BACKGROUND: Emergency medical service system (EMSS) is essential in providing acute care services for health conditions. However, trends of emergency and acute care in China haven’t been studied systematically. METHODS: Relevant literature was carefully reviewed, including original and review articles, letters, government reports, yearbooks, both in Chinese and in English. Data on the number of emergency visits, physicians and beds in emergency departments (EDs), and the workforce of pre-hospital emergency care were summarized and analyzed from China Health and Family Planning Statistical Yearbooks (2006-2018). RESULTS: Over the past decade, the number of ED visits tripled from 51.9 million to 166.5 million; and utilization of pre-hospital emergency care increased from 3.2 million to 6.8 million. In response to rapid increases in demand, the number of licensed emergency physicians raised from 20,058 to 59,409; the beds’ number increased from 10,783 to 42,367. For pre-hospital emergency care, the volume of health workforce increased from 3,687 to 8,671, with a 109% increase in the number of physicians from 1,774 to 3,712. However, overcrowding, the long length of stay in EDs, poor work environment, and work exhaustion were still the critical challenges faced by China’s EMSS. CONCLUSIONS: The number of emergency visits has grown with continual capability enhancement during the past decade. However, overcrowding, the long length of stay in EDs, poor work environment, and work exhaustion still need to be solved by China’s EMSS. These findings and comparison with the USA could offer experiences and lessons to EMSS development worldwide, especially for developing countries.

BACKGROUND: A pandemic of coronavirus disease (COVID-19) has been declared by the World Health Organization (WHO) and caring for critically ill patients is expected to be at the core of battling this disease. However, little is known regarding an early detection of patients at high risk of fatality. METHODS: This retrospective cohort study recruited consecutive adult patients admitted between February 8 and February 29, 2020, to the three intensive care units (ICUs) in a designated hospital for treating COVID-19 in Wuhan. The detailed clinical information and laboratory results for each patient were obtained. The primary outcome was in-hospital mortality. Potential predictors were analyzed for possible association with outcomes, and the predictive performance of indicators was assessed from the receiver operating characteristic (ROC) curve. RESULTS: A total of 121 critically ill patients were included in the study, and 28.9% (35/121) of them died in the hospital. The non-survivors were older and more likely to develop acute organ dysfunction, and had higher Sequential Organ Failure Assessment (SOFA) and quick SOFA (qSOFA) scores. Among the laboratory variables on admission, we identified 12 useful biomarkers for the prediction of in-hospital mortality, as suggested by area under the curve (AUC) above 0.80. The AUCs for three markers neutrophil-to-lymphocyte ratio (NLR), thyroid hormones free triiodothyronine (FT3), and ferritin were 0.857, 0.863, and 0.827, respectively. The combination of two easily accessed variables NLR and ferritin had comparable AUC with SOFA score for the prediction of in-hospital mortality (0.901 vs. 0.955, P=0.085). CONCLUSIONS: Acute organ dysfunction combined with older age is associated with fatal outcomes in COVID-19 patients. Circulating biomarkers could be used as powerful predictors for the in-hospital mortality.

BACKGROUND: The aim of the present study is to describe the clinical correlates of hypotension and its associated outcomes in patients with acute organophosphorus poisoning (AOPP). METHODS: In this retrospective cohort study, we analyzed data pertaining to 871 patients with AOPP who were treated at two hospitals. Data from hypotensive and non-hypotensive patients were compared to identify clinical correlates of hypotension. We also evaluated the association between clinical parameters (including hypotension) and in-hospital mortality. RESULTS: The incidence of hypotension in AOPP patients was 16.4%. Hypotensive patients showed significantly higher in-hospital mortality (1.1% vs. 39.9%, P<0.001). Advanced age (odds ratio [OR] 1.25, 95% confidence interval [CI] 1.08-1.44), history of diabetes (OR 2.65, 95% CI 1.14-5.96), and increased white blood cell count (OR 1.06, 95% CI 1.03-1.09), plasma cholinesterase (OR 0.91, 95% CI 0.84-0.94), plasma albumin (OR 0.88, 95% CI 0.85-0.92), serum amylase (OR 1.01, 95% CI 1.01-1.02), and blood pH (OR 0.64, 95% CI 0.54-0.75) were significantly associated with hypotension. After adjusting for potential confounders, hypotension was associated with increased in-hospital mortality (hazard ratio 8.77-37.06, depending on the controlled variables). CONCLUSIONS: Hypotension is a common complication of AOPP and is associated with increased in-hospital mortality. Advanced age, history of diabetes, and changes in laboratory parameters were associated with hypotension in AOPP patients.

