ObjectivesHyperlipidemic acute pancreatitis progresses rapidly to severe acute pancreatitis. Early identification of disease severity is critical for improving outcomes. This study aimed to investigate the risk factors associated with severe acute pancreatitis and to develop and validate a novel predictive model to support clinical decision making.MethodsThis retrospective cohort study included 502 patients with hyperlipidemic acute pancreatitis. A total of 502 patients with hyperlipidemic acute pancreatitis were retrospectively enrolled and randomly assigned to a training set (n = 351) and a validation set (n = 151) in a 7:3 ratio. Least absolute shrinkage and selection operator regression and multivariate logistic regression were used for model development. Model performance was comprehensively evaluated using the receiver operating characteristic curve, calibration curves, the Hosmer-Lemeshow test, Brier score, calibration slope, calibration-in-the-large, and decision curve analysis.ResultsMultivariate logistic regression confirmed the bedside index for severity in acute pancreatitis score (odds ratio = 7.042, 95% confidence interval: 3.850 to 14.145, p < 0.001) and metabolic score for insulin resistance (odds ratio = 1.053, 95% confidence interval: 1.023 to 1.087, p < 0.001) as independent risk factors for severe acute pancreatitis. The resulting predictive model demonstrated excellent discriminative ability in both the training set (area under the curve = 0.904, 95% confidence interval: 0.852 to 0.955) and the validation set (area under the curve = 0.885, 95% confidence interval: 0.812 to 0.958). In the training set, the area under the curve of the predictive model was significantly higher than those of the individual indicators, including metabolic score for insulin resistance, triglyceride-glucose index, triglyceride-glucose body mass index, triglycerides/high-density lipoprotein cholesterol, and the bedside index for severity in acute pancreatitis score (all p < 0.05). In the validation set, the model yielded only a minimal improvement in area under the curve over the bedside index for severity in acute pancreatitis score alone (difference = 0.020), which was not statistically significant (p = 0.326). The calibration slope and calibration-in-the-large were 1.00 and 0.00 in the training set and 0.82 and -0.54 in the validation set, respectively. Calibration curves, the Hosmer-Lemeshow test, and Brier scores collectively indicated good model fit and high predictive accuracy. Furthermore, decision curve analysis showed that the combined model provided superior net clinical benefit across a wide range of threshold probabilities.ConclusionThe combined model incorporating the bedside index for severity in acute pancreatitis score and metabolic score for insulin resistance serves as a preliminary risk stratification tool for the early identification of severe acute pancreatitis in patients with hyperlipidemic acute pancreatitis.

Acute gastric dilation (AGD) is a rare but critical medical condition characterized by a rapid and massive expansion of the stomach. While AGD secondary to binge-eating has been documented in literature, cases involving rapid consumption of carbonated beverages leading to acute gastric distention with subsequent pneumomediastinum are rarely reported. We present a case of a 17-year-old male who developed AGD following competitive ingestion of hamburgers and carbonated beverages, subsequently complicated by subcutaneous and mediastinal emphysema. Despite immediate gastric decompression via a nasogastric tube, the patient developed hemodynamic instability and oliguria. An emergency exploratory laparotomy was performed, during which a total of 3.6 liters of gastric contents were aspirated. The patient recuperated gradually under supportive care. This case highlights the necessity of early gastric decompression in binge-eating patients with significant carbonated beverage consumption who develop abdominal symptoms. The onset of hemodynamic instability or oliguria mandates urgent surgical intervention.

OBJECTIVES:This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To assess the benefits and harms of clarithromycin for treating sepsis in adults versus standard care with or without placebo or with an alternative active intervention, or clarithromycin in combination with antibiotic therapy versus standard care.

