Anqiang Zhang

Conventional flexible protective materials often fall short in addressing the increasingly demanding requirements for extreme impact protection across a broad temperature range. Here, we present a robustness/damping alternating multilayer ionogel with stable interlayer interfaces using sequential photopolymerization of different ionogel layers. The resulting ionogel exhibits outstanding comprehensive performance for extreme impact protection over a wide temperature range, including an exceptionally broad damping temperature range (−49°C to 154°C), a high maximum damping factor (tan δ _max = 1.31), as well as reliable mechanical properties. Moreover, the ionogel can withstand impact at a strain rate of 20 000 s ⁻¹ over a temperature span from −80°C to 120°C. At 25°C, its impact strength reaches 862.18 kJ m ⁻² under a strain rate of 28 000 s ⁻¹ , which is 7.48 times that at 4000 s ⁻¹ , demonstrating clear impact‐strengthening behavior. Shocktube tests reveal that the ionogel achieves a peak pressure attenuation rate of up to 76.54%. Further performance evaluations, including ultrasonic vibration damping, motor vibration suppression, and drop‐weight tests, confirm its effective vibration attenuation and low‐velocity rigid impacts protection. This work provides a new perspective for designing ionogel‐based protective materials suitable for extreme environments such as high‐explosive conditions, aerospace applications, and polar expeditions.

This study aimed to identify core differential proteins associated with severe hospital-acquired pneumonia (sHAP) complicating the hospitalization of traumatic brain injury (TBI) patients through proteomic analysis. It further explored their association with sHAP and evaluated their predictive value. This single-center cohort study collected general clinical characteristics and biological indicators from 153 TBI patients admitted to the neurosurgery department of Chongqing Emergency Medical Center between February 4, 2021, and May 10, 2024. We performed quantitative analysis of differential proteins associated with sHAP and identified Cystatin C (CysC) as a key differential protein. Logistic regression modeling assessed the correlation between serum CysC concentration at the 24-h cut-off point and the occurrence of sHAP. The predictive value of CysC for sHAP was evaluated using the Receiver Operating Characteristic (ROC) curve and the Kaplan-Meier method. The study included 153 TBI patients with a mean age of 48.7 ± 14.6 years, comprising 118 (77.1%) males and 35 (22.9%) females. Of these, 43 patients developed sHAP, with a mean CysC serum concentration of 120.8 ± 17.7 µg/L, while the 110 patients who did not develop sHAP had a mean CysC serum concentration of 92.7 ± 18.4 µg/L. After adjusting for multiple factors, each 1 µg/L increase in CysC levels was associated with a 9% increase in sHAP incidence (OR: 1.09, 95% CI: 1.06-1.13). In the ROC curve analysis, CysC demonstrated a sensitivity of 79.1% and specificity of 80.9% at a threshold of 111.75 µg/L, showing superior predictive efficacy compared with traditional inflammatory markers. Kaplan-Meier curves indicated a higher incidence of sHAP in TBI patients with CysC ≥111.75 µg/L. This study innovatively explored CysC at the proteomic level, identifying it as a key protein associated with sHAP in TBI patients. Our findings suggest that serum CysC levels may not only indicate renal function but also reflect systemic inflammation and other pathological states. Elevated CysC levels at 24 h post-admission were significantly linked to an increased risk of sHAP, with this association persisting after adjusting for relevant factors. Notably, CysC demonstrated superior accuracy in predicting sHAP compared with traditional inflammatory markers such as WBC and Neu#. Thus, CysC holds potential as a novel indicator for assessing sHAP risk in TBI patients post-admission. Further studies are needed to validate its clinical utility and broaden its application.