BACKGROUND: The study aims to investigate the performance of a metagenomic next-generation sequencing (NGS)-based diagnostic technique for the identification of potential bacterial and viral infections and effects of concomitant viral infection on the survival rate of intensive care unit (ICU) sepsis patients. METHODS: A total of 74 ICU patients with sepsis who were admitted to our institution from February 1, 2018 to June 30, 2019 were enrolled. Separate blood samples were collected from patients for blood cultures and metagenomic NGS when the patients’ body temperature was higher than 38 °C. Patients’ demographic data, including gender, age, ICU duration, ICU scores, and laboratory results, were recorded. The correlations between pathogen types and sepsis severity and survival rate were evaluated. RESULTS: NGS produced higher positive results (105 of 118; 88.98%) than blood cultures (18 of 118; 15.25%) over the whole study period. Concomitant viral infection correlated closely with sepsis severity and had the negative effect on the survival of patients with sepsis. However, correlation analysis indicated that the bacterial variety did not correlate with the severity of sepsis. CONCLUSIONS: Concurrent viral load correlates closely with the severity of sepsis and the survival rate of the ICU sepsis patients. This suggests that prophylactic administration of antiviral drugs combined with antibiotics may be beneficial to ICU sepsis patients.

BACKGROUND: We aim to investigate effects of metabolic syndrome on onset age and long-term outcomes in patients with acute coronary syndrome (ACS). METHODS: Patients with ACS (n=6,431) who underwent percutaneous coronary intervention from January to December 2013 were enrolled. After excluding patients with previous coronary artery disease, 1,558 patients were diagnosed with early-onset ACS (men aged ≤50 years; women aged ≤60 years) and 3,044 patients with late-onset ACS. Baseline characteristics and five-year clinical outcomes were measured. RESULTS: Body mass index, triglyceride, low-density lipoprotein cholesterol, and uric acid concentrations were significantly higher, while the high-density lipoprotein cholesterol (HDL-C) concentration was lower in the early-onset ACS group (P<0.001). Multivariate logistic regression revealed obesity (odds ratio [OR] 1.590, 95% confidence interval [CI] 1.345-1.881), hypertriglyceridemia (OR 1.403, 95% CI 1.185-1.660), and low HDL-C (OR 1.464, 95% CI 1.231-1.742) as independent risk factors for early-onset ACS (all P<0.001). The five-year follow-up showed that the incidences of all cause death (1.5% vs. 3.8%, P<0.001), cardiac death (1.1% vs. 2.0%, P=0.023), and recurrent stroke (2.2% vs. 4.2%, P<0.001) were lower, while bleeding events were more frequent in the early-onset ACS group. A subgroup analysis showed higher incidences of recurrent myocardial infarction (MI) and revascularization in patients with early-onset ACS and metabolic syndrome. CONCLUSIONS: Obesity, hypertriglyceridemia, and lower HDL-C level are independent risk factors for early-onset ACS, recurrent MI, and revascularization. The control of metabolic syndrome may reduce the incidence of early-onset ACS and improve the long-term prognosis.

BACKGROUND: Approximately 20% to 30% of patients with coronary artery disease (CAD) develop recurrent angina pectoris following successful and complete coronary revascularization utilizing percutaneous coronary intervention (PCI). We aim to investigate predictors of recurrent angina pectoris in patients who have undergone successful coronary revascularization using PCI, but on repeat coronary angiography have no need for secondary revascularization. METHODS: The study comprised 3,837 patients with CAD, who were enrolled from January 2007 to June 2019. They had undergone successful PCI; some of them redeveloped angina pectoris within one year after the procedure, but on repeat coronary angiography had no need for revascularization. Thrombolysis in myocardial infarction (TIMI) frame count was used to evaluate the velocity of coronary blood in the follow-up angiogram. Multivariate logistic regression was used to investigate risk factors for recurrent angina pectoris. Similarly, predictors of recurrent angina according to the TIMI frame count were assessed using multivariate linear regression. RESULTS: In this retrospective study, 53.5% of patients experienced recurrent angina pectoris. By multivariate logistic regression, the following characteristics were statistically identified as risk factors for recurrent angina pectoris: female sex, older age, current smoking, low-density lipoprotein cholesterol (LDL-C) ≥1.8 mmol/L, and an elevated TIMI frame count (P for all <0.05). Similarly, using multivariate linear regression, the statistical risk factors for TIMI frame count included: female sex, older age, diabetes, body mass index (BMI), post-procedural treatment without the inclusion of dual antiplatelet therapy. CONCLUSIONS: Patient characteristics of female sex, older age, diabetes, and elevated BMI are associated with an increased TIMI frame count, coronary microcirculation dysfunction, and recurrent angina pectoris after initially successful PCI. In addition, current smoking and LDL-C ≥1.8 mmol/L are risk factors for recurrent angina pectoris. In contrast, the treatment with dual antiplatelet therapy is negatively correlated with a higher TIMI frame count and the risk of recurrent angina pectoris.

