Developmental data from necrophagous flies are widely used to estimate the minimum postmortem interval (PMImin), but their reliability may be affected by larval feeding substrate and associated gut microbiota. Under controlled laboratory conditions, we investigated the effects of three porcine tissues (liver, lung, and muscle) on the development and gut microbial communities of Sarcophaga peregrina (Robineau-Desvoidy) (Diptera: Sarcophagidae). Developmental duration, larval body length, and pupal length were recorded, and gut samples from six developmental stages were analyzed by 16S rRNA gene sequencing. Feeding substrate affected development mainly during the feeding stages, with the second instar showing the greatest sensitivity. Larvae reared on liver developed significantly faster than those reared on muscle, whereas maximum larval length did not differ among groups; pupae from the liver group were significantly larger. Gut microbiota analysis showed that developmental stage was the primary driver of community succession, while feeding substrate further shaped microbial divergence during feeding. The dominant bacterial phyla across samples were Pseudomonadota, Bacillota, and Bacteroidota. The liver-fed group was enriched in Bacillota-associated taxa, including Vagococcus, Lactococcus, and Peptostreptococcus, whereas the lung- and muscle-fed groups showed greater enrichment of Wohlfahrtiimonas, Ignatzschineria, and Providencia. LEfSe, functional prediction, and random forest classification further supported clear substrate-associated differences. These findings show that tissue substrate influences both development and gut microbial succession in S. peregrina and may affect PMImin interpretation.

ObjectiveTo observe stage-specific changes in the intestinal microbiota of nude mice after death and to develop a postmortem interval （PMI） estimation model based on “rupture points”, thereby exploring a new model for PMI estimation.MethodsA total of 108 nude mice were sacrificed, and cecal contents were collected at 18 time points （0, 24, 41, 48, 55, 65, 72, 79, 89, 96, 103, 113, 120, 144, 168, 192, 216, and 240 h postmortem）. 16S rRNA gene amplicon sequencing was used to analyze the changes in intestinal microbiota. Based on microbial abundance, a random forest model was employed for cross-validation to identify signature bacterial genera. A segmented regression model was then constructed to estimate PMI and compared with a direct regression model.ResultsBoth α- diversity and β-diversity analyses indicated significant changes in the relative abundance of intestinal microbiota during the periods of 0-103 h and 113-240 h postmortem in nude mice. The segmented regression model built using the random forest algorithm achieved an R2 of 0.96 and a mean absolute error （MAE） of 9.83 h for PMI estimation. In contrast, the direct regression model yielded an R2 of 0.81 and an MAE of 16.91 h.ConclusionMicrobial succession during cadaver decomposition exhibits clear temporal and stage-specific characteristics. A segmented regression model for PMI estimation using “rupture points” can improve the accuracy of PMI estimation in nude mice.

Accurate classification of postmortem decomposition stages is a critical step in estimating the postmortem interval （PMI） and tracing the initial decomposition environment. Research on the decomposition staging methodological system is gradually shifting from empirical observation to the establishment of systems based on multidimensional quantitative indicators. This paper focuses on two key pathways, “macroscopic morphological evolution” and “microscopic molecular succession”, and systema-tically reviews the evolutionary patterns and applicability of the decomposition staging system in three typical environmental media: surface exposure, burial, and aquatic systems. It also summarizes research progress in constructing stage classification models utilizing microbiome and metabolomic features. Furthermore, it highlights the integrated application of decomposition characteristic quantification techniques, multi-omics data integration, and machine learning algorithms in decomposition analysis systems. It analyzes the prospects and challenges of applying these approaches to build a standardized and practical decomposition staging system, aiming to provide theoretical support for establishing a decomposition staging system with high accuracy and strong adaptability to different environments.

