Exertional heat stroke (EHS) is the most serious and life-threatening acute heat-related illness. It can develop from heat-related illnesses, and the prehospital management is a crucial in the diagnosis and treatment of EHS. The prognosis of EHS patients is largely determined by the rapid recognition, effective cooling, and standardized transportation during the prehospital period. Extensive research has demonstrated that medical security personnel still have fatal misconceptions in the prehospital recognition and management of EHS, mainly due to the lack of recognition and inappropriate treatment. This review summarizes the top 10 misconceptions in prehospital recognition and management of EHS, based on domestic and international research findings and combined with practical scenarios. It also provides an accurate prehospital management plan according to the China Expert Consensus on Diagnosis and Treatment of Heatstroke, aiming to reduce or avoid irreversible damage to EHS patients caused by these misunderstandings and to decrease the incidence, disability rate, and mortality rate of EHS.

Objective To elucidate the clinical significance of high expression levels of endonuclease meiosis 1 (EME1) in the prognosis of hepatocellular carcinoma (HCC). Methods The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to screen and analyze differential gene expression between HCC and non-tumor tissues. A retrospective collection of liver tissue samples from 80 HCC patients who underwent hepatectomy in the Fifth Medical Center of Chinese PLA General Hospital between January 2010 and December 2014 was performed. Immunohistochemistry analysis was employed to detect the EME1 expression levels. Survival analysis was then conducted to assess the impact of EME1 expression on 5-year postoperative survival rate of HCC patients. Additionally, gene enrichment analysis was applied to predict the function of EME1 in HCC. Results A total of 371 HCC tissue samples and 50 non-tumor liver tissue samples from TCGA database were analyzed, revealing significantly higher EME1 expression in HCC tissues. Microarray analysis of 107 samples within the GEO database (70 HCC tissues and 37 non-tumor tissues) confirmed that EME1 mRNA expression was markedly elevated in HCC tissues compared with non-tumor tissues (P<0.05). The 5-year overall survival (OS) rate was notably lower in high EME1 expression group than that in low expression group (44.1% vs. 53.0%, P<0.05). Semi-quantitative immunohistochemistry analysis demonstrated that patients with high EME1 expression had a significantly lower OS rate than those with low EME1 expression (32.8% vs. 45.0%, P<0.05). Multivariate COX regression analysis identified that high EME1 expression (HR=2.234, 95%CI 1.073-4.649, P=0.032) and advanced China liver caner (CNLC) staging (HR=4.317, 95%CI 1.799-10.359, P=0.001) were independent risk factors for the 5-year OS of post-operation patients with HCC. Conclusion Elevated EME1 expression in HCC tissues correlates with an adverse prognosis of HCC and suggests that EME1 could serve as a potential therapeutic target for HCC.

Objective To establish a dynamic prediction model of fatal massive hemorrhage in trauma based on the vital signs time series data and machine learning algorithms. Methods Retrospectively analyze the vital signs time series data of 7522 patients with trauma in the Medical Information Mart for Intensive Care-Ⅳ (MIMIC-Ⅳ) database from 2008 to 2019. According to the occurrence of posttraumatic fatal massive hemorrhage, the patients were divided into two groups: fatal massive hemorrhage group (n=283) and non-fatal massive hemorrhage group (n=7239). Six machine learning algorithms, including logistic regression (LR), support vector machine (SVM), random forests (RF), adaptive boosting (AdaBoost), gated recurrent unit (GRU), and GRU-D were used to develop a dynamic prediction models of fatal massive hemorrhage in trauma. The probability of fatal massive hemorrhage in the following 1, 2, and 3 h was dynamically predicted. The performance of the models was evaluated by accuracy, sensitivity, specificity, positive predictive value, negative predictive value, Youden index, and area under receiver operating characteristic curve (AUC). The models were externally validated based on the trauma database of the Chinese PLA General Hospital. Results In the MIMIC-Ⅳ database, the set of dynamic prediction models based on the GRU-D algorithm was the best. The AUC for predicting fatal major bleeding in the next 1, 2, and 3 h were 0.946±0.029, 0.940±0.032, and 0.943±0.034, respectively, and there was no significant difference (P=0.905). In the trauma dataset, GRU-D model achieved the best external validation effect. The AUC for predicting fatal major bleeding in the next 1, 2, and 3 h were 0.779±0.013, 0.780±0.008, and 0.778±0.009, respectively, and there was no significant difference (P=0.181). This set of models was deployed in a public web calculator and hospital emergency department information system, which is convenient for the public and medical staff to use and validate the model. Conclusion A set of dynamic prediction models has been successfully developed and validated, which is greatly significant for the early diagnosis and dynamic prediction of fatal massive hemorrhage in trauma.

