Sex disparities of clinical manifestations in acute pulmonary embolism and predictive value for in-hospital mortality: Insights from CURES.

BACKGROUND: Pulmonary embolism (PE) is a common and potentially fatal disease, with differences in mortality rates among PE patients of different sexes. This study aims to investigate the disparities in clinical manifestations and in-hospital mortality rates between sexes in PE patients, as well as the association of clinical symptoms with in-hospital mortality. METHODS: We analyzed data from the China pUlmonary thromboembolism REgistry Study (CURES), a nationwide, multicenter, prospective registry focusing on patients with acute PE. Using propensity score matching (PSM) to pair male and female patients with PE, we explored the correlation between clinical symptoms and in-hospital mortality through multivariable regression analysis. RESULTS: A total of 15,203 patients with acute PE were enrolled, and 380 died during hospitalization. The incidence of chest pain, hemoptysis, and palpitations was significantly higher in males compared to females. The incidence of dyspnea, fever, and syncope was higher in females. Hemoptysis and dyspnea were associated with increased in-hospital mortality in males, whereas dyspnea, fever, and palpitations were linked to higher mortality in females. Overall, males exhibited a higher in-hospital mortality than females (2.9 % vs. 2.1 %, p = 0.002). After matching 13,130 patients using the PSM method, the mortality rate of males remained higher than that of females (2.7 % vs. 2.1 %, p = 0.020). CONCLUSIONS: Our study demonstrates that male patients with PE have a higher risk of in-hospital mortality than females. Significant differences in clinical symptoms between sexes are associated with increased mortality risk, emphasizing the need for clinical awareness.

The significance of CD16+ monocytes in the occurrence and development of chronic thromboembolic pulmonary hypertension: insights from single-cell RNA sequencing.

Background: Chronic thromboembolic pulmonary hypertension (CTEPH) is a serious pulmonary vascular disease characterized by residual thrombi in the pulmonary arteries and distal pulmonary microvascular remodeling. The pathogenesis of CTEPH remains unclear, but many factors such as inflammation, immunity, coagulation and angiogenesis may be involved. Monocytes are important immune cells that can differentiate into macrophages and dendritic cells and play an important role in thrombus formation. However, the distribution, gene expression profile and differentiation trajectory of monocyte subsets in CTEPH patients have not been systematically studied. This study aims to reveal the characteristics and functions of monocytes in CTEPH patients using single-cell sequencing technology, and to provide new insights for the diagnosis and treatment of CTEPH. Methods: Single-cell RNA sequencing (scRNA-seq) were performed to analyze the transcriptomic features of peripheral blood mononuclear cells (PBMCs) from healthy controls, CTEPH patients and the tissues from CTEPH patients after the pulmonary endarterectomy (PEA). We established a CTEPH rat model with chronic pulmonary embolism caused by repeated injection of autologous thrombi through a central venous catheter, and used flow cytometry to detect the proportion changes of monocyte subsets in CTEPH patients and CTEPH rat model. We also observed the infiltration degree of macrophage subsets in thrombus tissue and their differentiation relationship with peripheral blood monocyte subsets by immunofluorescence staining. Results: The results showed that the monocyte subsets in peripheral blood of CTEPH patients changed significantly, especially the proportion of CD16+ monocyte subset increased. This monocyte subset had unique functional features at the transcriptomic level, involving processes such as cell adhesion, T cell activation, coagulation response and platelet activation, which may play an important role in pulmonary artery thrombus formation and pulmonary artery intimal remodeling. In addition, we also found that the macrophage subsets in pulmonary endarterectomy tissue of CTEPH patients showed pro-inflammatory and lipid metabolism reprogramming features, which may be related to the persistence and insolubility of pulmonary artery thrombi and the development of pulmonary hypertension. Finally, we also observed that CD16+ monocyte subset in peripheral blood of CTEPH patients may be recruited to pulmonary artery intimal tissue and differentiate into macrophage subset with high expression of IL-1ß, participating in disease progression. Conclusion: CD16+ monocytes subset had significant gene expression changes in CTEPH patients, related to platelet activation, coagulation response and inflammatory response. And we also found that these cells could migrate to the thrombus and differentiate into macrophages with high expression of IL-1ß involved in CTEPH disease progression. We believe that CD16+ monocytes are important participants in CTEPH and potential therapeutic targets.

