Colchicine poisoning: Case report of three homicides in a family.

Background: Colchicine is a common therapeutic agent for inflammatory conditions such as gout, yet its narrow therapeutic range frequently results in cases of overdose and subsequent poisoning. Acute colchicine poisoning can be difficult to identify due to its nonspecific clinical manifestations, posing a diagnostic challenge for emergency physicians without a clear history of colchicine ingestion. Case presentation: This report describes a tragic case of acute colchicine poisoning that resulted in three familial homicides. The patients presented with fever, abdominal pain, and diarrhea, which rapidly escalated to shock during their emergency department visits. Laboratory tests revealed a marked leukocytosis, mild elevation in procalcitonin (PCT), significantly elevated creatine kinase (CK) and CK-MB levels, and liver function abnormalities. Despite treatment with carbapenem antibiotics and aggressive fluid resuscitation, the patients' condition deteriorated, marked by a progressive decline in leukocytes and neutrophils. Initially misdiagnosed as septic shock, the ineffectiveness of the standard treatment protocols led to a fatal outcome for all three individuals. Conclusion: Emergency physicians should consider acute colchicine poisoning as a differential diagnosis in patients presenting with shock and the following clinical indicators: (1) pronounced increase in peripheral leukocytes with a disproportionate rise in neutrophils; (2) discordance between the level of serum procalcitonin and the severity of presumed septic shock; (3) early increase in serum creatine kinase (CK) and CK-MB; (4) poor response to antibiotics and resuscitative efforts, accompanied by a continuous decrease in white blood cells and neutrophils. This case underscores the critical need for awareness of colchicine toxicity in the emergency setting, particularly when the clinical presentation mimics septic shock but fails to respond to standard treatments.

Non-Canonical STING-PERK Pathway Modulation of Cellular Senescence and Therapeutic Response in Sepsis-Associated Acute Kidney Injury.

Abstract-This study explored the role of the non-canonical STING-PERK signaling pathway in sepsis-associated acute kidney injury (SA-AKI). Gene expression data from the GEO database and serum STING protein levels in patients with SA-AKI were analyzed. An LPS-induced mouse model and an in vitro model using HK-2 cells were used to investigate the role of STING in SA-AKI. STING expression was suppressed using shRNA silencing technology and the STING inhibitor C176. Kidney function, inflammatory markers, apoptosis, and senescence were measured. The role of the STING-PERK pathway was investigated by silencing PERK in HK-2 cells and administering the PERK inhibitor GSK2606414. STING mRNA expression and serum STING protein levels were significantly higher in patients with SA-AKI. Suppressing STING expression improved kidney function, reduced inflammation, and inhibited apoptosis and senescence. Silencing PERK or administering GSK2606414 suppressed the inflammatory response, cell apoptosis, and senescence, suggesting that PERK is a downstream effector in the STING signaling pathway. The STING-PERK signaling pathway exacerbates cell senescence and apoptosis in SA-AKI. Inhibiting this pathway could provide potential therapeutic targets for SA-AKI treatment.

H-151 attenuates lipopolysaccharide-induced acute kidney injury by inhibiting the STING-TBK1 pathway.

Sepsis is a severe systemic infectious disease that often leads to multi-organ dysfunction. One of the common and serious complications of sepsis is renal injury. In this study, we aimed to investigate the potential mechanistic role of a novel compound called H-151 in septic kidney injury. We also examined its impact on renal function and mouse survival rates. Initially, we confirmed abnormal activation of the STING-TBK1 signaling pathway in the kidneys of septic mice. Subsequently, we treated the mice with H-151 and observed significant improvement in sepsis-induced renal dysfunction. This was evidenced by reductions in blood creatinine and urea nitrogen levels, as well as a marked decrease in inflammatory cytokine levels. Furthermore, H-151 substantially improved the seven-day survival rate of septic mice, indicating its therapeutic potential. Importantly, H-151 also exhibited an inhibitory effect on renal apoptosis levels, further highlighting its mechanism of protecting against septic kidney injury. These study findings not only offer new insights into the treatment of septic renal injury but also provide crucial clues for further investigations into the regulatory mechanisms of the STING-TBK1 signaling pathway and potential drug targets.

