Single-cell RNA sequencing reveals immune cell dysfunction in the peripheral blood of patients with highly aggressive gastric cancer.

Highly aggressive gastric cancer (HAGC) is a gastric cancer characterized by bone marrow metastasis and disseminated intravascular coagulation (DIC). Information about the disease is limited. Here we employed single-cell RNA sequencing to investigate peripheral blood mononuclear cells (PBMCs), aiming to unravel the immune response of patients toward HAGC. PBMCs from seven HAGC patients, six normal advanced gastric cancer (NAGC) patients, and five healthy individuals were analysed by single-cell RNA sequencing. The expression of genes of interest was validated by bulk RNA-sequencing and ELISA. We found a massive expansion of neutrophils in PBMCs of HAGC. These neutrophils are activated, but immature. Besides, mononuclear phagocytes exhibited an M2-like signature and T cells were suppressed and reduced in number. Analysis of cell-cell crosstalk revealed that several signalling pathways involved in neutrophil to T-cell suppression including APP-CD74, MIF-(CD74+CXCR2), and MIF-(CD74+CD44) pathways were increased in HAGC. NETosis-associated genes S100A8 and S100A9 as well as VEGF, PDGF, FGF, and NOTCH signalling that contribute to DIC development were upregulated in HAGC too. This study reveals significant changes in the distribution and interactions of the PBMC subsets and provides valuable insight into the immune response in patients with HAGC. S100A8 and S100A9 are highly expressed in HAGC neutrophils, suggesting their potential to be used as novel diagnostic and therapeutic targets for HAGC.

Effect of electroacupuncture at "Neiguan" (PC 6) and "Zusanli" (ST 36) on gastrointestinal hormone in the antral tissue of rats with functional dyspepsia. / 电针"å† å ³""足三里"å¯¹åŠŸèƒ½æ€§æ¶ˆåŒ–ä¸è‰¯å¤§é¼ èƒƒçª¦ç»„ç»‡èƒƒè‚ æ¿€ç´ çš„å½±å“.

OBJECTIVES: To observe the effects of electroacupuncture (EA) at "Neiguan" (PC 6) and "Zusanli"(ST 36) on the gastric emptying rate, the level of serotonin (5-HT) and the protein expression of motilin (MTL), ghrelin, substance P (SP) and vasoactive intestinal peptide (VIP) in the antral tissue of the rats with functional dyspepsia (FD) and explore the effect mechanism of EA in treatment of FD. METHODS: A total of 21 SPF male SD rat pups were randomly divided into a normal group, a model group and an EA group, with 7 rats in each group. In the model group and the EA group, FD model was prepared by the gavage with 0.1% sucrose iodoacetamide solution combined with the modified small platform method. After the successful modeling, EA was applied to "Neiguan" (PC 6) and "Zusanli"(ST 36) in the rats of the EA group, with disperse-dense wave, 20 Hz/100 Hz in frequency, stimulated for 30 min, once daily, for 7 days consecutively. Before and after intervention, the general condition of the rats was observed in each group. After the completion of intervention, the gastric emptying rate was measured, the morphological changes of gastric antral tissue were observed using HE staining, the level of 5-HT was detected with ELISA method, and the protein expression of MTL, ghrelin, SP, and VIP was determined with Western blot method in the antral tissue of rats. RESULTS: In the normal group, the rats were in a good mental state, with lustrous fur, flexible movement and the increase of food intake and body mass. In the model group, the rats were poor in mental state, lack of lustre in fur, preference for the body curled up, reduced activity and response; and a part of rats had loose stool, obviously enlarged gastric body and gastric food retention. In the EA group, the general condition of rats, e.g. the mental state, food intake and activity, were improved, the gastric body got smaller obviously and the gastric food retention was reduced when compared with the model group. The antral structure was intact, the glands were rich and no injury of the gastric mucosa was found, e.g. inflammatory reaction and edema in the rats of each group. Compared with the normal group, the gastric emptying rate was decreased (P<0.01), 5-HT level was increased (P<0.01), the protein expression of MTL and ghrelin was reduced (P<0.01) and that of VIP was elevated (P<0.01) in the rats of the model group. The gastric emptying rate was increased (P<0.01), 5-HT level was decreased (P<0.01), and the protein expression of MTL and ghrelin was elevated (P<0.05, P<0.01) in the rats of the EA group when compared with those in the model group. CONCLUSIONS: Electroacupuncture at "Neiguan" (PC 6) and "Zusanli"(ST 36) may effectively relieve gastric dysfunction, strengthen gastric motility and promote gastric emptying so as to alleviate the symptoms of dyspepsia in FD rats, and its mechanism may be related to the regulation of gastrointestinal hormones in the antral tissue.

