A dataset for deep learning based detection of printed circuit board surface defect.

Printed circuit board (PCB) may display diverse surface defects in manufacturing. These defects not only influence aesthetics but can also affect the performance of the PCB and potentially damage the entire board. Thus, achieving efficient and highly accurate detection of PCB surface defects is fundamental for quality control in fabrication. The rapidly advancing deep learning (DL) technology holds promising prospects for providing accurate and efficient detection methods for surface defects on PCB. To facilitate DL model training, it is imperative to compile a comprehensive dataset encompassing diverse surface defect types found on PCB at a significant scale. This work categorized PCB surface defects into 9 distinct categories based on factors such as their causes, locations, and morphologies and developed a dataset of PCB surface defect (DsPCBSD+). In DsPCBSD+, a total of 20,276 defects were annotated manually by bounding boxes on the 10,259 images. This openly accessible dataset is aimed accelerating and promoting further researches and advancements in the field of DL-based detection of PCB surface defect.

Mesenchymal stem cell-derived exosomes ameliorate hypoxic pulmonary hypertension by inhibiting the Hsp90aa1/ERK/pERK pathway.

Hypoxic pulmonary hypertension (HPH) is a serious and life-threatening chronic cardiopulmonary disease characterized by progressive elevation of pulmonary artery pressure and pulmonary vascular remodeling. Mesenchymal stem cell- derived exosomes (MSC-Exos) can relieve HPH by reversing pulmonary vascular remodeling. The HPH model was established in healthy male Sprague-Dawley (SD) rats aged 6 to 8 weeks. The rats were placed in a room with oxygen concentration of (10 ± 1) % for 8 hours a day over 28 days, were then injected intravenously with MSC-Exos (100 ug protein/kg) or equal-volume phosphate buffer saline (PBS) once a day over 1 week. Right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI) and pulmonary vascular remodeling were observed after anesthesia. In addition, platelet-derived growth factor BB (PDGF-BB) was used to stimulate rat pulmonary artery smooth muscle cells (PASMCs) to construct HPH pathological cell models. The results showed that MSC-Exos could not only reduce the elevation of RVSP, right ventricular hypertrophy and the degree of pulmonary vascular remodeling in HPH rats, but also reduce the proliferation, migration and apoptosis resistance of PASMCs. Finally, GSE53408 and GSE113439 datasets were analyzed and showed that the expression of Hsp90aa1 and pERK/ERK were significantly increased in HPH, also could be inhibited by MSC-Exos. Meanwhile, inhibition of Hsp90aa1 also reduced PASMCs migration and pERK/ERK protein level. In conclusion, MSC-Exos alleviated HPH by suppressing PASMCs proliferation, migration and apoptosis resistance through inhibiting the Hsp90aa1/ERK/pERK pathway.

Exosomes derived from mesenchymal stromal cells exert a therapeutic effect on hypoxia-induced pulmonary hypertension by modulating the YAP1/SPP1 signaling pathway.

OBJECTIVE: Hypoxic pulmonary hypertension (HPH) is a progressive and life-threatening disease characterized by perivascular inflammation, pulmonary vascular remodeling, and occlusion. Mesenchymal stromal cell-derived exosomes (MSC-exo) have emerged as potential therapeutic agents due to their role in cell communication and the transportation of bioactive molecules. In this study, we aimed to investigate the therapeutic effects of MSC-exo against HPH and elucidate the underlying molecular mechanism. METHODS: Exosomes were isolated from conditioned media of human bone mesenchymal stromal cells using ultracentrifugation and characterized through western blotting, transmission electron microscopy (TEM), and nanoparticle tracking analysis (NTA). An HPH animal model was established in male SD rats, and MSC-exo or phosphate-buffered saline (PBS) were administered via the tail vein for three weeks. Subsequently, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and pulmonary vascular remodeling were evaluated. Lung tissues from HPH rats and normal rats underwent high-throughput sequencing and transcriptomic analysis. Gene Ontology (GO) analysis was employed to identify upregulated differentially expressed genes. Additionally, rat pulmonary artery smooth muscle cells (PASMC) exposed to platelet-derived growth factor-BB (PDGF-BB) were used to simulate HPH-related pathological behavior. In vitro cellular models were established to examine the molecular mechanism of MSC-exo in HPH. RESULTS: MSC-exo administration protected rats from hypoxia-induced increases in RVSP, RVHI, and pulmonary vascular remodeling. Additionally, MSC-exo alleviated PDGF-BB-induced proliferation and migration of PASMC. Transcriptomic analysis revealed 267 upregulated genes in lung tissues of HPH rats compared to control rats. Gene Ontology analysis indicated significant differences in pathways associated with Yes Associated Protein 1 (YAP1), a key regulator of cell proliferation and organ size. RT-qPCR and western blot analysis confirmed significantly increased expression of YAP1 in HPH lung tissues and PASMC, which was inhibited by MSC-exo treatment. Furthermore, analysis of datasets demonstrated that Secreted Phosphoprotein 1 (SPP1), also known as Osteopontin (OPN), is a downstream binding protein of YAP1 and can be upregulated by PDGF-BB. MSC-exo treatment reduced the expression of both YAP1 and SPP1. Lentivirus-mediated knockdown of YAP1 inhibited PDGF-BB-induced PASMC proliferation, migration, and SPP1 protein levels. CONCLUSION: Our findings demonstrate that MSC-exo exert a therapeutic effect against hypoxia-induced pulmonary hypertension by modulating the YAP1/SPP1 signaling pathway. The inhibition of YAP1 and downstream SPP1 expression by MSC-exo may contribute to the attenuation of pulmonary vascular remodeling and PASMC proliferation and migration. These results suggest that MSC-exo could serve as a potential therapeutic strategy for the treatment of HPH. Further investigations are warranted to explore the clinical applicability of MSC-exo-based therapies in HPH patients.

