sepsis-Associated Encephalopathy and ascertain if neuroglobin has any protective effects against Sepsis-Associated Encephalopathy. Randomized laboratory animal study. Research university animal laboratory. Two hundred and forty adult male Sprague-Dawley rats. Rats received cecal puncture and ligation (or sham) surgery to induce Sepsis, then broken up into groups based on whether or not the rat developed Sepsis-Associated Encephalopathy as determined by electroencephalograph and evoked potential recordings. The rats were then left untreated to examine the effect of Sepsis-Associated Encephalopathy on neuroglobin, treated with a neuroglobin antisense nucleotide to block gene expression, or given hemin, a neuroglobin inducer. Following Sepsis induction, diagnosis, and treatment, the brains were analyzed for both gross and ultrastructural morphology. Also, neuronal neuroglobin immunoreactivity and apoptosis (via terminal uridine nucleotide end-labeling) were examined. Blood serum levels were then analyzed for neuroglobin, superoxide dismutase, and malondialdehyde levels. We determined that Sepsis-Associated Encephalopathy induces damage evident when examining both gross and ultrastructural morphology, as well as induces neuronal neuroglobin expression. Also, blockade of neuroglobin expression via antisense treatment will exacerbate these pathological effects, while increasing neuroglobin levels via hemin will ameliorate them. Blood analysis found that levels of superoxide dismutase and malondialdehyde mirrored the level of pathology found in the brain, while plasma neuroglobin levels reflected the amount of neuronal neuroglobin immunoreactivity. We conclude that neuroglobin is involved in the pathogenesis of Sepsis-Associated Encephalopathy and has neuroprotective effects. We also determined that hemin has protective effects against Sepsis-Associated Encephalopathy as well, most probably due to its effect on neuroglobin.
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Expression and role of neuroglobin in rats with Sepsis-Associated Encephalopathy.
Critical care medicine, 2014Co-Authors: Li-na Zhang, Hua Gong, Li Huang, Qu-lian Guo, Zhiyong Liu, Bo YaoAbstract:Objectives To determine the role of neuroglobin in the pathology of Sepsis-Associated Encephalopathy and ascertain if neuroglobin has any protective effects against Sepsis-Associated Encephalopathy. Design Randomized laboratory animal study. Setting Research university animal laboratory. Subjects Two hundred and forty adult male Sprague-Dawley rats. Interventions Rats received cecal puncture and ligation (or sham) surgery to induce Sepsis, then broken up into groups based on whether or not the rat developed Sepsis-Associated Encephalopathy as determined by electroencephalograph and evoked potential recordings. The rats were then left untreated to examine the effect of Sepsis-Associated Encephalopathy on neuroglobin, treated with a neuroglobin antisense nucleotide to block gene expression, or given hemin, a neuroglobin inducer. Measurements and main results Following Sepsis induction, diagnosis, and treatment, the brains were analyzed for both gross and ultrastructural morphology. Also, neuronal neuroglobin immunoreactivity and apoptosis (via terminal uridine nucleotide end-labeling) were examined. Blood serum levels were then analyzed for neuroglobin, superoxide dismutase, and malondialdehyde levels. We determined that Sepsis-Associated Encephalopathy induces damage evident when examining both gross and ultrastructural morphology, as well as induces neuronal neuroglobin expression. Also, blockade of neuroglobin expression via antisense treatment will exacerbate these pathological effects, while increasing neuroglobin levels via hemin will ameliorate them. Blood analysis found that levels of superoxide dismutase and malondialdehyde mirrored the level of pathology found in the brain, while plasma neuroglobin levels reflected the amount of neuronal neuroglobin immunoreactivity. Conclusions We conclude that neuroglobin is involved in the pathogenesis of Sepsis-Associated Encephalopathy and has neuroprotective effects. We also determined that hemin has protective effects against Sepsis-Associated Encephalopathy as well, most probably due to its effect on neuroglobin.
Szilárd Szatmári - One of the best experts on this subject based on the ideXlab platform.
