Factors affecting do-not-attempt-resuscitation (DNAR) decisions among adult patients in the emergency department of a general tertiary teaching hospital in China: a retrospective observational study.

Objective: Do-not-attempt-resuscitation (DNAR) orders are designed to allow patients to opt out of receiving cardiopulmonary resuscitation in the event of a cardiac arrest. While DNAR has become a standard component of medical care, there is limited research available specifically focusing on DNAR orders in the context of emergency departments in China. This study aimed to fill that gap by examining the factors related to DNAR orders among patients in the emergency department of a general tertiary teaching hospital in China.

Severe Hypokalemia Complicated by Acute Myopathy: Initial Manifestation of Primary Sjögren's Syndrome-Associated Renal Tubular Acidosis.

BACKGROUND Severe hypokalemia, which often causes life-threatening malignant arrhythmias, is usually first diagnosed in the Emergency Department (ED). It is important to note that hypokalemia is often closely and complexly related to renal tubular acidosis (RTA) associated with autoimmune diseases such as Sjögren's syndrome (SS), especially in females with acute myopathy or acute liver injury (ALI). Severe hypokalemia can directly cause muscle injury, which can lead to hyper-creatine kinaseemia (HCK) and ALI, while SS can also directly cause hypokalemia, HCK, and even ALI and renal tubular/interstitial injury.

Angiotensin-(1-7) ameliorates sepsis-induced cardiomyopathy by alleviating inflammatory response and mitochondrial damage through the NF-κB and MAPK pathways.

Background: There is no available viable treatment for Sepsis-Induced Cardiomyopathy (SIC), a common sepsis complication with a higher fatality risk. The septic patients showed an abnormal activation of the renin angiotensin (Ang) aldosterone system (RAAS). However, it is not known how the Ang II and Ang-(1-7) affect SIC.

Losartan attenuates sepsis-induced cardiomyopathy by regulating macrophage polarization via TLR4-mediated NF-κB and MAPK signaling.

Sepsis-induced cardiomyopathy (SIC) is a serious complication of sepsis with high mortality but no effective treatment. The renin angiotensin (Ang) aldosterone system (RAAS) is activated in patients with sepsis but it is unclear how the Ang II/Ang II type 1 receptor (AT1R) axis contributes to SIC. This study examined the link between the Ang II/AT1R axis and SIC as well as the protective effect of AT1R blockers (ARBs).

Diagnostic Value of Metagenomic Next-Generation Sequencing for Pulmonary Infection in Intensive Care Unit and Non-Intensive Care Unit Patients.

Objective: To evaluate the diagnostic performance of metagenomic next-generation sequencing (mNGS) and culture in pathogen detection among intensive care unit (ICU) and non-ICU patients with suspected pulmonary infection.

Methods: In this prospective study, sputum samples were collected from patients with suspected pulmonary infection for 2 consecutive days and then subjected to DNA or RNA sequencing by mNGS or culture; 62 ICU patients and 60 non-ICU patients were admitted. In the end, comparisons were made on the pathogen species identified by mNGS and culture, the overall performance of these two methods in pathogen detection, and the most common pathogens detected by mNGS between the ICU and non-ICU groups.

Rutin Inhibits Cardiac Apoptosis and Prevents Sepsis-Induced Cardiomyopathy.

Rutin is a flavanol-type polyphenol that consists of flavanol quercetin and the disaccharide rutinose, which has been reported to exert various biological effects such as antioxidant and anti-inflammatory activities. It is not clear whether rutin has a protective effect on sepsis-induced cardiomyopathy (SIC). In this study, we used male C57BL/6 mice and cecal ligation and puncture (CLP) surgery to establish the model of SIC.

Insight Into Regulatory T Cells in Sepsis-Associated Encephalopathy.

Sepsis-associated encephalopathy (SAE) is a diffuse central nervous system (CNS) dysfunction during sepsis, and is associated with increased mortality and poor outcomes in septic patients. Despite the high incidence and clinical relevance, the exact mechanisms driving SAE pathogenesis are not yet fully understood, and no specific therapeutic strategies are available. Regulatory T cells (T) have a role in SAE pathogenesis, thought to be related with alleviation of sepsis-induced hyper-inflammation and immune responses, promotion of T helper (Th) 2 cells functional shift, neuroinflammation resolution, improvement of the blood-brain barrier (BBB) function, among others.

Regulatory T Cells: Angels or Demons in the Pathophysiology of Sepsis?

Sepsis is a syndrome characterized by life-threatening organ dysfunction caused by the dysregulated host response to an infection. Sepsis, especially septic shock and multiple organ dysfunction is a medical emergency associated with high morbidity, high mortality, and prolonged after-effects. Over the past 20 years, regulatory T cells (Tregs) have been a key topic of focus in all stages of sepsis research.

