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90 day mortality

WHAT WE ALREADY KNOW ABOUT THIS TOPIC Definitions and management strategies for septic shock continue to be updated as defined in Sepsis-2, Sepsis-3, and other guidelinesRecent randomized controlled trials of corticosteroids in septic shock report different treatment effects on 90-day mortality but use different inclusion criteria WHAT THIS ARTICLE TELLS US THAT IS NEW: In a post hoc analysis of the Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL) trial, in participants who fulfilled either the Sepsis-3 or -2 inclusion criteria or those with severe septic shock, a continuous infusion of hydrocortisone did not result in a lower 90-day mortality than placebo BACKGROUND:: Two recent randomized controlled trials (Adjunctive Glucocorticoid Therapy in Patients with Septic Shock [ADRENAL] and Activated Protein C and Corticosteroids for Human Septic Shock [APROCCHSS]) of corticosteroids in patients with septic shock reported different treatment effects on 90-day mortality.

Hydrocortisone Compared with Placebo in Patients with Septic Shock Satisfying the Sepsis-3 Diagnostic Criteria and APROCCHSS Study Inclusion Criteria: A Post Hoc Analysis of the ADRENAL Trial.

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Human Septic sentence examples within human septic shock

human septic shock

Endotoxin and its induced exaggerative responses of proinflammatory cytokines such as Tumor Necrosis Factor (TNF) cause human septic shock.

Generalized Shwartzman Reaction as an Experimental Endotoxin Shock Model: Role of Intermediate T Cell Receptor-Expressing Innate T Lymphocytes in its Pathogenesis

human septic shock

We explored the biological coherence of a large panel of sepsis mediators and their clinical relevance in septic myocardial dysfunction and organ failures during human septic shock.

A multiplex analysis of sepsis mediators during human septic shock: a preliminary study on myocardial depression and organ failures

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Human Septic sentence examples within human septic patient

human septic patient

INTERVENTIONS Prokineticin2 concentrations were measured and analyzed in human septic patients, patient controls, and healthy individuals.

Identifying Prokineticin2 as a Novel Immunomodulatory Factor in Diagnosis and Treatment of Sepsis.

human septic patient

scRNAseq analyses confirmed the expansion of Ly6Chi monocyte cluster, with elevation of pathogenic inflammatory genes previously observed in human septic patients.

Development of Exhausted Memory Monocytes and Underlying Mechanisms

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10.1038/s41598-021-93156-1

In vitro, canagliflozin was demonstrated to activate α1AMPK/p38MAPK/HSP27 pathway and to preserve VE-Cad’s integrity in human endothelial cells exposed to human septic plasma.

Canagliflozin protects against sepsis capillary leak syndrome by activating endothelial α1AMPK

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10.1097/CCM.0000000000005335

INTERVENTIONS Prokineticin2 concentrations were measured and analyzed in human septic patients, patient controls, and healthy individuals.

Identifying Prokineticin2 as a Novel Immunomodulatory Factor in Diagnosis and Treatment of Sepsis.

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10.1016/j.jss.2020.12.016

MATERIALS AND METHODS To explore the role of STIM1-gated SOCE in vascular endothelial cell calcium overload and inflammation, we established a human septic serum or lipopolysaccharide (LPS)-induced human umbilical vein endothelial cell (HUVEC) experimental system and derived ribonucleic acid interference (RNAi)-mediated STIM1, ORAI1 (orai gene [HGNC: 25896 Entrez Gene: 84876] coding protein, ORAI Calcium Release-Activated Calcium Modulator 1), and transient receptor potential channel 1 (TRPC1) (core components of store-operated Ca2+[SOC]) downregulated HUVECs, as well as STIM1 overinduced HUVECs.

STIM1 Regulates Endothelial Calcium Overload and Cytokine Upregulation During Sepsis.

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10.35248/2165-8056.21.S2.001

Endotoxin and its induced exaggerative responses of proinflammatory cytokines such as Tumor Necrosis Factor (TNF) cause human septic shock.

Generalized Shwartzman Reaction as an Experimental Endotoxin Shock Model: Role of Intermediate T Cell Receptor-Expressing Innate T Lymphocytes in its Pathogenesis

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10.3389/fimmu.2021.778830

scRNAseq analyses confirmed the expansion of Ly6Chi monocyte cluster, with elevation of pathogenic inflammatory genes previously observed in human septic patients.