Establishment and Validation of Prognostic Nomograms for Patients with Metastatic Pulmonary Large Cell Neuroendocrine Carcinoma.

PURPOSE: Metastatic pulmonary large cell neuroendocrine carcinoma (LCNEC) is an aggressive cancer with generally poor outcomes. Effective methods for predicting survival in patients with metastatic LCNEC are needed. This study aimed to identify independent survival predictors and develop nomograms for predicting survival in patients with metastatic LCNEC. PATIENTS AND METHODS: We conducted a retrospective analysis using the Surveillance, Epidemiology, and End Results (SEER) database, identifying patients with metastatic LCNEC diagnosed between 2010 and 2017. To find independent predictors of cancer-specific survival (CSS), we performed Cox regression analysis. A nomogram was developed to predict the 6-, 12-, and 18-month CSS rates of patients with metastatic LCNEC. The concordance index (C-index), area under the receiver operating characteristic (ROC) curves (AUC), and calibration curves were adopted with the aim of assessing whether the model can be discriminative and reliable. Decision curve analyses (DCAs) were used to assess the model's utility and benefits from a clinical perspective. RESULTS: This study enrolled a total of 616 patients, of whom 432 were allocated to the training cohort and 184 to the validation cohort. Age, T staging, N staging, metastatic sites, radiotherapy, and chemotherapy were identified as independent prognostic factors for patients with metastatic LCNEC based on multivariable Cox regression analysis results. The nomogram showed strong performance with C-index values of 0.733 and 0.728 for the training and validation cohorts, respectively. ROC curves indicated good predictive performance of the model, with AUC values of 0.796, 0.735, and 0.736 for predicting the 6-, 12-, and 18-month CSS rates of patients with metastatic LCNEC in the training cohort, and 0.795, 0.801, and 0.780 in the validation cohort, respectively. Calibration curves and DCAs confirmed the nomogram's reliability and clinical utility. CONCLUSION: The new nomogram was developed for predicting CSS in patients with metastatic LCNEC, providing personalized risk evaluation and aiding clinical decision-making.

Tissue factor regulates autophagy in pulmonary artery endothelial cells from chronic thromboembolic pulmonary hypertension rats via the p38 MAPK-FoxO1 pathway.

