Ischemic stroke, a leading cause of global mortality and disability, is exacerbated by cerebral ischemiareperfusion injury (CIRI), wherein ferroptosis drives irreversible neuronal loss. Curcumin, a potent natural polyphenol, holds promise for combating CIRI but is thwarted by poor solubility and low bioavailability. To overcome this, we have created a biomimetic macrophage-vectored nanoinducer (Cur-P @ MM) that can actively target the ischemic brain. By keeping the original membrane proteins such as CD47 and integrin alpha 4 beta 1, Cur-P @ MM can achieve effective immune evasion and inflammation-tropic delivery, which helps with crossing the blood-brain barrier and achieving site-specific drug release. In the cellular model, Cur-P @ MM improved neuronal survival under oxidative stress, scavenge ROS, and preserve mitochondrial integrity. In a rat stroke model, it mainly concentrated in the ischemic side, greatly reduced the infarction area, and restored the neurological and cognitive function. Mechanistically, Cur-P @ MM suppresses ferroptosis by alleviating lipid peroxidation, reducing iron overload, and enhancing the Nrf2-associated antioxidant defense program. This leads to the coordinated upregulation of the solute carrier family 7 member 11 / glutathione peroxidase 4 (SLC7A11/ GPX4) axis and downregulation of transferrin receptor 1. Our work unveils a targeted nanotherapeutic strategy that harnesses the body's own antioxidant machinery to combat ferroptosis, offering a transformative avenue for ischemic stroke treatment.

Decellularized artificial blood vessels prepared using physical and chemical methods often exhibit limitations, including poor mechanical performance, susceptibility to inflammation and calcification, and reduced patency. Cross-linking techniques can enhance the stiffness, as well as anti-inflammatory and anti-calcification properties of decellularized vessels. However, conventional cross-linking methods fail to effectively alleviate residual stress post-decellularization, which significantly impacts the patency and vascular remodeling following the implantation of artificial vessels. This study enhances vascular residual stress through varied conditions of proanthocyanidin (PC) cross-linking on decellularized vessels. Microstructural analysis and mechanical investigations across various scales of fresh, decellularized, and residual stress-recovered vessels are performed using atomic force microscopy (AFM), scanning electron microscopy (SEM), and uniaxial tensile testing. Results demonstrate substantial alterations in the morphology of elastic and collagen fibers post-decellularization, which remarkably resemble fresh vessels following residual stress recovery. Furthermore, both the micro- and macro-mechanical characteristics of vessels post-residual stress recovery, including Young's modulus, viscoelasticity, and adhesion, closely resemble those of fresh vessels. Finite element modeling (FEM) confirms the distribution of residual stress and its role in enhancing vascular mechanical integrity. This experimental investigation provides a theoretical foundation at both micro and macroscopic levels for the development of biomimetic blood vessels.

Tissue engineering and regenerative medicine field, which focuses on creating functional tissue constructs resembling native tissue to repair or replace damaged tissues or organs, has undergone rapid evolution in recent decades. Particularly, there has been a surge of interest in utilizing tissue engineering for treating cardiovascular diseases, utilizing both natural and synthetic blood vessels. Additionally, advancements in bio-printing hold promise for generating human-engineered tissues like bone and skin for clinical applications. However, traditional tissue engineering methods, involving the scaffolds used, growth factors, and cells, have faced challenges in fabricating complex 3D shapes and achieving in vivo organ regeneration, making them less feasible for clinical use due to logistical and economic constraints. Various techniques, such as Electrospinning, Molding, Cell Sheet Rolling, and Decellularization, have been explored, but they have limitations, prompting the investigation of 3D bioprinting techniques. The advantages of 3D bioprinting over other biofabrication techniques are manifold. Firstly, the technique enables the advanced and precise layer-by-layer assembly of cells and biomaterials. Secondly, the utilization of a 3D bioprinter to create replicas based on medical images allows for the fabrication of complex tissues. Thirdly, the construction of tissue models through layering provides control over the precise placement of biomaterials and cells. Additionally, the use of 3D bioprinting allows for significant advancements in bioink modification, resulting in more accurate tissue replicas for practical in vivo tissue regeneration. Furthermore, 3D bioprinting enables the printing of tissues from undifferentiated stem cells obtained from the patient, reducing the risk of tissue rejection in native vessels. This paper reviews the applications of 3D bioprinting in engineered human tissues such as skin, bones and artificial blood vessels for cardiovascular diseases treatments. It provides an overview of 3D bioprinting technology and strategies, including ink-jet printing, extrusion printing, and stereolithography. The review then focuses on the applications of 3D bioprinting in constructing various tissues and organs, including cardiac, skin, and bone, discussing the steps involved and the technological requirements based on recent review and research articles. Finally, the review underscores the merits of the 3D bioprinting technique and outlines its current state while providing insights into future innovations aimed at skin tissue, bone tissue and blood vessels bioprinting. It explores potential advancements in polymer and biomaterial usage, cell sources, oxygen provision to cells, hydrogel and scaffold utilization, integration of machine learning, combining 3D bioprinting with 4D bioprinting, and addressing the expenses associated with 3D bioprinting, along with recommended cost mitigation methodologies.