Induction of filopodia formation by α-Actinin-2 via RelA with a feedforward activation loop promoting overt bone marrow metastasis of gastric cancer.

BACKGROUND: Bone marrow metastasis (BMM) is underestimated in gastric cancer (GC). GC with BMM frequently complicate critical hematological abnormalities like diffused intravascular coagulation and microangiopathic hemolytic anemia, which constitute a highly aggressive GC (HAGC) subtype. HAGC present a very poor prognosis with peculiar clinical and pathological features when compared with not otherwise specified advanced GC (NAGC). But the molecular mechanisms underlying BMM from GC remain rudimentary. METHODS: The transcriptomic difference between HAGC and NAGC were analyzed. Genes that were specifically upregulated in HAGC were identified, and their effect on cell migration and invasion was studied. The function of ACTN2 gene were confirmed by GC cell lines, bone-metastatic animal model and patients' tissues. Furthermore, the molecular mechanism of ACTN2 derived-BMM was explored by multiple immunofluorescence staining, western blot, chromatin immunoprecipitation, and luciferase reporter assays. RESULTS: We elucidated the key mechanisms of BMM depending on the transcriptomic difference between HAGC and NAGC. Five genes specifically upregulated in HAGC were assessed their effect on cell migration and invasion. The ACTN2 gene encoding protein α-Actinin-2 was detected enhanced the metastatic capability and induced BMM of GC cells in mouse models. Mechanically, α-Actinin-2 was involved in filopodia formation where it promoted the Actin filament cross-linking by replacing α-Actinin-1 to form α-Actinin-2:α-Actinin-4 complexes in GC cells. Moreover, NF-κB subunit RelA and α-Actinin-2 formed heterotrimers in the nuclei of GC cells. As a direct target of RelA:α-Actinin-2 heterotrimers, the ACTN2 gene was a positive auto-regulatory loop for α-Actinin-2 expression. CONCLUSIONS: We demonstrated a link between filopodia, BMM and ACTN2 activation, where a feedforward activation loop between ACTN2 and RelA is established via actin in response to distant metastasis. Given the novel filopodia formation function and the new mechanism of BMM in GC, we propose ACTN2 as a druggable molecular vulnerability that may provide potential therapeutic benefit against BMM of GC.

A novel intergenic region (chr2: 30,193,816)-ALK fusion shows sensitivity to Alectinib in lung adenocarcinoma.

BACKGROUND: Anaplastic lymphoma kinase (ALK) rearrangement, which is mostly showed as fused with echinoderm microtubule-associated protein-like 4 gene (EML4), accounts 3-7% of all common mutations in non-small lung cancer (NSCLC). An intergenic region (chr2: 30,193,816), which located on upstream of the adjacent ALK gene, was never been reported as a ALK patterner before. CASE PRESENTATION: A 56-year-old female patient who had symptoms of persistent cough and shortness of breath visited our facility on April 24, 2022. The chest computerized tomography (CT) examination revealed a massive right hydrothorax. After draining pleural effusion, a hilar mass accompanied multiple nodules in both lungs could been seen in image. Tracheoscopy revealed neoplasm in the medial segment of the middle lobe of the right lung, and the patient was diagnosed as lung adenocarcinoma pathologically. It tested positive for cytokeratin (CK) 7, NapsinA, ALK, and thyroid transcription factor-1 (TTF-1). Next generation sequence testing confirmed the presence of the intergenic region (chr2: 30,193,816)-ALK fusion in the tumor tissue. The patient was subsequently treated with Alectinib, and her symptoms are obviously relieved, the right hilar mass and metastatic nodule were reduced in the reexamination after three months. CONCLUSIONS: The intergenic region (chr2: 30,193,816)-ALK fusion, which is firstly reported in lung adenocarcinoma, is a mutation with expression significance. It shows sensitivity to Alectinib.

Comparison Between Percutaneous Endoscopic Gastrostomy and Nasogastric Feeding in 160 Patients with Swallowing Disturbances: A Two-Year Follow-Up Study.