Objective To analyze the correlation of malondialdehyde (MDA), advanced oxidation protein products (AOPP), nuclear factor erythroid-2 related factor 2 (Nrf2), glutathione (GSH) levels with postoperative acute kidney injury (AKI) among patients undergoing laparoscopic partial nephrectomy (LPN). Methods A total of 110 patients with renal cell carcinoma who were admitted to the Department of Urology, the Third Medical Center of Chinese PLA General Hospital from February to August 2022 were included in the study. Patients were divided into AKI group (n=30) and non-AKI group (n=80) based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, and then divided into elderly AKI (>65 years old, n=14), middle-aged AKI (50-65 years old, n=16), elderly non-AKI (>65 years old, n=30), and middle-aged non-AKI (50-65 years old, n=50) four sub-groups based on age. Clinical characteristics and laboratory examination data were recorded. Venous blood was collected from the patients before the operation (T₁), immediately after the surgery (T₂), and 24 h after surgery (T₃), and MDA, AOPP, Nrf2 and GSH levels were measured. MDA, AOPP, Nrf2 and GSH levels were compared between the four subgroups at different time points, and their correlation with the occurrence of AKI after LPN were explored. The risk factors for AKI after LPN were analyzed using the univariate and multivariate logistic regression. Results Spearman correlation analysis revealed that AKI was not associated with the MDA level at each time point (P>0.05), was positively associated with AOPP-T₃ level (r=0.315, P=0.037), was negatively associated with the Nrf2-T₃ level (r=-0.365, P=0.015) and GSH-T₂ level (r=-0.338, P=0.025) in elderly patients after LPN. AKI was not associated with MDA, AOPP, Nrf2, and GSH levels (P>0.05) in middle-aged patients after LPN. Multivariate logistic regression analysis showed that BMI (OR=2.724, P=0.040) and surgically resected kidney volume (OR=1.309, P=0.049) were independent risk factors for AKI in elderly patients after LPN, GSH-T₂ (OR=0.271, P=0.042) was an independent protective factor for AKI in elderly patients after LPN. Intraoperative colloid fluid intake (OR=1.006, P=0.007) was an independent risk factor for AKI in middle-aged patients after LPN, intraoperative urine output (OR=0.104, P=0.007) was an independent protective factor for AKI in middle-aged patients after LPN. Conclusions The AKI after LPN may be related to the increase of AOPP level and the decrease of Nrf2 and GSH levels in elderly patients, and the postoperative GSH is an independent protective factor for AKI in elderly patients after LPN. The correlation of AKI after LPN is not significant with the levels of MDA, AOPP, Nrf2 and GSH in the middle-aged patients.

Objective To investigate the risk factors for early neurological deterioration (END) following intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) acute mild ischemic stroke (AMIS) patients. Methods Eighty-six patients with AMIS who underwent intravenous thrombolysis with rt-PA in the Department of Neurology, Civil Aviation General Hospital between January 2019 and October 2022 were retrospectively analyzed. Patients were categorized into END group (n=8) and non-END group (n=78) based on the presence of END within 24 hours after thrombolysis (NIHSS score increased by ≥2 points within 24 hours after intravenous thrombolysis). Baseline characteristics, including age, gender, past medical history (hypertension, diabetes, hyperlipidemia, etc.), smoking history, pre-thrombolysis NIHSS score, homocysteine level, fibrinogen level, and post-thrombolysis bleeding transformation were documented for each patient. A multivariate logistic regression analysis was conducted to access the risk factors associated with END following intravenous thrombolysis in AMIS. Results There were significant differences in homocysteine and fibrinogen levels, as well as bleeding transformation after thrombolysis between the two groups (P<0.05). In contrast, other factors such as age, gender, past medical history, pre-thrombolysis NIHSS score, and other imaging features were not statistically significant (P>0.05). Multivariate logistic regression analysis revealed that elevated homocysteine level was independently linked to risk of END after intravenous thrombolysis in AMIS, with an odds ratio of 1.074(95%CI 1.011-1.142, P=0.021). Conclusions Hyperhomocysteinemia emerges as an independent risk factor for END following intravenous thrombolysis in patients with AMIS.