AIMS: To detect the expression of autophagy components, p38 MAPK (p38) and phosphorylated forkhead box transcription factor O-1 (pFoxO1) in pulmonary vascular endothelial cells of chronic thromboembolic pulmonary hypertension (CTEPH) rats and to investigate the possible mechanism through which tissue factor (TF) regulates autophagy. METHODS: Pulmonary artery endothelial cells (PAECs) were isolated from CTEPH (CTEPH group) and healthy rats (control group (ctrl group)) which were cocultured with TF at different time points including 12 h, 24 h, 48 h and doses including 0 nM,10 nM, 100 nM, 1µM, 10µM, 100µM and cocultured with TFPI at 48 h including 0 nM, 2.5 nM, 5 nM. The expression of forkhead box transcription factor O-1 (FoxO1), pFoxO1, p38, Beclin-1 and LC3B in PAECs was measured. Coimmunoprecipitation (co-IP) assays were used to detect the interaction between FoxO1 and LC3. RESULTS: The protein expression of p-FoxO1/FoxO1 was significantly lower in the CTEPH groups (cocultured with TF from 0 nM to 100 µM) than in the ctrl group at 12 h, 24 h, and 48 h (P < 0.05) and was significantly lower in the CTEPH groups (cocultured with TFPI from 0 nM to 5 nM) than in the ctrl group at 48 h (P < 0.05). The protein expression of p38 in the CTEPH groups treated with 0 nM, 10 nM, 100 nM or 1 µM TF for 48 h significantly increased than ctrl groups (P < 0.05) and was significantly increased in the CTEPH groups (cocultured with TFPI concentration from 0 nM to 5 nM) than in the ctrl group at 48 h (P < 0.05). The protein expression of Beclin1 at the same concentration (cocultured with TF from 0 nM to 100 µM) was significantly lower in the CTEPH groups than ctrl groups after 24 h and 48 h (P < 0.05) and was significantly decreased in the CTEPH groups (cocultured with TFPI concentration from 2.5 nM to 5 nM) than in the ctrl group at 48 h (P < 0.05). The protein expression of LC3-II/LC3-I at the same concentration (cocultured with TF 0 nM, 1 µM, 10 µM, and 100 µM) was significantly lower in the CTEPH than in the ctrl groups after 12 h (P < 0.05) and was significantly lower in the CTEPH groups (cocultured with TFPI concentration from 0 nM to 5 nM) than in the ctrl group at 48 h (P < 0.05). There were close interactions between FoxO1 and LC3 in the control and CTEPH groups at different doses and time points. CONCLUSION: The autophagic activity of PAECs from CTEPH rats was disrupted. TF, FoxO1 and p38 MAPK play key roles in the autophagic activity of PAECs. TF may regulate autophagic activity through the p38 MAPK-FoxO1 pathway.

Whole-genome microRNA sequencing analysis in patients with pulmonary hypertension.

Pulmonary hypertension (PH) is a pathological disorder with multiple clinical manifestations that lead to cardiovascular and respiratory diseases in most patients. Recent studies have revealed that microRNAs (miRNAs) play important roles as upstream signaling molecules in several diseases, including PH. However, miRNAs that can be used as diagnostic or prognostic biomarkers for PH have not been identified. Thus, in this study, peripheral blood samples obtained from patients with PH and healthy individuals were subjected to genome-wide miRNA sequencing and transcriptome analysis. We screened 136 differentially expressed miRNAs in patients with PH and verified that four differentially expressed miRNAs, namely, hsa-miR-1304-3p, hsa-miR-490-3p, hsa-miR-11400, and hsa-miR-31-5p, could be used as clinical diagnostic biomarkers for pulmonary arterial hypertension. Our findings provide a basis for further in-depth investigations of the specific mechanisms of miRNAs in PH.

Bioinformatics and machine learning were used to validate glutamine metabolism-related genes and immunotherapy in osteoporosis patients.

BACKGROUND: Osteoporosis (OP), often referred to as the "silent disease of the twenty-first century," poses a significant public health concern due to its severity, chronic nature, and progressive course, predominantly affecting postmenopausal women and elderly individuals. The pathogenesis and progression of this disease have been associated with dysregulation in tumor metabolic pathways. Notably, the metabolic utilization of glutamine has emerged as a critical player in cancer biology. While metabolic reprogramming has been extensively studied in various malignancies and linked to clinical outcomes, its comprehensive investigation within the context of OP remains lacking. METHODS: This study aimed to identify and validate potential glutamine metabolism genes (GlnMgs) associated with OP through comprehensive bioinformatics analysis. The identification of GlnMgs was achieved by integrating the weighted gene co-expression network analysis and a set of 28 candidate GlnMgs. Subsequently, the putative biological functions and pathways associated with GlnMgs were elucidated using gene set variation analysis. The LASSO method was employed to identify key hub genes, and the diagnostic efficacy of five selected GlnMgs in OP detection was assessed. Additionally, the relationship between hub GlnMgs and clinical characteristics was investigated. Finally, the expression levels of the five GlnMgs were validated using independent datasets (GSE2208, GSE7158, GSE56815, and GSE35956). RESULTS: Five GlnMgs, namely IGKC, TMEM187, RPS11, IGLL3P, and GOLGA8N, were identified in this study. To gain insights into their biological functions, particular emphasis was placed on synaptic transmission GABAergic, inward rectifier potassium channel activity, and the cytoplasmic side of the lysosomal membrane. Furthermore, the diagnostic potential of these five GlnMgs in distinguishing individuals with OP yielded promising results, indicating their efficacy as discriminative markers for OP. CONCLUSIONS: This study discovered five GlnMgs that are linked to OP. They shed light on potential new biomarkers for OP and tracking its progression.