Plasma secretory proteins are associated with various diseases, including aortic dissection (AD). However, current research on the correlation between AD and plasma protein levels is scarce or lacks specificity. This study aimed to explore plasma secretory proteins as potential biomarkers for AD. Through genome-wide association studies, expression quantitative trait locus (eQTL) analysis, and human plasma protein profiling, we identified DBNL, NPC2, SUMF2, and TFPI as high-risk genes and CCN3, PRKCSH, TEX264, and TGFBR3 as low-risk genes for AD. Further cell localization and differential expression analysis of these eight genes were conducted using single-cell data. We also examined their expression in three Gene Expression Omnibus datasets, measured their mRNA levels in AD versus normal tissues using qPCR, and assessed their protein levels in patients’ blood versus healthy individuals using enzyme-linked immunosorbent assay. Our findings suggest that CCN3, consistently downregulated in both mRNA and plasma levels during AD, may have a protective role. Initial enrichment analyses of differentially expressed CCN3 cells suggested their involvement in focal adhesion, actin cytoskeleton regulation, and the PI3K-Akt signaling pathway.

The magnitude of vascular residual stress, an inherent characteristic exclusive to the vasculature, exhibits a strong correlation with vascular compliance, tensile resistance, vascular rigidity, and vascular remodeling subsequent to vascular transplantation. Vascular residual stress can be quantified by evaluating the magnitude of the opening angle within the vascular ring. For decellularized vessels, the vascular ring's opening angle diminishes, consequently reducing residual stress. The decellularization process induces a laxity in the vascular fiber structure within decellularized vessels. To investigate the interrelation between the magnitude of residual stress and the microstructure as well as mechanical properties of elastin and collagen within blood vessels, this study employed fresh blood vessels, stress-relieved vessels, and sections of decellularized blood vessels. Structural scanning and force map experiments on the surface of the sections were conducted using atomic force microscopy (AFM). The findings revealed well-organized arrangements of elastin and collagen within fresh vessels, wherein the regularity of collagen and elastin exhibited variability as residual stress declined. Furthermore, both stress-relieved and decellularized vessel sections exhibited a reduction in the mean Young's modulus to varying extents in comparison to fresh vessels. The validity of our experimental results was further corroborated through finite element simulations. Hence, residual stress assumes a crucial role in upholding the structural stability of blood vessels, and the intricate association between residual stress and the microstructural and micromechanical properties of blood vessels holds significant implications for comprehending the impact of vascular diseases on vascular structure and advancing the development of biomimetic artificial blood vessels that replicate residual stress.Research HighlightsIn this inquiry, we scrutinized the interconnection amid vascular residual stress and the microscale and nanoscale aspects of vascular structure and mechanical function, employing AFM. We ascertained that residual stress assumes a pivotal role in upholding vascular microstructure and mechanical attributes. The experimental outcomes were subsequently validated through finite element simulation. In this study, we utilized Atomic Force Microscopy (AFM) to investigate the correlation between residual stresses within blood vessels and the complexity of their internal microstructural composition and mechanical functionality. Subsequently, the experimental results were validated through finite element simulations. image