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Sepsis-Associated Encephalopathy
Orvosi hetilap, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, István Takács, Péter Siró, Béla FülesdiAbstract:Sepsis-Associated Encephalopathy is a common but neglected clinical symptom of systemic inflammatory reaction in the early phase. The clinical spectrum of diffuse cerebral dysfunction induced by systemic Sepsis--Sepsis-Associated Encephalopathy according to the new terms--varies from transient, reversible Encephalopathy, to severe irreversible brain damage. The aim of the present publication is to summarize the pathophysiology, frequent symptoms and possible treatments of the disease based on international and Hungarian articles on this topic. We want to emphasize the importance of monitoring the patient's mental status due to the fact that consciousness' disturbance of different severity is an early warning sign of Sepsis, so it has high clinical significance.
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impaired cerebrovascular reactivity in Sepsis Associated Encephalopathy studied by acetazolamide test
Critical Care, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, István Takács, Csilla Molnár, Akos Csomos, Judit Hallay, Béla FülesdiAbstract:Introduction The pathophysiology of Sepsis-Associated Encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.
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Acetazolamide-induced cerebrovascular reactivity is impaired in Sepsis-Associated Encephalopathy
Critical Care, 2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, Csilla Molnár, Béla FülesdiAbstract:The pathophysiology of Sepsis-Associated Encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with SAE.
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A szepszishez társuló encephalopathia = Sepsis-Associated Encephalopathy
2010Co-Authors: Szilárd Szatmári, Tamás Végh, Csaba Antek, István Takács, Péter Siró, Béla FülesdiAbstract:A szepszishez tarsulo encephalopathia a szisztemas gyulladasos reakcio korai szakaszaban jelentkező, gyakori, de klinikai szempontbol elhanyagolt tunete. A szisztemas szepszis okozta diffuz agyi műkodeszavar, ujabb elnevezes szerint a szepszishez tarsulo encephalopathia (Sepsis-Associated Encephalopathy – SAE) valtozatos megjelenesű lehet: az atmeneti, reverzibilis encephalopathiaval jellemezhető formatol egeszen a visszafordithatatlan agyi karosodassal jaro sulyos formaig terjedhet a klinikai spektrum. A jelen kozlemenyben a hazai es a nemzetkozi szakirodalom attekintese alapjan ossze kivantuk foglalni a korkep korelettani hatteret, a leggyakrabban előfordulo klinikai tuneteket es a kezeles lehetseges modjait. Fel kivantuk hivni a figyelmet arra, hogy szepszisben a kulonboző sulyossagu tudatzavar az egyik legkorabbi figyelmeztető tunet, ezert a szepszis szempontjabol veszelyeztetett betegekben felismerese nagy klinikai jelentősegű. | Sepsis-Associated Encephalopathy is a common but neglected clinical symptom of systemic inflammatory reaction in the early phase. The clinical spectrum of diffuse cerebral dysfunction induced by systemic Sepsis – Sepsis-Associated Encephalopathy according to the new terms- varies from transient, reversible Encephalopathy, to severe irreversible brain damage. The aim of the present publication is to summarize the pathophysiology, frequent symptoms and possible treatments of the disease based on international and Hungarian articles on this topic. We want to emphasize the importance of monitoring the patient’s mental status due to the fact that consciousness’ disturbance of different severity is an early warning sign of Sepsis, so it has high clinical significance.
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Sepsis-Associated Encephalopathy studied by acetazolamide test
2010Co-Authors: Szilárd Szatmári, Tamás Végh, István Takács, Csilla Molnár, Akos Csomos, Judit Hallay, Béla FülesdiAbstract:Introduction: The pathophysiology of Sepsis-Associated Encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE. Methods: Patients fulfilling the criteria of clinical Sepsis and showing disturbance of consciousness of any severity were included (n = 14). Non-septic persons whithout previous diseases affecting cerebral vasoreactivity served as controls (n = 20). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity, CVR) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity, CRC) were compared among the groups. Results: Absolute blood flow velocities after adminsitration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that patients with SAE reacted to a lesser extent to the drug than did control subjects (CRC controls:46.2 ± 15.9%, CRC SAE: 31,5 ± 15.8%, P < 0.01). Conclusions: We conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.