A tunable perfect absorber based on a black phosphorus/bowtie shaped cavity hybrid metasurface.

The practical application of black phosphorus (BP) is limited by its low absorption characteristics. In this work, we propose a perfect absorber based on a BP and bowtie shaped cavity, which has high tunability and excellent optical performance. This absorber effectively increases the light-matter interaction and achieves perfect absorption by using a monolayer BP and a reflector to form a Fabry-Perot cavity. We study the influence of structural parameters on the absorption spectrum and realize the adjustment of frequency and absorption in a certain range. Applying an external electric field on the surface of BP by electrostatic gating, we can change its carrier concentration to control its optical properties. In addition, we can flexibly tune the absorption and Q-factor by varying the polarization direction of incident light. This absorber has promising applications in optical switches, sensing, and slow light, which provides a new perspective for the practical application of BP and a foundation for future research, offering possibilities for more applications.

Pulmonary thromboembolic disease or pulmonary artery intimal sarcoma: Case report and literature review.

The present case study reported on a patient initially diagnosed with pulmonary embolism at the First Affiliated Hospital of Fujian Medical University (Fuzhou, China) in May 2021. Furthermore, a relevant literature review was performed. The patient was a 57-year-old Chinese male who presented with dyspnea and wheezing following exercise. Physical examination revealed pulmonary valve second heart sound > aortic valve second heart sound but lack of swelling on both lower limbs, while the imaging results suggested pulmonary artery filling defects. Initially, the patient was diagnosed with pulmonary embolism and was administered anticoagulation treatment, which lasted for 3 months but proved to be ineffective. Subsequent re-examination via chest computed tomography further indicated multiple nodules in the left hilum and lung. Therefore, the patient was hospitalized for lung aspiration biopsy, which led to the final diagnosis of pulmonary artery intimal sarcoma based on the pathological review.

Mechanism of Herb Pairs Astragalus mongholicus and Curcuma phaeocaulis Valeton in Treating Gastric Carcinoma: A Network Pharmacology Combines with Differential Analysis and Molecular Docking.

Background: Gastric carcinoma (GC) is a kind of digestive tract tumor that is highly malignant and has a very poor prognosis. Although both Astragalus mongholicus (AM, huáng qí) and Curcuma phaeocaulis Valeton (CPV, é zhú) can slow the onset and progression of GC, the mechanism by which AM-CPV works in the treatment of GC is uncertain. Materials and Methods: The traditional Chinese medicine network databases TCMSP, TCMID, and ETCM were used to identify the key functional components and associated targets of AM and CPV. To establish a theoretical foundation, the development of gastric cancer (GC) was predicted utilizing a GEO gene chip and TCGA difference analysis mixed with network pharmacology. A herbal-ingredient-target network and a core target-signal pathway network were created using GO and KEGG enrichment analyses. The molecular docking method was used to evaluate seventeen main targets and their compounds. Results: Cell activity, reactive oxygen species modification, metabolic regulation, and systemic immune activation may all be involved in the action mechanism of the AM-CPV drug-pair in the treatment of GC. It inhibits the calcium signaling route, the AGE-RAGE signaling system, the cAMP signaling pathway, the PI3K-Akt signaling network, and the MAPK signaling pathway, slowing the progression of GC. The number of inflammatory substances in the tumor microenvironment is reduced, GC cell proliferation is deprived, apoptosis is promoted, and GC progression is retarded through controlling the IL-17 signaling route, TNF signaling pathway, and other inflammation-related pathways. Conclusions: The AM-CPV pharmaceutical combination regulates GC treatment via a multitarget, component, and signal pathway with a cooperative and bidirectional regulatory mechanism. Its active constituents may treat GC by regulating the expression of STAT1, MMP9, IL6, HSP90AA1, JUN, CCL2, IFNG, CXCL8, and other targets, as well as activating or inhibiting immune-inflammatory and cancer signaling pathways.