Background: Sepsis is a life‐threatening organ dysfunction caused by a dysregulated host response to infection and progressive immunosuppression with high mortality. HLA‐DR, CD64, and PD‐1 were assumed to be useful biomarkers for sepsis prediction. However, the ability of a combination of these biomarkers has not been clarified.Methods: An observational case‐control study was conducted that included 30 sepsis patients, 30 critically ill patients without sepsis admitted to the intensive care unit (ICU), and 32 healthy individuals. The levels of HLA‐DR, CD64, and PD‐1 expression in peripheral blood immune cells and subsets was assayed on Days 1, 3, and 5, and the clinical information of patients was collected. We compared these biomarkers between groups and evaluated the predictive validity of single and combined biomarkers on sepsis mortality.Results: The results indicate that PD‐1 expression on CD4⁻CD8⁻T (PD‐1⁺CD4⁻CD8⁻T) (19.19% ± 10.78% vs. 9.88% ± 1.79%, p = .004) cells and neutrophil CD64 index (nCD64 index) (9.15 ± 5.46 vs. 5.33 ± 2.34, p = .001) of sepsis patients were significantly increased, and HLA‐DR expression on monocytes (mHLA‐DR⁺) was significantly reduced (13.26% ± 8.06% vs. 30.17% ± 21.42%, p = 2.54 × 10⁻⁴) compared with nonsepsis critically ill patients on the first day. Importantly, the expression of PD‐1⁺CD4⁻CD8⁻T (OR = 0.622, 95% CI = 0.423–0.916, p = .016) and mHLA‐DR⁺ (OR = 1.146, 95% CI = 1.014–1.295, p = .029) were significantly associated with sepsis mortality. For sepsis diagnosis, the mHLA‐DR⁺, PD‐1⁺CD4⁻CD8⁻T, and nCD64 index showed the moderate individual performance, and combinations of the three biomarkers achieved greater diagnostic value (AUC = 0.899, 95% CI = 0.792–0.962). When adding PCT into the combined model, the AUC increased to 0.936 (95% CI = 0.840–0.983). For sepsis mortality, combinations of PD‐1⁺CD4⁻CD8⁻T and mHLA‐DR⁺, have a good ability to predict the prognosis of sepsis patients, with an AUC = 0.921 (95% CI = 0.762–0.987).Conclusion: These findings indicate that the combinations of HLA‐DR, CD64, and PD‐1 outperformed each of the single indicator in diagnosis and predicting prognosis of sepsis.

Immunotherapies have emerged as potential treatments for metastatic castration-resistant prostate cancer (mCRPC). However, it is still unclear to identify the efficacy and safety of immunotherapy in large-scale samples. We performed a meta-analysis of 7 phase III randomized trials and 3 phase II trials comparing immunotherapy to placebo in mCRPC. Searching the PubMed, ClinicalTrials and Cochrane Library, completed III/IV phase trials were identified. Data extraction was conducted according to the PRISMA statement. The measured outcomes were OS, PFS, ORR and AE. Based on the results of phase III randomized trials, 3 II phase trials with results were identified. A total of 4185 patients were available for evaluation of OS, and 3320 for PFS. Compared to placebo, immunotherapies were not able to improve OS (HR = 0.90; 95%CI 0.79–1.03; p = 0.13). However, immunotherapies, especially ICBs were able to decrease the risk of progression over placebo by 18% (HR = 0.82; 95%CI 0.68–1.00; p = 0.04). Significant ORR improvement was found in patients treated in ICBs (RR = 1.90; 95%CI 1.30–2.78; p < 0.001). Immunotherapies (OR = 1.01, 95% CI = 0.40–2.56; OR = 1.27, 95% CI = 0.72–2.25) were not associated with significant any grade TRAEs and 3–4 grade TRAEs. However, in subgroup analysis, ICBs (OR = 2.85, 95% CI = 2.27–3.57) and vaccines (OR = 0.78, 95% CI = 0.64–0.53) were associated with significant 3–4 grade TRAEs respectively. Moreover, ICBs alone induced positive PSA response [OR = 2.43(1.09–5.43), P = 0.03(I2 = 0%, P = 0.83)] and was effective in advanced PC even without classical therapies based on three phase II clinical trials about ICBs. Immunotherapies are not able to improve OS, but significantly improve PFS and ORR especially in ICBs treatment. Immunotherapies were not associated with significant TRAEs. However, in subgroup analysis, ICBs and vaccines were associated with significant 3–4 grade TRAEs.

