scholarly journals Reduced Flow-Mediated Dilatation Is Not Related to COVID-19 Severity Three Months after Hospitalization for SARS-CoV-2 Infection

2021 ◽  
Vol 10 (6) ◽  
pp. 1318
Author(s):  
Marianne Riou ◽  
Walid Oulehri ◽  
Cedric Momas ◽  
Olivier Rouyer ◽  
Fabienne Lebourg ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Matched Control ◽  
Acute Infection ◽  
Critical Role ◽  
Lung Damage ◽  
Vascular Effect ◽  
Flow Mediated Dilatation ◽  
Artery Flow

The coronavirus disease 2019 (COVID-19) pandemic has spread rapidly worldwide, with more than two million deaths. Evidence indicates the critical role of the vascular endothelium in its pathophysiology but, like potential changes in functional vasodilation, the vascular effect of SARS-CoV-2 at a given distance from the acute infection is largely unknown. We assessed brachial artery flow-mediated dilatation (FMD) in 27 COVID-19 patients needing conventional or intensive care unit hospitalization, three months after SARS-CoV-2 infection diagnosis and in nine age- and sex- matched control subjects. Interestingly, the FMD was lower in COVID-19 patients as compared to controls (8.2 (7.2–8.9) vs. 10.3 (9.1–11.7)); p = 0.002, and half of the hospitalized COVID-19 survivors presented with a reduced FMD < 8% at three months of COVID-19 onset. Impaired FMD was not associated with severe or critical SARS-CoV-2 infection, reflected by ICU hospitalization, total hospitalization duration, or severity of lung damage. In conclusion, reduced FMD is often observed even three months after hospitalization for SARS-CoV-2 infection, but such alteration predominantly appears to not be related to COVID-19 severity. Longer and larger follow-up studies will help to clarify the potential prognosis value of FMD among COVID-19 patients, as well as to further determine the mechanisms involved.

scholarly journals Acute Myeloid and Lymphoblastic Leukemia Cell Interactions with Endothelial Selectins: Critical Role of PSGL-1, CD44 and CD43

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1253 ◽  
Author(s):  
Caroline Spertini ◽  
Bénédicte Baïsse ◽  
Marta Bellone ◽  
Milica Gikic ◽  
Tatiana Smirnova ◽  
...  
Keyword(s):  
Acute Leukemia ◽  
Vascular Endothelium ◽  
Lymphoblastic Leukemia ◽  
Critical Role ◽  
Leukemia Cell ◽  
Hematologic Malignancies ◽  
Selectin Ligands ◽  
Blast Cells ◽  
Acute Myeloid

Acute myeloid and lymphoblastic leukemia are poor prognosis hematologic malignancies, which disseminate from the bone marrow into the blood. Blast interactions with selectins expressed by vascular endothelium promote the development of drug resistance and leukostasis. While the role of selectins in initiating leukemia blast adhesion is established, our knowledge of the involved selectin ligands is incomplete. Using various primary acute leukemia cells and U937 monoblasts, we identified here functional selectin ligands expressed by myeloblasts and lymphoblasts by performing biochemical studies, expression inhibition by RNA interference and flow adhesion assays on recombinant selectins or selectin ligands immunoadsorbed from primary blast cells. Results demonstrate that P-selectin glycoprotein ligand-1 (PSGL-1) is the major P-selectin ligand on myeloblasts, while it is much less frequently expressed and used by lymphoblasts to interact with endothelial selectins. To roll on E-selectin, myeloblasts use PSGL-1, CD44, and CD43 to various extents and the contribution of these ligands varies strongly among patients. In contrast, the interactions of PSGL-1-deficient lymphoblasts with E-selectin are mainly supported by CD43 and/or CD44. By identifying key selectin ligands expressed by acute leukemia blasts, this study offers novel insight into their involvement in mediating acute leukemia cell adhesion with vascular endothelium and may identify novel therapeutic targets.

scholarly journals Standardized Protocol for Hemodialysis Vascular Access Assessment: The Role of Ultrasound and ColorDoppler

2018 ◽  
Vol 45 (1-3) ◽  
pp. 260-269 ◽  
Author(s):  
Federico Nalesso ◽  
Francesco Garzotto ◽  
Ilaria Petrucci ◽  
Sara Samoni ◽  
Grazia Maria Virzì ◽  
...  
Keyword(s):  
Early Diagnosis ◽  
Vascular Access ◽  
Hemodynamic Parameters ◽  
Non Invasive ◽  
Standardized Protocol ◽  
Hemodialysis Vascular Access ◽  
Simple Step ◽  
Artery Flow