BACKGROUND Multilocular thymic cyst (MTC) is a rare mediastinal lesion which is considered to occur in the process of acquired inflammation. It is usually characterized by well-defined cystic density and is filled with transparent liquid. CASE SUMMARY We report on a 39-year-old male with a cystic-solid mass in the anterior mediastinum. Computer tomography (CT) imaging showed that the mass was irregular with unclear boundaries. After injection of contrast agent, there was a slight enhancement of stripes and nodules. According to CT findings, it was diagnosed as thymic cancer. CONCLUSION After surgery, MTC accompanied by bleeding and infection was confirmed by pathological examination. The main lesson of this case was that malignant thymic tumor and MTC of the anterior mediastinum sometimes exhibit similar CT findings. Caution is necessary in clinical work to avoid misdiagnosis.

Cell mechanics plays a key role in determining physical performances and physiological functions of cells, as well as the early detection of diseases and development of biomedical engineering. In this study, we utilized a combination of atomic force microscopy (AFM) and finite element method (FEM) to compare the cellular elasticity (Young's modulus) and viscoelasticity (stress-relaxation time) of living and fixed endothelial cells (ECs) across varying loading rates. The results showed that both mechanical properties of normal ECs are more sensitive to loading speed compared with fixed ECs. The Young's modulus of normal endothelial cells (ECs) exhibits an increasing trend with the growing loading rate, whereas the Young's modulus of fixed ECs is almost not affected by the loading rate. Among various viscoelastic properties of cells under varying loading rates, the long-term relaxation time, especially at a loading rate of 5 mu m s-1, showed the most significant difference between living and fixed cells. This work comprehensively evaluated the effectiveness of using different mechanical properties to distinguish cells with different physiological characteristic. This research would improve our knowledge of single-cell mechanical behaviors and provide new ideas for distinguishing various types of cells by AFM-based cellular elastic and viscoelastic properties with varying loading rates.

The incidence of heart failure with preserved ejection fraction (HFpEF) increases with the ageing of populations. This study aimed to explore ageing-associated gene signatures in HFpEF to develop new diagnostic biomarkers and provide new insights into the underlying mechanisms of HFpEF. Mice were subjected to a high-fat diet combined with L-NG-nitroarginine methyl ester (l-NAME) to induce HFpEF, and next-generation sequencing was performed with HFpEF hearts. Additionally, separate datasets were acquired from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were used to identify ageing-related DEGs. Support vector machine, random forest, and least absolute shrinkage and selection operator algorithms were employed to identify potential diagnostic genes from ageing-related DEGs. The diagnostic value was assessed using a nomogram and receiver operating characteristic curve. The gene and related protein expression were verified by reverse transcription PCR and western blotting. The immune cell infiltration in hearts was analysed using the single-sample gene-set enrichment analysis algorithm. The results showed that the merged HFpEF datasets comprised 103 genes, of which 15 ageing-related DEGs were further screened in. The ageing-related DEGs were primarily associated with immune and metabolism regulation. AGTR1a, NR3C1, and PRKAB1 were selected for nomogram construction and machine learning-based diagnostic value, displaying strong diagnostic potential. Additionally, ageing scores were established based on nine key DEGs, revealing noteworthy differences in immune cell infiltration across HFpEF subtypes. In summary, those results highlight the significance of immune dysfunction in HFpEF. Furthermore, ageing-related DEGs might serve as promising prognostic and predictive biomarkers for HFpEF.

This study utilized the freeze-drying method to create a chitosan (CS) and polyvinyl alcohol (PVA) sponge. To enhance its antibacterial properties, curcumin and nano silver (Cur@Ag) were added for synergistic antibacterial. After adding curcumin and nano silver, the mechanical properties of the composite sponge dressing (CS-PVA-Cur@Ag) were improved. The porosity of the composite sponge dressing was closed to 80%, which was helpful for drug release, and it had good water absorption and water retention rate. The nano silver diameter was 50-80 nm, which was optimal for killing bacteria. Antibacterial tests usedEscherichia coliandStaphylococcus aureusdemonstrated that little nano silver was required to eliminate bacteria. Finally, in the rat full-thickness skin wound model, the composite sponge dressing can promote wound healing in a short time. In summary, CS-PVA-Cur@Ag wound dressing could protect from bacterial infection and accelerate wound healing. Thus, it had high potential application value for wound dressing.

