scholarly journals Quantification Series of Procalcitonin Decides the Conceivable Bacterial Infection among Vital Organs

2021 ◽  
Vol 8 (4) ◽  
pp. 475-483
Author(s):  
Cinthiaha S ◽  
Fahima Sheerin SMH ◽  
Divya S
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Bacterial Infection ◽  
Organ Dysfunction ◽  
Liver Enzymes ◽  
Pancreatic Enzymes ◽  
Bacterial Sepsis ◽  
Renal Markers ◽  
Key Factor ◽  
Huge Impact

Sepsis is the occurrence of infection in association with the systemic inflammatory response syndrome (SIRS). Bacterial sepsis is one of the major illnesses that shows severe symptoms which leads to organ dysfunction. Procalcitonin (PCT) the precursor of the hormone calcitonin shows a huge impact on the diagnosis of sepsis caused by the bacterial infection. Many studies have also insisted the importance of PCT as a biomarker for sepsis. As early diagnosis is the key factor to overcome the difficulties of the sepsis, PCT acts a prominent diagnostic tool to acquire the desired results. This study focused on the role of PCT in correlation with supporting parameters of the vital organs such as renal markers, liver enzymes and pancreatic enzymes to reduce the organ dysfunction and its complications. Keywords: Sepsis, procalcitonin, renal markers, liver enzymes, pancreatic enzymes.

scholarly journals Monitoring of Organ Dysfunction in Sepsis/Systemic Inflammatory Response Syndrome: Novel Strategies

2001 ◽  
Vol 12 (suppl 1) ◽  
pp. S53-S59
Author(s):  
THEA KOCH ◽  
STEFAN GEIGER ◽  
MAX J. R. RAGALLER
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Systemic Inflammatory Response ◽  
Therapeutic Consequences ◽  
Key Factor ◽  
Therapeutic Procedures ◽  
Organ Specific ◽  
Recent Developments

Abstract. Sepsis and systemic inflammatory response syndrome—induced severe disruption of microcirculation and consecutive tissue hypoxia is considered a key factor in the development of organ dysfunction and multiple organ failure. The conventionally measured global variables such as lactate or macrohemodynamic parameters using a pulmonary artery catheter do not adequately mirror microcirculatory disturbances. Evaluation of the severity of microcirculatory distress and the effectiveness of resuscitation strategies requires new clinical technologies aimed at the microcirculation. It is anticipated that novel techniques such as optical spectroscopy and intelligent biosensors will play a major role in the development of new monitoring systems. In general, the current monitoring of organ dysfunction is characterized by a trend from invasive to noninvasive and “safe” techniques, which provide bedside or even on-line monitoring and allow a more precise and earlier detection of organ dysfunction. Techniques for the assessment of regional perfusion and microcirculatory bioenergetics to direct therapeutic procedures are expected to refine and optimize clinical treatment of critically ill patients in the future. This article addresses the question of which variables should be monitored, what is feasible, and what is valid for therapeutic consequences. Recent developments in monitoring of macro- and microcirculation and organ-specific dysfunction, e.g., lung, kidney, are described with respect to their advantages and limitations, and future directions are outlined.

The Janus Face of Neutrophil Specific Antigen CD177 in Bacterial Infection: Focal Disease Versus Systemic Disease

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1108-1108
Author(s):  
Behnaz Bayat ◽  
Vanessa Santoso ◽  
Beate Kehrel ◽  
Ulrich J Sachs ◽  
Sentot Santoso
Keyword(s):  
Bacterial Infection ◽  
Conflicts Of Interest ◽  
Systemic Disease ◽  
Specific Antigen ◽  
Favourable Effect ◽  
Bacterial Sepsis ◽  
Migration Ability ◽  
Significant Difference ◽  
The Impact