Factors influencing ultrasound cardiac output monitor waveform quality in patients admitted to the emergency intensive care unit.

Objective: The ultrasonic cardiac output monitor (USCOM), an instrument that monitors the evolution of a patient's hemodynamic status and determines the type of shock, has become an important tool for assessing cardiac pathology and predicting changes in disease, but there are some variations in the instrumental findings for different physical conditions of patients. This article examines whether there are differences in the quality of USCOM waveforms measured in different types of critically ill patients based on clinical characteristics and test parameters. Methods: Baseline data, diagnoses, echocardiograms, ventilation patterns, and USCOM results were retrospectively collected from patients in the emergency intensive care unit. Waveform quality was quantified using the Fremantle score to determine the extent to which age, body mass index (BMI), chronic obstructive pulmonary disease (COPD), respiratory failure, cardiac enlargement, valvular heart disease, and ventilation pattern influenced USCOM waveform quality. Results: Age, body mass index, chronic obstructive pulmonary disease, respiratory failure, right and left heart enlargement, aortic valve disease (excluding aortic stenosis), and ventilation mode did not have a significant effect on USCOM waveform quality in critically ill patients (P > 0.05). Conclusions: Various physical conditions of critically ill patients may have limited effect on the quality of the USCOM waveform, potentially rendering USCOM suitable for early assessment of hemodynamic status during ICU admission.

Clinical and Epidemiological Characteristics of Rhabdomyolysis: A Retrospective Study.

Background: Rhabdomyolysis (RM) refers to a clinical syndrome in which muscle cells are damaged by various causes and the clinical manifestations are mainly muscle pain, weakness, and dark urine. Acute kidney injury (AKI) is a serious complication of RM with complex mechanisms and high mortality. Therefore, understanding the pathogenesis and clinical manifestations, early diagnosis and treatment of RM are crucial to improve its prognosis. Method: Analysis of medical records of RM patients admitted to Tianjin Medical University General Hospital from October 2019 to October 2022. Statistical software SPSS 25.0 was used to analyze the data. The risk factors of RM-complicated AKI were analyzed by logistic regression. The receiver operating characteristic (ROC) curve was plotted, the area under the curve (AUC) was calculated, and the optimal cutoff value was determined by the Youden index. P < 0.05 indicates a statistically significant difference between the groups. Result: Among the 71 patients, the median age of the patients was 53.0 (30.0, 71.0) years and was 2.5 times higher in men than in women. Infection was the most common etiology. History of alcohol consumption, CK, and creatinine were independent influencing factors for AKI due to RM. Logistic regression analysis showed that CK combined with creatinine had a better predictive value than the single index. Conclusion: Our study revealed the clinical and laboratory characteristics of RM in the population attending the Tianjin Medical University General Hospital in the last three years, which is a reference for future multicenter, prospective studies.

Construction and validation of machine learning models for sepsis prediction in patients with acute pancreatitis.

BACKGROUND: This study aimed to construct predictive models for the risk of sepsis in patients with Acute pancreatitis (AP) using machine learning methods and compared optimal one with the logistic regression (LR) model and scoring systems. METHODS: In this retrospective cohort study, data were collected from the Medical Information Mart for Intensive Care III (MIMIC III) database between 2001 and 2012 and the MIMIC IV database between 2008 and 2019. Patients were randomly divided into training and test sets (8:2). The least absolute shrinkage and selection operator (LASSO) regression plus 5-fold cross-validation were used to screen and confirm the predictive factors. Based on the selected predictive factors, 6 machine learning models were constructed, including support vector machine (SVM), K-nearest neighbour (KNN), multi-layer perceptron (MLP), LR, gradient boosting decision tree (GBDT) and adaptive enhancement algorithm (AdaBoost). The models and scoring systems were evaluated and compared using sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), accuracy, and the area under the curve (AUC). RESULTS: A total of 1, 672 patients were eligible for participation. In the training set, 261 AP patients (19.51%) were diagnosed with sepsis. The predictive factors for the risk of sepsis in AP patients included age, insurance, vasopressors, mechanical ventilation, Glasgow Coma Scale (GCS), heart rate, respiratory rate, temperature, SpO2, platelet, red blood cell distribution width (RDW), International Normalized Ratio (INR), and blood urea nitrogen (BUN). The AUC of the GBDT model for sepsis prediction in the AP patients in the testing set was 0.985. The GBDT model showed better performance in sepsis prediction than the LR, systemic inflammatory response syndrome (SIRS) score, bedside index for severity in acute pancreatitis (BISAP) score, sequential organ failure assessment (SOFA) score, quick-SOFA (qSOFA), and simplified acute physiology score II (SAPS II). CONCLUSION: The present findings suggest that compared to the classical LR model and SOFA, qSOFA, SAPS II, SIRS, and BISAP scores, the machine learning model-GBDT model had a better performance in predicting sepsis in the AP patients, which is a useful tool for early identification of high-risk patients and timely clinical interventions.