INTRODUCTION:Chlorfenapyr is a pyrrole insecticide metabolized to the active toxin tralopyril. Reports of poisoning have increased recently. This retrospective study analyzed clinical data to examine clinical features and describe characteristics observed in fatal outcomes. METHODS:Clinical data were collected from patients with chlorfenapyr poisoning at the First Affiliated Hospital of Zhengzhou University (2020-2024). Patients were categorized into survivors and non-survivors to describe demographic, clinical, laboratory, and imaging findings. RESULTS:Twenty-one patients were included (case fatality: 28.6%). Among oral exposures, non-survivors ingested a higher estimated dose than survivors, with median 122.5 mL (IQR 105-125 mL) versus 20.0 mL (IQR 20.0-30.0 mL). Non-survivors exhibited longer symptom latency, median 24.0 versus 1.0 h and a delay in neurological symptoms, with median of 2.5 days. Plasma concentrations of chlorfenapyr and tralopyril were numerically higher in non-survivors, median 293 versus 147 ng/mL and 946 versus 531 ng/mL, respectively, compared to survivors. Clinically, non-survivors universally (100%) exhibited fever, diaphoresis, and impaired consciousness; they also showed higher frequencies of paresthesia (50%), bowel/bladder dysfunction (50%), and muscle weakness (50%). Laboratory analysis in non-survivors revealed higher creatine kinase, median 1266.0 versus 72.0 U/L, aspartate aminotransferase, lactate dehydrogenase, myoglobin, prothrombin time, and lipase. Abnormal magnetic resonance imaging signals were observed in all non-survivors (3/3) compared to only 12.5% (1/8) of survivors. DISCUSSION:In this cohort, the observed latent period followed by a hypermetabolic state aligns with the delayed conversion of chlorfenapyr to tralopyril and its uncoupling of mitochondrial respiration. The specific pattern of elevated muscle enzymes and central nervous system lesions reflects injury primarily to tissues with high metabolic demand. Furthermore, the sustained plasma toxin concentrations despite extracorporeal clearance indicate a large total body burden and prolonged toxicity. CONCLUSION:Fatal chlorfenapyr poisoning was characterized by a latency period followed by a hypermetabolic state (fever, diaphoresis) and severe neurological/muscular injury. Fever, impaired consciousness, elevated muscle enzymes (notably CK), and specific brainstem/spinal cord MRI abnormalities were observed in fatal cases, whereas these features were largely absent in survivors.

BACKGROUND:Sepsis is a highly heterogeneous organ dysfunction syndrome. There is limited evidence regarding phenotypes and clinical outcomes in sepsis patients with initial normal lactate levels. We sought to identify the lactate-based clinical phenotypes and outcomes of sepsis patients. METHODS:The Medical Information Mart for Intensive Care IV (MIMIC-IV) and eICU databases were used to conduct a retrospective cohort study. Adult sepsis patients were included. Lactate was measured via blood gas, and the same assay type was used across both databases. Serial lactate measurements were analyzed via a two-point classification system based on the highest values recorded during two consecutive 24-hour periods following ICU admission. The first measurement window (T1) comprised the initial 24 h post-admission, whereas the second window (T2) covered 24-48 h post-admission. The lactate difference was defined as the numerical change between the highest lactate level at T2 and the highest level at T1. The time interval between these two measurements was fixed, with T2 commencing immediately after T1, together encompassing the first 48 h post-ICU admission. A normal lactate level was defined as ≤2 mmol/L, and an elevated level was defined as >2 mmol/L. Sepsis patients were stratified into four trajectory phenotypes: (1) normal‒normal (N‒N); (2) normal-elevated (N‒E); (3) elevated-normal (E‒N); and (4) elevated-elevated (E‒E). The primary outcome was in-hospital mortality. RESULTS:This study enrolled 6,926 sepsis patients. The clinical phenotypes of the sepsis patients were as follows: N‒N (24.4%), N‒E (3.8%), E‒N (36.4%), and E‒E (35.3%). The in-hospital mortality rates of sepsis patients with the four phenotypes from the MIMIC-IV and eICU databases were as follows (N‒N: 18.9% vs. 17.6%, P=0.66; N‒E: 35.3% vs. 29.2%, P=0.45; E‒N: 16.6% vs. 14.2%, P=0.14; E‒E: 43.6% vs. 37.8%, P=0.01). After adjusting for age, sex, Sequential Organ Failure Assessment (SOFA) score, vasopressor therapy, and infection sites, the N‒E phenotype was associated with a higher risk of in-hospital mortality (odds ratio [OR] 1.44; 95% confidence intervals [95% CI] 1.11-1.86; P=0.006; adjusted OR 1.61; 95% CI 1.23-2.11; P<0.001). The E‒N phenotype was associated with the most favorable outcomes for in-hospital mortality in the multivariable analysis (adjusted OR 0.41; 95% CI 0.36-0.46; P<0.001). The E‒E phenotype was associated with the highest risk of in-hospital mortality in the overall cohort (adjusted OR 3.00; 95% CI2.67-3.37; P<0.001). CONCLUSION:In sepsis patients with normal initial lactate levels, serial lactate measurements could be valuable for prognostic assessment.