Accurately estimating the postmortem interval (PMI) is a pivotal forensic challenge, as the precision of “chemical clocks” based on volatile organic compounds (VOCs) is confounded by intrinsic factors like age and extrinsic factors like insect colonization. This study aimed to disentangle these effects using TD-GC-MS with multivariate analysis to profile VOCs from rats of three ages with and without Sarcophaga peregrina (Robineau-Desvoidy, 1830) (Diptera: Sarcophagidae) colonization. While decomposition time was the principal driver of VOC succession, exhibiting stage-specific signatures like early-phase 2-hexanone and mid-phase aromatics, age and insects modulated this timeline via distinct mechanisms. Age increased the chemical complexity of VOC profiles, with adult rats showing significantly more diverse VOC profiles than younger cohorts during days 10–14 (p < 0.05). In contrast, insect colonization acted as a potent accelerator, advancing the chemical timeline by approximately 6 days, with the day 4 profile of colonized rats mirroring the day 10 profile of insect-free ones. We demonstrate that age increases the chemical heterogeneity of VOC profiles while insects accelerate temporal progression. Both factors must therefore be integrated as critical variables in VOC-based PMI models to ensure accuracy.

Microbial communities play a crucial role in decomposition, yet their patterns in human tissues remain underexplored. Most previous research has often focused on animal models such as mice and swine, with limited studies on human samples, primarily targeting specific environments like the gut and skin. Consequently, gaps persist in understanding postmortem microbial dynamics within internal human organs. The 2bRAD-M sequencing technology offers a powerful approach for human thanatomicrobiome research, overcoming key limitations of 16S rRNA and metagenomic sequencing methods. In this study, we used 2bRAD-M to profile microbial succession across seven human tissues-heart, liver, spleen, lung, kidney, calf muscle, and gut-at various postmortem intervals (PMIs). Significant variations in microbial community composition were observed across organs and decomposition stages, with Proteobacteria dominating early and Firmicutes later. A comparison of frozen and unfrozen cadavers (PMI 1-7 days) revealed divergent microbial shifts in the liver and spleen, while other tissues exhibited limited variation. These findings highlight complex, organ-specific microbial trajectories and suggest that microbial signatures could serve as biomarkers for PMI estimation. This research deepens our understanding of the microbial succession within internal human organs postmortem and contributes to elucidating the identity and role of microorganisms in human decomposition.IMPORTANCEHumans host a diverse array of microbial communities that play a crucial role in the decomposition process after death. Understanding these postmortem microbial dynamics is essential, as they offer valuable insights into the progression of decomposition with significant implications for forensic science. The role of microorganisms in corpse decomposition has gained increasing attention in both forensic and ecological research, but studies in this area remain in their early stages, requiring further in-depth exploration. This work pioneers the use of 2bRAD-M sequencing to investigate microbial changes across various human organs over increasing postmortem intervals. By enhancing knowledge of postmortem microbiota dynamics, the study contributes to refining and improving the accuracy of forensic methodologies.

IntroductionSenescent cells (SCs) accumulate with age and play a causative role in age-related diseases, such as idiopathic pulmonary fibrosis (IPF). Clearance of SCs attenuates lung fibrogenesis and favors fibrosis resolution, suggesting that targeting of SCs is recognized as a promising therapeutic approach for IPF. Isothiocyanates (ITCs) are natural compounds with anticancer and anti-aging properties, but their role in IPF remains unclear. The aim of our study to investigate whether benzyl isothiocyanate (BITC), a type of ITCs, can act as a senolytic agent thereby attenuating pulmonary fibrosis in aged mice.MethodsPrimary lung fibroblasts from IPF patients and controls were cultured and treated with various ITCs to identify potential senolytic agents. Senescence-associated β-galactosidase staining, Cell viability assays, Annexin V/PI double staining, Caspase 3 activity assay, Western blot analysis, and qPCR were performed to evaluate senescence markers, cell viability, and apoptosis-related proteins after BITC treatment of senescent IPF lung fibroblasts in vitro. HE staining, Masson staining, Hydroxyproline assay, and Western blot analysis were used to assess the pathological progress, collagen content of lung tissues, and fibrotic gene expression changes after BITC treatment in C57BL/6 aged mice.ResultsUsing senescent IPF fibroblasts, we screened and identified BITC as a potent senolytic drug. We show that BITC selectively induces apoptosis in senescent IPF fibroblasts by targeting AKT signal pathway. Intraperitoneal administration of BITC to an age-related lung fibrosis mouse model effectively depleted senescent lung fibroblasts and reversed persistent pulmonary fibrosis.DiscussionOur study reveals that BITC may be a promising therapeutic option for IPF and other age-related disease that progress with the accumulation of senescent fibroblasts.