The early diagnosis and pathogenic mechanisms of sepsis-related acute kidney injury.

Sepsis is a syndrome caused by an imbalance in the inflammatory response of the body caused by an infection that leads to organ dysfunction, with the kidney being one of the most commonly affected organs. Sepsis-related acute kidney injury (SAKI) is strongly linked to increased mortality and poor clinical outcomes. Early diagnosis and treatment can significantly reduce patient mortality. On the other hand, the pathogenesis of SAKI is not fully understood, and early diagnosis of SAKI is a clinical challenge. Therefore, the current review describes biomarkers of acute kidney injury in sepsis and discusses the various pathogenic mechanisms involved in the progression of acute kidney injury in sepsis to develop new clinical treatment avenues.

The roles of interleukin-17A in risk stratification and prognosis of patients with sepsis-associated acute kidney injury.

BACKGROUND: The aim of this study was to evaluate the roles of interleukin (IL)-17A in risk stratification and prognosis of patients with sepsis-associated acute kidney injury (SAKI). METHODS: We enrolled 146 sepsis patients (84 non-SAKI and 62 SAKI patients) admitted to the emergency department from November 2020 to November 2021. Patients with SAKI were differentiated based on the severity of acute kidney injury. All clinical parameters were evaluated upon admission before administering antibiotic treatment. Inflammatory cytokines were assessed using flow cytometry and the Pylon 3D automated immunoassay system (ET Healthcare). In addition, a receiver operating characteristic (ROC) curve was utilized to determine the prognostic values of IL-17A in SAKI. RESULTS: The levels of creatinine, IL-2, IL-4, IL-6, IL-17A, tumor necrosis factor alpha, C-reactive protein, and procalcitonin (PCT) were significantly higher in the SAKI group than in the non-SAKI group (p < 0.05). The level of IL-17A revealed significant differences among stages 1, 2, and 3 in SAKI patients (p < 0.05). The mean levels of PCT, IL-4, and IL-17A were significantly higher in the non-survival group than in the survival group in SAKI patients (p < 0.05). In addition, the area under the ROC curve of IL-17A was 0.811. Moreover, the IL-17A cutoff for differentiating survivors from non-survivors was 4.7 pg/mL, of which the sensitivity and specificity were 77.4% and 71.0%, respectively. CONCLUSION: Elevated levels of IL-17A could predict that SAKI patients are significantly prone to worsening kidney injury with higher mortality. The usefulness of IL-17A in treating SAKI requires further research.

Exploration of m6A methylation regulators as epigenetic targets for immunotherapy in advanced sepsis.

