Shock (Augusta, Ga.)最新文献

{"title":"EARLY INITIATION OF VASOPRESSIN REDUCES ORGAN FAILURE AND MORTALITY IN SEPTIC SHOCK.","authors":"Alexandria C Rydz,&nbsp;Jessica L Elefritz,&nbsp;Megan Conroy,&nbsp;Kathryn A Disney,&nbsp;Christopher J Miller,&nbsp;Kyle Porter,&nbsp;Bruce A Doepker","doi":"10.1097/SHK.0000000000001978","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001978","url":null,"abstract":"<p><strong>Abstract: </strong>Purpose : The aim of the study is to determine whether initiating vasopressin earlier in septic shock reduces organ dysfunction and in-hospital all-cause mortality. Methods : This multicenter, retrospective, cohort study evaluated patients admitted to the medical intensive care unit between October 2011 and August 2018 with septic shock who received vasopressin within 48 hours of shock onset. The primary composite outcome was the proportion of patients with a change in the Sequential Organ Failure Assessment score greater than 3 from baseline to 72 hours after initiation of vasopressin and/or in-hospital all-cause mortality. Secondary outcomes included time to hemodynamic stability, acute kidney injury, and intensive care unit length of stay. Results : A total of 385 patients included in the final evaluation with a mean Acute Physiology and Chronic Health Evaluation II score of 31 and a mean baseline Sequential Organ Failure Assessment score of 13. Median time to initiation of vasopressin after norepinephrine was 7.3 hours. The primary composite outcome was significantly reduced in patients who had vasopressin initiated earlier in septic shock (odds ratio = 1.08, 95% confidence interval = 1.03-1.13, P &lt; 0.001). After controlling for baseline data in a multivariable regression model the primary outcome remained statistically significant (odds ratio = 1.04, 95% confidence interval = 1.02-1.07, P = 0.001). Conclusions : Early initiation of vasopressin in septic shock may reduce the risk of in-hospital all-cause mortality and/or organ dysfunction.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"269-274"},"PeriodicalIF":3.1,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33438424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RECOVERY OF ENDOTHELIOPATHY AT 24 HOURS IN AN ESTABLISHED MOUSE MODEL OF HEMORRHAGIC SHOCK AND TRAUMA.","authors":"Mark Barry,&nbsp;Alpa Trivedi,&nbsp;Lindsay R Vivona,&nbsp;Jenna Chui,&nbsp;Praneeti Pathipati,&nbsp;Byron Miyazawa,&nbsp;Shibani Pati","doi":"10.1097/SHK.0000000000001984","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001984","url":null,"abstract":"<p><strong>Abstract: </strong>Introduction: The endotheliopathy of trauma develops early after injury and consists of increased vascular permeability, inflammation, and dysfunctional coagulation. Persistence of these abnormalities ultimately leads to multiorgan failure. We hypothesized that extending an established 3-hour acute mouse model of hemorrhagic shock and trauma (HS/T) to a 24-hour survival model would allow for evaluation of persistent endotheliopathy and organ injury after HS/T. Methods: Adult male C57BL/6J mice underwent laparotomy, femoral artery cannulation, and blood withdrawal to induce HS to a MAP of 35 mm Hg for 90 minutes. Mice were resuscitated with either lactated Ringer's (LR) or fresh frozen plasma (FFP). Vascular permeability in the lung and gut was assessed by measuring extravasation of a fluorescent dextran dye. Lungs were evaluated for histopathologic injury, and immunofluorescent staining was used to evaluate intercellular junction integrity. Pulmonary inflammatory gene expression was evaluated using NanoString (Seattle, WA). All endpoints were evaluated at both 3 and 24 hours after initiation of shock. Results: Lactated Ringer's- and FFP-treated mice had an equal mortality rate of 17% in the 24-hour model. Lactated Ringer's-treated mice demonstrated increased vascular permeability in the lung and gut at 3 hours compared with sham mice (lung, P &lt; 0.01; gut, P &lt; 0.001), which was mitigated by FFP treatment (lung, P &lt; 0.05; gut, P &lt; 0.001). Twenty-four hours after shock, however, there