Introduction: Ultrasound and colorDoppler technique, which is relatively inexpensive, rapid, non-invasive and repeatable is a powerful tool used for early diagnosis of vascular access (VA) complications in hemodialysis patients. To date a standard and widely comprehensible echocolorDoppler (ECD) protocol is not available. Materials and Methods: A simple step-by-step protocol based on anatomical and hemodynamic parameters of VA has been developed during a 3-years VA ECD follow-up. It consists of an ECD study scheme. The algorithm created involves the calculation of brachial artery flow, description of artero-venous and/or graft-vascular anastomosis and efferent vessel and/or graft. Results: The algorithm allows to formulate a medical report that takes into account both anatomic and hemodynamic parameters of the VA. Reduction of complications and the prevention of chronic complications as well as the early detection of acute problems were achieved. Discussion and Conclusion: The creation of a step-by-step protocol may simplify the multidisciplinary management of VA, its monitoring and the early diagnosis of its complications.

CRITICAL ROLE OF THROMBOXANE A2 IN MONOCYTE RECRUITMENT TO VASCULAR ENDOTHELIUM UNDER FLOW

2004 ◽  
Vol 13 (3) ◽  
pp. 101
Author(s):  
Noriko Nitta ◽  
Keiko Takahashi ◽  
Kentaro Shimokado ◽  
Masayuki Yoshida
Keyword(s):  
Vascular Endothelium ◽  
Critical Role ◽  
Thromboxane A2 ◽  
Monocyte Recruitment

scholarly journals Reversible Acute Fontan Circulation Failure Secondary to Retroconducted Junctional Rhythm. Clinical Echocardiographic Correlation

2021 ◽  
Author(s):  
Paolo Ferrero ◽  
Isabelle Piazza ◽  
Youcef Sadou ◽  
Matteo Ciuffreda
Keyword(s):  
Heart Rate ◽  
Critical Role ◽  
Circadian Variation ◽  
Fontan Circulation ◽  
Atrial Pacing ◽  
Junctional Rhythm ◽  
Echocardiographic Evaluation ◽  
Low Threshold

Abstract Background: Sequential atrioventricular activation plays a critical role in the physiology of Fontan circulation. Although bradycardia is usually well tolerated, retroconducted junctional rhythm may acutely increase atrial pressure impairing cardiac output. Echocardiographic evaluation can reveal clues of this hemodynamic condition. The clinical impact of arrhythmic disturbance on the follow up of patients who had undergone total cavo-pulmonary connection is well recognized but the role of, transient periods of retroconducted junctional rhythm on the immediate post-operative course is less defined. Case presentation: We describe two cases of acute Fontan circulatory failure due to postoperative retroconducted escaping junctional rhythm despite an adequate heart rate and circadian variation. The patients rapidly improved after atrial pacing, allowing discharge with a minimal dose of diuretic.Conclusion: In the absence of any hemodynamic target, hearth rhythm should be systematically checked after TCPC irrespective of adequacy of heart rate. Likewise, efficiency of temporary atrial pacing should be granted and surgeons should have a low threshold for epicardial lead implantation.

scholarly journals Secreted Antibody Is Required for Immunity to Plasmodium berghei

2008 ◽  
Vol 77 (1) ◽  
pp. 414-418 ◽  
Author(s):  
Julia K. Nunes ◽  
Michael N. Starnbach ◽  
Dyann F. Wirth
Keyword(s):  
Adaptive Immunity ◽  
Plasmodium Berghei ◽  
Acute Infection ◽  
Critical Role ◽  
Challenge Infection ◽  
Blood Stage ◽  
Wild Type ◽  
Homologous Blood ◽  
Immunodeficient Mice

ABSTRACT Infection with Plasmodium berghei is lethal to mice, causing high levels of parasitemia, severe anemia, and death. However, when mice are treated with antimalarial drugs during acute infection, they have enhanced immunity to subsequent infections. With this infection and cure model of immunity, we systematically examined the basis of adaptive immunity to infection using immunodeficient mice. In order to induce adaptive immunity, mice were infected with blood-stage parasites. When the mice developed 2 to 3% parasitemia, they were treated with chloroquine to cure the infection. These convalescent mice were then challenged with homologous blood-stage parasites. Immunized wild-type mice were able to control the level of infection. In contrast, mice lacking mature B cells and T cells were unable to control a challenge infection, indicating the critical role of lymphocytes in immunity to P. berghei. Furthermore, mice lacking secreted antibody were unable to control the level of parasitemia following a challenge infection. Our results indicate that secreted antibody is a requirement for immunity to P. berghei.

scholarly journals Interleukin-27R Signaling Mediates Early Viral Containment and Impacts Innate and Adaptive Immunity after Chronic Lymphocytic Choriomeningitis Virus Infection

