SHOCK最新文献

{"title":"NINJ1: A NOVEL SEPSIS SEVERITY AND MORTALITY BIOMARKER.","authors":"Yongbin Wu, Tao Li, Sichuang Tan, Ruoyu Song, Kaiyuan Song, Jiankang Zhou, Xianzhong Xiao, Kangkai Wang, Huali Zhang, Sipin Tan","doi":"10.1097/SHK.0000000000002460","DOIUrl":"10.1097/SHK.0000000000002460","url":null,"abstract":"<p><strong>Abstract: </strong>Background : Multiple cell death modalities are implicated in sepsis pathobiology. However, the clinical relevance of NINJ1, a key mediator of plasma membrane rupture during lytic cell death, in sepsis progression and outcomes has remained poorly explored. Methods: Circulating NINJ1 levels were measured in 116 septic intensive care unit (ICU) patients, 16 nonseptic ICU controls, and 16 healthy controls. Comparative analysis of serum NINJ1 across these groups was performed. Correlations between NINJ1 and clinical disease severity scores (Sequential Organ Failure Assessment [SOFA], Acute Physiology and Chronic Health Evaluation [APACHE II]) as well as laboratory parameters were examined in the sepsis cohort. Furthermore, we assessed the prognostic performance of NINJ1 for predicting 28-day mortality in septic patients using receiver operating characteristic (ROC) analyses. Results: Circulating NINJ1 levels were elevated in septic patients and positively correlated with sepsis severity scores. NINJ1 also showed positive correlations with liver injury markers (aspartate transaminase/alanine aminotransferase) and coagulation parameters (D-dimer, activated partial thromboplastin time, prothrombin time, thrombin time) in sepsis. Further analysis using the International Society on Thrombosis and Hemostasis overt disseminated intravascular coagulation scoring system revealed an association between NINJ1 and sepsis-induced coagulopathy. ROC analysis demonstrated that NINJ1 outperformed traditional inflammatory biomarkers procalcitonin and C-reactive protein in predicting 28-day sepsis mortality, although its prognostic accuracy was lower than SOFA and APACHE II scores. Combining NINJ1 with SOFA improved mortality prediction from an area under the curve of 0.6843 to 0.773. Conclusions: Circulating NINJ1 serves as a novel sepsis biomarker indicative of disease severity, coagulopathy and mortality risk, and its integration with SOFA and APACHE II scores substantially enhances prognostic risk stratification. These findings highlight the prospective clinical utility of NINJ1 for sepsis prognostication and monitoring, warranting further validation studies to facilitate implementation.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"527-532"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142081394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"INTESTINAL EPITHELIAL-SPECIFIC OCCLUDIN DELETION WORSENS GUT PERMEABILITY AND SURVIVAL FOLLOWING SEPSIS.","authors":"Tetsuya Yumoto, Takehiko Oami, Zhe Liang, Eileen M Burd, Mandy L Ford, Jerrold R Turner, Craig M Coopersmith","doi":"10.1097/SHK.0000000000002531","DOIUrl":"10.1097/SHK.0000000000002531","url":null,"abstract":"<p><strong>Abstract: </strong>Sepsis induces intestinal hyperpermeability, which is associated with higher mortality. Occludin is a tight junction protein that plays a critical role in regulating disease-associated intestinal barrier loss. This study examined the role of intestinal occludin on gut barrier function and survival in a preclinical model of sepsis. Intestinal epithelial-specific occludin knockout (occludin KO IEC ) mice and wild type controls were subjected to intra-abdominal sepsis and sacrificed at predetermined endpoints for mechanistic studies or followed for survival. Occludin KO IEC mice had a significant increase in intestinal permeability, which was induced only in the setting of sepsis as knockout mice and control mice had similar baseline permeability. The worsened barrier was specific to the leak pathway of permeability, without changes in either the pore or unrestricted pathways. Increased sepsis-induced permeability was associated with increased levels of the tight junction ZO-1 in occludin KO IEC mice. Occludin KO IEC mice also had significant increases in systemic cytokines IL-6 and MCP-1 