Knowledge mapping of surgical smoke from 2003 to 2022: a bibliometric analysis.

PURPOSE: The purpose of this study is to identify and characterize the literature on surgical smoke, visualize the data and sketch a certain trending outline. METHODS: In the Web of Science Core Collection (WoSCC), all the data were acquired from January 1st 2003 to December 31st 2022. VOSviewer and CiteSpace were employed to visualize data, based on publications, bibliographic coupling, co-citation, or co-authorship relations. Microsoft Excel 2019 was used to comb and categorize all the statistics. RESULT: A total 363 of journal papers were retrieved. The publication number was in a slow but steady growth between 2003 and 2019, followed by a sharp surge in 2020, and then the publication kept in a productive way. Surgical endoscopy and other interventional techniques was the most active journal on surgical smoke. USA played an important role among all the countries/regions. There were 1847 authors for these 363 papers, among whom 44 authors published more than three articles on surgical smoke. "Surgical smoke", "covid-19" and "surgery" were the top 3 appeared keywords, while the latest hot-spot keywords were "COVID-19", "virus", "transmission", "exposure" and "risk". There were 1105 co-cited references and 3786 links appeared in all 363 articles. Among them, 38 references are cited more than 10 times. The most co-cited article was "Detecting hepatitis B virus in surgical smoke emitted during laparoscopic surgery." Based on the titles of references and calculated by CiteSpace, the top 3 cluster trend network are "laparoscopic surgery", "COVID-19 pandemic" and "surgical smoke". CONCLUSION: According to bibliometric analysis, the research on surgical smoke has been drawing attention of more scholars in the world. Increasing number of countries or regions added in this field, and among them, USA, Italy, and China has been playing important roles, however, more wide and intense cooperation is still in expectation.

M-CSF secreted by gastric cancer cells exacerbates the progression of gastric cancer by increasing the expression of SHP2 in tumor-associated macrophages.

OBJECTIVE: To investigate the effect of Src homology 2 domain-containing tyrosine phosphatase-2 (SHP2) in tumor-associated macrophages (TAMs), which is mediated by macrophage colony-stimulating factor (M-CSF) secreted by gastric cancer cells, on the development of gastric cancer and its molecular mechanism. METHODS: The progression of gastric cancer was detected by nude mouse tumor-bearing experiments. Colony formation assay and cell counting kit-8 (CCK8) assay were used to detect the proliferation capacity of gastric cancer cells. The migration capacity of gastric cancer cells was examined by wound healing assay. Transwell migration and invasion assays were performed on gastric cancer cells. Detection of relevant protein expression using western blotting. RESULTS: Overexpression of SHP2 could promote the progression of gastric cancer in nude mice. The results of colony formation assay and CCK8 assay showed that overexpression of SHP2 could enhance the proliferation of gastric cancer cells. It was found by wound healing assay and Transwell assay that overexpression of SHP2 could facilitate the migration and invasion of gastric cancer cells. The results of Western blotting revealed that overexpression of SHP2 could increase the expressions of p-STAT3, s-PD-1, p-Src, p-Lyn, p-PI3K, p-AKT, Arginase-1, MMP1 and MMP3 but decrease the expressions of TBK1 and SOCS1 in TAMs, and also increase the expressions of CD9, TSG101 and s-PD-1 in exosomes. CONCLUSION: M-CSF secreted by gastric cancer cells can promote the proliferation, invasion and migration of gastric cancer cells by increasing the expression of SHP2 in TAMs.

The effect and mechanism of dl-3-n-butylphthalide on angiogenesis in a rat model of chronic myocardial ischemia.

OBJECTIVE: To assess the effect of dl-3-n-butylphthalide (NBP) on angiogenesis and its underlying mechanism in a rat model of chronic myocardial ischemia (CMI). METHODS: Forty Sprague-Dawley rats were randomly divided into four groups: model, low-dose NBP (L-NBP), middle-dose NBP (M-NBP), or high-dose NBP (H-NBP) (n=10/group). All groups received intraperitoneal injections of isoprinosine hydrochloride daily for 14 days. Additionally, the L-NBP, M-NBP, and H-NBP groups received NBP at 3, 6, and 12 mg per kg body weight, respectively, by intraperitoneal injection. An additional 10 rats (control group) received 0.9% sodium chloride via intraperitoneal injection for 14 consecutive days. Echocardiography was used for the measurement of heart function. Immunohistochemical staining for factor VIII-related antigen and microvascular density determination were performed. The protein and mRNA expression of hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in CMI areas were measured by western blot and RT-PCR, respectively. RESULTS: Electrocardiograms showed that NBP improved cardiac function by regulating left ventricular end-diastolic and end-systolic diameters, ejection fraction, and fractional shortening. Compared with the control and model groups, the L-NBP, M-NBP, and H-NBP groups showed increased mRNA and protein expression of VEGFA and HIF-1α in myocardial tissue. The mRNA and protein expression of VEGFA and HIF-α in the H-NBP group were the highest. CONCLUSION: NBP treatment promotes VEGF and HIF-1α protein expression during myocardial ischemia, which may represent useful biomarkers for coronary collateral establishment and offer potential targets for therapeutic induction of angiogenesis in patients with CMI.