Pulmonary embolism with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease. The incidence of COPD is growing annually in China, and it is a significant and growing public health burden. Multivariate analysis showed that COPD was one of the independent risk factors for the occurrence of pulmonary embolism (PE), and the incidence of PE was significantly higher in COPD patients than in normal subjects. However, PE is often overlooked in patients with acute exacerbation of COPD (AECOPD) because there are many similarities in clinical symptoms between PE and AECOPD, which are difficult to distinguish, resulting in the failure of timely treatment and poor prognosis. Therefore, it is of great significance to understand the clinical manifestations, diagnosis, and treatment of COPD combined with PE for making a more accurate diagnosis, providing timely and effective treatment, and improving the prognosis of such patients.

The role of ß-catenin in pulmonary artery endothelial-mesenchymal transformation in rats with chronic thromboembolic pulmonary hypertension.

ß-catenin and endothelial mesenchymal transformation play an important role in the formation of pulmonary hypertension. To explore the role of ß-catenin in chronic thromboembolic pulmonary hypertension (CTEPH), we first established a rat model of CTEPH by repeated autologous thromboembolization and then treated these rats with a ß-catenin specific inhibitor, XAV939, for two or four weeks. We further examined the expression of ß-catenin, α-SMA and CD31, mean pulmonary artery pressure (mPAP), and histopathology in the pulmonary artery, and analyzed their correlation. In the thrombus group without treatment of the inhibitor, the expression of ß-catenin and α-SMA in pulmonary artery was increased with time; mPAP, the thickness of pulmonary artery wall, and the area/total area of pulmonary artery (WA/TA) were also increased; however, the expression of CD31 was decreased. Interestingly, these symptoms could be improved by treatment with XAV939. In this study, in CTEPH rat model, the expression of ß-catenin signal affects pulmonary vascular remodeling and pulmonary artery pressure, and positively correlated with pulmonary arterial endothelial mesenchymal transformation (EMT), indicating that ß-catenin signal may play an important role in the occurrence and development of CTEPH. The inhibition of ß-catenin signal and the improvement of pulmonary arterial EMT may provide therapeutic ideas for CTEPH.

The role of inflammation in a rat model of chronic thromboembolic pulmonary hypertension induced by carrageenan.

BACKGROUND: Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening condition arising from the thrombus and obstructive remodeling of the pulmonary arteries, which causes a significant morbidity and mortality. Although the modern treatment in CTEPH has been significant advanced both in surgical and medical treatment, none can claim to cure the disease, largely because of our limited understanding of the underlying pathogenesis of the disease and lack of a reliable CTEPH animal model to study for. Recently, inflammation has been accepted as a common pathway through which various risk factors trigger venous thrombo-embolism (VTE) formation, we describe a novel mouse model of CTEPH which reproduces a frequent trigger and resembles the time course, histological features, and clinical presentation of CTEPH in humans, to open a new horizons of inflammation in CTEPH. METHODS: By administering a pulmonary embolism (PE) protocol (comprising 3 sequential left jugular vein injections of autologous blood clots) to 8-week-old male Sprague Dawley (SD) rats using tranexamic acid (200 mg/kg.d) to inhibit fibrinolysis and injecting additional carrageenan (20 mg/kg, once a week) to create perivascular inflammation, we successfully generated a CTEPH animal model. By monitoring the mean pulmonary artery pressure (mPAP) and the histopathological change to evaluate the CTEPH model. By detecting the RT-PCR, western blot, TUNEL, and immunohistochemistry in the sub-groups to find the potential mechanism of inflammation may work in the pulmonary vascular remolding. RESULTS: In this study, rats with CTEPH exhibited pronounced pulmonary vascular remolding with higher vessel wall area/total area (WA/TA) ratio in comparison to the control rats (85.41%±7.37% vs. 76.41%±5.97%, P<0.05), the mPAP (25.51±1.13 vs. 15.92±1.13 mmHg, P<0.05). Significant differences in mean pulmonary artery pressure (mPAP) values were observed between rats injected solely with clots and those injected with both clots and carrageenan (25.51±1.13 vs. 29.82±1.26 mmHg, P<0.05, respectively). Furthermore, following the third embolization, thrombi and intimal hyperplasia occurred in the pulmonary artery. In addition, repeated embolization elevated mRNA and protein levels of tumor necrosis factor-α (TNF-α), NF-κB/p65, and B-cell lymphoma-2 (BCL-2), but decreased BAX expression in a time-dependent manner. CONCLUSIONS: Take advantage of the inflammation to trigger VTE formation, we successfully generated a CTEPH animal model. Inflammation may play a crucial role in the pathogenesis and progression of CTEPH by inhibiting endothelial cell apoptosis. Understanding the role of inflammation in CTEPH may not only help to determine the optimal treatment options but also may aid in the development of future preventative strategies, since current anticoagulation treatment regimens are not designed to inhibit inflammation.