BACKGROUND: This study aims to deeply explore the relationship between m6A methylation modification and peripheral immune cells in patients with advanced sepsis and mine potential epigenetic therapeutic targets by analyzing the differential expression patterns of m6A-related genes in healthy subjects and advanced sepsis patients. METHODS: A single cell expression dataset of peripheral immune cells containing blood samples from 4 patients with advanced sepsis and 5 healthy subjects was obtained from the gene expression comprehensive database (GSE175453). Differential expression analysis and cluster analysis were performed on 21 m6A-related genes. The characteristic gene was identified based on random forest  algorithm, and the correlation between the characteristic gene METTL16 and 23 immune cells in patients with advanced sepsis was evaluated using single-sample gene set enrichment analysis. RESULTS: IGFBP1, IGFBP2, IGF2BP1, and WTAP were highly expressed in patients with advanced sepsis and m6A cluster B. IGFBP1, IGFBP2, and IGF2BP1 were positively correlated with Th17 helper T cells. The characteristic gene METTL16 exhibited a significant positive correlation with the proportion of various immune cells. CONCLUSION: IGFBP1, IGFBP2, IGF2BP1, WTAP, and METTL16 may accelerate the development of advanced sepsis by regulating m6A methylation modification and promoting immune cell infiltration. The discovery of these characteristic genes related to advanced sepsis provides potential therapeutic targets for the diagnosis and treatment of sepsis.

The role of IL-17 in acute kidney injury.

Acute kidney injury (AKI) is a common clinical kidney disease with a high mortality rate. AKI is caused by a variety of factors, including sepsis, ischemia, and nephrotoxic drugs, and can progress to chronic kidney disease and end-stage renal disease. Numerous studies have suggested that cytokines can be used as therapeutic targets for AKI. IL-17 is a pro-inflammatory cytokine that not only participates in the host defense and the development of autoimmune diseases but also is linked to AKI due to a variety of factors. This review will give an overview of the structure, signaling pathways, and biological functions of IL-17, as well as its role in AKI, to show that IL-17 is a potential target for the prevention and treatment of AKI.

A novel role of DOT1L in kidney diseases.

BACKGROUND: We systematically summarized the structure and biological function of DOT1L in detail, and further discussed the role of DOT1L in kidney diseases through different mechanisms. METHODS AND RESULTS: We first described the role of DOT1L in various kidney diseases including AKI, CKD, DN and kidney tumor diseases. CONCLUSIONS: A better understanding of DOT1L as a histone methylase based on characteristics of regulating telomere silencing, transcriptional extension, DNA damage repair and cell cycle could lead to the development of new therapeutic targets for various kidney diseases, thereby improving the prognosis of kidney disease patients.

A case of pulmonary infection with Prevotella melanogenica having the paving stone symptom.

Prevotella melanogenica is a typical organism present in the human oral cavity and female reproductive tract, which is responsible for causing periodontal disease and the inflammation of the female reproductive tract. The present report discusses the case of a young female patient who presented with cough and fever as the main clinical symptoms. Computed Tomography (CT) revealed multiple clusters of ground glass density shadows in both lungs, with network-like and paving stone-like changes. The alveolar lavage fluid was collected for next-generation sequencing, which revealed the presence of Prevotella melanogenica. The patient received treatments, CT revealed that the density of multiple flakes of ground glass density in both lungs was lower than the previously observed density. Prevotella melanogenica pneumonia is rare, and the paving stone symptom observed in CT is not specific. Therefore, the case reported here provides a novel perspective regarding the diagnosis of pneumonia.

Neutrophilia with subclinical Cushing's disease: A case report and literature review.

The increase in the level of neutrophils following subclinical Cushing's disease is an uncommon clinical phenomenon that is characterized by insignificant biochemical or clinical evidence of hypercortisolism. In this study, we reported a 37-year-old female patient who presented with palpitations and fatigue, and showed increased neutrophils that were unaffected by anti-infection therapy. The patient was suspected of having a urinary tract infection because of occasionally with urinary frequency, urgency, increased procalcitonin, leukocytosis, and an increased proportion of neutrophils. The ineffectiveness of anti-infection therapy ruled out the possibility of urinary tract infection. Further examination of the bone marrow excluded the possibility of blood disease. However, the levels of blood cortisol and adrenocorticotropic hormone (ACTH) increased, and a magnetic resonance imaging examination revealed lesions in the sphenoidal sinus and sella area of the sphenoidal bone, which confirmed the relationship between increased glucocorticoids and increased neutrophils. This was further confirmed by follow-up surgery and pathological examination, which revealed silent corticotropin adenomas, which are characterized by the lack of biochemical or clinical evidence of hypercortisolism with positive immunostaining for ACTH.