Despite significant progress in human medicine, certain diseases remain challenging to promptly diagnose and treat. Hence, the imperative lies in the development of more exhaustive criteria and tools. Tissue and cellular mechanics exhibit distinctive traits in both normal and pathological states, suggesting that "force" represents a promising and distinctive target for disease diagnosis and treatment. Atomic force microscopy (AFM) holds great promise as a prospective clinical medical device due to its capability to concurrently assess surface morphology and mechanical characteristics of biological specimens within a physiological setting. This review presents a comprehensive examination of the operational principles of AFM and diverse mechanical models, focusing on its applications in investigating tissue and cellular mechanics associated with prevalent diseases. The findings from these studies lay a solid groundwork for potential clinical implementations of AFM. RESEARCH HIGHLIGHTS: By examining the surface morphology and assessing tissue and cellular mechanics of biological specimens in a physiological setting, AFM shows promise as a clinical device to diagnose and treat challenging diseases.

Cerebral ischemia/reperfusion (I/R) injury can result in different levels of cerebral impairment, and in severe cases, death. Curcumin, an essential bioactive component of turmeric, has a rich history as a traditional medicine for various ailments in numerous countries. Experimental and clinical research has established that curcumin offers a protective effect against cerebral I/R injury. Curcumin exerts its protective effects by acting on specific mechanisms such as antioxidant, anti-inflammatory, inhibition of ferroptosis and pyroptosis, protection of mitochondrial function and structure, reduction of excessive autophagy, and improvement of endoplasmic reticulum (ER) stress, which ultimately help to preserve the blood-brain barrier (BBB) and reducing apoptosis. There is currently a shortage of drugs undergoing clinical trials for the treatment of cerebral I/R injury, highlighting the pressing need for research and development of novel treatments to address this injury. The primary objective of this study is to establish a theoretical basis for future clinical applications of curcumin by delineating the mechanisms and protective effects of curcumin against cerebral I/R injury. Adapted with permission from [1].

Background We have reported a positive correlation between S100 calcium-binding protein (S100) A8/S100A9 and sepsis-induced lung damage before. However, limited knowledge exists concerning the biological role of S100A8/A9 in pulmonary vascular endothelial barrier dysfunction, as well as the diagnostic value of S100A8/A9 in sepsis. Methods Sepsis was induced in C57BL/6J mice and S100A9-knockout (KO) mice through the cecal ligation and puncture (CLP). Pulmonary vascular leakage was determined by measuring extravasated Evans blue (EB). Reverse transcription polymerase chain reaction and the histological score were used to evaluate inflammation and lung injury, respectively. Recombinant S100A8/A9 (rhS100A8/A9) was used to identify the effects of S100A8/A9 on endothelial barrier dysfunction in human umbilical vein endothelial cells (HUVECs). Additionally, the diagnostic value of S100A8/A9 in sepsis was assessed using receiver operating characteristic. Results S100A8/A9 expression was up-regulated in the lungs of CLP-operated mice. S100A9 KO significantly reversed CLP-induced hypothermia and hypotension, resulting in an improved survival rate. S100A9 KO also decreased the inflammatory response, EB leakage, and histological scores in the lungs of CLP-operated mice. Occludin and VE-cadherin expressions were decreased in the lungs of CLP-operated mice; However, S100A9 KO attenuated this decrease. Moreover, CLP-induced signal transducer and activator of transcription 3 (STAT3) and p38/extracellular signal-regulated kinase (ERK) signalling activation and apoptosis were mitigated by S100A9 KO in lungs. In addition, rhS100A8/A9 administration significantly decreased occludin and VE-cadherin expressions, increased the phosphorylated (p)-ERK/ERK, p-p38/p38, and B-cell leukaemia/lymphoma 2 protein (Bcl-2)-associated X protein/Bcl-2 ratios in HUVECs. Conclusion The present study demonstrated S100A8/A9 aggravated sepsis-induced pulmonary inflammation, vascular permeability, and lung injury. This was achieved, at least partially, by activating the P38/STAT3/ERK signalling pathways. Moreover, S100A8/A9 showed the potential as a biomarker for sepsis diagnosis.