Design and analysis of refractive index sensors based on slotted photonic crystal nanobeam cavities with sidewall gratings.

We propose and numerically investigate a refractive index sensor based on a one-dimensional slotted photonic crystal nanobeam cavity with sidewall gratings for refractive index sensing in a gaseous environment. By using the three-dimensional finite-difference time-domain method, we demonstrate that our proposed sensor simultaneously possesses a high quality factor of $ 3.71 \times {10^6} $3.71×106 and a high sensitivity of 508 nm/RIU (refractive index unit) at the resonant wavelength near 1583 nm, yielding a detection limit as low as $ 1.97 \times {10^{ - 6}} $1.97×10-6 RIU. Moreover, the mode volume of the cavity's fundamental resonant mode is found to be as small as $ 0.022(\lambda /n)^3 $0.022(λ/n)3, resulting in a very compact effective sensing area. We finally study and assess the effect of fabrication disorder on the performances of our proposed sensor. We believe our proposed sensor will be a promising candidate for applications not only in multiplexed biochemical sensing and multielement mixture detection, but also in optical trapping of single biomolecules or nanoparticles.

Simulation study on active control of electromagnetically induced transparency analogue in coupled photonic crystal nanobeam cavity-waveguide systems integrated with graphene.

We proposed and numerically investigated a coupled photonic crystal nanobeam (PCN) cavity-waveguide system which is composed of a bus waveguide and two one-dimensional PCN cavities, acting as bright and dark mode cavities, to achieve a distinct electromagnetically induced transparency analogue (EIT-like) effect by changing the near-field coupling strength between two cavities. By further integrating with graphene on top of the dark mode cavity, the three-dimensional finite-difference time-domain simulation results show that the generated EIT-like transparency window can be actively tuned and a complete on-to-off modulation of the EIT-like effect is realized by electrically tuning the graphene's Fermi level without reoptimizing or refabricating the structure. Theoretical analysis based on the coupled mode theory is then conducted and the results are highly consistent with the numerical results. In addition, we demonstrated that the group delay of the system can also be actively modulated by changing the Fermi level of graphene, achieving a well-controlled slow light effect. Our proposed coupled PCN cavity-waveguide system, combining the merits of PCN cavity and graphene in a single device, may provide a new platform for applications in chip-integrated slow light devices, tunable switches, optical modulators and high-sensitive sensors.

Analysis of PROC and PROS1 single nucleotide polymorphisms in a thrombophilia family.