Inhibitory effect of siRNA-Annexin A7 on growth, migration, and invasion in BGC823 cells and gastric cancer xenograftsin nude mice.

OBJECTIVE: To explore the inhibitory effect of siRNA-Annexin A7 on growth, migration, and invasion of transplanted gastric cancer in nude mice. METHODS: The siRNA sequence targeting to human Annexin A7 gene was designed, and based on that a pair of complementary oligonucleotides were synthesized, annealed, and cloned into plasmid pGenesil-1.1 to construct recombinant plasmid siRNA-Annexin A7. Transplanted gastric cancer model was established by injecting s.c. nude mice with human gastric cancer BGC823 cells, and siRNA-Annexin A7 was injected into the tumors formed. The nude mice were observed for clinical manifestation relying on the size and weight of transplanted tumors. The tumor tissue and angiogenesis were examined by pathologic sections. Flow cytometry was used to detect the changes of cell cycle. Western blot and qRT-PCR were used to analyze the expression of PCNA, P27, MMP-2, and TIMP-2. RESULTS: Both the size and weight of transplanted tumors of nude mice injected with siRNA-Annexin A7 were less than those of control groups (P<0.05). The examination of pathologic sections showed that, compared with in the control group, obvious necrosis of tumor cells was observed in siRNA-Annexin A7 group. The cells in stage S were fewer in siRNA-Annexin A7 group than those in the other two groups, while the cells in stage G0/G1 were much more in siRNA-Annexin A7 group. The results of western blot and qRT-PCR confirmed that the expression of PCNA and MMP-2 was down-regulated, whereas the expression of p27 was up-regulated. CONCLUSION: Gastric cancer xenografts were established in nude mice with human gastric cancer BGC823 cells. The volume and weight of tumor were decreased after inhibition of Annexin A7 expression in BGC823 cells. Tumor cells were arranged sparsely after inhibition of Annexin A7 expression in BGC823 cells. The siRNA-Annexin A7 inhibits Annexin A7 expression in transplanted gastric cancer of nude mice, and influences the growth, migration, and invasion of tumors by down-regulating the expression of PCNA and MMP-2, as well as up-regulating the expression of p27.

Downregulation of annexin A7 decreases proliferation, migration, and invasion of gastric cancer cells by reducing matrix metalloproteinase 1 and 9 expression.

High annexin A7 expression is a potential indicator of lymphatic metastasis and poor prognosis in patients with gastric cancer (GC). The mechanism underlying the effects of annexin A7 on GC cells remains unclear. In patients with GC, primary adenocarcinoma tissues had higher annexin A7 expression than adjacent non-cancerous tissues (P < 0.05). Among three human GC cell lines with high, moderate, and low levels of differentiation, respectively, the cell line with the lowest level of differentiation displayed the highest level of annexin A7 expression. We transfected cells of the human GC cell line BGC823 with short interfering RNAs (siRNAs) targeting annexin A7 and investigated the effects on signaling pathways related to cancer progression by quantitative real-time PCR and western blot. The silencing of endogenous annexin A7 suppressed the proliferation, migration, and invasion abilities of the BGC823 cells. In the cells treated with annexin A7 siRNA, the expression of p16, p21, and p27 was significantly upregulated while that of proliferating cell nuclear antigen (PCNA), cyclin A, cyclin D1, cyclin E1, matrix metalloproteinase-2 (MMP-2), MMP-9, and intercellular cell-adhesion molecule-1 (ICAM-1) was significantly downregulated compared with that in control cells. Our results suggest that the downregulation of endogenous annexin A7 inhibits GC cell proliferation, migration, and invasion by impacting cell cycle regulators and the expression of MMP-1, MMP-2, and ICAM-1. Targeting annexin A7 may represent a valuable strategy for the diagnosis and clinical treatment of GC.

Associations between Single Nucleotide Polymorphisms in the Mitochondrial DNA D-Loop Region and Outcome of Gastroenteropancreatic Neuroendocrine Neoplasm.