and increased bacteremia. Furthermore, occludin KO IEC mice had higher levels of jejunal IL-1β and MCP-1 as well as increased MCP-1 and IL-17A in the peritoneal fluid although peritoneal bacteria levels were unchanged. Notably, 7-day mortality was significantly higher in occludin KO IEC mice following sepsis. Occludin thus plays a critical role in preserving gut barrier function and mediating survival during sepsis, associated with alterations in inflammation and bacteremia. Agents that preserve occludin function may represent a new therapeutic strategy in the treatment of sepsis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"597-605"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IMPELLA COMPARED TO VENOARTERIAL EXTRACORPOREAL MEMBRANE OXYGENATION IN CARDIOGENIC SHOCK: A SYSTEMATIC REVIEW AND META-ANALYSIS OF PROPENSITY SCORE-MATCHED STUDIES.","authors":"Dion Stub, William Chan, Jocasta Ball, Aidan Burell, Josh Ihle, Steven Theng, Stelios Tsintzos, David M Kaye, Tahlia Seage, Mia Mudge","doi":"10.1097/SHK.0000000000002540","DOIUrl":"10.1097/SHK.0000000000002540","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Veno-arterial extracorporeal membrane oxygenation (VA ECMO) and Impella, a transluminal microaxial ventricular assist device, are well-established in the management of cardiogenic shock. No randomized controlled trials (RCTs) directly compare Impella versus VA ECMO to inform their safety and efficacy in cardiogenic shock. Purpose: This study aims to conduct a systematic review and meta-analysis of propensity score-matched/adjusted studies to compare the clinical outcomes of Impella versus VA ECMO in cardiogenic shock patients. Methods: A systematic review was undertaken to identify comparative studies of Impella and VA ECMO in cardiogenic shock, which in the absence of RCTs, was limited to observational trials with propensity-matched or adjusted outcomes to account for important confounding factors between populations. In-hospital/30-day survival and bleeding events requiring transfusion were meta-analyzed using the random effects method. Results: Five propensity score-matched/adjusted studies comparing short-term survival following treatment with Impella versus VA ECMO were included. A statistically significant difference in in-hospital/30-day mortality was detected between patients treated with Impella (39.6%) versus VA ECMO (53.8%) (odds ratio [95% confidence interval]: 0.57 [0.44, 0.74]; P < 0.0001). Impella was associated with significantly fewer bleeding events requiring transfusion compared with VA ECMO (19.9% vs. 28.8%, respectively) (OR [95% confidence interval]: 0.61 [0.46, 0.80]; P = 0.0004). Conclusion: In the absence of RCTs, this meta-analysis of propensity matched/adjusted observational trials represents the highest level of evidence available to date. Impella was associated with improved short-term survival and decreased bleeding events compared to VA ECMO in patients with cardiogenic shock.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"512-519"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11939094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143450030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EARLY AND CONCOMITANT ADMINISTRATION OF NOREPINEPHRINE AND ILOMEDIN IMPROVES MICROCIRCULATORY PERFUSION WITHOUT IMPAIRING MACROCIRCULATION IN AN INTESTINAL ISCHEMIA-REPERFUSION INJURY SWINE MODEL: A RANDOMIZED EXPERIMENTAL TRIAL.","authors":"Stéphane Bar, John Diaper, Fabienne Fontao, Xavier Belin, Stanislas Abrard, Gergely Albu, Hervé Dupont, Walid Habre, Eduardo Schiffer","doi":"10.1097/SHK.0000000000002533","DOIUrl":"10.1097/SHK.0000000000002533","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Intestinal ischemia-reperfusion injury is associated with both macrocirculatory and microcirculatory failure. Association of a vasoconstrictor in combination with a vasodilator such as ilomedin may improve macrocirculation parameters, microcirculation perfusion and reduce endothelial dysfunction. The primary objective was to demonstrate a difference in mean arterial pressure (MAP) after intestinal reperfusion with the concomitant administration of norepinephrine