OBJECTIVE: The aim of this study was to assess the association of single nucleotide polymorphisms (SNPs) in protein C (PROC) and protein S (PROS1) genes with deep venous thrombosis (DVT) in a thrombophilia family. METHODS: DNA were extracted from blood of participants. Five PROC SNPs and 11 PROS1 SNPs were selected from the Hapmap and 1000 Genomes databases. The minor allele frequencies (MAFs) of SNPs in the thrombophilia family (Group I) and healthy controls (Group II) were detected. SNPs were analysed by Chi-square, logistic regression and linkage disequilibrium patterns. RESULTS: MAFs for all 16 SNPs were greater than 0.05. Chi-square analysis showed significant differences between Group I and Group II in the frequency of mutant alleles of rs1799808, rs5936, rs6123, rs12634349, rs6441600 and rs13062355 SNPs (P < .05). Logistic regression analysis found that mutant alleles of rs1799808, rs6441600 and rs13062355 SNPs may contribute to DVT in this family (OR > 1, L95 > 1). Linkage disequilibrium was found among 15 of the PROC and PROS SNPs. CONCLUSIONS: Single nucleotide polymorphisms (SNPs) of PROC and PROS1 may be closely associated with DVT in this thrombophilia family. Mutant alleles of rs1799808, rs6441600 and rs13062355 SNPs may contribute to DVT, whereas mutant alleles of rs1799810, rs6123 and rs12634349 may protect individuals from DVT. With the exception of rs9681204, there was linkage disequilibrium between PROC and PROS1 SNPs. We found that 12 haplotypes were in linkage disequilibrium, but linkage disequilibrium was strong in only eight of these (frequency >5%).

Role of monocyte tissue factor on patients with non-small cell lung cancer.

BACKGROUND: To examine the expression of D-dimer, fibrinogen (FIB), leukocyte, C-reactive protein (CRP) and tissue factor (TF) released from monocyte in non-small cell lung cancer (NSCLC) patients with or without venous thromboembolism (VTE) and analyse the correlation, to explore the possible mechanisms. METHODS: Seventy-two patients confirmed the diagnosis of lung cancer, among whom 10 with VTE were enrolled into the study from November 2012 to January 2014 in the First Affiliated Hospital of Fujian Medical University and 30 healthy subjects were also enrolled as the control group. Ficoll and Percoll density gradient centrifugation separated of peripheral blood monocyte. Monocyte TF mRNA expression was detected using reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: There were significant differences in different stages of the cancer (P < .05) and no significance among the histopathologic types (P > .05) for the expression of monocyte TF mRNA in NSCLC patients, its expression was significantly higher in cancer with lymph node metastasis than those without lymph node metastasis (P < .01). Meanwhile, in NSCLC patients with VTE, the expression of monocyte TF mRNA was significantly higher than that in patients without VTE (P < .01). Difference of the survival curves between the low monocyte TF mRNA expression and the high monocyte TF mRNA expression was significant (Log-rank x2 = 4.923, P < .05). CONCLUSIONS: Monocyte TF may be a relevant source of TF-mediated thrombogenicity in NSCLC patients and may be associated with prognosis in NSCLC.

Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension.

To explore the role of FoxO1 and apoptosis in a rat model of chronic thromboembolic pulmonary hypertension (CTEPH). Rats were randomly divided into a sham group (n = 45) and an experimental group (n = 45). Autologous blood clots were injected into rats three times to induce CTEPH. Rats were further divided into three subgroups: a 1-week subgroup (n = 15), a 2-week subgroup (n = 15), and a 4-week subgroup (n = 15). Mean pulmonary arterial pressure (mPAP) and histopathology were evaluated at each time point. FoxO1, Bad, and Bcl-2 levels were examined at each time point using reverse transcription PCR and western blotting. The mPAP and vessel wall area/total area (WA/TA) ratio in the experimental group gradually increased in a time-dependent manner (P < 0.05). Both the mRNA and protein levels of FoxO1 decreased in the CTEPH rats compared to in the sham group. In addition, embolization led to the up-regulation of Bad and the down-regulation of Bcl-2 (P < 0.05). FoxO1 and apoptosis play an important role in the pathogenesis of CTEPH. Apoptosis-resistant pulmonary artery endothelial cells may play an important role in remodeling of the rat pulmonary artery.