Recent studies highlight the critical role of gut microbiota in sepsis pathogenesis and its potential link to neurological disorders, particularly sepsis-associated encephalopathy (SAE). However, the exact relationship between gut microbiota, their metabolites, and SAE’s etiology and progression remains enigmatic. We aimed to elucidate how gut bacteria, fungi, and their metabolites contribute to the development and progression of SAE. This study was a prospective cohort study. Patients who met the criteria for sepsis 3.0 were included and were divided into SAE and non-SAE groups according to the presence or absence of SAE. Baseline characteristics were collected and mortality was followed up for 28 days. We conducted 16 S and ITS rRNA sequencing of rectal swabs, fecal and plasma metabolomic analysis in septic patients with and without SAE to identify differential bacteria, fungi and microbiota-related metabolites. And we identified potential biomarkers of bacteria and fungi through LEfSe analysis. Differential metabolites were screened and their sources were identified using MetOrigin, followed by identification of KEGG pathways related to gut microbiota, host, and co-metabolism that might play important roles in SAE. Lastly, correlation analysis was performed among differential bacteria, fungi, gut metabolites, plasma metabolites and clinical indicators and we revealed vital flora and metabolites. The study included 42 SAE patients, 129 non-SAE patients, and 35 age-matched healthy volunteers. The 28-day mortality rate of SAE patients was higher than that of non-SAE patients (28.57

BACKGROUND: Although the Confusion Assessment Methods for the Intensive Care Unit (CAM-ICU) is a recommended tool for diagnosing sepsis-associated encephalopathy (SAE), it has several limitations. Mismatch-negativity (MMN) and P3a are components of event-related potentials (ERPs) used with electroencephalography (EEG) and are associated with cerebral function changes in critically ill patients. This study aimed to provide a quantitative, non-invasive method to guide SAE diagnosis in non-sedated patients. METHODS: From January 2022 to March 2023, sepsis patients without sedation were enrolled and assessed via the CAM-ICU, Glasgow Coma Scale (GCS), and ERP under standard procedures. Both MMN and P3a data were collected. The diagnostic value of MMN and P3a was assessed with processed ERP data. RESULTS: Thirty-six patients were included in this study, comprising 19 patients with SAE and 17 patients without SAE (NSAE). MMN and P3a amplitudes decreased, and only FzMMN amplitude significantly decreased in SAE patients (2.03 [1.08, 2.93] mV vs. 3.21 [1.92, 4.34] mV, P=0.040). After median dichotomization, low F3P3a and FzP3a amplitudes were associated with higher CAM-ICU positivity rates and APACHE II scores. Both amplitude in F3P3a (AUC=0.710, 95%CI: 0.527-0.893, P=0.034) and FzP3a (AUC=0.700, 95%CI: 0.519-0.881, P=0.041) exhibited moderate diagnostic efficacy for SAE, while FzMMN amplitude lacks effective diagnostic value. CONCLUSION: In this pilot study, ERP components F3P3a and FzP3a amplitudes demonstrated moderate diagnostic value for SAE. These exploratory findings require confirmation in larger and powered cohorts.