Body fluids are commonly found biological traces at crime scenes. Differentiating body fluid types-especially saliva (SA) from vaginal secretions (VA)-remains a forensic challenge. Currently, microbes play an increasingly vital role in forensic science. In this study, we analyzed bacterial communities from various samples, including SA, VA, semen (SE) and skin (SK), using Illumina HiSeq sequencing of 16S rRNA gene amplicons. We validated the ability to distinguish SA samples from VA samples using real-time quantitative PCR (qPCR) for specific biomarkers. We obtained 8,211,062 tags and identified 4427 operational taxonomic units (OTUs). Bacteria at the phylum level were similar across the four body fluid types, but their abundances varied. At the genus level, different bacteria dominated. Principal coordinates analysis (PCoA) and cluster analysis revealed significant differences among sample types. Additionally, linear discriminant analysis effect size (LEfSe) identified specific bacterial variations across the four body fluids. qPCR validation of the sequencing-derived markers confirmed that eight specific biomarkers reliably distinguish SA from VA. This work enhances the fundamental understanding of microorganisms in different body fluids and aids in distinguishing SA and VA.

Microbial communities are critical drivers of mammalian carcass decomposition in natural ecosystems. Many studies have attempted to establish a microbial clock to estimate the postmortem interval (PMI); however, several obstacles remain to be solved. This study examines how age and insect activity influence microbial dynamics and emphasizes the role of ‘rupture’ in the decay. Notably, microbial diversity exhibited more pronounced shifts in immature cadavers, while insect activity suppressed overall diversity. Conversely, older age and insect colonization promoted the dominance of the Pseudomonadota phylum. We constructed random forest models (MAE: 0.62–0.95 days, R²: 0.976–0.987) for PMI estimation. These findings provide novel insights into refining PMI estimation in forensic contexts. Future research will further investigate the mechanisms behind these changes. Additionally, it will explore how other factors influence the decay, improving the accuracy and applicability of PMI estimation in various contexts.