An irregular pulmonary nodule was confirmed diagnosis of aspiration pneumonia by finding plant cells through rapid on-site evaluation.

BACKGROUND: Rapid on-site evaluation (ROSE) is a method which is often used in quick-staining cytology in the tumour diagnostic field, and results in a significant decrease in diagnostic time and cost. However, we have not found any previous report on the ROSE method for diagnosing aspiration pneumonia. METHODS: We would like to discuss the case of a patient with an irregular pulmonary nodule in the left lower lobar bronchus who had a confirmed diagnosis of aspiration pneumonia through ROSE stained by Diff-Quik methods during bronchoscopy. RESULTS: Through ROSE, which we were able to perform within just 1 min, we observed the plant cells on the smear under the microscope. The Giemsa stain of the specimen, which would take much more time than Diff-Quik, also revealed the plant cells. CONCLUSION: ROSE for the specimen from the bronchoscopy could be done for the patient who has developed an unexplained pulmonary nodule and is helpful. If the non-human cells such as plant cells are found from the ROSE, aspiration pneumonia can be diagnosed immediately and the corresponding therapy may be performed, which may significantly shorten hospital stay, reduce hospital costs and improve patient outcomes.

Small lung lesions invisible under fluoroscopy are located accurately by three-dimensional localization technique on chest wall surface and performed bronchoscopy procedures to increase diagnostic yields.

BACKGROUND: Nowadays, small peripheral pulmonary lesions (PPLs) are frequently detected and the prognosis of lung cancer depends on the early diagnosis. Because of the high fee and requiring specialized training, many advanced techniques are not available in many developing countries and rural districts. METHODS: Three sets of opaque soft copper wires visible under the fluoroscopy (Flu) in the Flu-flexible bronchoscopy (FB) group (n = 24), which determined the three planes of the lesion, were respectively placed firmly on the surface of the chest wall with adhesive tape on the chest wall. The FB tip was advanced into the bronchus toward the crosspoint of the three perpendicular planes under Flu with careful rotation of a C-arm unit. Then the specimen were harvested focusing around the crosspoint for pathologic diagnosis. The rapid on-site evaluation (ROSE) procedure was also performed. The average Flu time during FB procedures were recorded and diagnostic accuracy rates in the Flu-FB group were compared with the other group guided by radial endobronchial ultrasound (R-EBUS) (n = 23). RESULTS: The location of the core point of the lesion, whether it was visible or not under the fluoroscopy could be recognized by three-dimensional localization technique. The accuracy rates of diagnostic yields were 62.5% in the Flu-FB group, and was similar as 65.2% in the R-EBUS group (P > 0.05). However, in the Flu-FB group, there was a decreasing tendency on accurate diagnosis rates of lower lobe (LL) lesions when comparing with non-LL lesions (3/8 = 37.5% vs 12/16 = 75%, P = 0.091) while in the R-EBUS group it was similar (9/12 = 75% vs 6/11 = 54.6%, P = 0.278). In the Flu-FB group, fluoroscopy time was negatively correlated with the lesion length (r = -0.613, P = 0.001), however, there was no significant difference between the lesions invisible or not (5.83 ± 1.45 min vs 7.67 ± 2.02 min, P = 0.116) under the fluoroscopy, as well as no significant difference among SPN, mGGO and GGO (6.12 ± 2.05 min, 7.25 ± 1.33 min and 7.80 ± 2.02 min, P > 0.05). CONCLUSIONS: Small PPL whether it is visible or not under fluoroscopy can be located accurately by our three-dimensional localization technique on chest wall surface and performed bronchoscopy procedures to increase diagnostic yields. It is more convenient, economical and reliable with the similar diagnostic yields than R-EBUS guided method. TRIAL REGISTRATION: Current Controlled Trials ChiCTR-DDD-16009715 . The date of registration: 3rd Nov, 2016. Retrospectively registered.