Purpose: We retrospectively compared the complications, blood biochemical indexes and outcomes in patients with swallowing disturbances receiving nasogastric tube (NGT) feeding and percutaneous endoscopy gastrostomy (PEG). Methods: Among 160 patients, 72 cases received PEG and 88 cases received NGT. All patients were followed up for two years. We collected their clinical data from the medical records. Indicators, such as body mass index (BMI), white blood cell (WBC), hemoglobin (HGB), complications, including recurrent aspiration pneumonia, gastrointestinal bleeding, reflux esophagitis, and outcomes (survival or death) were compared between the two groups semi-annually. Results: SAt both six months and one year after receiving treatment, there was no statistical difference between the two groups in indicators, complications and outcomes, with all P >0.05. It can be seen that, when the patients were followed up for one and a half years18 months, ALB was lower in the NGT group (33.81±0.46) compared with the PEG group (36.14±0.50) (P <0.05). After two years of follow-up, differences between the NGT and PEG group could be seen in a variety of indicators, including BMI (20.08±0.27 vs 21.03±0.25), WBC (9.12±0.56 vs 7.08±0.29), ALB (33.11±0.43 vs 35.75±0.49), creatinine (55.07±1.83 vs 63.21±2.94), and the complications, such as aspiration pneumonia, gastrointestinal bleeding, reflux esophagitis, and electrolyte disorder, in the PEG group were significantly reduced compared to the NGT groupthan that in its counterpart, P <0.05. In the two-year follow-up period, there were 13 and 22 patients died in the PEG group and NGT group, respectively. Conclusion: Both techniques are safe and effective in the short term. However, on a longer-term basis, PEG is shown to be superior to NGT feeding in improving nutrition and preventing common complications for patients with swallowing disturbances.

Intravenous Hemostats: Foundation, Targeting, and Controlled-Release.

Uncontrollable blood loss is the greatest cause of mortality in prehospital patients and the main source of disability and death in hospital care. Compared with external hemostats, intravenous hemostats are more appropriate for preventing and treating uncontrolled bleeding in vivo and large bleeding on the body surface. This Review initially establishes intravenous hemostats' response basis, including the coagulation mechanism, fibrinolytic pathway, and protein corona. Second, the study of advancement of intravenous hemostat targeting was expanded from two perspectives, cellular hemostatic agents and synthetic hemostatic agents. Meanwhile, after discussing the progress of controlled-release intravenous hemostats with platelets as the stimuli, this Review offers insight into the possibility of controlled-release intravenous hemostats with microenvironment as the stimuli, combining the studies of controlled-release targeted thrombolysis.

Value of ultrasonography in determining the nature of pleural effusion: Analysis of 582 cases.

To explore the value of ultrasonography in the auxiliary diagnosis of pleural effusion, we retrospectively analyzed the ultrasonographic findings of 275 exudates and 307 transudates and summarized the ultrasonographic image features of pleural effusion according to patients' primary diseases. The findings of thoracic ultrasonography performed before the initial thoracentesis in 582 patients with subsequently confirmed exudative/transudative pleural effusion were analyzed with regard to the sonographic features of pleural effusion. In 275 cases with exudates, thoracic ultrasonography showed a complex septate appearance in 19 cases (6.9%), complex nonseptate appearance in 100 cases (36.4%), complex homogenous sign in 46 cases (16.7%), and pleural thickness > 3 mm in 105 cases. In contrast, in 307 patients with transudates, most patients (97.1%) had bilateral pleural effusion. Ultrasonographic images displayed anechoic appearance and absence of pleural thickening in a vast majority of cases (306, 99.7%; 301, 98%). These positive findings in the exudate were statistically higher than those in their counterparts (P < .05). In the empyema subgroup, the proportion of complex septate appearance, complex nonseptate appearance, complex homogenous sign, and pleural thickening was the highest, at 19/41, 12/41, 10/41, and 30/41, respectively. Ultrasonography is valuable in defining the nature of pleural effusion. Some sonographic features of pleural effusion, such as echogenicity, septation, and pleural thickening, may indicate a high risk of exudative pleural effusion.

Practical Security of High-Dimensional Quantum Key Distribution with Intensity Modulator Extinction.

Quantum key distribution (QKD) has attracted much attention due to its unconditional security. High-dimensional quantum key distribution (HD-QKD) is a brand-new type of QKD protocol that has many excellent advantages. Nonetheless, practical imperfections in realistic devices that are not considered in the theoretical security proof may have an impact on the practical security of realistic HD-QKD systems. In this paper, we research the influence of a realistic intensity modulator on the practical security of HD-QKD systems with the decoy-state method and finite-key effects. We demonstrate that there is a certain impact in the secret key rate and the transmission distance when taking practical factors into security analysis.