BACKGROUND:Advanced hepatocellular carcinoma (HCC) has been treated with targeted therapy, immunotherapy, or a combination of both, however, the overall clinical efficacy is still unsatisfactory. Hepatic arterial infusion chemotherapy (HAIC), as a localized treatment modality, has demonstrated favorable therapeutic efficacy in patients with advanced HCC accompanied by portal vein tumor thrombus and extensive intrahepatic metastasis. In recent years, the combination of HAIC with immune and targeted therapy has gradually gained acceptance in East Asian countries. However, further investigation is necessary to assess the efficacy and safety of this triple therapy. METHOD:PubMed, Embase, the Cochrane Library, and Web of Science databases were systematically searched for studies conducted within the past 5 years on HAIC combined with immunotherapy and targeted therapy as first-line treatment for advanced HCC. According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we conducted this meta-analysis. Additionally, the quality of included studies was assessed using the Joanna Briggs Institute (JBI) scale. Outcomes such as overall response rate (ORR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and adverse events (AEs)were extracted and pooled from eligible studies. RESULT:Twelve studies involving 1072 patients were enrolled in this meta-analysis. In terms of tumor response, the pooled ORR and DCR were 65.7% (95% CI, 58.7%-72.7%) (I2 = 83%, P = 0.000) and 89.2% (95% CI, 83.9%-93.6%) (I2 = 83%, P = 0.000), respectively. When analyzing PFS, the upper limit of 95% confidence interval of PFS in one study was not reached, which could potentially impact the statistical analysis. Therefore, we analyzed the remaining 11 studies a total of 1019 patients to pool mPFS, ultimately the pooled mPFS was 9.77months (95% CI, 7.73-11.80) (I2 = 93.9%, P = 0.000). Follow-up time in some studies was insufficient, only eight studies reported OS, we systematically analyzed these eight studies and extracted the pooled mOS was 16.65 months (95% CI, 14.17-19.14) (I2 = 76.9%, P = 0.000). In terms of safety, the incidence rates of any grade AEs, ranked from high to low, were as follows: aminotransferase increased (61.3%), nausea and vomiting (40.5%), hypertension (37.8%), thrombocytopenia (37.4%), hyperbilirubinemia (36.7%), abdominal pain (35.6%), leukopenia (34.6%), hypothyroidism (19.0%), rash (14.4%). Grade 3-4 AEs ranked from high to low were as follows: aminotransferase increased (10.8%), thrombocytopenia (7.9%), hypertension (7.4%), leukopenia (5.0%). No treatment-related deaths occurred, patients receiving this triple therapy demonstrated favorable tolerability. CONCLUSION:The combination of hepatic arterial infusion chemotherapy with tyrosine kinase inhibitors and immune checkpoint inhibitors as a first-line therapy for unresectable advanced HCC demonstrates promising therapeutic efficacy and favorable safety.

The estimation of postmortem interval (PMI) has long been a focal point in the field of forensic science. Following the death of an organism, microorganisms exhibit a clock-like proliferation pattern during the course of cadaver decomposition, forming the foundation for utilizing microbiology in PMI estimation. The establishment of PMI estimation models based on datasets from different seasons is of great practical significance. In this experiment, we conducted microbiota sequencing and analysis on gravesoil and mouse intestinal contents collected during both the winter and summer seasons and constructed a PMI estimation model using the Random Forest algorithm. The results showed that the MAE of the gut microbiota model in summer was 0.47 ± 0.26 d, R2 = 0.991, and the MAE of the gravesoil model in winter was 1.04 ± 0.22 d, R2 = 0.998. We propose that, in practical applications, it is advantageous to selectively build PMI estimation models based on seasonal variations. Additionally, through a combination of morphological observations, gravesoil microbiota sequencing results, and soil physicochemical data, we identified the time of cadaveric rupture for mouse cadavers, occurring at around days 24–27 in winter and days 6–9 in summer. This study not only confirms previous research findings but also introduces novel insights, contributing to the foundational knowledge necessary to advance the utilization of microbiota for PMI estimation.

BACKGROUNDStress granules (SGs) could be formed under different stimulation to inhibit cell injury.AIMTo investigate whether SGs could protect hepatocytes from hypoxia-induced damage during acute liver failure (ALF) by reducing endoplasmic reticulum stress (ERS) mediated apoptosis.METHODSThe agonist of SGs, arsenite (Ars) was used to intervene hypoxia-induced hepatocyte injury cellular model and ALF mice models. Further, the siRNA of activating transcription factor 4 (ATF4) and SGs inhibitor anisomycin was then used to intervene in cell models.RESULTSWith the increase of hypoxia time from 4 h to 12 h, the levels of HIF-1 alpha, ERS and apoptosis gradually increased, and the expression of SGs marker G3BP1 and TIA-1 was increased and then decreased. Compared with the hypoxia cell model group and ALF mice model, the levels of HIF-1 alpha, apoptosis and ERS were increased in the Ars intervention group. After siRNA-ATF4 intervention, the level of SGs in cells increased, and the levels of HIF-1 alpha, ERS and apoptosis decreased. Compared with the siRNA-ATF4 group, the levels of G3BP1 in the siRNA-ATF4+anisomycin group were decreased, and the levels of HIF-1 alpha, ERS and apoptosis were increased. Moreover, compared with the ALF group, the degree of liver injury and liver function, the levels of HIF-1 alpha, ERS and apoptosis in the Ars intervention group were decreased, the level of SGs was increased.CONCLUSIONSGs could protect hepatocytes from hypoxia-induced damage during ALF by reducing ERS-mediated apoptosis.