Abstract Abstract 1108 CD177, also known as NB1 (or HNA-2) is a GPI-linked glycoprotein, which is exclusively expressed on neutrophils. Approximately 3 to 5% of healthy individuals do not express this antigen on their neutrophils (NBnull). Recent data demonstrated a strong upregulation of NB1 on neutrophils in patients with bacterial, but not viral infections. The mechanism underlying this phenomenon, however, is unknown. Our previous studies showed that NB1 functions as a partner of endothelial PECAM-1 and therefore plays a role on neutrophil diapedesis. Consequently, neutrophils carrying NB1 (NB1plus) migrate faster through endothelial cells than NBnull neutrophils. However, several studies have documented an abrogation of neutrophil migratory abilities in sepsis conditions. In this study, we aim to clarify the impact of neutrophil NB1 expression in bacterial sepsis. To mimic this condition in vitro, we first compared the transendothelial migration ability of NB1 phenotyped neutrophils after stimulation with the bacterial peptide fMLP in a transwell system. Lower transmigration ability (75% vs. 40%) was observed in fMLP-treated NB1plus neutrophils (n = 5) in comparison to untreated neutrophils. In contrast, no significant difference in the migration ability was observed between fMLP-treated and untreated NB1null neutrophils (n = 3). Expression analysis by flow cytometry showed a dose-dependent upregulation of NB1 after stimulation with fMLP (10−6 to 10−8 μM) in NB1plus neutrophils. Interestingly, down regulation of PECAM-1 expression was observed in these treated cells. Contrary, no PECAM-1 downregulation was detected in NBnull fMLP-treated neutrophils. These results could be confirmed by immunoblotting analysis using specific antibodies directed against different epitopes on NB1 (mabs 7D8, MEM166) and against different PECAM-1 Ig domains (mabs PECAM1.1, 1.2 and 1.3). Analysis of the supernatants of fMLP-treated neutrophils demonstrated the shedding of PECAM-1 from NB1plus, but not from NB1null neutrophils. These results indicate that shedding of PECAM-1 from neutrophils during bacterial infections depends on NB1 expression. Recent studies showed that a single nucleotide polymorphism (42C>G) located in NB1 promoter region is associated with the regulation of NB1 expression. Individuals homozygous for C allele express high NB1 surface density in comparison to individuals homozygous for G allele. Our association study showed higher frequency of C allele in patients with bacterial sepsis (n=98) compared with healthy cohort (n = 132) (8.16% vs. 12.88%; P<0.03). This observation indicates the role of C42 allele (or high NB1 expression) as genetic risk factor for bacterial sepsis. All together, these data demonstrate a reverse role of NB1 expression in focal and systemic infection, indicating favourable effect of low NB1 in systemic bacterial infection. This phenomenon may be caused by reduction of neutrophil directionality and motility due to NB1-mediated PECAM-1 shedding. Disclosures: No relevant conflicts of interest to declare.

Relationship between Procalcitonin Levels and Severity of DIC Induced by Bacterial Infection.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3976-3976
Author(s):  
Kazuo Kawasugi ◽  
Ryousuke Shirasaki ◽  
Mizuho Noguti ◽  
Haruko Tashiro ◽  
Naoki Shirafuji
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Bacterial Infection ◽  
Thrombin Generation ◽  
Serum Levels ◽  
Promyelocytic Leukemia ◽  
Clinical Marker ◽  
Functional Studies ◽  
The Past ◽  
Generation Capacity

Abstract <Background and Methods> In the past few years, structural and functional studies have demonstrated an increasingly tight interplay between the coagulation and inflammatory systems. These studies support an important role of systemic inflammatory response syndrome (SIRS) in the development of disseminated intravascular coagulation (DIC) in these critically ill patients. Although PCT is important clinical marker, it role in the DIC process is unkown. We measured serum levels of PCT in septic patients with DIC (n=15) and acute promyelocytic leukemia (APL)-induced DIC (n=5). Serum levels of PCT were determined by the EIA (BIOMERIEMX, France). <Results> The thrombin antithrombin complexes (TAT) levels were higher in both DIC patients as reported by others. ?Levels of PCT elevated in all patients with bacterial infection. In the septic patients with DIC, we found significant elevations of serum PCT levels (97.3±72.3 ng/ml) as compared with septic patients with non overt DIC (30.5±42.4 ng/ml). All the patients that levels of PCT increased than 100 ng/ml died. However, we did not find any difference serum levels of PCT in the APL and EB virus infected patients with DIC. <Conclusion> These results suggest that assess of thrombin generation capacity may be helpful in the making the diagnosis in septic patients with DIC. It appears that serum levels of PCT may contribute to the severity of DIC induced bacterial infection.

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Excitatory Amino Acid ◽  
Ischemia Reperfusion ◽  
Thiol Group ◽  
Protective Role ◽  
Key Factor ◽  
Rate Limiting ◽  
Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

scholarly journals Changing Technology or Behavior? The Impacts of a Behavioral Disruption

2021 ◽  
Vol 13 (11) ◽  
pp. 5861
Author(s):  
Marianne Pedinotti-Castelle ◽  
Pierre-Olivier Pineau ◽  
Kathleen Vaillancourt ◽  
Ben Amor
Keyword(s):  
Energy Transition ◽  
Energy System ◽  
Behavior Changes ◽  
Ghg Emission ◽  
The North ◽  
Behavioral Disruption ◽  
Transportation Sector ◽  
Key Factor ◽  
Additional Costs