2018 ◽  
Vol 92 (12) ◽  
Author(s):  
James A. Harker ◽  
Kurt A. Wong ◽  
Simone Dallari ◽  
Phuc Bao ◽  
Aleksandr Dolgoter ◽  
...  
Keyword(s):  
Acute Infection ◽  
Critical Role ◽  
Myeloid Cells ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Host Immune System ◽  
Adaptive Immune ◽  
Interleukin 27 ◽  
Immune Alterations

ABSTRACTChronic viral infections represent a major challenge to the host immune response, and a unique network of immunological elements, including cytokines, are required for their containment. By using a model persistent infection with the natural murine pathogen lymphocytic choriomeningitis virus clone 13 (LCMV Cl13) we investigated the role of one such cytokine, interleukin-27 (IL-27), in the control of chronic infection. We found that IL-27 receptor (IL-27R) signaling promoted control of LCMV Cl13 as early as days 1 and 5 after infection and thatil27p28transcripts were rapidly elevated in multiple subsets of dendritic cells (DCs) and myeloid cells. In particular, plasmacytoid DCs (pDCs), the most potent type 1 interferon (IFN-I)-producing cells, significantly increasedil27p28in a Toll-like receptor 7 (TLR7)-dependent fashion. Notably, mice deficient in an IL-27-specific receptor, WSX-1, exhibited a pleiotropy of innate and adaptive immune alterations after chronic lymphocytic choriomeningitis virus (LCMV) infection, including compromised NK cell cytotoxicity and antibody responses. While, the majority of these immune alterations appeared to be cell extrinsic, cell-intrinsic IL-27R was necessary to maintain early pDC numbers, which, alongside lower IFN-I transcription in CD11b+DCs and myeloid cells, may explain the compromised IFN-I elevation that we observed early after LCMV Cl13 infection in IL-27R-deficient mice. Together, these data highlight the critical role of IL-27 in enabling optimal antiviral immunity early and late after infection with a systemic persistent virus and suggest that a previously unrecognized positive-feedback loop mediated by IL-27 in pDCs might be involved in this process.IMPORTANCEPersistently replicating pathogens, such as human immunodeficiency virus, hepatitis B virus, and hepatitis C virus, represent major health problems worldwide. These infections impose a long-term challenge on the host immune system, which must be heavily and continuously regulated to keep pathogen replication in check without causing fatal immunopathology. Using a persistently replicating rodent pathogen, LCMV, in its natural host, we identified the cellular sources and effects of one important regulatory pathway, interleukin-27 receptor WSX-1 signaling, that is required for both very early and late restriction of chronic (but not acute) infection. We found that WSX-1 was necessary to promote innate immunity and the development of aberrant adaptive immune responses. This not only highlights the role of IL-27 receptor signaling in regulating distinct host responses that are known to be necessary to control chronic infections, but also positions IL-27 as a potential therapeutic target for their modulation.

scholarly journals No difference in learning retention in manikin-based simulation based on role

2016 ◽  
Vol 30 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Dominic Giuliano ◽  
Marion McGregor DC
Keyword(s):  
Repeated Measures ◽  
Critical Role ◽  
Learning Retention ◽  
Time Points ◽  
Repeated Measures Analysis ◽  
Significant Difference ◽  
Simulation Based ◽  
Data Points

Objective: We evaluated learning retention in interns exposed to simulation. It was hypothesized that learning would degrade after 6 months and there would be a difference in retention between interns who played a critical role versus those who did not. Methods: A total of 23 groups of 5 to 9 interns underwent a cardiac scenario twice during 1 simulation experience and again 6 months later. We captured 69 recordings (23 before debrief at baseline [PrDV], 23 after debrief at baseline [PoDV], and 23 at 6-month follow-up [FUV]). Students were assigned different roles, including the critical role of “doctor” in a blinded, haphazard fashion. At 6-month follow-up, 12 interns who played the role of doctor initially were assigned that role again, while 11 interns who played noncritical roles initially were newly assigned to doctor. All videos of intern performance were scored independently and in a blinded fashion, by 3 judges using a 15-item check list. Results: Repeated-measures analysis of variance for interns completing all 3 time points indicated a significant difference between time points (F2,22 = 112, p = .00). Contrasts showed a statistically significant difference between PrDV and PoDV (p = .00), and PrDV and FUV (p = .00), but no difference between PoDV and FUV (p = .98). This was consistent with results including all data points. Checklist scores were more than double for PoDV recordings (16) and FUV (15), compared to PrDV recordings (6.6). Follow-up scores comparing old to new doctors showed no statistically significant difference (15.4 vs 15.2 respectively, t21 = 0.26, p = .80, d = .11). Conclusions: Learning retention was maintained regardless of role.

scholarly journals Interaction among estrogen, IGF-1, and H2S on smooth muscle cell proliferation