Development of Exhausted Memory Monocytes and Underlying Mechanisms

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10.1186/s13613-019-0538-3

We explored the biological coherence of a large panel of sepsis mediators and their clinical relevance in septic myocardial dysfunction and organ failures during human septic shock.

A multiplex analysis of sepsis mediators during human septic shock: a preliminary study on myocardial depression and organ failures

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10.1097/SHK.0000000000001395

This preliminary data supports myocardial edema as a potentially relevant and largely unexplored mechanism of human septic cardiomyopathy.

Myocardial Edema: An Overlooked Mechanism of Septic Cardiomyopathy?

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10.1093/ajhp/zxz017

The recently published Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL) and Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trials provide valuable but opposing insight into this ongoing debate.

Low-dose corticosteroids in septic shock: Has the pendulum shifted?

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10.1097/ALN.0000000000002955

WHAT WE ALREADY KNOW ABOUT THIS TOPIC Definitions and management strategies for septic shock continue to be updated as defined in Sepsis-2, Sepsis-3, and other guidelinesRecent randomized controlled trials of corticosteroids in septic shock report different treatment effects on 90-day mortality but use different inclusion criteria WHAT THIS ARTICLE TELLS US THAT IS NEW: In a post hoc analysis of the Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL) trial, in participants who fulfilled either the Sepsis-3 or -2 inclusion criteria or those with severe septic shock, a continuous infusion of hydrocortisone did not result in a lower 90-day mortality than placebo BACKGROUND:: Two recent randomized controlled trials (Adjunctive Glucocorticoid Therapy in Patients with Septic Shock [ADRENAL] and Activated Protein C and Corticosteroids for Human Septic Shock [APROCCHSS]) of corticosteroids in patients with septic shock reported different treatment effects on 90-day mortality.

Hydrocortisone Compared with Placebo in Patients with Septic Shock Satisfying the Sepsis-3 Diagnostic Criteria and APROCCHSS Study Inclusion Criteria: A Post Hoc Analysis of the ADRENAL Trial.

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10.1164/rccm.201811-2169LE

Ventriculoarterial decoupling in human septic shock.

Acute and Chronic Effects of Cigarette Smoking on sRAGE

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10.1111/vcp.12807

Paraoxonase-1 (PON-1) and butyrylcholinesterase (BChE) activities have been identified as significant biomarkers to monitor such disorders in human septic patients.

The diagnostic and prognostic value of paraoxonase-1 and butyrylcholinesterase activities compared with acute-phase proteins in septic dogs and stratified by the acute patient physiologic and laboratory evaluation score.

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10.1159/000500418

We hypothesized that the inflammatory response differs according to organism in human septic shock.

The Specific Organism: Not Bacterial Gram Type: Drives the Inflammatory Response in Septic Shock

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Human Septic
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What is/are Human Septic?

Human Septic - In vitro, canagliflozin was demonstrated to activate α1AMPK/p38MAPK/HSP27 pathway and to preserve VE-Cad’s integrity in human endothelial cells exposed to human septic plasma. [1] INTERVENTIONS Prokineticin2 concentrations were measured and analyzed in human septic patients, patient controls, and healthy individuals. [2] MATERIALS AND METHODS To explore the role of STIM1-gated SOCE in vascular endothelial cell calcium overload and inflammation, we established a human septic serum or lipopolysaccharide (LPS)-induced human umbilical vein endothelial cell (HUVEC) experimental system and derived ribonucleic acid interference (RNAi)-mediated STIM1, ORAI1 (orai gene [HGNC: 25896 Entrez Gene: 84876] coding protein, ORAI Calcium Release-Activated Calcium Modulator 1), and transient receptor potential channel 1 (TRPC1) (core components of store-operated Ca2+[SOC]) downregulated HUVECs, as well as STIM1 overinduced HUVECs. [3] Endotoxin and its induced exaggerative responses of proinflammatory cytokines such as Tumor Necrosis Factor (TNF) cause human septic shock. [4] scRNAseq analyses confirmed the expansion of Ly6Chi monocyte cluster, with elevation of pathogenic inflammatory genes previously observed in human septic patients. [5] We explored the biological coherence of a large panel of sepsis mediators and their clinical relevance in septic myocardial dysfunction and organ failures during human septic shock. [6] This preliminary data supports myocardial edema as a potentially relevant and largely unexplored mechanism of human septic cardiomyopathy. [7] The recently published Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL) and Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trials provide valuable but opposing insight into this ongoing debate. [8] WHAT WE ALREADY KNOW ABOUT THIS TOPIC Definitions and management strategies for septic shock continue to be updated as defined in Sepsis-2, Sepsis-3, and other guidelinesRecent randomized controlled trials of corticosteroids in septic shock report different treatment effects on 90-day mortality but use different inclusion criteria WHAT THIS ARTICLE TELLS US THAT IS NEW: In a post hoc analysis of the Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL) trial, in participants who fulfilled either the Sepsis-3 or -2 inclusion criteria or those with severe septic shock, a continuous infusion of hydrocortisone did not result in a lower 90-day mortality than placebo BACKGROUND:: Two recent randomized controlled trials (Adjunctive Glucocorticoid Therapy in Patients with Septic Shock [ADRENAL] and Activated Protein C and Corticosteroids for Human Septic Shock [APROCCHSS]) of corticosteroids in patients with septic shock reported different treatment effects on 90-day mortality. [9] Ventriculoarterial decoupling in human septic shock. [10] Paraoxonase-1 (PON-1) and butyrylcholinesterase (BChE) activities have been identified as significant biomarkers to monitor such disorders in human septic patients. [11] We hypothesized that the inflammatory response differs according to organism in human septic shock. [12]