Microbial communities can undergo significant successional changes during decay and decomposition, potentially providing valuable insights for determining the postmortem interval (PMI). The microbiota produce various gases that cause cadaver bloating, and rupture releases nutrient-rich bodily fluids into the environment, altering the soil microbiota around the carcasses. In this study, we aimed to investigate the underlying principles governing the succession of microbial communities during the decomposition of pig carcasses and the soil beneath the carcasses. At early decay, the phylum Firmicutes and Bacteroidota were the most abundant in both the winter and summer pig rectum. However, Proteobacteria became the most abundant in the winter pig rectum in late decay. Using genus as a biomarker to estimate the PMI could get the MAE from 1.375 days to 2.478 days based on the RF model. The abundance of bacterial communities showed a decreasing trend with prolonged decomposition time. There were statistically significant differences in microbial diversity in the two periods (pre-rupture and post-rupture) of the four groups (WPG 0–8Dvs. WPG 16–40D, p < 0.0001; WPS 0–16Dvs. WPS 24–40D, p = 0.003; SPG 0D vs. SPG 8–40D, p = 0.0005; and SPS 0D vs. SPS 8–40D, p = 0.0208). Most of the biomarkers in the pre-rupture period belong to obligate anaerobes. In contrast, the biomarkers in the post-rupture period belong to aerobic bacteria. Furthermore, the genus Vagococcus shows a similar increase trend, whether in winter or summer. Together, these results suggest that microbial succession was predictable and can be developed into a forensic tool for estimating the PMI.

Cardiovascular disease remains the leading cause of disability and mortality worldwide and a significant global burden. Many lines of evidence suggest complex remodeling responses to cardiovascular disease, such as myocardial ischemia, hypertension and valve disease, which lead to poor clinical outcomes, including heart failure, arrhythmia and sudden cardiac death (SCD). The mechanisms underlying cardiac remodeling are closely related to reactive oxygen species (ROS) and inflammation. Myeloid differentiation protein 1 (MD1) is a secreted glycoprotein known as lymphocyte antigen 86. The complex of MD1 and radioprotective 105 (RP105) is an important regulator of inflammation and is involved in the modulation of vascular remodeling and atherosclerotic plaque development. A recent study suggested that the expression of MD1 in hypertrophic cardiomyopathy (HCM) patients is decreased compared with that in donor hearts. Therefore, MD1 may play an important role in the pathological processes of cardiovascular disease and have potential clinical value. Here, this review aims to discuss the current knowledge regarding the role of MD1 in the regulation of cardiac pathophysiology.

Polysaccharides are rich in Panax notoginseng residue after extraction. This study aims to explore the structural characteristics of PNP-20, which is a homogeneous polysaccharide, separated from P. notoginseng residue by fractional precipitation and evaluate the anti-enteritis effect of PNP-20. The structure of PNP-20 was determined by spectroscopic analyses. A mouse model with enteritis induced by restraint stress (RS) and lipopolysaccharide (LPS) was used to evaluate the pharmacological effect of PNP-20. The results indicated that PNP-20 consisted of glucose (Glc), galactose (Gal), Mannose (Man) and Rhamnose (Rha). PNP-20 was composed of Glcp-(1→, →4)-α-Glcp-(1→, →4)-α-Galp-(1→, →4,6)-α-Glcp-(1→, →4)-Manp-(1→ and →3)-Rhap-(1→, and contained two backbone fragments of →4)-α-Glcp-(1→4)- α-Glcp-(1→ and →4)-α-Galp-(1→4)-α-Glcp-(1→. PNP-20 reduced intestinal injury and inflammatory cell infiltration in RS- and LPS-induced enteritis in mice. PNP-20 decreased the expression of intestinal tumor necrosis factor-α, NOD-like receptor family pyrin domain containing 3, and nuclear factor-κB and increased the expression of intestinal superoxide dismutase 2. In conclusion, PNP-20 may be a promising material basis of P. Notoginseng for the treatment of inflammatory bowel disease.