2021 ◽  
Vol 248 (1) ◽  
pp. 17-30
Author(s):  
Tian Shuang ◽  
Ming Fu ◽  
Guangdong Yang ◽  
Ying Huang ◽  
Zhongming Qian ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Critical Role ◽  
Insulin Like Growth Factor ◽  
Vascular Effects ◽  
Vascular Effect ◽  
Vascular Smcs ◽  
Underlying Mechanisms

Both estrogen and hydrogen sulfide (H2S) inhibit the proliferation of vascular smooth muscle cells (SMCs) and development of atherosclerosis. In the absence of endogenous H2S as occurred in CSE-knockout (KO) mouse, however, estrogen stimulates the proliferation of vascular SMCs. The underlying mechanisms for this seemingly controversial vascular effect of estrogen are unclear. In the present study, we demonstrated that the stimulatory effect of estrogen on the proliferation of CSE-KO SMCs was suppressed by the inhibitor of insulin-like growth factor-1 receptor (IGF-1R) or knockdown of IGF-1R protein expression. Estrogen downregulated the expression of insulin-like growth factor-1 (IGF-1) and IGF-1R in aortic tissues or aortic SMCs isolated from WT and CSE-KO mice. Furthermore, endogenous H2S downregulated IGF-1R, but upregulated estrogen receptor (ER)-α, in aortic tissues or SMCs. ER-α and IGF-1R were co-located in SMCs and co-immunoprecipitated, which was decreased by H2S. Finally, both endogenous and exogenous H2S induced the S-sulfhydration of IGF-1R, but not ER-α, in WT-SMCs and CSE-KO SMCs, which underlies the decreased formation of IGF-1R/ER-α hybrid in the presence of H2S. Thus, the absence of H2S favors the interaction of estrogen with IGF-1R/ER-α hybrid to stimulate SMCs proliferation. The appreciation of a critical role of H2S in preventing estrogen-induced SMCs proliferation will help better understand the regulation of complex vascular effects of estrogen and sex-related cardiovascular diseases.

Perceptions of Smoking and Nonsmoking Peers: The Value of Smoker and Nonsmoker Prototypes in Predicting Smoking Onset and Regular Smoking Among Adolescents

2006 ◽  
Vol 34 (6) ◽  
pp. 897-910 ◽  
Author(s):  
Renske Spijkerman ◽  
Regina J. J. M. Van Den Eijnden ◽  
Rutger C. M. E. Engels
Keyword(s):  
Logistic Regression ◽  
High Schools ◽  
Critical Role ◽  
Smoking Behavior ◽  
Regression Analyses ◽  
Smoking Onset ◽  
Reported Data ◽  
Additional Role

Adolescents' perceptions of persons their age who smoke cigarettes (also known as prototypes of smoking peers) play a critical role in an adolescent's decision to start smoking. However, adolescents' perceptions of their peers who do not smoke (prototypes of nonsmoking peers) could be implicated in adolescents' smoking decisions as well. In the present study, the authors examined the additional role of nonsmoker prototypes in adolescents' smoking onset and regular smoking. At seven high schools, Dutch students ( n = 1,035) between the ages of 12 and 15 years who were attending the eighth grade provided self-reported data on their smoker and nonsmoker prototypes and smoking behavior during a baseline and 6-month follow-up measurement. Logistic regression analyses showed that both smoker and nonsmoker prototypes assessed at Time 1 predicted smoking onset by Time 2 among nonsmoking adolescents. However, only nonsmoker prototypes predicted regular smoking among adolescents who smoked occasionally at baseline.

scholarly journals Metabolic profiling during malaria reveals the role of the aryl hydrocarbon receptor in regulating kidney injury

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Michelle M Lissner ◽  
Katherine Cumnock ◽  
Nicole M Davis ◽  
José G Vilches-Moure ◽  
Priyanka Basak ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Metabolic Response ◽  
Acute Infection ◽  
Critical Role ◽  
Kidney Injury ◽  
High Plasma ◽  
Metabolic Reprogramming ◽  
Aryl Hydrocarbon ◽  
Specific Effects

Systemic metabolic reprogramming induced by infection exerts profound, pathogen-specific effects on infection outcome. Here, we detail the host immune and metabolic response during sickness and recovery in a mouse model of malaria. We describe extensive alterations in metabolism during acute infection, and identify increases in host-derived metabolites that signal through the aryl hydrocarbon receptor (AHR), a transcription factor with immunomodulatory functions. We find that Ahr-/- mice are more susceptible to malaria and develop high plasma heme and acute kidney injury. This phenotype is dependent on AHR in Tek-expressing radioresistant cells. Our findings identify a role for AHR in limiting tissue damage during malaria. Furthermore, this work demonstrates the critical role of host metabolism in surviving infection.

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