Background: Sterile inflammation contributes to the pathogenesis of cardiac dysfunction caused by various conditions including pressure overload in hypertension. Mitochondrial DNA (mtDNA) released from damaged mitochondria has been implicated in cardiac inflammation. However, the upstream mechanisms governing mtDNA release and how mtDNA activates sterile inflammation in pressure-overloaded hearts remain largely unknown. Here, we investigated the role of inducible NO synthase (iNOS) on pressure overload-induced cytosolic accumulation of mtDNA and whether mtDNA activated inflammation through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway. Methods: To investigate whether the cGAS-STING cascade was involved in sterile inflammation and cardiac dysfunction upon pressure overload, cardiomyocyte-specific STING depletion mice and mice injected with adeno-associated virus-9 (AAV-9) to suppress the cGAS-STING cascade in the heart were subjected to transverse aortic constriction (TAC). iNOS null mice were used to determine the role of iNOS in cGAS-STING pathway activation in pressure-stressed hearts. Results: iNOS knockout abrogated mtDNA release and alleviated cardiac sterile inflammation resulting in improved cardiac function. Conversely, activating the cGAS-STING pathway blunted the protective effects of iNOS knockout. Moreover, iNOS activated the cGAS-STING pathway in isolated myocytes and this was prevented by depleting cytosolic mtDNA. In addition, disruption of the cGAS-STING pathway suppressed inflammatory cytokine transcription and modulated M1/M2 macrophage polarization, and thus mitigated cardiac remodeling and improved heart function. Finally, increased iNOS expression along with cytosolic mtDNA accumulation and cGAS-STING activation were also seen in human hypertensive hearts. Conclusion: Our findings demonstrate that mtDNA is released into the cytosol and triggers sterile inflammation through the cGAS-STING pathway leading to cardiac dysfunction after pressure overload. iNOS controls mtDNA release and subsequent cGAS activation in pressure-stressed hearts.

Background: S100 calcium-binding protein A9 (S100A9) is a danger-associated molecular pattern molecule that mediates the inflammatory response. Inflammation is essential in aging-related cardiovascular diseases. How-ever, less is known regarding the role of S100A9 in vascular aging. Methods: S100A9 null mice were used to investigate the role of S100A9 in aging-related pathologies. Artery rings were used to measure the functional characteristics of vascular with a pressurized myograph. Telomere length, Sirtuin activity, oxidative stress, and endothelial nitric oxide synthetase (eNOS) activity were used to elevate vascular senescence. Intraperitoneal glucose tolerance (IPGTT) and insulin sensitivity test (IST) were employed to investigate the effects of S100A9 on insulin resistance. Inflammation response was reflected by the concen-tration of inflammatory cytokines. The Toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE) inhibitors were used to identify the downstream molecular mechanisms of S100A9 in aging -induced senescence in endothelial cells. Results: S100A9 expression in vascular increased with aging in mice and humans. Deficiency of S100A9 alleviated vascular senescence in aged mice, as evidenced by increased telomere length, Sirtuin activity, and eNOS activity. Meanwhile, S100A9 knockout improved endothelium-dependent vasodilatation and endothelial continuity in aged mice. Moreover, the increased insulin resistance, oxidative stress, and inflammation were mitigated by S100A9 deletion in aged mice. In vitro, S100A9 induced senescence in endothelial cells, and that effect was blunted by TLR4 but not RAGE inhibitors. Conclusion: The present study suggested that S100A9 may contribute to aging-related pathologies and endothelial dysfunction via the TLR4 pathway. Therefore, targeting S100A9/TLR4 signaling pathway may represent a crucial therapeutic strategy to prevent age-related cardiovascular diseases.