Dasatinib protects against acute respiratory distress syndrome via Nrf2-regulated M2 macrophages polarization.

Dasatinib, a tyrosine kinase inhibitor, has a protective effect on experimental acute respiratory distress syndrome (ARDS). This study investigated the effect and mechanism of dasatinib in ARDS. C57BL/6 mice were administered with dasatinib (1 and 10 mg/kg) after lipopolysaccharide (LPS) treatment to evaluate the effect of dasatinib on white blood cells (WBC), neutrophils, lymphocytes and macrophages in bronchoalveolar lavage fluid (BALF). The levels and mRNA expressions of inflammation-related cytokines in lung tissues and RAW 264.7 cells were detected by enzyme-linked immunosorbent assay and quantitative real-time PCR, respectively. The protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO1) were determined by Western blot. MTT assay was performed to detect the viability of RAW 264.7 cell. Rescue experiments were used to assess the effect of Nrf2 silencing on the LPS- and dasatinib-treated mice. Under LPS treatment, levels of the WBC, neutrophils, lymphocytes and macrophages in BALF and mRNA expressions of IL-6, TNF-α and IL-10 as well as expression of iNOS were increased, but the expression of arginase-1 was inhibited, while no obvious changes of the protein expressions of Nrf2 and HO1 were observed. Dasatinib partially reversed the effects of LPS above, and further promoted the mRNA expression of IL-10 and the protein expressions of Nrf2 and HO1, while Nrf2 silencing counteracted the effect of dasatinib. Dasatinib induced the polarization of M2 subtype of macrophages and alleviated LPS-induced ARDS through activating Nrf2 signaling pathway, which may provide a new strategy for the treatment of ARDS.

The S100 protein family in lung cancer.

The S100 protein family is involved in the pathogenesis of several malignancies including lung cancer. Recent studies have shown that one member, S100A2, was over-expressed in advanced stage non-small cell lung cancer (NSCLC). Another, S100A6, demonstrated variable expression in different lung cancer subtypes. Research using NSCLC cell lines reported that SIX3 inhibited cell metastasis and proliferation via S100P down-regulation. This review represents an update on S100 proteins in lung cancer from 2017 to 2021 and includes the aforementioned as well as S100A4, S100A7, and S100B. Inconsistencies in mechanisms of action for S100A8/S100A9 are highlighted and a comprehensive evaluation of the most recent evidence for the S100 proteins in lung cancer is presented.

S100A6 represses Calu-6 lung cancer cells growth via inhibiting cell proliferation, migration, invasion and enhancing apoptosis.

S100 calcium binding protein A6 (S100A6) has been reported to involve in many kinds of cancers through regulating intracellular calcium homeostasis. Previous studies found that S100A6 increased in lung cancer patients' plasma and pleural effusion. This study focused on its function in Calu-6 lung cancer cells. S100A6 gene was transferred into Calu-6 lung cancer cell line by lentivirus vector, the empty vector transfected cells and the blank cells were set as control groups. MTT was evaluating cell proliferation. The transwell assay was reflecting cell migration and cell invasion. The flow cytometric analysis was detecting cell apoptosis and cell cycle of three groups (Calu-6, Calu-6/neo, Calu-6/S100A6). Nude mouse tumorigenicity was then applied to evaluate S100A6's effect on cellular tumorigenicity. Compared with control groups, Calu-6/S100A6 cells showed a weakening trend in the cell behaviours of proliferation, migration and invasiveness, while had an enhancement of cell apoptosis, with all P < .05. The cell cycle of Calu-6/S100A6 cells had a reduction of S phase and an increase of G1 phase (P < .05). In animal study, after 5 weeks of cell injection, the tumour bulk of Calu-6/S100A6 group was smaller than controls, with P < .05. Our results demonstrate S100A6 inhibits the growth of Calu-6 lung cancer cells, as well as impairs Calu-6's ability in tumorigenesis. At cellular level, S100A6 is supposed to act as a tumour suppressor gene in lung cancer.

T cell-derived exosomes induced macrophage inflammatory protein-1α/ß drive the trafficking of CD8+ T cells in oral lichen planus.