In spite of the great progress in the management of critical diseases in recent years, its associated prevalence and mortality of multiple organ failure still remain high. As an endocrine hormone, fibroblast growth factor 21 (FGF21) functions to maintain homeostasis in the whole body. Recent studies have proved that FGF21 has promising potential effects in critical diseases. FGF21 has also been found to have a close relationship with the progression of critical diseases and has a great predictive function for organ failure. The level of FGF21 was elevated in both mouse models and human patients with sepsis or other critical illnesses. Moreover, it is a promising biomarker and has certain therapeutic roles in some critical diseases. We focus on the emerging roles of FGF21 and its potential effects in critical diseases including acute lung injury/acute respiratory distress syndrome (ALI/ARDS), acute myocardial injury (AMI), acute kidney injury (AKI), sepsis, and liver failure in this review. FGF21 has high application value and is worth further studying. Focusing on FGF21 may provide a new perspective for the management of the critical diseases.

Background/Aims: Daphnetin (7,8-dihydroxycoumarin, DAP) exhibits various bioactivities, such as anti-inflammatory and antioxidant activities. However, the role of DAP in myocardial ischaemia/reperfusion (I/R) injury and I/R-related arrhythmia is still uncertain. This study aimed to investigate the mechanisms underlying the effects of DAP on myocardial I/R injury and electrophysiological properties in vivo and in vitro. Methods: Myocardial infarct size was measured by triphenyltetrazolium chloride staining. Cardiac function was assessed by echocardiographic and haemodynamic analyses. The levels of creatine kinase-MB, lactate dehydrogenase, malondialdehyde, superoxide dismutase, interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α) were detected using commercial kits. Apoptosis was measured by terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labelling staining and flow cytometry. The viability of H9c2 cells was determined by the Cell Counting Kit-8 assay. In vitro, the levels of IL-6 and TNF-α were measured by quantitative PCR. The expression levels of proteins associated with apoptosis, inflammation, and the Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappa B (TLR4/MyD88/NF-κB) signalling pathway were detected by Western blot analysis. The RR, PR, QRS, and QTc intervals were assessed by surface ECG. The 90% action potential duration (APD90), threshold of APD alternans, and ventricular tachycardia inducibility were measured by the Langendorff perfusion technique. Results: DAP preconditioning decreased myocardial I/R injury and hypoxia/reoxygenation (H/R) injury in cells. DAP preconditioning improved cardiac function after myocardial I/R injury. DAP preconditioning also suppressed apoptosis, attenuated oxidative stress, and inhibited inflammatory responses in vivo and in vitro. Furthermore, DAP preconditioning decreased the susceptibility to ventricular arrhythmia after myocardial I/R. Finally, DAP preconditioning inhibited the expression of TLR4, MyD88, and phosphorylated NF-κB (p-NF-κB)/P65 in mice subjected to I/R and cells subjected to H/R. Conclusions: DAP preconditioning protected against myocardial I/R injury and decreased susceptibility to ventricular arrhythmia by inhibiting the TLR4/MyD88/NF-κB signalling pathway.