Thyroid hormone disorders: a predictor of mortality in patients with septic shock defined by Sepsis-3?

Decreased serum thyroid hormone levels and their prediction of mortality in septic patients are still controversial, especially with the evolution of the definition of sepsis. This study aimed to assess the ability of thyroid hormone disorders to predict the early mortality of patients with septic shock defined by Sepsis-3. Sixty-three adult patients with septic shock admitted to a university hospital emergency intensive care unit (EICU) were studied.

Targeting Neuropilin-1 Suppresses the Stability of CD4 CD25 Regulatory T Cells via the NF-κB Signaling Pathway in Sepsis.

Neuropilin-1 (Nrp-1) contributes to maintaining the stability of CD4 CD25 regulatory T cells (T). We investigated the impact of Nrp-1 on the stability of CD4 CD25 T, and the underlying signaling pathways, in a model of sepsis. Splenic CD4 CD25 T were either treated with anti-Nrp-1, transfected to silence Nrp-1 and inhibitor of NF-κB kinase subunit beta (IKKβ), or administered ammonium pyrrolidine dithiocarbamate (PDTC), followed by recombinant semaphorin 3A (rSema3A), in a simulation of sepsis.

Quick Sequential Organ Failure Assessment as a prognostic factor for infected patients outside the intensive care unit: a systematic review and meta-analysis.

Quick Sequential Organ Failure Assessment (qSOFA) was proposed to replace SIRS as a new screening tool for the identification of septic patients at high mortality. However, researches from infected patients outside of ICU especially in Emergency Department (ED) drew contradictory conclusions on the prognostic value of qSOFA. This systematic review evaluated qSOFA as a prognostic marker of infected patients outside of ICU.

Recent Advances in the Molecular Mechanisms Underlying Pyroptosis in Sepsis.

Sepsis is recognized as a life-threatening organ dysfunctional disease that is caused by dysregulated host responses to infection. Up to now, sepsis still remains a dominant cause of multiple organ dysfunction syndrome (MODS) and death among severe condition patients. Pyroptosis, originally named after the Greek words "" and "" in 2001, has been defined as a specific programmed cell death characterized by release of inflammatory cytokines.

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression.

Cellular immunosuppression appears to be involved in sepsis and sepsis-induced multiple organ dysfunction syndrome (MODS). Recent evidence showed that parenteral vitamin C (Vit C) had the ability to attenuate sepsis and sepsis-induced MODS. Herein, we investigated the impact of parenteral Vit C on cellular immunosuppression and the therapeutic value in sepsis.

Tuftsin prevents the negative immunoregulation of neuropilin-1highCD4+CD25+Regulatory T cells and improves survival rate in septic mice.

Our previous research showed that neuropilin (Nrp) -1highCD4+CD25+Regulatory T cells (Tregs) exhibited primary negative immunoregulation in sepsis induced immune dysfunction. Tuftsin is the typical ligand of Nrp-1. Herein, we investigated the potential therapeutic value and mechanisms of tuftsin in sepsis.

Neuropilin-1highCD4⁺CD25⁺ Regulatory T Cells Exhibit Primary Negative Immunoregulation in Sepsis.

Regulatory T cells (Tregs) appear to be involved in sepsis-induced immune dysfunction; neuropilin-1 (Nrp-1) was identified as a surface marker for CD4(+)CD25(+)Tregs. In the current study, we investigated the negative immunoregulation of Nrp-1(high)CD4(+)CD25(+)Tregs and the potential therapeutic value of Nrp-1 in sepsis. Splenic CD4(+)CD25(+)Tregs from cecal ligation and puncture (CLP) mouse models were further segregated into Nrp-1(high)Tregs and Nrp-1(low)Tregs; they were cocultured with CD4(+)CD25(-)  T cells.

Tuftsin-derived T-peptide prevents cellular immunosuppression and improves survival rate in septic mice.

The primary mechanisms of sepsis induced cellular immunosuppression involve immune dysfunction of T lymphocytes and negative immunoregulation of regulatory T cells (Tregs). It has been found that tuftsin is an immune modulating peptide derived from IgG in spleen. T-peptide is one of tuftsin analogs.

[Advancement in the research of mechanism of immune dysfunction in sepsis and the regulatory effects of Xuebijing injection].

Sepsis is a systemic inflammatory response syndrome resulting from a host response to infection. The early stage of sepsis is characterized by excessive inflammatory response, accompanied by immune dysfunction characterized by aggravating cellular immunosuppression. The vast majority of patients with sepsis survive the initial excessive inflammatory response, but die of hospital-acquired infection, opportunistic pathogenic bacteria infection, latent virus reactivation, and multiple organ dysfunction syndrome.