Chronic pulmonary aspergillosis is an uncommon form of Aspergillus infection. It typically occurs in people with a weakened immune system and underlying lung disease. Our case demonstrates that pulmonary aspergillosis can occur in immunocompetent middle-aged men with a rare pleural effusion as the main imaging manifestation. A 45-year-old Chinese man with chronic exposure to wet crops presented to our emergency department with a two-year history of cough which worsened over the past 10 days. An initial chest CT showed right pleural effusion with compressive pulmonary atelectasis. Bronchoscopy was unremarkable, but next-generation sequencing of bronchoalveolar-lavage fluid revealed Aspergillus fumigatus. Chronic pulmonary aspergillosis was diagnosed based on typical personal contact history, clinical manifestations and microbiological results. The patient responded well to voriconazole and was discharged 20 days later with oral voriconazole medicine. The case illustrates that bloody pleural effusion could be a rare condition of chronic pulmonary aspergillosis.

AIMS:The objective of this study is to explore the regulatory role of DNA methylation in delayed encephalopathy after carbon monoxide poisoning (DEACMP) and to identify candidate epigenetic biomarkers. METHODS:In this study, multi-omics analyses such as methylomics, transcriptomics, pyrophosphate sequencing, qRT-PCR, immunohistochemistry, and western blotting were utilized to investigate the role of epigenetic regulation and altered gene expression in the pathogenesis of DEACMP. RESULTS:Using integrated analysis, we identified 168 differentially methylated CpGs sites, 334 differentially expressed genes, and two differentially methylated and differentially expressed genes (DAB2IP and SMYD3) in the DEACMP group. The pyrosequencing results further revealed hypomethylation of DAB2IP and hypermethylation of SMYD3. Moreover, we verified the upregulation of DAB2IP expression accompanied by the downregulation of SMYD3 expression in the DEACMP rats model. CONCLUSION:This study, based on dysregulated DNA methylation and gene expression profiles, identified and validated two DEACMP-related genes (DAB2IP and SMYD3) that could serve as epigenetic biomarkers and potential therapeutic targets for DEACMP.

BACKGROUND:Sepsis, a common acute and critical disease, leads to 11 million deaths annually worldwide. Probiotics are living microorganisms that are beneficial to the host and may benefit sepsis outcomes, but their effects are still inconclusive. This study aimed to evaluate the overall effect of probiotics on the prognosis of patients with sepsis. DATA RESOURCES:We searched several sources for published/presented studies, including PubMed, EMBASE, Web of Science, the Cochrane Library and the US National Library of Medicine Clinical Trials Register (www.clinicaltrials.gov) updated through July 30, 2023, to identify all relevant randomized controlled trials (RCTs) or observational studies that assessed the effectiveness of probiotics or synbiotics in patients with sepsis and reported mortality. We focused primarily on mortality during the study period and analyzed secondary outcomes, including 28-day mortality, in-intensive care unit (ICU) mortality and other outcomes. RESULTS:Data from 405 patients in five RCTs and 108 patients in one cohort study were included in the analysis. The overall quality of the studies was satisfactory, but clinical heterogeneity existed. All adult studies reported a tendency for probiotics to reduce the mortality of patients with sepsis, and most studies reported a decreasing trend in the incidence of infectious complications, length of ICU stay and duration of antibiotic use. There was only one RCT involving children. CONCLUSION:Probiotics show promise for improving the prognosis of patients with sepsis, including reducing mortality and the incidence of infectious complications, particularly in adult patients. Despite the limited number of studies, especially in children, these findings will be encouraging for clinical practice in the treatment of sepsis and suggest that gut microbiota-targeted therapy may improve the prognosis of patients with sepsis.

The blood‒brain barrier (BBB) is a critical selective interface between the central nervous system (CNS) and the blood circulation. BBB dysfunction plays an important role in the neurological damage caused by sepsis. However, the mechanisms underlying the disruption of the BBB during sepsis remain unclear. We established a human induced pluripotent stem cell (iPSC)-derived BBB model and reported that treating with sepsis patient serum leads to structural and functional disruption of the BBB. In a cecal ligation and puncture (CLP)-induced mouse model of sepsis, we also observed disruption of the BBB, inflammation in the brain, and impairments in cognition. In both models, we found that the expression of TREM-1 was significantly increased in endothelial cells. TREM-1 knockout specifically in endothelial cells alleviated BBB dysfunction and cognitive impairments. Further study revealed that TREM-1 affects the expression of genes involved in the PI3K/Akt signaling pathway. The protective effects of TREM-1 inhibition on the BBB and cognition were abrogated by PI3K inhibitors. Our findings suggest that endothelial TREM-1 induces sepsis-induced BBB disruption and cognitive impairments via the PI3K/Akt signaling pathway. Targeting endothelial TREM-1 or the PI3K/Akt signaling pathway may be a promising strategy to maintain BBB integrity and improve cognitive function in sepsis patients.