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. METHODS: Peripheral plasma was collected from the Healthy Control (HC) and septic patients and Ang II and Ang-(1-7) protein concentrations were measured. The in vitro and in vivo models of SIC were developed using Lipopolysaccharide (LPS) to preliminarily explore the relationship between the SIC state, Ang II, and Ang-(1-7) levels, along with the protective function of exogenous Ang-(1-7) on SIC. RESULTS: Peripheral plasma Ang II and the Ang II/Ang-(1-7) levels in SIC-affected patients were elevated compared to the levels in HC and non-SIC patients, however, the HC showed higher Ang-(1-7) levels. Furthermore, peripheral plasma Ang II, Ang II/Ang-(1-7), and Ang-(1-7) levels in SIC patients were significantly correlated with the degree of myocardial injury. Additionally, exogenous Ang-(1-7) can attenuate inflammatory response, reduce oxidative stress, maintain mitochondrial dynamics homeostasis, and alleviate mitochondrial structural and functional damage by inhibiting nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, thus alleviating SIC. CONCLUSIONS: Plasma Ang-(1-7), Ang II, and Ang II/Ang-(1-7) levels were regarded as significant SIC biomarkers. In SIC, therapeutic targeting of RAAS, for example with Ang-(1-7), may exert protective roles against myocardial damage.

Omega-3 polyunsaturated fatty acids inhibit cardiomyocyte apoptosis and attenuate sepsis-induced cardiomyopathy.

OBJECTIVES: Sepsis can cause myocardial injury, which is one of the leading causes of death in critically ill patients. Fish oil rich in omega-3 polyunsaturated fatty acids (PUFAs) in ultralong chains has immunomodulatory effects and can inhibit the production of various critically ill proinflammatory cytokines. Therefore, this study focused on whether ω-3 PUFAs have a protective effect on sepsis-induced cardiomyopathy (SIC). METHODS: Male 6-8 weeks old C57BL/6 mice were pretreated with 3% special fish oil supplement rat food for seven consecutive days prior to surgery. Cecal ligation and puncture (CLP) was perfromed to induce polymicrobial sepsis.The cardiac function was assessed by echocardiography, apoptosis of cardiomyocyte were detected by TUNEL assay and Western blotting, and the level of TNF-α, IL-6, and IL-1ß in plasma was determined 24h after CLP. RESULTS: Pretreatment with omega-3 PUFAs attenuated cardiomyocyte apoptosis, decreased the production of proinflammatory cytokines, attenuated the SIC, and improved the survival rate of septic mice induced by CLP. CONCLUSIONS: ω-3 PUFAs alleviate SIC through attenuating cardiomyocyte apoptosis, which provides a new direction for the prevention and treatment of 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). The Ang II level in peripheral plasma and AT1R expression on monocytes were significantly higher in patients with SIC compared with those in non-SIC patients and healthy controls and were correlated with the degree of myocardial injury. The ARB losartan reduced the infiltration of neutrophils, monocytes, and macrophages into the heart and spleen of SIC mice. Additionally, losartan regulated macrophage polarization from the M1 to the M2 subtype via nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, thereby maintaining the mitochondrial dynamics balance in cardiomyocytes and reducing oxidative stress and cardiomyocyte apoptosis. In conclusion, the plasma Ang II level and AT1R expression on plasma monocytes are an important biomarker in SIC. Therapeutic targeting of AT1R, for example with losartan, can potentially protect against myocardial injury in SIC.

Use of Quantitative Metagenomics Next-Generation Sequencing to Confirm Fever of Unknown Origin and Infectious Disease.

A body temperature >38.3°C that lasts ≥3 weeks and lacks a clear diagnosis after 1 week of standard hospital examination and treatment is called "fever of unknown origin" (FUO). The main causes of FUO are infections, hematological diseases, autoimmune diseases, and other non-infectious inflammatory diseases. In recent years, quantitative metagenomics next-generation sequencing (Q-mNGS) has been used widely to detect pathogenic microorganisms, especially in the contribution of rare or new (e.g., severe acute respiratory syndrome-coronavirus-2) pathogens. This review addresses the undetermined cause of fever and its evaluation by Q-mNGS.