在我国所有癌症中,肺癌的发病率及病死率均为第一,绝大多数患者就诊时已属晚期,这与缺乏筛查及规范治疗有关.随着胸部薄层CT的普及,近年来肺结节检出率逐年增加,而手术切除是肺结节最有效的治疗手段.单孔胸腔镜手术是微创手术的重要方式之一,为进一步规范重庆地区临床诊疗行为,保障诊疗质量,促进该技术规范,重庆市医药生物技术协会肺癌专业委员会组织重庆地区肺癌领域专家学者编写该共识,供广大胸外科同仁参考.

目的基于CT肺动脉造影(CTPA)检查,探讨肺动脉内对比剂浓度达峰时间(TTP)影响因素,构建肺动脉TTP预测模型.资料与方法采用前瞻性研究,纳入2019年9月—2020年9月于重庆市中医院行CTPA检查的153例疑似肺栓塞(PE)患者.采用时间-密度曲线软件计算肺动脉TTP;采用相关分析和多元线性逐步回归分析研究肺动脉TTP与影响因素的关系,并建立回归预测模型.结果相关分析结果显示,身高、性别、对比剂总量、对比剂浓度和体重与肺动脉TTP均呈正相关(r=0.363、0.330、0.179、0.168、0.164,均P<0.05).多元线性逐步回归分析结果表明,性别、身高和对比剂浓度可以独立预测肺动脉TTP(β=0.909、0.065、0.026,均P<0.05),并进一步建立肺动脉TTP回归预测模型,该模型检验结果显示拟合较好(F=11.721,P=0.012,调整R2=0.175).结论性别、身高和对比剂浓度是预测肺动脉TTP的独立影响因素.基于这3个指标建立的预测模型对肺动脉TTP具有较高预测价值.

BACKGROUND The number of patients with bronchial trauma (BT) who survived to hospital admission has increased with the improvement of prehospital care; early diagnosis and treatment should be considered, especially among blunt trauma patients, whose diagnosis is frequently delayed. AIM To describe the early recognition and surgical management considerations of blunt and penetrating BTs, and to elaborate the differences between them. METHODS All patients with BTs during the past 15 years were reviewed, and data were retrospectively analyzed regarding the mechanism of injury, diagnostic and therapeutic procedures, and outcomes. According to the injury mechanisms, the patients were divided into two groups: Blunt BT (BBT) group and penetrating BT (PBT) group. The injury severity, treatment procedures, and prognoses of the two groups were compared. RESULTS A total of 73 patients with BT were admitted during the study period. The proportion of BTs among the entire cohort with chest trauma was 2.4% (73/3018), and all 73 underwent thoracotomy. Polytrauma patients accounted for 81.6% in the BBT group and 22.9% in the PBT group, and the mean Injury Severity Score was 38.22 ± 8.13 and 21.33 ± 6.12, respectively. Preoperative three-dimensional spiral computed tomography (CT) and/or fiberoptic bronchoscopy (FB) were performed in 92.1% of cases in the BBT group (n = 38) and 34.3% in the PBT group (n = 35). In the BBT group, a delay in diagnosis for over 48 h occurred in 55.3% of patients. In the PBT group, 31 patients underwent emergency thoracotomy due to massive hemothorax, and BT was confirmed during the operation. Among them, 22 underwent pulmo-tractotomy for hemostasis, avoiding partial pneumonectomy. In this series, the overall mortality rate was 6.9% (5/73), and it was 7.9% (3/38) and 5.7% (2/35) in the BBT group and PBT group, respectively (P > 0.05). All 68 survivors were followed for 6 to 42 (23 ± 6.4) mo, and CT, FB, and pulmonary function examinations were performed as planned. All patients exhibited normal lung function and healthy conditions except three who required reoperations. CONCLUSION The difference between blunt and penetrating BTs is obvious. In BBT, patients generally have no vessel injury, and the diagnosis is easily missed, leading to delayed treatment. The main cause of death is ventilation disturbance due to tension pneumothorax early and refractory atelectasis with pneumonia late. However, in PBT, most patients require emergency thoracotomy because of simultaneous vessel trauma and massive hemothorax, and delays in diagnosis are infrequent. The leading cause of death is hemorrhagic shock.