Background:Sepsis is a life-threatening organ dysfunction syndrome, with an overall mortality rate of 32.8%. Platelets have been shown to have a central role in the pathogenesis of a diverse array of immune-mediated and infectious diseases, and both thrombocytopenia and platelet hyperreactivity independently correlate with elevated sepsis-related morbidity and mortality. Methods:From February 2021 to June 2022, patients diagnosed with sepsis (according to the Sepsis 3.0 criteria) from the emergency department were screened and enrolled in a prospective observational cytokine analysis cohort. "Bio-Plex Pro Human Cytokine Grp I Panel 17-plex" was used for cytokines analysis. Patients were stratified into high- and low-platelet groups using a discharge platelet threshold of 150 × 109/L. Data were analyzed with R 4.4.0 and GraphPad Prism 9, calculating medians and frequencies for variables. Results:Fifty-seven patients were enrolled and were classified into high- and low-platelet groups (31 vs 26). IL-6 had a significant difference between the two groups after adjusting for admission platelet level and length of stay in hospital (2072 vs 107.1, q < 0.05). Receiver operating characteristic curve also showed IL-6 had high degrees of sensitivity and specificity for predicting higher platelet levels. Conclusion:Higher IL-6 levels at admission for sepsis were associated with higher platelet levels at discharge.

Acute lung injury (ALI) is a life‐threatening condition with excessive immune activation and dysregulated inflammation. Dendritic cells (DCs) play a pivotal role in immune regulation; however, their exact contribution to ALI pathogenesis remains unclear. This study demonstrates that the upregulation of the glycolytic regulator 6‐phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase 2 (PFKFB2) by hypoxia‐inducible factor‐1α (HIF‐1α) enhances glycolysis, drives DC maturation, and exacerbates inflammation, contributing to the pathogenesis of ALI. The findings reveal that HIF‐1α directly binds to the PFKFB2 promoter and drives its transcription, leading to increased glycolysis, accelerated DC maturation, and amplified immune activation. In paraquat (PQ)‐ALI and lipopolysaccharide (LPS)‐ALI mouse models, DC‐specific PFKFB2 knockout and DC‐targeted delivery of HIF‐1α inhibitor‐loaded nanoparticles each significantly suppressed DC maturation and alleviated ALI severity. Analyses of lung tissues from patients with PQ poisoning, secondary bacterial pneumonia (2°BP), and Coronavirus Disease 2019 (COVID‐19), as well as from normal controls, confirmed these findings, showing increased PFKFB2 expression and DC maturation during ALI. These findings highlight the HIF‐1α–PFKFB2 signaling pathway as a critical regulator of glycolysis‐driven DC maturation and immune activation, offering novel insights into immunometabolic regulation and a promising therapeutic target for ALI.

Background: Septic shock is a life-threatening disease with high mortality rates, and the relevant hub genes and biomarkers are poorly understood. We aimed to identify hub genes and prognostic biomarkers of mRNAs/lncRNAs in septic shock to rapidly and accurately diagnose infection, identify patients at a high risk of developing septic shock, and predict prognosis. Methods: Gene expression profiles of 279 patients with septic shock and 100 healthy controls were analyzed using bioinformatics methods. We screened for differentially expressed genes (DEGs), identified hub genes, and investigated the correlations between mRNA/lncRNA expression and disease severity/prognosis. Protein level validation was performed using blood proteomic data from an independent cohort study. Results: The protein-protein interaction network constructed using upregulated DEGs contained 102 nodes and 222 edges, with LTF, MMP8, MMP9, CEACAM8, CTSG, LCN2, and PRTN3 identified as hub genes. There was a possible association between LCN2 mRNA upregulation and increased severity of septic shock (odds ratio: 1.518; 95% confidence interval: 0.999-2.305; P = 0.050), approaching statistical significance, and BCL2A1 mRNA upregulation correlated with higher mortality risk (odds ratio: 1.178; 95% confidence interval: 1.035-1.341; P = 0.013). No significant prognostic correlation was observed for lncRNAs. The validation cohort confirmed significant upregulation of MMP9, CTSG, LCN2, LTF, and MMP8 proteins in patients with septic shock, with MMP9, LCN2, CTSG, and LTF exhibiting strong diagnostic performance (area under the curve >0.8). Conclusion: Seven hub genes related to septic shock were identified, including MMP9, LCN2, CTSG, and LTF, which could potentially function as candidate biotargets and biomarkers for the diagnosis and prognostic prediction of septic shock, though further validation is needed. Notably, LCN2 showed a trend toward association with disease severity, while BCL2A1 correlated with mortality risk.

Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis, often leading to poor neurological outcomes. Lipid molecules are increasingly recognized for their potential involvement in both sepsis and cognitive impairment. However, the relationship between lipidomic alterations and SAE remains incompletely understood. This study aims to investigate lipidomic changes in patients with SAE and explore potential associations between lipid metabolism and the development of SAE. Sepsis patients without pre-existing central nervous system disorders were prospectively enrolled. SAE was defined as a positive result on the Confusion Assessment Method for the ICU (CAM-ICU) or a Glasgow Coma Scale (GCS) score < 15. Blood samples were collected at enrollment and upon any change in cognitive status. Cerebrospinal fluid (CSF) samples were collected based on the physician assessment. Lipid metabolites were analyzed using high-performance liquid chromatography coupled with mass spectrometry. A total of 98 sepsis patients were enrolled, with 39 classified into the SAE group and 59 into the non-SAE group. Plasma levels of phosphatidylethanolamines (PE) and phosphatidylcholines (PC) were significantly decreased in SAE patients. Among these, LPC (18:2), LPC (16:0), LPE (22:6), and LPE (20:4) showed the most notable reductions. Additionally, 3-hydroxy-3-methylglutaryl coenzyme A(HMG-CoA) levels were decreased in SAE patients, while proinflammatory cytokines such as IFN-γ, IL-1ra, MCP-1, and IP-10 were elevated. Reduced levels of PC and PE lipids in SAE patients may reflect underlying inflammatory processes. The observed downregulation of HMG-CoA and upregulation of IP-10 and MCP-1 suggest a potential therapeutic role for statins in the management of SAE. Clinical Trial Registry number and website where it was obtained: Clinical Trial NCT04230447 (Registration Date: 01/02/2021; https://www.clinicaltrials.gov/study/NCT04230447?cond=Sepsis ).

Radiofrequency microneedle (RFMN) could mechanically penetrates the epidermis and emits radiofrequency energy to the target skin layer. This innovative system offers the capability to deliver precisely controlled radiofrequency energy at varying depths within the skin in a single insertion. We hypothesized that the new RFMN could improve both pore size and skin laxity simultaneously by single insertion and multiple discharges, thus reducing the number of treatment passes and improving the treatment efficiency. Therefore, we carried out this pilot study to confirm the clinical effects and corresponding histological changes. In clinical part, 3 subjects received a single RFMN treatment. Subjects’ faces were randomly divided into superficial base-energy and deep high-energy side or superficial high-energy and deep base-energy side. Facial characteristics were documented using standardized photographic techniques at various points in the study. In animal experiment, the abdomen of Bama miniature pig was divided into 4 treatment zones: the blank control group; superficial base-energy and deep high-energy group; superficial high-energy and deep base-energy group; no energy control group. Skin samples were collected immediately and 1 month post-treatment for histological analysis to observe the corresponding histological changes. Immediately after treatment, we found that the severity of erythema and petechiae may be related to the parameter settings. 1 month after treatment, improvement in skin laxity and facial pore size on both sides of the face was observed. The treatment resulted in a more significant improvement in relaxation on the superficial base-energy and deep high-energy side, but the pore improvement appeared to be more pronounced on the superficial high-energy and deep base-energy side. A trend of decreasing intensity in vascular dilatation was observed across the treatment groups, with the superficial high-energy and deep base-energy group exhibiting the most pronounced dilation. Histological observations immediately after treatment revealed that 2 seperated injury zones, which was caused by the same needle discharged electric twice, and one charge in the deep and one in the shallow. Immediate post-treatment dilation of blood vessels in all treatment groups was observed. A trend of decreasing intensity in vascular dilatation was observed across the treatment groups, with the superficial high-energy and deep base-energy group exhibiting the most pronounced dilation. 1 month post-treatment, histological analysis revealed an increase in dermal thickness, elastin, collagen fiber thickness and density, perivascular inflammatory cell infiltration across all treatment groups. Overall, our study demonstrated that variations in energy delivered at different depths by a new RFMN could induce distinct histological changes and corresponding clinical efficacy. This finding holds promise for optimizing the clinical application of RFMN. By tailoring the depth and energy settings in one insertion, specific concerns such as enlarged pores or facial laxity can be addressed more efficiently.

