In the Catheterization Laboratory, Most Iatrogenic Cardiac Tamponades Require Only Pericardiocentesis: A Single-Center Experience.

Background: Cardiac tamponade (CT) is a rare but life-threatening complication of cardiac interventions, requiring immediate pericardial cavity pressure relief. While pericardiocentesis often suffices, and some cases necessitate open-chest surgery. This decision is frequently based on individual physician's experience. This study aims to identify high-risk CT patients following cardiac intervention, advocating for early, decisive surgical intervention. Methods: A retrospective analysis was conducted on 51 patients who developed iatrogenic CT at our center between October 2013 and October 2023. Patients were classified based on the necessity for open-chest surgery. The study evaluated a variety of factors, including baseline characteristics, therapeutic approaches, and outcomes. Results: Of the 51 patients with iatrogenic CT, 49 patients were successfully treated without open-chest surgery, with an average immediate drainage volume of 208.2 ± 173.8 mL. In contrast, the two patients requiring open-chest surgery had significantly higher drainage volumes, exceeding 500 mL, with over 300 mL drained in the first hour, indicating laceration injuries. Patients not requiring open-chest surgery demonstrated favorable outcomes. Conclusions: The majority of patients with iatrogenic CT and non-lacerated injuries experienced a favorable prognosis following pericardiocentesis. However, in cases of lacerated injuries with drainage volume was above 300 mL per hour, pericardiocentesis alone could not stabilize the hemodynamics due to persistent bleeding. Immediate surgery may be needed in these cases.

Boosting the capacity and stability of a MoO3 cathode via valence regulation and polypyrrole coating for a rechargeable Zn ion battery.

Molybdenum trioxide (MoO3) is emerging as a hugely competitive cathode material for aqueous zinc ion batteries (ZIBs) for its high theoretical capacity and electrochemical activity. Nevertheless, owing to its undesirable electronic transport capability and poor structural stability, the practical capacity and cycling performance of MoO3 are yet unsatisfactory, which greatly blocks its commercial use. In this work, we report an effective approach to first synthesise nanosized MoO3-x materials to provide more active specific surface areas, while improving the capacity and cycle life of MoO3 by introducing low valence Mo and coated polypyrrole (PPy). MoO3 nanoparticles with low-valence-state Mo and PPy coating (denoted as MoO3-x@PPy) are synthesized via a solvothermal method and subsequent electrodeposition process. The as-prepared MoO3-x@PPy cathode delivers a high reversible capacity of 212.4 mA h g-1 at 1 A g-1 with good cycling life (more than 75% capacity retention after 500 cycles). In contrast, the original commercial MoO3 sample only obtains a capacity of 99.3 mA h g-1 at 1 A g-1, and a cycling stability of 10% capacity retention over 500 cycles. Additionally, the fabricated Zn//MoO3-x@PPy battery obtains a maximum energy density of 233.6 W h kg-1 and a power density of 11.2 kW kg-1. Our results provide an efficient and practical approach to enhance commercial MoO3 materials as high-performance cathodes for AZIBs.

Neutrophil extracellular traps drive epithelial-mesenchymal transition of human colon cancer.

Neutrophil extracellular traps (NETs) are extracellular structures, composed of nuclear DNA and various proteins released from neutrophils. Evidence is growing that NETs exert manifold functions in infection, immunity and cancer. Recently, NETs have been detected in colorectal cancer (CRC) tissues, but their association with disease progression and putative functional impact on tumourigenesis remained elusive. Using high-resolution stimulated emission depletion (STED) microscopy, we showed that citrullinated histone H3 (H3cit) is sufficient to specifically detect citrullinated NETs in colon cancer tissues. Among other evidence, this was supported by the close association of H3cit with de-condensed extracellular DNA, the hallmark of NETs. Extracellular DNA was reliably differentiated from nuclear condensed DNA by staining with an anti-DNA antibody, providing a novel and valuable tool to detect NETs in formalin-fixed paraffin-embedded tissues. Using these markers, the clinical association of NETs was investigated in a cohort of 85 patients with colon cancer. NETs were frequently detected (37/85, 44%) in colon cancer tissue sections and preferentially localised either only in the tumour centre or both in the tumour centre and the invasive front. Of note, citrullinated NETs were significantly associated with high histopathological tumour grades and lymph node metastasis. In vitro, purified NETs induced filopodia formation and cell motility in CRC cell lines. This was associated with increased expression of mesenchymal marker mRNAs (vimentin [VIM], fibronectin [FN1]) and epithelial-mesenchymal transition promoting transcription factors (ZEB1, Slug [SNAI2]), as well as decreased expression of the epithelial markers E-cadherin (CDH1) and epithelial cell adhesion molecule (EPCAM). These findings indicated that NETs activate an epithelial-mesenchymal transition-like process in CRC cells and may contribute to the metastatic progression of CRC. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Hypoxia-induced microRNA-10b-3p promotes esophageal squamous cell carcinoma growth and metastasis by targeting TSGA10.