Transportation is a key factor in the fight against climate change. Consumer behavior changes in transportation are underrepresented in energy policies, even if they could be essential to achieve the fixed GHG emission reduction targets. To help quantify the role of behaviors in energy transition and their implications on the dynamics of an energy system, this study is conducted using the North American TIMES Energy Model, adapted to Quebec (Canada). A behavioral disruption scenario (an increase in carpooling) is introduced in the model’s transportation sector and is compared to a massive electrification scenario. Our results highlight the fact that a behavioral disruption can lead to the same GHG emission reductions (65%) by 2050 as an electrification policy, while alleviating different efforts (such as additional electrical capacity and additional costs) associated with massive electrification. Moreover, the results are sensitive to behavior-related parameters, such as social discount rates and car lifetimes.

scholarly journals sFasL—The Key to a Riddle: Immune Responses in Aging Lung and Disease

2021 ◽  
Vol 22 (4) ◽  
pp. 2177
Author(s):  
Shulamit B. Wallach-Dayan ◽  
Dmytro Petukhov ◽  
Ronit Ahdut-HaCohen ◽  
Mark Richter-Dayan ◽  
Raphael Breuer
Keyword(s):  
Cell Death ◽  
Lung Disease ◽  
Fas Ligand ◽  
Death Receptor ◽  
Mesenchymal Cells ◽  
Soluble Form ◽  
Cell Accumulation ◽  
Key Factor ◽  
Aged Subjects

By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL+ T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment.

scholarly journals Innovative Work Behavior—A Key Factor in Business Performance? The Role of Team Cognitive Diversity and Teamwork Climate in This Relationship

2021 ◽  
Vol 14 (4) ◽  
pp. 185
Author(s):  
Nadežda Jankelová ◽  
Zuzana Joniaková ◽  
Juraj Mišún
Keyword(s):  
Business Performance ◽  
Main Tool ◽  
Work Behavior ◽  
Cognitive Diversity ◽  
Staff Perceptions ◽  
Innovative Work Behavior ◽  
Positive Effects ◽  
Key Factor ◽  
Innovative Work

The aim of our paper is to examine whether the support of innovative work behavior by management is positively related to business performance and at the same time, whether this relationship is mediated by the teamwork climate and cognitive diversity of teams. Cognitive diversity is defined as differences in knowledge and perspective, which arise from professional diversity and account for its positive effects. A teamwork climate represents staff perceptions of collaboration between personnel. Business performance is defined by the level of sales. Our sample consisted of 211 managers of companies operating in Slovakia, and data collection took place in the form of a questionnaire. The main tool for examining the mechanism of operation of the investigated relationships is mediation using regression analysis and the Sobel test to determine the significance of the indirect effect of mediation variables. The findings point to a significant direct relationship between the innovative work behavior of company employees and business performance. The intensity of this relationship can be partly influenced by promoting cognitive diversity, especially in the area of knowledge and ways of thinking. The significant role of a teamwork climate was not demonstrated in the examined model.

scholarly journals HIF-1α promoted vasculogenic mimicry formation in lung adenocarcinoma through NRP1 upregulation in the hypoxic tumor microenvironment

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Ran Fu ◽  
Wenwen Du ◽  
Zongli Ding ◽  
Yi Wang ◽  
Yue Li ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Vasculogenic Mimicry ◽  
Tube Formation ◽  
Luciferase Reporter ◽  
Vimentin Expression ◽  
Cell Metastasis ◽  
Therapeutic Value ◽  
Key Factor ◽  
Important Form

AbstractNeovascularization is a key factor that contributes to tumor metastasis, and vasculogenic mimicry (VM) is an important form of neovascularization found in highly invasive tumors, including lung cancer. Despite the increasing number of studies focusing on VM, the mechanisms underlying VM formation remain unclear. Herein, our study explored the role of the HIF-1α/NRP1 axis in mediating lung adenocarcinoma metastasis and VM formation. HIF-1α, NRP1 expression, and VM in lung adenocarcinoma (LUAD) patient samples were examined by immunohistochemical staining. Quantitative real-time (qRT-PCR), western blot, transwell assay, wound healing assay, and tube formation assay were performed to verify the role of HIF-1α/NRP1 axis in LUAD metastasis and VM formation. ChIP and luciferase reporter assay were used to confirm whether NRP1 is a direct target of HIF-1α. In LUAD tissues, we confirmed a positive relationship between HIF-1α and NRP1 expression. Importantly, high HIF-1α and NRP1 expression and the presence of VM were correlated with poor prognosis. We also found that HIF-1α could induce LUAD cell migration, invasion, and VM formation by regulating NRP1. Moreover, we demonstrated that HIF-1α can directly bind to the NRP1 promoter located between −2009 and −2017 of the promoter. Mechanistically, MMP2, VE-cadherin, and Vimentin expression were affected. HIF-1α plays an important role in inducing lung adenocarcinoma cell metastasis and VM formation via upregulation of NRP1. This study highlights the potential therapeutic value of targeting NRP1 for suppressing lung adenocarcinoma metastasis and progression.

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