Accumulation of single-nucleotide polymorphisms (SNPs) in the displacement loop (D-loop) of mitochondrial DNA (mtDNA) may be associated with cancer risk and disease outcome. We evaluated the predictive value of these SNPs for GEP-NEN outcome. Three SNP sites of nucleotides 16257C/A, 150C/T and 151C/Tdel were identified for statistically significant prediction of postoperative survival in GEP-NEN by univariate analysis with log-rank test. In addition, the minor haplotype of nucleotides 16257A in the hypervariable segment 1(HV1) region of the D-loop was identified for their association with lower survival rate of GEP-NEN (relative risk, 3.390; 95% CI, 1.071~10.729; p=0.038) by multivariate analysis with COX hazards model. The analysis of genetic polymorphisms in the mitochondrial D-loop can help identify patient subgroups with a high risk of GEP-NEN outcome.

Annexin A7 expression is downregulated in late-stage gastric cancer and is negatively correlated with the differentiation grade and apoptosis rate.

Annexin A7 is a member of the Annexin A family, which participates in various biological processes. Accumulating evidence has demonstrated that Annexin A7 serves an important role in tumorigenesis and is dysregulated in multiple types of cancer. However, the role of Annexin A7 in the tumorigenesis of gastric cancer remains to be determined. The present study revealed that Annexin A7 expression is downregulated in late-stage gastric cancer and is negatively correlated with the differentiation grade and apoptosis. There was a significant difference in Annexin A7 mRNA and protein expression in gastric cancer samples with distinct differentiation grades, with the lowest expression being observed in the highly differentiated cases. A terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling assay demonstrated that the apoptosis indices of highly, moderately and poorly differentiated gastric cancers were 18.12±2.40, 9.73±1.73 and 4.13±0.83%, respectively, with statistical significance (P<0.05). Flow cytometric analysis demonstrated that the apoptosis rates of gastric cancer MKN74, SGC7901 and BGC823 cells were 10.07±1.21, 7.11±1.04 and 4.25±1.02%, respectively, with statistical significance (P<0.05). Spearman's rank correlation analysis revealed that the Annexin A7 mRNA and protein levels were negatively correlated with the differentiation grade of the gastric cancer tissues, while the apoptosis index was positively correlated with the differentiation grade of the gastric cancer tissues. Furthermore, the apoptosis index was negatively correlated with Annexin A7 mRNA and protein expression. Similar associations were observed among Annexin A7 expression, differentiation grades and apoptosis in gastric cancer cell lines. The results of the present study demonstrated that Annexin A7 expression is downregulated, while apoptosis is upregulated, with the progression of gastric adenocarcinoma. These observations suggested that Annexin A7 may inhibit apoptosis during tumorigenesis and that it is a potential biomarker for the diagnosis, prognosis and treatment of gastric adenocarcinoma.

Upregulation of miR­185 promotes apoptosis of the human gastric cancer cell line MGC803.

MicroRNA (miR)-185, which has been reported to be abnormally expressed in some types of cancer, exerts significant effects on the proliferation, apoptosis, drug resistance and metastasis of cancer cells. The present study aimed to explore the effects and underlying molecular mechanisms of miR­185 upregulation on the apoptosis of gastric cancer (GC) cells. Quantitative polymerase chain reaction (qPCR) and western blotting were used to detect the expression levels of miR­185 in GC and adjacent normal tissues. In addition, miR­185 expression was detected in the following GC cell lines: MKN74, SGC7901, BGC823, MGC803, as well as in the gastric epithelial cell line GES­1. Subsequently, miR­185 mimics were transfected into MGC803 cells. Post­transfection, the following experiments were conducted: MTT assay was applied to test cell viability; flow cytometry (FCM) was used to determine the apoptotic rate of the cells; and qPCR and western blotting were conducted to detect the expression levels of the following apoptosis­associated factors: B­cell lymphoma 2 (Bcl­2), Bcl­2­associated X protein (Bax), survivin, X­linked inhibitor of apoptosis protein (XIAP), livin, caspase­3 and caspase­8. The results demonstrated that miR­185 was downregulated in GC tissues compared with the adjacent tissues. In cell lines, miR­185 expression was higher in GES­1 cells compared with in the GC cell lines; in the 4 GC cell lines, the strongest miR­185 expression was in MKN74 cells, followed by SGC7901 and BGC823 cells, and the weakest was in MGC803 cells (P<0.05). Expression of miR­185 was associated with tumor size, differentiation and lymphatic metastasis. Post-transfection with miR­185 mimics, miR­185 expression was significantly increased in a time­ and concentration­dependent manner. MGC803 cell viability was significantly decreased following miR­185 mimics transfection. The results of FCM demonstrated that post­transfection with miR­185 mimics, the apoptotic rate of MGC803 cells was significantly increased. Post­transfection with miR­185 mimics, the expression levels of Bcl­2, survivin and XIAP were significantly decreased in MGC803 cells, whereas the expression levels of Bax and livin were not altered, and caspase­3 and caspase­8 expression was significantly increased. Spectrophotometry indicated that caspase­3 and caspase­8 activity was significantly increased in MGC803 cells following transfection with miR­185 mimics. In conclusion, the present study suggested that miR­185 upregulation in GC cells may promote apoptosis of tumor cells via gene expression regulation.