Oral lichen planus (OLP) is a T cell-mediated chronic inflammatory disease with uncertain aetiology. Exosomes are nanosized particles with biological capacities. Here, we aimed to study the effects of T cell-derived exosomes (T-exos) on the pathogenesis of OLP and its mechanism. T-exos were incubated with Jurkat cells for 48 hours, and 26 cytokines in the supernatant were measured by luminex assay. The expression of macrophage inflammatory protein (MIP)-1α/ß was detected using immunohistochemistry and ELISA; that of CCR1/3/5 on peripheral T cells was determined by flow cytometry. Transwell assay was performed to investigate the chemotactic effect of MIP-1α/ß, and cells in the lower chambers were examinated by flow cytometry. As a result, OLP T-exos elevated the production of MIP-1α/ß, which were highly expressed in OLP tissues and plasma. CCR1/5 were markedly expressed on OLP peripheral T cells, and the majority of CCR1/5+ T cells were CD8+ T cells. Besides, MIP-1α/ß promoted the migration of OLP mononuclear cells, while inhibiting CCR1/5 significantly decreased the trafficking of mononuclear cells, especially that of CD8+ T cells. Conclusively, OLP T-exos-induced MIP-1α/ß may drive the trafficking of CD8+ T cells after binding with CCR1/5 in OLP, contributing to the development of OLP.

Correction: A rapid hemostatic sponge based on large, mesoporous silica nanoparticles and N-alkylated chitosan.

Correction for 'A rapid hemostatic sponge based on large, mesoporous silica nanoparticles and N-alkylated chitosan' by Zihao Chen et al., Nanoscale, 2018, 10, 20234-20245, DOI: .

A rapid hemostatic sponge based on large, mesoporous silica nanoparticles and N-alkylated chitosan.

Rapid bleeding control is increasingly important in current civilian and military emergency medicine, but the rapid hemostasis achieved with current hemostatic products is often unsafe. In this study, mesoporous silica nanoparticles (MSNs) with large pores were coordinated with a glycerol-modified N-alkylated chitosan sponge (GACS) to develop a rapid and safe hemostatic sponge. Due to its coagulation-promoting structure, MSN-GACS exhibited unique hemostatic potency in serial in vitro coagulation tests. In addition to enhanced platelet adhesion and whole blood absorption, MSN-GACS exhibited better biocompatibility than Combat Gauze (CG), which is popular in the US military. Furthermore, in rabbit femoral artery and liver injury in vivo models, MSN-GACS showed better hemostatic efficiency and lower cardiovascular toxicity than CG. In conclusion, MSN-GACS is an excellent prehospital hemostatic agent for first-aid applications.

Activated Akt/mTOR-autophagy in local T cells of oral lichen planus.

Oral lichen planus (OLP) is a chronic inflammatory disease regulated by T cell-mediated immune response. Autophagy and its major inhibitory pathway Akt/mTOR participate in T cell metabolism and homeostasis, which has been implicated in autoimmune diseases. In this study, the potential involvement of autophagy and its regulatory Akt/mTOR pathway were investigated in local T cells of OLP. The expression of Akt/mTOR pathway and autophagy-related proteins in OLP local lesions, as well as in T cells, were measured by immunohistochemistry and double-labeling immunofluorescence, respectively. Furthermore, the associations of p-Akt, p-mTOR, ULK1, and LC3B expression with RAE scores representing the disease severity of OLP were assessed. The expression of p-Akt, p-mTOR, ULK1, and LC3B in OLP lesions, as well as in local T cells, was significantly increased compared with that in controls. In addition, the level of LC3B was negatively correlated with RAE scores of OLP, and LC3B was higher in nonerosive OLP than erosive ones and controls. Our results suggested that activated Akt/mTOR-autophagy may have a role in the local T cell-mediated immunoregulatory mechanism of OLP. LC3B might be a valuable marker to monitor the disease severity of OLP.

Increased circulating CXCR5+ CD4+ T follicular helper-like cells in oral lichen planus.

BACKGROUND: CD4+ T-helper cell is crucial for the inflammatory autoimmune condition of oral lichen planus (OLP). Recently, the pathogenetic functions of T follicular helper (Tfh) cells, a subtype of CD4+ T-helper cells, have been revealed in autoimmune diseases for their pivotal regulation on humoral immunity. To explore the potential pathophysiological role of Tfh cells in OLP, the expression of circulating Tfh-like cells and its correlations with IL-21 and B cells were investigated. METHODS: The frequencies of CXCR5+ CD4+ Tfh-like cells and CD19+ B cells were analyzed in peripheral blood of patients with OLP and controls by flow cytometry, respectively. Besides, the serum IL-21 concentration was measured using ELISA technology. Furthermore, the correlations of CXCR5+ CD4+ Tfh-like cells with CD19+ B cells and serum IL-21 expression levels were evaluated. RESULTS: This study showed significant increased circulating Tfh-like cells (P < 0.05) and B cells (P < 0.0001), as well as decreased serum IL-21 expression (P < 0.001) in OLP. Besides, the frequency of Tfh-like cells exhibited negative correlation with B cells in OLP (r = -0.435, P < 0.05). In particular, the proportion of CXCR5+ CD4+ Tfh-like cells in peripheral blood mononuclear cells of erosive OLP was higher than non-erosive OLP and controls (P = 0.012 and 0.021, respectively). CONCLUSIONS: Increased circulating Tfh-like cells may be involved in the pathogenesis of OLP through abnormal modulation on B-cell proliferation and IL-21 production, and associated with different clinical forms of OLP.