were no differences in vascular permeability between groups. Similarly, although at 3 hours, the lungs of LR-treated mice demonstrated significant histopathologic injury, loss of tight and adherens junctions, and a pro-inflammatory gene expression profile at 3 hours, these endpoints in LR mice were similar to sham mice by 24 hours. Conclusions: In an established mouse model of HS/T, endotheliopathy and lung injury are evident at 3 hours but recover by 24 hours. Polytrauma models or larger animal models allowing for more severe injury coupled with supportive care are likely necessary to evaluate endotheliopathy and organ injury outside of the acute period.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"313-320"},"PeriodicalIF":3.1,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40339534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"INTESTINAL DAMAGE AND IMMUNE RESPONSE AFTER EXPERIMENTAL BLUNT ABDOMINAL TRAUMA.","authors":"Felix Haussner,&nbsp;Alexander Maitz,&nbsp;Volker Rasche,&nbsp;Andrea Hoffmann,&nbsp;Sonja Braumüller,&nbsp;Ludmila Lupu,&nbsp;Anita Ignatius,&nbsp;Thomas A Neff,&nbsp;Annette Palmer,&nbsp;Markus Huber-Lang","doi":"10.1097/SHK.0000000000001986","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001986","url":null,"abstract":"<p><strong>Abstract: </strong>Abdominal trauma (AT) is of major global importance, particularly because the civil, terroristic, and military traumatic potential of blast injuries has increased. The consequences of blunt abdominal injuries are highly variable and frequently underestimated or even overlooked. However, the underlying path mechanisms and subsequent innate immune response remain poorly understood. Therefore, we investigated the spatiotemporal local and systemic effects of a standardized blast-induced blunt AT on the intestine and innate immune response. In an established AT model, 66 male C57Bl6 mice were anesthetized and exposed to either a single blast wave centered on the epigastrium or control treatment (sham). At 2, 6, or 24 hours after trauma induction, animals were sacrificed. In 16 of 44 (36%) AT animals, one or more macroscopically visible injuries of the intestine were observed. Epithelial damage was detected by histological analysis of jejunum and ileum tissue samples, quantified by the Chiu score and by increased plasma concentrations of the intestinal fatty acid-binding protein, an enterocyte damage marker. Moreover, in the early posttraumatic period, elevated syndecan-1, claudin-5, and mucin-2 plasma levels also indicated alterations in the gut-blood barrier. Increased levels of pro-inflammatory cytokines such as TNF and macrophage inflammatory protein 2 in tissue homogenates and plasma indicate a systemic immune activation after blunt AT. In conclusion, we detected early morphological intestinal damage associated with high, early detectable intestinal fatty acid-binding protein plasma levels, and a considerable time- and dose-dependent impairment of the gut-blood barrier in a newly established mouse model of blunt AT. It appears to be a sufficient model for further studies of the intestinal immunopathophysiological consequences of AT and the evaluation of novel therapeutic approaches.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"332-340"},"PeriodicalIF":3.1,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33439203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IMPACT OF TIME TO EMERGENCY DEPARTMENT RESUSCITATIVE AORTIC OCCLUSION AFTER NONCOMPRESSIBLE TORSO HEMORRHAGE.","authors":"Jacob M Broome,&nbsp;Ayman Ali,&nbsp;John T Simpson,&nbsp;Sherman Tran,&nbsp;Danielle Tatum,&nbsp;Sharven Taghavi,&nbsp;Joseph DuBose,&nbsp;Juan Duchesne","doi":"10.1097/SHK.0000000000001988","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001988","url":null,"abstract":"<p><strong>Abstract: </strong>Introduction: Time is an essential element in outcomes of trauma patients. The relationship of time to treatment in management of noncompressible torso hemorrhage (NCTH) with resuscitative endovascular balloon occlusion of the aorta (REBOA) or resuscitative thoracotomy (RT) has not been previously described. We hypothesized that shorter times to intervention would reduce mortality. Methods: A review of the Aortic Occlusion for Resuscitation in Trauma and Acute Care Surgery registry from 2013 to 2022 was performed to identify patients who underwent emergency department aortic occlusion (AO). Multivariate logistic regression was used to examine the impact of time to treatment on mortality. Results: A total of 1,853 patients (1,245 [67%] RT, 608 [33%] REBOA) were included. Most patients were male (82%) with a median age of 34 years (interquartile range, 30). Median time from injury to admission and admission to successful AO were 31 versus 11 minutes, respectively. Patients who died had shorter median times from injury to successful AO (44 vs. 72 minutes, P &lt; 0.001) and admission to successful AO (10 vs. 22 minutes, P &lt; 0.001). Multivariate logistic regression demonstrated that receiving RT was the strongest predictor of mortality (odds ratio [OR], 6.6; 95% confidence interval [CI], 4.4-9.9; P &lt; 0.001). Time from injury to admission and admission to successful AO were not significant. This finding was consistent in subgroup analysis of RT-only and REBOA-only populations. Conclusions: Despite expedited interventions, time to aortic occlusion did not significantly impact mortality. This may suggest that rapid in-hospital intervention was often insufficient to compensate for severe exsanguination and hypovolemia that had already occurred before emergency department presentation. Selective prehospital advanced resuscitative care closer to the point of injury with \"scoop and control\" efforts including hemostatic resuscitation warrants special consideration.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"275-279"},"PeriodicalIF":3.1,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40339533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FLUOROFENIDONE ATTENUATES PULMONARY INFLAMMATION AND FIBROSIS BY INHIBITING THE IL-11/MEK/ERK SIGNALING PATHWAY.","authors":"Cheng Song,&nbsp;Xiaofan Liu,&nbsp;Weijun Tan,&nbsp;Xiaoqun Guo,&nbsp;Yahui Mao,&nbsp;Qi Zhou,&nbsp;Shuang Geng,&nbsp;Yi Hu","doi":"10.1097/SHK.0000000000001960","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001960","url":null,"abstract":"<p><strong>Abstract: </strong>Idiopathic pulmonary fibrosis is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause. Interleukin (IL)-11 plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. In this study, we explore whether a potential antifibrotic agent fluorofenidone (FD) exerts its anti-inflammatory and antifibrotic effects through suppressing activation of the IL-11/MEK/ERK signaling pathway in vivo and in vitro. Male C57BL/6 J mice were intratracheally injected with bleomycin or saline. Fluorofenidone was administered throughout the course of the experiment. Lung tissue sections were stained with hemotoxylin and eosin, and Masson trichrome. Cytokines were measured using the enzyme-linked immunosorbent assay. The α-smooth muscle actin (α-SMA), fibronectin, and collagen I were measured using immunohistochemistry, and the phosphorylated extracellular signal-regulated kinase, phosphorylated mitogen-activated protein kinase, IL-11RA, and gp130 were measured using Western blot. The RAW264.7 cells and the normal human lung fibroblasts were treated with IL-11 and/or FD, IL-11RA-siRNA, or MEK inhibitor. The expressions of phosphorylated extracellular signal-regulated kinase, phosphorylated mitogen-activated protein kinase, IL-11RA, gp130, α-SMA, fibronectin, and collagen I were measured using Western blot and/or real-time polymerase chain reaction, and the cytokines were measured using enzyme-linked immunosorbent assay. Results showed that FD markedly reduced the expressions of IL-8, IL-18, IL-11, monocyte chemotactic protein-1, α-SMA, fibronectin, and collagen I in mice lung tissues. In addition, FD attenuated IL-11-induced expressions of α-SMA, fibronectin, and collagen I and inhibited IL-11RA, gp130, and phosphorylation of the ERK and MEK protein expression, as well as reduced the expressions of IL-8, IL-18, and monocyte chemotactic protein-1 in vitro. This study demonstrated that FD attenuated bleomycin-induced pulmonary inflammation and fibrosis in mice by inhibiting the IL-11/MEK/ERK signaling pathway.