Effect of annexin A7 suppression on the apoptosis of gastric cancer cells.

Understanding the molecular mechanism of gastric cancer cell apoptosis is pivotal for the development of precise therapies targeting this disease. In the present study, we examined the effects of annexin A7 inhibition on the apoptosis of gastric cancer cells and the growth of tumour xenografts in vivo. Expression of annexin A7 in BGC823 cells was suppressed by small interference RNA, and cells apoptosis was assessed by flow cytometry. The mechanism by which annexin A7 mediates apoptosis in BGC823 cells was explored by determining the expression of key apoptosis regulators. In addition, by suppressing annexin A7 in BGC823 cells with small hairpin RNA, we studied the effects of annexin A7 inhibition on in vivo tumour growth. Our results showed that inhibiting annexin A7 expression induced more than fivefold increase in BGC823 cell apoptosis in vitro. This was in concord with a significant decrease of Bcl-2 expression and increases of Bax, Caspase-3, and Caspase-9. The activities of caspase-3 and caspase-9 were increased by 2.95 ± 0.18 and 3.70 ± 0.33 times, respectively, upon the annexin A7 downregulation in BGC823 cells. Importantly, suppressing annexin A7 showed the same apoptotic mechanism in vivo and significantly inhibited the growth of BGC823 xenografts in mice. These data suggest that annexin A7 likely protects gastric cells from apoptosis and targeting it may represent a valuable strategy in future therapeutic development.

Fluid Resuscitation and Markers of Glycocalyx Degradation in Severe Sepsis.

BACKGROUND: The aim of this study was to determine the relationship between fluid resuscitation and glycocalyx degradation in severe sepsis. METHODOLOGY: 15 post-thoracotomy patients with severe sepsis and 11 patients in recovery after open chest surgery (controls) were enrolled. RESULTS: Plasma syndecan-1 concentrations were significantly higher in the sepsis group than that in control group, and were correlated with fluid balance in the sepsis group (P=0.026). Survival was not related to trends in plasma syndecan-1 concentrations (ascending/descending) in the sepsis group (P = 0.409). Fluid balance at 24 h was significantly higher in sepsis patients who died than in those who survived (P = 0.010). Acute Physiology and Chronic Health Evaluation II scores, Sequential Organ Failure Assessment scores, duration of mechanical ventilation, and length of intensive care unit stay did not differ with the trend of plasma syndecan-1 concentrations. Compared with plasma syndecan-1 concentrations, lactate clearance at a cutoff of 0.40% had a higher diagnostic value. CONCLUSIONS: In patients with severe sepsis, the glycocalyx plays an important role in liquid distribution in different phases. With time, it changes as well. At present, lactate clearance has greater diagnostic value than plasma syndecan-1 concentrations in severe sepsis. A better indicator of endothelial glycocalyx is therefore required.

Expression of annexin A7 and its clinical significance in differentiation and metastasis of gastric carcinoma.

OBJECTIVE: To investigate the expression and clinical significance of annexin A7 in the differentiation and lymphatic metastasis of gastric cancer (GC). METHODS: The clinical and pathological data were recorded for analysis. Immunohistochemical staining and Western blot were performed to analyze the expression of ANXA 7 in primary GC tissues. Logistic regression analyses were conducted to evaluate the associations between annexin A7 expression levels and differentiations of GC. Analyses of the ROC were conducted to determine the cut-off value of the ratio of pixel density of annexin A7 for predicting lymphatic metastasis of GC. RESULTS: A total of 162 GC patients were enrolled in this study, and expression rate of annexin A7 was 65.4% in GC. The survival rate of patients with positive expression of annexin A7 was lower than that in patients with negative expression (P=0.000). The results of COX regression showed that the positive expression of annexin A7, submucosal confinement and pathological stage of GC were associated with poor clinical outcomes. The ratio of pixel density value of primary GC tissues with PN 1-3 lymphatic spread was significantly higher than those in tissues with PN 0 lymphatic spread (0.56±0.09 vs. 0.42±0.07, P < 0.05). ROC analysis showed a high area under the curve for the ratio of pixel density value of annexin A7 in primary GC tissues. At a cut-off level of > 0.505, the ratio of pixel density value of annexin A7 exhibited 76.7% sensitivity and 88.3% specificity for detecting lymphatic metastasis of GC. CONCLUSION: High annexin A7 expression is associated with poor differentiation in GC patients, and it may be a predictor for lymphatic metastasis of GC.