BACKGROUND: This study aims to investigate whether small balloon aortic valvuloplasty (BAV) reduces the need for permanent pacemaker implantation (PPMI) after transcatheter aortic valve implantation (TAVI). METHODS: This was a retrospective analysis using data from our local TAVI database. Small BAV was defined as a small balloon size (=18 mm) pre-dilatation. Normal BAV was defined as a balloon size >18 mm. The primary endpoint was the incidence of new PPMI. RESULTS: Of 99 consecutive TAVI patients, five patients were excluded due to pre-existing permanent pacemaker. Patients in the small BAV group (n=57) had a significantly lower PPMI rate compared with the normal BAV group (n=37) (3.5% vs. 18.9%, P=0.026). Moderate or severe aortic valve regurgitation post-procedure was similar between the small BAV and normal BAV groups (5.3% vs. 8.1%, P=0.480); likewise, the mean aortic gradient post-procedure did not differ significantly (11.5±5.2 mmHg vs. 12.2±7.3 mmHg, 1 mmHg=0.133 kPa, P=0.580) between the groups. Device success rates were also similar (94.7% vs. 91.8%, P=0.680). In multivariable analysis, small BAV (P=0.027), the ratio of prosthesis diameter to annulus diameter (P=0.048), and mean aortic gradient by echo in the basement (P=0.021) were independent predictors of PPMI. CONCLUSIONS: The small BAV strategy is associated with a low rate of permanent pacemaker implantation after transcatheter self-expanding valve implantation in this single-center observational study.

BACKGROUND: Acute respiratory distress syndrome (ARDS) causes substantial mortalities. Alveolar epithelium is one of the main sites of cell injuries in ARDS. As an important kind of microRNAs (miRNAs), microRNA-145 (miR-145) has been studied in various diseases, while its role in ARDS has not been investigated. METHODS: Lipopolysaccharide (LPS) was intratracheally instilled to establish a rat ARDS model. Cytokines from bronchoalveolar lavage fluid (BALF) were measured using rat tumor necrosis factor-α and interleukin-6 enzyme-linked immunosorbent assay kits (R&D Systems), and the pathological structures were evaluated using hematoxylin and eosin (H&E) staining and transmission electron microscope; the lung miR-145 messenger RNA (mRNA) was detected using quantitative polymerase chain reaction. Bioinformatics focused on the target genes and possible pathways of gene regulation. RESULTS: A rat model of LPS-induced ARDS was successfully established. The miR-145 was down-regulated in the LPS-induced ARDS lung, and mitochondrial dysfunction was observed in alveolar epithelial cells, most obviously at 72 hours after LPS. TargetScan and miRDB databases were used to predict the target genes of miR-145. A total of 428 overlapping genes were identified, seven genes were associated with mitochondrial function, and Ogt, Camk2d, Slc8a3, and Slc25a25 were verified. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were enriched in the mitogen-activated protein kinase (MAPK) signaling pathway, and Gene Ontology (GO) biological process was mainly enriched in signal transduction and transcription regulation. CONCLUSIONS: The miR-145 is down-regulated in LPS-induced ARDS, and affects its downstream genes targeting mitochondrial functions.

BACKGROUND: Small extracellular vesicles (sEVs) from bone marrow mesenchymal stem cells (BMSCs) have shown therapeutic potential for cerebral ischemic diseases. However, the mechanisms by which BMSC-derived sEVs (BMSC-sEVs) protect neurons against cerebral ischemia/reperfusion (I/R) injury remain unclear. In this study, we explored the neuroprotective effects of BMSC-sEVs in the primary culture of rat cortical neurons exposed to oxygen-glucose deprivation and reperfusion (OGD/R) injury. METHODS: The primary cortical neuron OGD/R model was established to simulate the process of cerebral I/R in vitro. Based on this model, we examined whether the mechanism through which BMSC-sEVs could rescue OGD/R-induced neuronal injury. RESULTS: BMSC-sEVs (20 μg/mL, 40 μg/mL) significantly decreased the reactive oxygen species (ROS) productions, and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Additionally, BMSC-sEVs prevented OGD/R-induced neuronal apoptosis in vivo, as indicated by increased cell viability, reduced lactate dehydrogenase (LDH) leakage, decreased terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining-positive cells, down-regulated cleaved caspase-3, and up-regulated Bcl-2/Bax ratio. Furthermore, Western blot and flow cytometry analysis indicated that BMSC-sEV treatment decreased the expression of phosphorylated calcium/calmodulin-dependent kinase II (p-CaMK II)/CaMK II, suppressed the increase of intracellular calcium concentration ([Ca2+]i) caused by OGD/R in neurons. CONCLUSIONS: These results demonstrate that BMSC-sEVs have significant neuroprotective effects against OGD/R-induced cell injury by suppressing oxidative stress and apoptosis, and Ca2+/CaMK II signaling pathways may be involved in this process.

Over the past few decades, traumatic brain injuries (TBIs) have become one of the leading causes of death and the leading cause of injury-related death in the USA.[1,2] It is estimated that 1.70 million people are subject to TBIs each year.[2] Males are more likely to sustain TBIs (59%); the most common age groups are 0-5 years, 15-19 years, and >65 years.[2] Approximately 1.36 million people present to the emergency department (ED), 275,000 are admitted to the hospital, and 52,000 people die from TBIs.[2] The leading causes of TBIs are falling (35.2%), motor vehicle collisions (MVCs, 17.3%), struck by/against an object (16.5%), and assault (10.0%).[2] These statistics combine to make TBIs the leading cause of injury-related death in the USA at 30.5%.[2] It has been estimated that, with specific guidelines from the Brain Trauma Foundation, up to 50.0% of the 52,000 TBI-related deaths may be prevented.[3]