The inherited polyglutamine (polyQ) expansion diseases are characterized by progressive accumulation of aggregation-prone polyQ proteins, which may provoke proteostasis imbalance and result in significant neurotoxicity. Using polyQ transgenic Caenorhabditis elegans models, we find that Kai-Xin-San (KXS), a well-known herbal formula traditionally used to treat mental disorders in China, can alleviate polyQ-mediated neuronal death and associated chemosensory deficiency. Intriguingly, KXS does not reduce polyQ aggregation in vitro as demonstrated by Thioflavin-T test, but does inhibit polyQ aggregation in C. elegans models, indicating an indirect aggregation-inhibitory mechanism. Further investigation reveals that KXS can modulate two key arms of the protein quality control system, that is, heat shock response and autophagy, to clear polyQ aggregates, but has little effect on proteasome activity. In addition, KXS is able to reduce oxidative stress, which is involved in proteostasis and neurodegeneration, but has no effect on life span or dietary restriction response. To examine potential interaction of the four component herbs of KXS, a dissection strategy was used to study the effects of differential herbal combinations in C. elegans polyQ models. While the four herbs do contribute additively to KXS function, Panax ginseng is found to be the most effective constituent. Taken together, these findings not only demonstrate the neuroprotective ability of KXS but also suggest its potential as a proteostasis regulator in protein aggregation disorders and provide an insight into the mechanism studies of traditionally used complex prescriptions and their rationality.

AIMS:To investigate the characteristics and clinical significance of myocardial injury in patients with severe coronavirus disease 2019 (COVID-19). METHODS AND RESULTS:We enrolled 671 eligible hospitalized patients with severe COVID-19 from 1 January to 23 February 2020, with a median age of 63 years. Clinical, laboratory, and treatment data were collected and compared between patients who died and survivors. Risk factors of death and myocardial injury were analysed using multivariable regression models. A total of 62 patients (9.2%) died, who more often had myocardial injury (75.8% vs. 9.7%; P < 0.001) than survivors. The area under the receiver operating characteristic curve of initial cardiac troponin I (cTnI) for predicting in-hospital mortality was 0.92 [95% confidence interval (CI), 0.87-0.96; sensitivity, 0.86; specificity, 0.86; P < 0.001]. The single cut-off point and high level of cTnI predicted risk of in-hospital death, hazard ratio (HR) was 4.56 (95% CI, 1.28-16.28; P = 0.019) and 1.25 (95% CI, 1.07-1.46; P = 0.004), respectively. In multivariable logistic regression, senior age, comorbidities (e.g. hypertension, coronary heart disease, chronic renal failure, and chronic obstructive pulmonary disease), and high level of C-reactive protein were predictors of myocardial injury. CONCLUSION:The risk of in-hospital death among patients with severe COVID-19 can be predicted by markers of myocardial injury, and was significantly associated with senior age, inflammatory response, and cardiovascular comorbidities.

With the high operating temperature in power electronics devices, the reliability of lead-free solder joints in electronic packages at high temperatures is important. Solder joint reliability depends on a large extent on the mechanical properties of the thin intermetallic compound layer, especially hardness and Young's modulus. In this paper, the mechanical properties of Cu6Sn5, the main component of IMC, at high temperature are measured by nanoindentation. After being processed and analyzed, data are compared with the room temperature one. The results show that temperature changes have effect on the mechanical properties of lead-free solder joints.

为有效抑制恶劣服役环境中输电塔线体系的断线事故,首先建立输电塔线体系的分析模型,提出断线动力效应的非线性分析方法及其导线与地面之间的非线性接触力计算方法,准确模拟断线过程中的接触效应,评估冲击力作用下输电杆塔的服役安全性;然后通过在杆塔上安装黏滞阻尼器,提出一种输电塔线体系断线效应的减振控制方法,减小结构振动并提高安全储备;最后以某输电塔线体系为实例,评估断线作用下该塔线体系的安全性.结果表明:塔线体系在断线作用下动力冲击效应较为显著,采用黏滞阻尼器可有效减小结构的断线动力效应,使位移、速度和加速度峰值的减振率达15％,35％和60％.