BACKGROUND AND AIMS:Liver injury is one of the common complications of paraquat (PQ) poisoning, but whether the degree of liver injury is related to patient prognosis is still controversial. This study aimed to investigate whether liver injury was a risk factor for death in PQ-poisoned patients. METHODS:We conducted a retrospective cohort study of PQ-poisoned patients from the past 10 years (2011-2020) from a large tertiary academic medical centre in China. PQ-poisoned patients were divided into a normal liver function group (n = 580) and a liver injury group (n = 60). Propensity score matching (PSM) analysis was then performed. RESULTS:A total of 640 patients with PQ poisoning were included in this study. To reduce the impact of bias, dose of PQ, urinary PQ concentration and time from poisoning to hospital admission were matched between the two groups. A 3:1 PSM analysis was performed, ultimately including 240 patients. Compared with the normal liver function group, patients in the liver injury group were older, had a higher R value ([ALT/ULN]/[ALP/ULN]) (p < .001) and had a higher mortality rate. Cox regression analysis showed that there was no significant association between alanine aminotransferase, alkaline phosphatase, total bilirubin levels and hazard of death, but age, PQ dose, creatine kinase isoenzyme, creatine kinase, white blood cell count, neutrophil percentage and lymphocyte percentage were associated with mortality in patients with PQ poisoning. CONCLUSIONS:The occurrence of liver injury within 48 h after PQ poisoning was a risk factor for mortality, and such liver injury was likely of a hepatocellular nature. Age, PQ dose, creatine kinase isoenzyme and white blood cell count were positively correlated with mortality, while creatine kinase, percentage of neutrophils and lymphocytes were inversely correlated.

ObjectivesThis study aims to evaluate the safety of the radiofrequency device and its efficacy in various treatment and refrigeration modes.MethodsFour 4-week Bama miniature pigs were used in this study, and four repeated treatment sites were selected on the pig's abdomen, each site consisting of 6 different treatment and cooling modes, with radiofrequency device (YouMagic; WE Medical Technology Co., Ltd.) administered every 3-5 s for a total of five treatments. The handheld infrared thermometer (HIKMICRO; Hangzhou Hikmicro Sensing Technology Co., Ltd.) was used to monitor the surface temperature of skin. Twenty minutes after the completion of treatment, a biopsy of the treatment and control area was performed on the pigs using a 4-mm biopsy punch. One-month after the treatment, samples were obtained using surgical scalpels. After that we used proper staining to estimate the therapeutic efficacy. At last, SPSS and Image J were used to proceed to the next step of analysis.ResultsDuring the therapy, no side effects were observed apart from mild transient erythema caused by the heating of skin temperature, staining of biopsy samples taken 20 min after treatment showed no serious damage of dermis. After 1 month of treatment, it can increase collagen I and elastin production. In addition, increases in energy setting at a standard pass number also increased the expression of collagen I. Meanwhile, we also found an increase in the thickness of the dermal layer among all treatment groups.ConclusionsThe new monopolar radiofrequency instrument possesses excellent therapeutic safety. After 1 month of treatment, it can increase collagen I and elastin production in 2-month-old Bama miniature pigs.