Objective To report the clinicopathological features, gene mutation sites, diagnosis and treatment of a case of hereditary myopathy with early respiratory failure (HMERF), and review the literature to enhance the understanding of the disease. Methods A retrospective analysis was conducted on the clinical data, imaging examinations, histopathological and genetic sequencing results, as well as the diagnosis and treatment of a case of HMERF as the initial presenting symptom, admitted to Sichuan Provincial People's Hospital in April 2021. The clinical characteristics of Chinese patients with HMERF were summarized in conjunction with literature reports. Results This patient presented with limb weakness and progressive dyspnea. Magnetic resonance imaging (MRI) showed selective fat infiltration of the medial head of calf gastrocnemius muscle. Two mutation sites in titin (TTN) gene inherited from both parents were identified, exon 341 c.94828G>A (P.a31610t) and exon 50 c.14915C>T (P.S.4972L), leading to the diagnosis of HMERF. The patient received supportive therapy. The PubMed database was searched and 15 cases of HMERF were diagnosed in Chinese patients over the past decade. The onset age of these patients was (26.1±17.0) years, predominantly affecting males. All patients exhibited mutations in TTN gene. The most prevalent mutation was identified as c.95195C>T (p.P31732L), followed by c.95134T>C (p.C31712R). Conclusions HMERF is a rare genetic disease caused by genetic mutation, with skeletal muscle weakness and respiratory muscle weakness as the main clinical manifestations. Clinical symptoms can be atypical, and exon 344 of TTN gene is a common mutation site. The mutation sites in this case, located at exon 341 c.94828G>A (P.a31610t) and exon 50 c.14915C>T (P.S4972L) of the TTN gene, may represent novel genetic markers for HMERF.

Hepatic fibrosis refers to repeated or persistent inflammation and necrosis of liver parenchymal cells and excessive deposition of liver fibrous connective tissue caused by various etiologies, which is a necessary stage for chronic liver disease to develop into cirrhosis. Etiological treatment as antiviral therapy can reduce the inflammation of the liver tissues to a certain degree, but cannot completely stop the process of liver fibrosis. In recent years, researchers have found that intrahepatic macrophages play an important role in the occurrence and progression of hepatic fibrosis, among which M1/M2 macrophages have become the key to exploring macrophages to regulate hepatic fibrosis. This article will focus on the role and mechanism of intrahepatic M1/M2 macrophages in hepatic fibrosis.

Objective To investigate the short-term efficacy and safety of chemotherapy induced by nimotuzumab (NTZ) combined with TP regimen and sequential concurrent chemoradiotherapy in patients with epidermal growth factor receptor positive(EGFR-positive) locally advanced nasopharyngeal carcinoma. Methods A total of 48 patients with stage Ⅲ to IV A nasopharyngeal carcinoma in Guizhou Provincial People's Hospital from January 2020 to December 2022 were prospectively enrolled, and were randomized into two groups: NTP (NTZ+docetaxel/albumin-paclitaxel+cisplatin) group and TP (Docetaxel/albumin-paclitaxel+cisplatin) group(24 cases per group) by random number table method. After 2 or 3 cycles of induction chemotherapy in NTP group, NTZ was sequentially used in combination with cisplatin for concurrent chemoradiotherapy. Immunohistochemistry was used to detect the EGFR expression level, exploring EGFR expression intensity and the therapeutic effect of NTZ in NTP group patients. Meanwhile, short-term efficacy, withdrawal rate and toxic side effects were compared between the two groups after induction chemotherapy. Results In NTP group, the positive expression rate of EGFR was 100%, and EGFR expression intensity significantly correlated with the efficacy of NTZ-combined induction therapy (P<0.05). After induction chemotherapy, the objective response rate (ORR) of cervical lymph nodes in NTP group was significantly higher than that in TP group (75% vs. 45.8%, P=0.039). The primary lesion ORR and overall (primary lesion and cervical lymph node) ORR showed no significant difference between the two groups (P>0.05). Comparison of adverse reactions between the two groups during induction therapy: leukopenia and gastrointestinal reaction in NTP group were lower than those in TP group (P<0.05), but rash was higher than those in TP group (P<0.05). There was no significant difference in liver function, hemoglobin and thrombocytopenia between two groups (P>0.05). Conclusions EGFR expression intensity varies in nasopharyngeal carcinoma tissues, with higher levels indicating greater clinical benefit of combined induction therapy with NTZ. NTZ combined with TP induction regimen demonstrates good short-term efficacy and safety for cervical lymph nodes in patients with locally advanced nasopharyngeal carcinoma.