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"137-146"},"PeriodicalIF":3.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40378080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MECHANISM OF MIR-25-3P CARRIED BY EXTRACELLULAR VESICLES DERIVED FROM PLATELET-RICH PLASMA IN IL-1β-INDUCED NUCLEUS PULPOSUS CELL DEGENERATION VIA THE SOX4/CXCR7 AXIS.","authors":"Baoshan Hu, Lianxin Wang, Naikun Sun, Shengrong Lin, Gang Rui","doi":"10.1097/SHK.0000000000001947","DOIUrl":"10.1097/SHK.0000000000001947","url":null,"abstract":"<p><strong>Abstract: </strong>Objectives: Nucleus pulposus (NP) cell degeneration promotes the progression of intervertebral disc (IVD) degeneration. MicroRNAs (miRs) are associated with IVD degeneration. This study expounded the mechanism of microRNA (miR)-25-3p carried by extracellular vesicles (EVs) derived from platelet-rich plasma (PRP) in interleukin (IL)-1β-induced NP cell degeneration. Methods: Platelet-rich plasma from mouse blood was obtained, and EVs were isolated from PRP (EVs derived from PRP [PRP-EVs]) and identified. Nucleus pulposus cells were isolated from the mouse lumbar IVD and treated with IL-1β to induce NP cell degeneration. Extracellular vesicles derived from PRP were added into NP cell culture medium. Afterward, intracellular miR-25-3p, sex determining region Y-related high-mobility-group box 4 (SOX4), and CXC chemokine receptor 7 (CXCR7) levels were examined. Nucleus pulposus cell viability, apoptosis, and inflammation were detected. Extracellular vesicles derived from PRP were labeled by PKH67 to obverse the uptake of EVs by NP cells. The binding relations between SOX4 and miR-25-3p and CXCR7 were predicted and examined. Functional rescue experiments were performed to investigate the roles of miR-25-3p, SOX4, and CXCR7 in NP cell degeneration. Results: miR-25-3p was downregulated, whereas SOX4 and CXCR7 were upregulated in IL-1β-induced NP cells. Extracellular vesicles derived from PRP increased the cell viability, and decreased apoptosis and inflammation. miR-25-3p carried by PRP-EVs into NP cells alleviated NP cell degeneration. miR-25-3p inhibited SOX4 expression and limited CXCR7 transcription. Silencing miR-25-3p or overexpressing SOX4 or CXCR7 reversed the alleviating role of PRP-EVs in NP cell degeneration. Conclusion: miR-25-3p carried by PRP-EVs into NP cells elevated intracellular miR-25-3p expression, which suppressed SOX4 expression and further limited CXCR7 transcription, thus alleviating IL-1β-induced NP cell degeneration. Extracellular vesicles derived from PRP containing miR-25-3p may be a new method for IVD treatment.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"56-67"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40721848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA UBAP2 (hsa_circ_0007367) Correlates with Microcirculatory Perfusion and Predicts Outcomes of Cardiogenic Shock Patients Undergoing Extracorporeal Membrane Oxygenation Support.","authors":"Jiani Li,&nbsp;Zhexuan Yu,&nbsp;Jianfeng Zeng,&nbsp;Zhaoyuan Liu,&nbsp;Zongkai Zhao,&nbsp;Yu Zhang,&nbsp;Guanhua Li","doi":"10.1097/SHK.0000000000001937","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001937","url":null,"abstract":"<p><strong>Background: </strong>Severe microcirculatory disturbance is common in patients with cardiogenic shock necessitating extracorporeal membrane oxygenation (ECMO), however, biomarkers linked to microcirculation and clinical outcome are scarce. Herein we identified a circular RNA, hsa_circ_0007367, rooted from the ubiquitin-associated protein 2 (UBAP2) gene, namely circUBAP2, and evaluated its biological function and the associations with microcirculation and the prognosis.