90 day mortality

WHAT WE ALREADY KNOW ABOUT THIS TOPIC Definitions and management strategies for septic shock continue to be updated as defined in Sepsis-2, Sepsis-3, and other guidelinesRecent randomized controlled trials of corticosteroids in septic shock report different treatment effects on 90-day mortality but use different inclusion criteria WHAT THIS ARTICLE TELLS US THAT IS NEW: In a post hoc analysis of the Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL) trial, in participants who fulfilled either the Sepsis-3 or -2 inclusion criteria or those with severe septic shock, a continuous infusion of hydrocortisone did not result in a lower 90-day mortality than placebo BACKGROUND:: Two recent randomized controlled trials (Adjunctive Glucocorticoid Therapy in Patients with Septic Shock [ADRENAL] and Activated Protein C and Corticosteroids for Human Septic Shock [APROCCHSS]) of corticosteroids in patients with septic shock reported different treatment effects on 90-day mortality. [1]

human septic shock

Endotoxin and its induced exaggerative responses of proinflammatory cytokines such as Tumor Necrosis Factor (TNF) cause human septic shock. [1] We explored the biological coherence of a large panel of sepsis mediators and their clinical relevance in septic myocardial dysfunction and organ failures during human septic shock. [2] The recently published Adjunctive Corticosteroid Treatment in Critically Ill Patients with Septic Shock (ADRENAL) and Activated Protein C and Corticosteroids for Human Septic Shock (APROCCHSS) trials provide valuable but opposing insight into this ongoing debate. [3] WHAT WE ALREADY KNOW ABOUT THIS TOPIC Definitions and management strategies for septic shock continue to be updated as defined in Sepsis-2, Sepsis-3, and other guidelinesRecent randomized controlled trials of corticosteroids in septic shock report different treatment effects on 90-day mortality but use different inclusion criteria WHAT THIS ARTICLE TELLS US THAT IS NEW: In a post hoc analysis of the Adjunctive Glucocorticoid Therapy in Patients with Septic Shock (ADRENAL) trial, in participants who fulfilled either the Sepsis-3 or -2 inclusion criteria or those with severe septic shock, a continuous infusion of hydrocortisone did not result in a lower 90-day mortality than placebo BACKGROUND:: Two recent randomized controlled trials (Adjunctive Glucocorticoid Therapy in Patients with Septic Shock [ADRENAL] and Activated Protein C and Corticosteroids for Human Septic Shock [APROCCHSS]) of corticosteroids in patients with septic shock reported different treatment effects on 90-day mortality. [4] Ventriculoarterial decoupling in human septic shock. [5] We hypothesized that the inflammatory response differs according to organism in human septic shock. [6]

human septic patient

INTERVENTIONS Prokineticin2 concentrations were measured and analyzed in human septic patients, patient controls, and healthy individuals. [1] scRNAseq analyses confirmed the expansion of Ly6Chi monocyte cluster, with elevation of pathogenic inflammatory genes previously observed in human septic patients. [2] Paraoxonase-1 (PON-1) and butyrylcholinesterase (BChE) activities have been identified as significant biomarkers to monitor such disorders in human septic patients. [3]