Rib fracture is the most common injury in chest trauma. Most of patients with rib fractures were treated conservatively, but up to 50% of patients, especially those with combined injury such as flail chest, presented chronic pain or chest wall deformities, and more than 30% had long-term disabilities, unable to retain a full-time job. In the past two decades, surgery for rib fractures has achieving good outcomes. However, in clinic, there are still some problems including inconsistency in surgical indications and quality control in medical services. Before the year of 2018, there were 3 guidelines on the management of regional traumatic rib fractures were published at home and abroad, focusing on the guidance of the overall treatment decisions and plans; another clinical guideline about the surgical treatment of rib fractures lacks recent related progress in surgical treatment of rib fractures. The Chinese Society of Traumatology, Chinese Medical Association, and the Chinese College of Trauma Surgeons, Chinese Medical Doctor Association organized experts from cardiothoracic surgery, trauma surgery, acute care surgery, orthopedics and other disciplines to participate together, following the principle of evidence-based medicine and in line with the scientific nature and practicality, formulated the Chinese consensus for surgical treatment of traumatic rib fractures (STTRF 2021). This expert consensus put forward some clear, applicable, and graded recommendations from seven aspects: preoperative imaging evaluation, surgical indications, timing of surgery, surgical methods, rib fracture sites for surgical fixation, internal fixation method and material selection, treatment of combined injuries in rib fractures, in order to provide guidance and reference for surgical treatment of traumatic rib fractures.

Decellularization method based on trypsin-digestion is widely used to construct small diameter vascular grafts. However, this method will reduce the opening angle of the blood vessel and result in the reduction of residual stress. Residual stress reduced has an adverse effect on the compliance and permeability of small diameter vascular grafts. To improve the situation, acellular blood vessels were treated with glutaraldehyde and photooxidation crosslinking respectively, and the changes of opening angle, circumferential residual strain of native blood vessels, decellularized arteries and crosslinked blood vessels were measured by means of histological examination, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) in this study. The opening angle of decellularized arteries significantly restored after photooxidation crosslinking (P=0.0216), while that of glutaraldehyde crosslinking blood vessels reduced. The elastic fibers inside the blood vessels became densely rearranged after photooxidation crosslinking. The results of finite element simulation showed that the residual stress increased with the increase of opening angle. In this study, we found at the first time that photooxidation crosslinking method could significantly increase the residual stress of decellularized vessels, which provides biomechanical support for the development of new biomaterials of vascular grafts.

AbstractBackgroundS100 calcium binding protein A9 (S100A9) is a pro-inflammatory alarmin associated with several inflammation-related diseases. However, the role of S100A9 in lung injury in sepsis has not been fully investigated. Therefore, the present study aimed to determine the role of S100A9 in a lipopolysaccharide (LPS)-induced lung injury murine model and its underlying molecular mechanisms.MethodsLPS was utilized to induce sepsis and lung injury in C57BL/6 or NOD-like receptor family pyrin domain containing 3 (NLRP3)−/−mice. To investigate the effects of S100A9 blockade, mice were treated with a specific inhibitor of S100A9. Subsequently, lung injury and inflammation were evaluated by histology and enzyme‑linked immunosorbent assay (ELISA), respectively. Furthermore, western blot analysis and RT-qPCR were carried out to investigate the molecular mechanisms underlying the effects of S100A9.ResultsS100A9 was upregulated in the lung tissues of LPS-treated mice. However, inhibition of S100A9 alleviated LPS-induced lung injury. Additionally, S100A9 blockade also attenuated the inflammatory responses and apoptosis in the lungs of LPS-challenged mice. Furthermore, the increased expression of NLRP3 was also suppressed by S100A9 blockade, while S100A9 blockade had no effect on NLRP3−/−mice. In vitro, S100A9 downregulation mitigated LPS-induced inflammation. Interestingly, these effects were blunted by NLRP3 overexpression.ConclusionThe results of the current study suggested that inhibition of S100A9 could protect against LPS-induced lung injury via inhibiting the NLRP3 pathway. Therefore, S100A9 blockade could be considered as a novel therapeutic strategy for lung injury in sepsis.