and ilomedin during ischemia compared with traditional hemodynamic treatment strategies (fluid resuscitation and vasopressors only). Secondary objectives were to demonstrate an improvement in peripheral and intestinal microcirculatory perfusion and endothelial dysfunction after intestinal reperfusion using this association. Methods: We conducted a randomized preclinical trial in 21 large white pigs, in which a 2-h small bowel ischemia was performed using a segmental mesenteric occlusion model, followed by a 2-h reperfusion. Pigs were randomized into the following three groups: goal-directed fluid therapy, early administration of norepinephrine before reperfusion and early administration of ilomedin and norepinephrine before reperfusion. Macrocirculatory (MAP and Cardiac Index (CI), microcirculatory (Sublingual with SideStream Dark Field system and intestinal hemoglobin oxygen saturation with hyperspectral imaging) measurements and biological analysis (biomarkers of endothelial dysfunction) were performed. Results: There were no significant differences in the MAP ( P = 0.499) and the CI ( P = 0.659) between the three groups. Perfused vessel density in sublingual microcirculation was significantly higher immediately after reperfusion and 2 h after reperfusion in the early administration of ilomedin and norepinephrine group compared with the other two groups ( P < 0.05). Hemoglobin oxygen saturation measured at the intestinal level was significantly higher immediately after reperfusion in the early administration of ilomedin and norepinephrine group compared with the other two groups ( P < 0.01). There were no significant differences in biomarkers of endothelial dysfunction between the three groups. Creatinine, AST and alkaline phosphatases increased significantly 2 h after reperfusion in the early administration of ilomedin and norepinephrine group compared with baseline ( P < 0.05). Conclusions: Early administration of norepinephrine and ilomedin during ischemia improved short-term postreperfusion sublingual and intestinal microcirculation without worsening macrocirculatory parameters in an intestinal ischemia-reperfusion injury model. However, use of this strategy seemed to worsen both liver and kidney function.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"606-613"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COMBINED EFFECTS OF OXANDROLONE AND EXERCISE ON MUSCLE RECOVERY IN RATS WITH SEVERE BURN AND HINDLIMB UNLOADING.","authors":"Alen Palackic, Amina El Ayadi, Charles E Wade, Lisa A Baer, Ludwik K Branski, Gabriel Hundeshagen, Julia Kleinhapl, Steven E Wolf, Juquan Song","doi":"10.1097/SHK.0000000000002541","DOIUrl":"10.1097/SHK.0000000000002541","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Loss of muscle mass and strength in patients who have experienced severe burns is dramatic and associated with subsequent functional impairment. Past work has shown that exercise and oxandrolone, an anabolic steroid, individually improve muscle function and muscle mass in severely burned patients. This study aims to evaluate the effect of oxandrolone treatment combined with resistance exercise on muscle atrophy and investigate the protein synthesis and mitochondrial biogenesis pathways in a hindlimb suspension model. Methods: Twenty-four Sprague-Dawley rats received 40% total body surface area (%TBSA) scald burns and were then placed for hindlimb unloading. All animals were randomly grouped into vehicle (corn oil) without exercise (V/NEX), oxandrolone administration (0.1 mg/kg/d) without exercise (OX/NEX), vehicle with exercise (V/EX), or oxandrolone with exercise (OX/EX) (n = 6/group). On day 14, isometric forces of the left plantaris and soleus muscle were measured by using a muscle lever system with dynamic muscle control and analysis software. Fatigue measurement was only performed in the soleus muscle. The tissue of the muscle was then collected for protein extraction. Western blots were performed to study signal alternations and mitochondrial biogenesis pathways. Results: Tetanic force (Po) was significantly increased in the plantaris with exercise rather than with oxandrolone treatment. Fatigue index (FI) was lower, and integration was significantly elevated in the soleus with exercise but not with oxandrolone treatment. Fatigue curve in the soleus further revealed that the average maximum force was achieved in soleus with either oxandrolone treatment or exercise alone independently. Raptor and p-Akt levels are elevated in the OX/EX group, whereas PGC1a expression was not altered. Conclusion: Oxandrolone and resistance exercise have independent positive effects on muscle function recovery in this clinically relevant rodent model of severe burn. Both treatments combined increased signaling pathways by increasing protein synthesis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"622-627"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WHOLE TRANSCRIPTION ANALYSIS IDENTIFIED THE REGULATION OF HYPOXIA-INDUCIBLE FACTORS IN MONOCYTES WITH IMMUNE SUPPRESSION: IMPLICATIONS FOR CLINICAL OUTCOMES.","authors":"Shuai Zhao, Hui Li, Wei Luo, Zhaolan Hu, Yulu Wang, Tao Liu, Yanling Zhang, RuPing Dai","doi":"10.1097/SHK.0000000000002479","DOIUrl":"10.1097/SHK.0000000000002479","url":null,"abstract":"<p><strong>Abstract: </strong>Aims: Sepsis progression is marked by a complex immune response, where the involvement of hypoxia-inducible factors (HIFs) plays an uncertain role. The study aims to elucidate the involvement of HIF-1α in monocyte function during sepsis and its potential as a prognostic indicator. Methods and Results: Transcriptomic data from healthy individuals and septic patients in datasets GSE54514, GSE167363, and GSE46955 were analyzed. Additionally, human monocytes were employed to elucidate how HIF regulates immune responses in the context of sepsis. Septic nonsurvivors exhibited sustained upregulation of HIF-1α expression alongside compromised inflammatory response and antigen presentation, with downregulation of NF-κB and HLADRB1 genes associated with poor sepsis prognosis. Conversely, septic survivors displayed an increased proportion of classical monocytes and enhanced inflammation and expression of antigen presentation-related genes. During the recovery phase of sepsis, monocytes continued to demonstrate elevated HIF-1α expression. In cultured THP1 cells and septic CD14 + monocytes, HIF hindered inflammatory responses and antigen presentation, while also suppressing the proportion of classical monocytes after LPS stimulation. Mechanistically, HIF significantly attenuated LPS-induced immune responses in monocytes by inhibiting the phosphorylation of IKK. Conclusions: HIF in monocytes acts as a suppressor of immune-inflammatory responses and antigen presentation, and may serve as a negative molecular marker for sepsis development.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"541-551"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11939089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLATELET TRAITS AND SEPSIS RISK AND PROGNOSIS: A BIDIRECTIONAL TWO-SAMPLE MENDELIAN RANDOMIZATION STUDY.","authors":"Zhonghai Song, Hua Li, Jing Zhang, Yaomeng Huang, Shichao Gao","doi":"10.1097/SHK.0000000000002447","DOIUrl":"10.1097/SHK.0000000000002447","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Sepsis is a critical medical condition characterized by a dysregulated host response to infection. Platelet abnormalities frequently manifest in sepsis patients, but the causal role of platelets in sepsis remains unclear. This study employed a bidirectional two-sample Mendelian randomization (MR) approach to investigate the causal direction between platelets and sepsis. Methods: MR analysis was used to investigate the causal effect of four platelet traits-platelet count (PLT), platelet crit (PCT), mean platelet volume (MPV), and platelet distribution width (PDW)-on sepsis risk and prognosis. Additionally, the study explored the reverse causality, assessing the impact of sepsis on these platelet traits. Genetic variants from large-scale genome-wide association studies served as instrumental variables to infer causality. Sensitivity analyses and heterogeneity tests were conducted to ensure the validity and robustness of the results. Results: Genetically predicted decreased PCT (OR = 0.938, P = 0.044) and