Evidence has shown that hypoxia promotes esophageal squamous cell carcinoma (ESCC) growth and metastasis, but the molecular mechanisms underlying that response remain poorly understood. MicroRNAs (miRNAs) are post-transcriptional regulators that participate in various cancer-related processes. Here, we demonstrated that hypoxia along with hypoxia-inducible factor 1α significantly increased expression of miR-10b-3p. Inhibition of miR-10b-3p weakened the effects of hypoxia on ESCC cell proliferation, migration and invasion, while miR-10b-3p overexpression had the opposite effects. Mechanistically, miR-10b-3p acted as cancer-promoting gene by targeting testis specific 10. Using a xenograft model, we observed that administration of miR-10b-3p agomir to tumors enhanced their growth and metastasis in vivo. These findings verified the potent regulatory role played by hypoxia-induced miR-10b-3p expression in ESCC progression. These results suggest that miR-10b-3p may be a useful therapeutic target for treating ESCC.

Hepatic radiofrequency ablation causes an increase of circulating histones in patients with hepatocellular carcinoma.

BACKGROUND: Radiofrequency ablation (RFA) has been increasingly accepted for the treatment of hepatocellular carcinoma (HCC). However, RFA has been associated with an obvious systemic inflammatory response, but little is known about the underlying mechanisms. Circulating histones are recently identified as pivotal inflammatory mediators. Hence, we investigated whether circulating histones are involved in RFA-related inflammation. METHODS: Serial blood samples were collected from 42 HCC patients undergoing RFA at 3 time points: pre-RFA, post-RFA (within 24 h), and in 4-week follow up after RFA. Plasma histones, myeloperoxidase (MPO), inflammatory cytokines (IL-1ß, IL-6, IL-10, TNF-α), liver damage parameters (ALT, AST), and creatinine were measured. RESULTS: Compared to pre-RFA (0.837 µg/ml), there was a significant increase in the levels of circulating histones within 24 h post-RFA (4.576 µg/ml, p < 0.0001); histones decreased to pre-RFA levels in 4-week follow up after RFA. Meanwhile, MPO, IL-6, and IL-10 were elevated remarkably within 24 h post-RFA, indicative of an occurrence of the inflammatory response. Notably, histone levels correlated well with MPO (r = 0.5678), IL-6 (r = 0.4851), and IL-10 (r = 0.3574), respectively. In addition, there was a significant damage of liver function in patients within 24 h post-RFA, evidenced by the increased levels of ALT and AST. No changes in creatinine levels were observed. CONCLUSIONS: These data demonstrate that circulating histones are excessively released in HCC patients treated with RFA, which may lead to systemic inflammation by stimulating neutrophil activation and promoting cytokine production. Circulating histones may act as a novel marker to indicate the extent of inflammation related to RFA.

miR-137 inhibits proliferation of melanoma cells by targeting PAK2.