S100A9 and SOCS3 as diagnostic biomarkers of acute myocardial infarction and their association with immune infiltration.

Acute myocardial infarction (AMI) is one of the leading causes of death globally, with a mortality rate of over 20%. However, the diagnostic biomarkers frequently used in current clinical practice have limitations in both sensitivity and specificity, likely resulting in delayed diagnosis. This study aimed to identify potential diagnostic biomarkers for AMI and explored the possible mechanisms involved. Datasets were retrieved from the Gene Expression Omnibus. First, we identified differentially expressed genes (DEGs) and preserved modules, from which we identified candidate genes by LASSO (least absolute shrinkage and selection operator) regression and the SVM-RFE (support vector machine-recursive feature elimination) algorithm. Subsequently, we used ROC (receiver operating characteristic) analysis to evaluate the diagnostic accuracy of the candidate genes. Thereafter, functional enrichment analysis and an analysis of immune infiltration were implemented. Finally, we assessed the association between biomarkers and biological processes, infiltrated cells, clinical traits, tissues and time points. We identified nine preserved modules containing 1,016 DEGs and managed to construct a diagnostic model with high accuracy (GSE48060: AUC = 0.923; GSE66360: AUC = 0.973) incorporating two genes named S100A9 and SOCS3. Functional analysis revealed the pivotal role of inflammation; immune infiltration analysis indicated that eight cell types (monocytes, epithelial cells, neutrophils, CD8+ T cells, Th2 cells, NK cells, NKT cells and platelets) were likely involved in AMI. Furthermore, we observed that S100A9 and SOCS3 were correlated with inflammation, variably infiltrated cells, clinical traits of patients, sampling tissues and sampling time points. In conclusion, we suggested S100A9 and SOCS3 as diagnostic biomarkers of AMI and discovered their association with inflammation, infiltrated immune cells and other factors.

Dynamic changes of emergency visits: a retrospective observational study.

BACKGROUND: With more emergency visits, there is increasing pressure to provide emergency medical services globally and locally. This study aimed to investigate the epidemiological characteristics and the disease spectrum of patients presenting in the last three years to the Department of Emergency Medicine of Tianjin Medical University General Hospital, a tertiary hospital in Tianjin, China, to improve the services of the emergency medicine department. METHODS: A retrospective study was conducted on all patients in the Department of Emergency Medicine of Tianjin Medical University General Hospital from Jan 1, 2017, 00:00:00 to Dec 31, 2020, 23:59:59, including variables like medical record number, gender, age, date of admission, principal diagnosis. The data were analyzed by SPSS statistical software; statistical charts were prepared by GraphPad Prism9.0 and SPSS 20.0; statistical tables were made by Microsoft Excel. RESULTS: A total of 1,314,916 patients presented to the Department of Emergency Medicine of Tianjin Medical University General Hospital from Jan 1, 2017, 00:00:00 to Dec 31, 2020, 23:59:59. In terms of gender distribution, the male-female ratio was 0.78∶1. As for age distribution, patients aged 60-69 were the most (23.47%), and patients younger than 20 years were the least (2.80%). Concerning monthly data, the number of visits peaked during January and December. The distribution of daily visits showed the feature of three highs and a low. The top three prevalence diseases in the emergency disease spectrum were respiratory, cardiovascular, and digestive diseases. The respiratory system was the most common in patients with infectious diseases (200,912, accounting for 86.97%). Among the patients suffering from infectious diseases, the number of patients with respiratory infections peaked in 2019 (73,530) and was the lowest in 2020 (20,078). CONCLUSIONS: From 2017 to 2019, the demand for emergency services in Tianjin Medical University General Hospital continued to increase, but it was greatly affected by COVID-19 in 2020. This emergency department is mainly for patients with respiratory system, circulatory system and digestive system diseases, and its treatment time is relatively centralized. The prevention of diseases for people of all ages, especially female patients and the elderly, should be strengthened, and emergency medical resources should be allocated reasonably according to the peak months and crowed periods of patients.