MPV (OR = 0.410, P = 0.006) were associated with an increased risk of sepsis. In the reverse direction, 28-day sepsis mortality was significantly associated with decreased PLT (OR = 0.986, P = 0.034). No significant causal relationships were observed between sepsis and other platelet traits. Conclusions: This study suggests a causal association between low PCT and MPV levels and increased risk of sepsis. Additionally, sepsis with a poor prognosis was causally linked to decreased PLT. These findings provide novel evidence for the causal relationship between platelet traits and sepsis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"520-526"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DL-3-N-BUTYLPHTHALIDE ALLEVIATES CARDIAC DYSFUNCTION AND INJURY POSSIBLY BY INHIBITING CELL PYROPTOSIS AND INFLAMMATION VIA THE CGAS-STING-TBK1 PATHWAY IN A PORCINE MODEL OF HEMORRHAGE-INDUCED CARDIAC ARREST.","authors":"Ting Zhou, Yong Liu, Lijun Zhu, Jian Jiang, Qijiang Chen, Lulu Li, Xianlong Wu, Jiefeng Xu, Jianjiang Fang","doi":"10.1097/SHK.0000000000002539","DOIUrl":"10.1097/SHK.0000000000002539","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Abstract: &lt;/strong&gt;Introduction: Dl-3-n-butylphthalide (NBP), a small molecular compound extracted from celery seeds, has been shown to exhibit diverse pharmacological activities, including anti-inflammatory, antioxidative, and anti-apoptotic effects. Recent studies have highlighted its efficacy in treating various cardiovascular conditions, such as myocardial infarction, hypertrophy, heart failure, and cardiotoxicity. This study aimed to investigate whether NBP could alleviate cardiac dysfunction and injury following hemorrhage-induced cardiac arrest (HCA) in a porcine model and elucidate its potential mechanisms. Methods: Seventeen pigs were randomized into three groups: sham (n = 5), HCA + vehicle (n = 5), and HCA + NBP (n = 7). In the HCA + vehicle and HCA + NBP groups, the HCA model was established by continuous bleeding at a rate of 2 mL/kg/min to induce cardiac arrest. Cardiac arrest was maintained for 7 min, followed by the reinfusion of 50% of the shed blood at a rate of 5 mL/kg/min. After successful resuscitation, the HCA + NBP group received an intravenous dose of 2.5 mg/kg of NBP within 120 min. Post-resuscitation cardiac function (stroke volume, global ejection fraction) and injury biomarkers (cardiac troponin I, creatine kinase-MB) were assessed at regular intervals. At the end of the post-resuscitation observation, cardiac tissue samples were collected to assess: histopathological injury; cellular apoptosis; levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18); the expression levels of NOD-like receptor pyrin domain 3 (NLRP3), caspase 1, gasdermin D (GSDMD), cyclic-GMP-AMP synthase (cGAS), stimulator of interferon genes (STING), and tank-binding kinase 1 (TBK1); and the integrated optical density (IOD) of GSDMD N-terminal (GSDMD-N), phosphorylated STING (p-STING), and phosphorylated TBK1 (p-TBK1). Results: Following resuscitation, both stroke volume and global ejection fraction were significantly reduced, while serum levels of cardiac troponin I and creatine kinase-MB were markedly elevated in the HCA + vehicle and HCA + NBP groups compared with the sham group. However, the extent of cardiac dysfunction and injury was significantly attenuated in the HCA + NBP group relative to the HCA + vehicle group. At 24 h post-resuscitation, substantial cardiac pathological injury and apoptosis were observed. Additionally, pyroptosis-related proteins (NLRP3, caspase-1, GSDMD, GSDMD-N) were upregulated, inflammatory markers (TNF-α, IL-1β, IL-6, IL-18) were elevated, and the activation of the cGAS-STING-TBK1 pathway (cGAS, STING, TBK1, p-STING, p-TBK1) were noted in both the HCA + vehicle and HCA + NBP groups compared with the sham group. Notably, these pathological changes were significantly attenuated in the HCA + NBP group compared with the HCA + vehicle group. Conclusions: NBP provided substantial cardiac protection following HCA an","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"614-621"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time course