TLR4-induced B7-H1 on keratinocytes negatively regulates CD4+ T cells and CD8+ T cells responses in oral lichen planus.

Oral lichen planus (OLP) is a T-cell-mediated autoimmune mucocutaneous disease affected by the interactions among the keratinocytes, CD4+ T cells and CD8+ T cells. B7-H1 induced by Toll-like receptors (TLRs) can suppress T-cell immune reaction, thereby resulting in immune tolerance. However, the role of TLR-mediated B7-H1 on keratinocytes in the immune response of OLP is still unknown. The present study showed that TLR4 could induce time-coursed B7-H1 expression on oral keratinocytes, and blocking NF-κB or PI3K/mTOR pathway downregulated B7-H1 transcriptional expression. Moreover, TLR4-stimulated oral keratinocytes inhibited the proliferation of OLP CD4+ T cells and OLP CD8+ T cells, and simultaneously prompted their apoptosis. Blockade of keratinocyte-associated B7-H1 restored the declined proliferation of OLP CD4+ T cells and OLP CD8+ T cells, and prevented their increased apoptosis. Therefore, TLR4-upregulated B7-H1 on keratinocytes could decelerate immune responses of CD4+ T cells and CD8+ T cells in OLP.

Altered Autophagy-Associated Genes Expression in T Cells of Oral Lichen Planus Correlated with Clinical Features.

Oral lichen planus (OLP) is a T cell-mediated inflammatory autoimmune disease. Autophagy has emerged as a fundamental trafficking event in mediating T cell response, which plays crucial roles in innate and adaptive immunity. The present study mainly investigated the mRNA expression of autophagy-associated genes in peripheral blood T cells of OLP patients and evaluated correlations between their expression and the clinical features of OLP. Five differentially expressed autophagy-associated genes were identified by autophagy array. Quantitative real-time RT-PCR results confirmed that IGF1 expression in the peripheral blood T cells of OLP patients was significantly higher than that in controls, especially in female and middle-aged (30-50 years old) OLP patients. In addition, ATG9B mRNA levels were significantly lower in nonerosive OLP patients. However, no significant differences were found in the expression of HGS, ESR1, and SNCA between OLP patients and controls. Taken together, dysregulation of T cell autophagy may be involved in immune response of OLP and may be correlated with clinical patterns.

Blood clot initiation by mesoporous silica nanoparticles: dependence on pore size or particle size?

Mesoporous silica nanoparticles (MSNs) with controllable pore size and particle size were prepared using a vesicle-organic template method. Transmission electron microscopy (TEM), nitrogen adsorption measurements, X-ray diffraction (XRD) and Fourier transform infrared (FTIR) spectra were used to characterize the coagulation-promoting surface chemistry, topologies and porous structure of the MSNs. The clotting blood tests (CBTs) showed that the pore sizes of the MSNs varying from 5 nm to 15 nm greatly affected the blood clot rate of rabbit plasma, while variation of the particle size from 60 nm to 220 nm had little influence on coagulation. Associated with the blood coagulation factor XII (FXII) tests, it could be inferred that the accessibility and diffusion of clotting were mainly dependent on the pore size of the MSNs. Proper pore size could readily promote the blood proteins to contact the huge interior surfaces of the MSNs and then initiate the quick blood clot. Furthermore, the perfect biocompatibility of the MSNs was achieved through a CCK-8 and cellular uptake study, indicating that cell viability could be promoted by MSNs and MSNs with larger pore size showed better biocompatibility. Rapid hemostasis in rabbit femoral artery injury testified the superb hemostatic efficiency of the MSNs. We demonstrated that MSNs with a pore size of 15 nm showed the best hemostatic efficiency and it would be probably an optimal candidate for the first aid of hemorrhage in the field or pre-hospital.