</p><p><strong>Methods: </strong>Patients on ECMO with cardiogenic shock were included if qualified sublingual microcirculation parameters could be obtained and were categorized into the survivor group or non-survivor group. Macro-circulatory, microcirculatory data, cytokine levels, and relative circUBAP2 expressions were collected before, at 24 h, and at ECMO weaning off, respectively. The effects of circUBAP2 on the migration, polarization, cytokine productions, and inflammatory pathways in macrophage NR8383 cells were investigated using in vitro methods.</p><p><strong>Results: </strong>Thirty-three patients with an average age of 58.0 years were enrolled, including 19 survivors and 14 non-survivors. The survivors had higher small vessel density, perfused small vessel density (PSVD), and microvascular flow index (MFI) throughout the ECMO course than did the non-survivors. Relative expression of circUBAP2 (hsa_circ_0007367) correlated with the microcirculatory parameters and satisfactorily predicted the 30-day in-hospital mortality. A multivariable logistic model was developed, showing following four predictors: age (odds ratio [OR] 1.06, 95% confidence interval [CI] 1.00-1.12), time from shock to ECMO (OR 1.10, 95% CI 1.01-1.20), PVSD (OR 0.14, 95% CI 0.02-0.89), and the circUBAP2 expression (OR 0.25, 95% CI 0.08-0.78). In addition, circUBAP2 inhibited the migratory activity and promoted M2 polarization in macrophages, declining the productions of cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and monocyte chemotactic protein [MCP]-1) and the PI3K/Akt/mTOR pathway.</p><p><strong>Conclusion: </strong>The expression of circUBAP2 correlates with microcirculatory perfusion and has the potential in predicting outcomes for on-ECMO patients with cardiogenic shock.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"200-210"},"PeriodicalIF":3.1,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40404251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining Sepsis Phenotypes-Two Murine Models of Sepsis and Machine Learning.","authors":"Allan E Stolarski,&nbsp;Jiyoun Kim,&nbsp;Jacob Nudel,&nbsp;Sophia Gunn,&nbsp;Daniel G Remick","doi":"10.1097/SHK.0000000000001935","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001935","url":null,"abstract":"<p><strong>Introduction: </strong>The immunobiology defining the clinically apparent differences in response to sepsis remains unclear. We hypothesize that in murine models of sepsis we can identify phenotypes of sepsis using non-invasive physiologic parameters (NIPP) early after infection to distinguish between different inflammatory states.</p><p><strong>Methods: </strong>Two murine models of sepsis were used: gram-negative pneumonia (PNA) and cecal ligation and puncture (CLP). All mice were treated with broad spectrum antibiotics and fluid resuscitation. High-risk sepsis responders (pDie) were defined as those predicted to die within 72 h following infection. Low-risk responders (pLive) were expected to survive the initial 72 h of sepsis. Statistical modeling in R was used for statistical analysis and machine learning.</p><p><strong>Results: </strong>NIPP obtained at 6 and 24 h after infection of 291 mice (85 PNA and 206 CLP) were used to define the sepsis phenotypes. Lasso regression for variable selection with 10-fold cross-validation was used to define the optimal shrinkage parameters. The variables selected to discriminate between phenotypes included 6-h temperature and 24-h pulse distention, heart rate (HR), and temperature. Applying the model to fit test data (n = 55), area under the curve (AUC) for the receiver operating characteristics (ROC) curve was 0.93. Subgroup analysis of 120 CLP mice revealed a HR of <620 bpm at 24 h as a univariate predictor of pDie. (AUC of ROC curve = 0.90). Subgroup analysis of PNA exposed mice (n = 121) did not reveal a single predictive variable highlighting the complex physiological alterations in response to sepsis.</p><p><strong>Conclusion: </strong>In murine models with various etiologies of sepsis, non-invasive vitals assessed just 6 and 24 h after infection can identify different sepsis phenotypes. Stratification by sepsis phenotypes can transform future studies investigating novel therapies for sepsis.