MicroRNAs (miRNA) are key players in a variety of cancers including malignant melanoma. miR-137 has been reported to be a tumor suppressor in melanoma and several targets have been identified for this miRNA. We previously developed a novel proteomics technology, (35) S in vivo/vitro labelling analysis for dynamic proteomics (SiLAD). Because of its high sensitivity in analysing protein expression rates, SiLAD has the potential to unravel miRNA effects on mRNAs coding for proteins with long half-lives or high abundance. Using SiLAD, we discovered that miR-137 significantly downregulated the expression rate of p21-activated kinase 2 (PAK2) in melanoma cells. Bioinformatics analysis predicted PAK2 as a direct target of miR-137, which was confirmed by luciferase reporter assay and Western blot analysis. We found that overexpression of miR-137 inhibited the proliferation of melanoma cells, which could be phenocopied by knockdown of PAK2 using siRNAs. Furthermore, overexpression of PAK2 restored miR-137-mediated suppression of cell proliferation. These findings indicate that miR-137 could inhibit proliferation through targeting PAK2 in melanoma cells.

Clinical significance of plasma lysophosphatidic acid levels in the differential diagnosis of ovarian cancer.

OBJECTIVE: To investigate the value of lysophosphatidic acid (LPA) in the diagnosis of ovarian cancer. MATERIALS AND METHODS: We first performed a hospital-based, case-control study involving 123 ovarian cancer patients and 101 benign ovarian tumor patients, and then conducted a meta-analysis with 19 case-control studies to assess the correlation between ovarian cancer and plasma LPA levels. RESULTS: The case-control study results demonstrated that ovarian cancer patients have increased LPA and cancer antigen (CA)-125 levels compared to patients with benign ovarian tumor (LPA: Ovarian cancer vs benign ovarian tumor: 5.28 ± 1.52 vs 1.82 ± 0.77 µmol/L; CA-125: Ovarian cancer vs benign ovarian tumor: 87.17 ± 45.81 vs. 14.03 ± 10.14 U/mL), which showed statistically significant differences (both P < 0.05). LPA with advanced sensitivity, specificity, positive predictive value, negative predictive value, and accuracy rate of diagnosis excelled CA-125 in the diagnosis of ovarian cancer (both P < 0.05). The areas under the receiver operating characteristic (ROC) curve in the diagnosis of ovarian cancer (LPA: 0.983; CA-125: 0.910) were statistically significant compared with the reference (both P < 0.001) and the difference of the areas of ROC curve between LPA and CA-125 in the diagnosis of ovarian cancer showed statistically significant difference (P < 0.05). The meta-analysis results suggested that plasma LPA levels were higher in ovarian cancer tissues than in benign tissues (standardized mean difference (SMD) =2.36, 95% confidence interval (CI): 1.61-3.11, P < 0.001) and normal tissues (SMD = 2.32, 95% CI: 1.77-2.87, P < 0.001). CONCLUSION: LPA shows greater value in the diagnosis of ovarian cancer compared to CA-125 and may be employed as a biological index to diagnose ovarian cancer.

The Type VI Secretion System Modulates Flagellar Gene Expression and Secretion in Citrobacter freundii and Contributes to Adhesion and Cytotoxicity to Host Cells.

The type VI secretion system (T6SS) as a virulence factor-releasing system contributes to virulence development of various pathogens and is often activated upon contact with target cells. Citrobacter freundii strain CF74 has a complete T6SS genomic island (GI) that contains clpV, hcp-2, and vgr T6SS genes. We constructed clpV, hcp-2, vgr, and T6SS GI deletion mutants in CF74 and analyzed their effects on the transcriptome overall and, specifically, on the flagellar system at the levels of transcription and translation. Deletion of the T6SS GI affected the transcription of 84 genes, with 15 and 69 genes exhibiting higher and lower levels of transcription, respectively. Members of the cell motility class of downregulated genes of the CF74ΔT6SS mutant were mainly flagellar genes, including effector proteins, chaperones, and regulators. Moreover, the production and secretion of FliC were also decreased in clpV, hcp-2, vgr, or T6SS GI deletion mutants in CF74 and were restored upon complementation. In swimming motility assays, the mutant strains were found to be less motile than the wild type, and motility was restored by complementation. The mutant strains were defective in adhesion to HEp-2 cells and were restored partially upon complementation. Further, the CF74ΔT6SS, CF74ΔclpV, and CF74Δhcp-2 mutants induced lower cytotoxicity to HEp-2 cells than the wild type. These results suggested that the T6SS GI in CF74 regulates the flagellar system, enhances motility, is involved in adherence to host cells, and induces cytotoxicity to host cells. Thus, the T6SS plays a wide-ranging role in C. freundii.