Background:Current research indicated Annexin A3 (ANXA3) was involved in innate immunity. Nevertheless, the comprehensive expression of ANXA3 in sepsis patients remain uncertain.Methods:We performed a meta-analysis utilizing public datasets form Array Express and Gene Expression Omnibus (GEO) to summarize and evaluate the expression level of ANXA3 in sepsis patients. Then, we investigated the associations between plasma ANXA3 and sepsis via a retrospective study. The predictive ability of plasma ANXA3 for sepsis was evaluated using the Area Under the Curve (AUC).Results:Totally, the meta-analysis including 2612 sepsis and 2259 controls indicated sepsis patients were with markedly higher levels of ANXA3 mRNA expression (SMD=2.04 (1.54-2.55); p<0.00001). Meanwhile, sepsis deaths (n=500) were with limited higher expression of ANXA3 mRNA than sepsis survivors (n=1711) (SMD=0.11(0.01-0.22); p=0.03). Furthermore, our results indicated plasma ANXA3 on admission were significantly associated with the incidence of sepsis in critically ill patients (OR=2.41(1.75-3.32), p<0.001). As a predictive biomarker, plasma ANXA3 resulted in a better AUC 0.815(0.745-0.886) than procalcitonin (PCT) (0.673(0.584-0.761)) and interleukin-6 (IL-6) (0.672(0.585-0.759)) and SOFA score (0.668(0.577-0.759)). Additionally, patients with high plasma ANXA3 had a poorer overall 28-day survival in critically ill patients (HR=2.16(1.09-4.28); p=0.028), but not for sepsis patients (HR=1.63(0.65-4.06); p=0.276).Conclusions:This study evaluated and validated ANXA3 was increased in sepsis. As a predictive biomarker, plasma ANXA3 obtained a good predictive ability for sepsis. Meanwhile, plasma ANXA3 was associated with outcomes of critically ill patients, but not sepsis patients.

Background: The study aimed to establish the profiles of cytokines in trauma patients to characterize the nature of the immune responses to sepsis, which might enable early prediction and individualized treatments to be developed and targeted.Methods: A 15-plex human cytokine magnetic bead assay system was used to measure analytes in citrated plasma samples. Analysis of these cytokine kinetics was performed on 40 patients with severe blunt trauma admitted to our trauma center between March 2016 and February 2017 with Injury Severity Score (ISS) more than 20 with regard to sepsis (Sepsis-3) over a 14-day time course.Results: In total, six cytokines changed in trauma patients between the different timepoints at day 1, 3, 5, 7, and 14. Additionally, IL-6, IL-10, IL-15, MDC, GRO, sCD40L, G-CSF, and FGF-2 significantly distinguished between sepsis and nonsepsis at day 3 and afterward with an area under the curve of up to 0.90 when the eight biomarkers (P < 0.001) were combined. Event-related analysis demonstrated 1.5- to 4-fold serum level changes for these cytokines within 72 hours before clinically apparent sepsis. Conclusion: Cytokine profiles demonstrate high discriminatory ability to timely identify evolving traumatic sepsis. These abrupt changes allow sepsis detection up to 72 hours before clinically overt deterioration. Measurement of these cytokines might enable future studies to better predict, diagnose, and characterize traumatic sepsis, as well as confer the potential for physicians to timely initiate treatment with reduced mortality and costs.Trial registration: Clinicaltrials, NCT01713205. Registered 22 October 2012, https://register.clinicaltrials.gov/NCT01713205

Purpose: CXC chemokines are mediators which mediate immune cells migration to sites of inflammation and injury. Chemokine C-X-C motif ligand 16 (CXCL16) plays an important role in the occurrence and development of sepsis through leukocyte chemotaxis, leukocyte adhesion and endotoxin clearance. In this study, we selected a set of tagging single nucleotide polymorphisms (tag SNPs) in the CXCL16 gene and investigated their clinical relevance to the development of sepsis and multiple organ dysfunction syndrome (MODS) in patients with major trauma in three independent Chinese Han populations.Methods: A total of 1,620 major trauma patients were enrolled in this study. Among these patients, 920 came from Chongqing in western China, 350 came from Zhejiang Province in eastern China, and 350 came from Guizhou Province in southwestern China. The improved multiplex ligation detection reaction (iMLDR) method was employed in the genotyping and genetic association analyses to determine the associations between CXCL16 haplotypes and sepsis morbidity rate and higher MOD scores in three cohorts.Results: Only CXCL16 T123V181 haplotype was associated with an increased risk for sepsis morbidity and higher MOD scores in the three cohorts (OR = 1.89,P= 0.001 for the Chongqing cohort; OR = 1.76,P= 0.004 for the Zhejiang cohort; OR = 1.55,P= 0.012 for the Guizhou cohort). The effect of T123V181 haplotype on the chemotaxis, migration and endotoxin clearance of immune cells were further observed. Protein modeling analysis showed that T123 and V181 might alter the structure of the CXCL16 active center. Thus it enhanced the chemotaxis and adhesion ability of immunocytes.Conclusion: We demonstrate the mechanism of CXCL16 T123V181 haplotype which regulates the sepsis morbidity rate and thus provide a new biomarker for early diagnosis of sepsis and MODS.Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT01713205 (https://www.clinicaltrials.gov/ct2/results?cond=&term=+NCT01713205&cntry=&state= &city=&dist=).