of red blood cell deformability during diabetic ketoacidosis.","authors":"Dorian Leroy, Bruno Sirault, Alexandre Rousseau, Patrick Biston, Karim Zouaoui Boudjeltia, Michaël Piagnerelli","doi":"10.1097/SHK.0000000000002572","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002572","url":null,"abstract":"<p><strong>Background: </strong>Diabetic ketoacidosis (DKA) is a life-threatening emergency. Microvascular hyporeactivity has been reported in these patients and is completely reversible when acidosis is corrected with aggressive treatment. The shape of the red blood cell (RBC), a sensor of local hypoxia and a component of the microcirculation, is altered in diabetic patients, but no data are available concerning RBC deformability in DKA during treatment.</p><p><strong>Methods: </strong>In this prospective observational study, we included all adult patients admitted with DKA to a 32-bed medico-surgical ICU over a 6-month period. We excluded patients with infection. We measured RBC deformability in the DKA patients and compared results with those from patients with type 1 diabetes (DM1) and from a group of healthy volunteers (HV). RBC deformability was assessed using ektacytometry. In the DKA patients, it was assessed at ICU admission, 8 and 24 hours after admission, and prior to ICU discharge (48-72 h). The RBC elongation index (EI) was determined based on the laser diffraction pattern changes. A higher EI indicates greater RBC deformability.</p><p><strong>Results: </strong>A total of 46 diabetic patients (15 DKA and 31 DM1 patients) and 20 HV were included. RBC deformability was more altered at ICU admission in DKA patients, with significantly lower EI values than in the other groups, and these alterations persisted during the ICU stay despite treatment. There were no correlations between these alterations and the quantity of fluids or insulin received.</p><p><strong>Conclusions: </strong>In contrast to the reversible microvascular hyporeactivity observed in DKA, RBC deformability was already altered at ICU admission in patients with DKA and remained altered despite treatment. These alterations may contribute to the blood flow abnormalities observed in these patients.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BAICALIN ALLEVIATES LPS-INDUCED CYTOTOXICITY IN ACUTE LUNG INJURY THROUGH MEDIATING METTL14/SOX6 AXIS.","authors":"Yuexuan Chen, Yuhai Gu, Zhihan Gao","doi":"10.1097/SHK.0000000000002518","DOIUrl":"10.1097/SHK.0000000000002518","url":null,"abstract":"<p><strong>Abstract: </strong>Background : Baicalin (C 21 H 18 O 11 ) is a flavonoid component extracted from Scutellaria baicalensis with biological activity in various types of diseases, including acute lung injury (ALI). The relevant mechanism behind baicalin in ALI needs further investigation. Methods : ALI model in vitro was established by LPS in WI-38 cells (lung fibroblast). Cell growth was determined via MTT assay and EdU assay. Apoptosis was assessed using flow cytometry, caspase 3 assay, and TUNEL assay. Oxidative indicators and inflammatory cytokines were detected by commercial kits. Interaction between methyltransferase-like 14 (METTL14) and SRY-box transcription factor 6 (SOX6) was studied using methylated RNA immunoprecipitation and dual-luciferase reporter assay. Reverse transcription-quantitative polymerase chain reaction and Western blot were applied for examining gene levels. Results : Baicalin enhanced cell growth and reduced apoptosis and oxidative stress; inflammation after ALI was induced by LPS. Downregulation of SOX6 weakened LPS-induced cytotoxicity in WI-38 cells. Baicalin prevented from LPS-induced lung cell injury via reducing SOX6 expression. SOX6 expression was stabilized by METTL14 through its methylation modification. METTL14/SOX6 axis was related to the regulation of baicalin in LPS-treated WI-38 cells. Conclusion : Therefore, baicalin played an important role to inhibit LPS-induced cytotoxicity in vitro via METTL14-mediated methylation of SOX6.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"566-572"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142772115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}