CYP1A1 Ile462Val polymorphism and the risk of non-small cell lung cancer in a Chinese population.

AIMS AND BACKGROUND: Cytochrome P450 (CYP) 1A1 enzyme plays an important role in the metabolism of carcinogens, such as polycyclic aromatic hydrocarbons, nitroaromatics and arylamines. METHODS: The study examined the association of CYP1A1 Ile462Val polymorphism with the risk of developing non-small cell lung cancer in a Chinese population. We conducted a case-control study including 526 non-small cell lung cancer cases and 526 cancer-free controls. The odds ratios and 95％ confidence intervals were calculated by logistic regression models. RESULTS: Compared with 462Ile/Ile genotype carriers, subjects with CYP1A1 462Ile/Val or Val/Val genotype had a decreased risk of developing non-small cell lung cancer with odds ratios of 0.57 (95% CI, 0.44-0.75) and 0.54 (95% CI, 0.36-0.81), respectively. When stratified by smoking status, the decreased risk of non-small cell lung cancer associated with CYP1A1 462Ile/Val or Val/Val genotype was observed among non-smokers (OR = 0.62, 95% CI, 0.45-0.87) and among smokers (OR = 0.54, 95% CI, 0.37-0.78). When stratified by smoking-dose, the correlation between CYP1A1 genotypes and the risk of non-small cell lung cancer was detected among light smokers (OR = 0.30, 95% CI, 0.19-0.48) but not among heavy smokers (OR = 0.93, 95% CI, 0.61-1.43). CONCLUSIONS: The CYP1A1 Ile462Val variant was associated with a low risk of developing non-small cell lung cancer in a Chinese population.

[Cyclooxygenase 2 genetic variant interacting with tobacco smoking and the risk of lung cancer].

OBJECTIVE: To explore the association of -1195G > A genetic variant in the promoter region of cyclooxygenase 2 genetic (COX2) with the genetic susceptibility of lung cancer and its interaction with smoking. METHODS: Totally, 956 lung cancer patients recruited between January 2000 and December 2008 at Cancer Hospital, Chinese Academy of Medical Science as the case group, and 994 frequency-matched controls were randomly selected from a pool of cancer-free subjects recruited from a nutritional survey. All subjects were ethnic Han Chinese. There was no sex, age restrictions. Case group and control group were matched. Informed consent was obtained and 2 ml peripheral blood was collected from each subject. All samples were genotyped by polymerase chain reaction-restriction fragment length polymorphism method, smoking status of the subjects was surveyed.While the OR and 95% CI were estimated by logistic regression to evaluate the relation of COX2 -1195G > A variant and the risk of lung cancer. RESULTS: The genetic allele COX2 -1195AA of control group and case group were 24.9% (247/994) and 28.3% (271/956) . Case-control analysis showed an increased risk of developing lung cancer for -1195AA genotype carriers (OR = 1.36, 95% CI: 1.03-1.79), compared with -1195GG carriers. When stratified by smoking status, the significant increased risk of lung cancer was found among smokers with COX2-1195AA genotype, with the OR (95%CI) was 1.56 (1.08-2.25); while among non-smokers, difference of lung cancer risk was not found among different genotypes (OR = 1.17; 95%CI: 0.77-1.61). Among heavy smokers (pack-year >20), -1195AA and -1195AG genotype carriers have significant increased risk of lung cancer with 1.85 (1.16-2.95) and 1.62(1.08-2.43) of OR (95%CI), respectively; among light smokers (pack-year ≤ 20), the OR (95%CI) of lung cancer risk in -1195AG and -1195AA genotype carriers were 0.78 (0.47-1.30) and 1.08 (0.60-1.94), respectively. CONCLUSION: Genetic polymorphism in the promoter of COX2 gene interacting with smoking factor plays an important role in the development of lung cancer.