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"268-273"},"PeriodicalIF":3.1,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40404181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Necroptosis, Pyroptosis, Ferroptosis in Sepsis and Treatment.","authors":"Mengdi Qu,&nbsp;Yanghanzhao Wang,&nbsp;Zhiyun Qiu,&nbsp;Shuainan Zhu,&nbsp;Kefang Guo,&nbsp;Wankun Chen,&nbsp;Changhong Miao,&nbsp;Hao Zhang","doi":"10.1097/SHK.0000000000001936","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001936","url":null,"abstract":"<p><strong>Abstract: </strong>As a global major health problem and a leading cause of death, sepsis is defined as a failure of homeostasis, which is mainly initiated by an infection and followed by sustained excessive inflammation until immune suppression. Despite advances in the identification and management of clinical sepsis, morbidity, and mortality remain high. In addition, clinical trials have failed to yield promising results. In recent years, the mechanism of regulated cell death (RCD) in sepsis has attracted more and more attention, because these dying cells could release a large number of danger signals which contribute to inflammatory responses and exacerbation of sepsis, providing a new direction for us to make treatment strategy. Here we summarize mechanisms of several forms of RCD in sepsis including necroptosis, pyroptosis, ferroptosis. In conclusion, targeting RCD is considered a promising approach to treat sepsis.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"161-171"},"PeriodicalIF":3.1,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40404249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Limited Role for AMD3100 Induced Stem Cell Mobilization for Modulation of Thoracic Trauma Outcome.","authors":"Mona Vogel,&nbsp;Bettina Möhrle,&nbsp;Vadim Sakk,&nbsp;Andreas Brown,&nbsp;Annette Palmer,&nbsp;Sonja Braumüller,&nbsp;Markus Huber-Lang,&nbsp;Andreas Allgöwer,&nbsp;Jose A Cancelas,&nbsp;Hartmut Geiger","doi":"10.1097/SHK.0000000000001933","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001933","url":null,"abstract":"<p><strong>Abstract: </strong>Thoracic trauma is a major cause of mortality due to the associated inflammatory acute respiratory distress syndrome and morbidity due to impaired tissue regeneration. Trauma-induced lung inflammation is characterized by the early recruitment of cells with pro- or anti-inflammatory activity to the lung. Therapeutic interventions reducing the level of tissue inflammation may result in decreased tissue damage and improved healing and recovery. Stem cells might be able to improve trauma outcome via immunomodulation or by enhancing tissue regeneration.Here, we describe the migratory dynamics of murine mesenchymal, hematopoietic and endothelial stem and progenitor cells (SPCs) as well as mature inflammatory cells (monocytes, neutrophils, lymphocytes) to peripheral blood (PB) and lung tissue between 0.2 and 48 h post-blunt chest trauma (TXT). We demonstrate that the kinetics of immune cell and SPC distribution upon trauma are both cell-type and tissue-dependent. We identified a transient, early increase in the number of inflammatory cells in PB and lung at 2 h post-TXT and a second wave of infiltrating SPCs in lungs by 48 h after TXT induction, suggesting a role for SPCs in tissue remodeling after the initial inflammatory phase. Cxcl12/Cxcr4 blockade by AMD3100 within the first 6 h after TXT, while inducing a strong and coordinated mobilization of SPCs and leukocytes to PB and lung tissue, did not significantly affect TXT associated inflammation or tissue damage as determined by inflammatory cytokine levels, plasma markers for organ function, lung cell proliferation and survival, and myofibroblast/fibroblast ratio in the lung. Further understanding the dynamics of the distribution of endogenous SPCs and inflammatory cells will therefore be indispensable for stem cell-based or immunomodulation therapies in trauma.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"260-267"},"PeriodicalIF":3.1,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40404180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}