Objective To investigate the differentially expressed genes (DEGs) and their molecular interactions in unstable carotid atherosclerotic plaques. Methods Gene expression datasets related to carotid atherosclerotic plaques (GSE41571, GSE118481, and E-MTAB-2055) were downloaded from Gene Expression Omnibus (GEO) and European Bioinformatics Institute (EBI) ArrayExpress databases. The co-regulated DEGs in at least two datasets of unstable carotid plaques were merged and analyzed using Gene Ontology Biological Process (GO-BP), Kyoto Encyclopedia of Genes and Genomes (KEGG), Protein-Protein Interaction (PPI) Networks and subnetwork analysis, relationships between miRNAs/transcription factors and target genes, and drug-gene interaction database. Quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect the expression levels of some DEGs in carotid plaques and plasma from 58 patients with carotid atherosclerosis. Results GO enrichment analysis showed that DEGs in unstable carotid atherosclerotic plaques were mainly enriched in genes related to inflammatory response and extracellular matrix structure genes. KEGG enrichment analysis indicated that upregulated DEGs in unstable carotid plaques were enriched in extracellular matrix receptor (ECM-receptor) interaction, PI3K-Akt, Hippo and transforming growth factor-β (TGF-β) signaling pathways, while downregulated DEGs were primarily enriched in lysosomes, phagosomes, and chemokines processes. PPI network analysis suggested that COL1A2, COL4A2, insulin-like growth factor binding protein 6 (IGFBP6), COL4A5, C1QA, CXCL10, CXCL2, CXCR4, and CSF1R may play important roles in PPI networks. Prediction of drug-gene interactions revealed that CSF1R had the most drug interaction, CXCL2 was most antagonized by drugs, and IGFBP6 was most activated by drugs. qRT-PCR showed that the expression level of IGFBP6 in unstable carotid plaques group was significantly lower than that in stable carotid plaques group (P<0.001). ELISA results showed that plasma concentration of IGFBP6 in unstable carotid plaques group was significantly lower than that in stable carotid plaques group (P<0.0001). Receiver operating characteristic (ROC) suggested that the area under the curve (AUC) for plasma IGFBP6 levels to identify unstable plaques was 0.894 (95%CI 0.810-0.977), with a cutoff value of 142.08 ng/ml. Conclusion IGFBP6 may become an important biomarker for predicting unstable carotid atherosclerotic plaques.

Takeda G protein-coupled receptor 5 (TGR5) is a bile acid receptor located on the surface of cell membrane, widely distributed in many tissues and cells in the body, and can be directly activated by most bile acids in vivo. TGR5 plays an important role in various physiological and pathophysiological processes, including cellular Ca²⁺ transport, oxidative stress, cell proliferation, inflammatory responses, and mitochondrial metabolism, thereby maintaining mitochondrial homeostasis and vascular endothelial function, and inhibiting the progression of cardiovascular diseases such as atherosclerosis, myocardial hypertrophy, and cardiac remodeling after myocardial infarction. Currently, with the gradual clinical application of numerous bile acid and bile acid derivatives drugs, it is necessary to further investigate the role of TGR5 in the cardiovascular system, which is an important basis for clinical application of these new drugs. This review discusses the relationship between TGR5 and cardiovascular system from five perspectives: TGR5's involvement in regulating macrophages, endothelial function, vascular smooth muscle cells, cardiomyocytes, and mitochondrial metabolism. It summarizes the recent research progress, aiming to provide the theoretical basis for TGR5 as a novel therapeutic target for cardiovascular diseases.