CEMIP promotes small cell lung cancer proliferation by activation of glutamine metabolism via FBXW7/c-Myc-dependent axis.

Small cell lung cancer (SCLC) is the most malignant lung cancer with rapid growth and early metastasis, but still lacks effective targeted therapies to improve the prognosis. Here, we demonstrated that a novel oncogenic protein, cell migration inducing hyaluronic binding protein (CEMIP), was robustly overexpressed in SCLC tissues than that in noncancerous tissues and high expression of CEMIP predicted poor outcomes in clinical specimens and in large sample size cohorts from public databases (GEPIA 2 and CPTAC). Liquid chromatography mass spectrometry (LC-MS) and in vitro/in vivo functional assays indicated that CEMIP contributed to the proliferation by increasing glutamine consumption and their metabolites (glutamate and glutathione) levels in SCLC cells. Moreover, the addition of a GLS1 inhibitor CB-839 dramatically reduced CEMIP-induced SCLC cell proliferation. Mechanistically, beyond as a scaffold protein, CEMIP facilitates glutamine-dependent cell proliferation through inhibiting c-Myc ubiquitination and increasing c-Myc stabilization and nuclear accumulation via hindering the interaction between FBXW7 (a E3 ubiquitin ligase) and its target substrate c-Myc. Taken together, our findings reveal a novel oncogenic role of CEMIP in sustaining SCLC growth via FBXW7/c-Myc-dependent axis, and provide new evidence that inhibition of CEMIP might be a potential therapeutic strategy for the treatment of SCLC.

KIAA1199 Correlates With Tumor Microenvironment and Immune Infiltration in Lung Adenocarcinoma as a Potential Prognostic Biomarker.

Background: KIAA1199 has been considered a key regulator of carcinogenesis. However, the relationship between KIAA1199 and immune infiltrates, as well as its prognostic value in lung adenocarcinoma (LUAD) remains unclear. Methods: The expression of KIAA1199 and its influence on tumor prognosis were analyzed using a series of databases, comprising TIMER, GEPIA, UALCAN, LCE, Prognoscan and Kaplan-Meier Plotter. Further, immunohistochemistry (IHC), western blot (WB) and receiver operating characteristic (ROC) curve analyses were performed to verify our findings. The cBioPortal was used to investigate the genomic alterations of KIAA1199. Prediction of candidate microRNA (miRNAs) and transcription factor (TF) targeting KIAA1199, as well as GO and KEGG analyses, were performed based on LinkedOmics. TIMER and TISIDB databases were used to explore the relationship between KIAA1199 and tumor immune infiltration. Results: High expression of KIAA1199 was identified in LUAD and Lung squamous cell carcinoma (LUSC) patients. High expression of KIAA1199 indicated a worse prognosis in LUAD patients. The results of IHC and WB analyses showed that the expression level of KIAA1199 in tumor tissues was higher than that in adjacent tissues. GO and KEGG analyses indicated KIAA1199 was mainly involved in extracellular matrix (ECM)-receptor interaction and extracellular matrix structure constituent. KIAA1199 was positively correlated with infiltrating levels of CD4+ T cells, macrophages, neutrophil cells, dendritic cells, and showed positive relationship with immune marker subsets expression of a variety of immunosuppressive cells. Conclusion: High expression of KIAA1199 predicts a poor prognosis of LUAD patients. KIAA1199 might exert its carcinogenic role in the tumor microenvironment via participating in the extracellular matrix formation and regulating the infiltration of immune cells in LUAD. The results indicate that KIAA1199 might be a novel biomarker for evaluating prognosis and immune cell infiltration in LUAD.

Nitidine chloride induces caspase 3/GSDME-dependent pyroptosis by inhibting PI3K/Akt pathway in lung cancer.

BACKGROUND: As the increasing mortality and incidence of lung cancer (LC), there is an urgent need to discover novel treatment agent. In this study, we aimed to investigate the anti-LC effects of nitidine chloride (NC), a small molecular compound extracted from Chinese herbal medicine, while detailing its underlying mechanisms. METHODS: Cell viability was detected by MTT assays and five cell death inhibitors, including ferrostatin-1 (Fer-1), Z-VAD-FMK, necrostatin-1 (Nec-1), disulfiram (DSF) and IM-54 were used to explore the type of cell death induced by NC. The microscopic features of NC-induced pyroptosis were assessed by transmission electron microscopy (TEM) and the pyroptotic-related proteins such as caspase and gasdermin family, were examined by western blot. Network pharmacology was employed to predict the potential mechanisms of NC in lung cancer treatment. CETSA and DARTs were used to determine the activity of NC binding to targeted protein. Xenograft mice model was established to further investigate the inhibitory effect and mechanism of NC against LC. RESULTS: The pyroptosis inhibitor (DSF) and apoptosis inhibitor (Z-VAD-FMK) but not IM-54, necrostatin-1, or Ferrostatin-1 rescued NC-induced cell death. Morphologically, H1688 and A549 cells treated with NC showed notably pyroptotic features, such as cell swelling and large bubbles emerging from the plasma membrane. Gasdermin E (GSDME) rather than GSDMC or GSDMD was cleaved in NC-treated H1688 and A549 cells with an increased cleavage of caspase 3. Combined with network pharmacology and molecule docking, PI3K/Akt signaling axis was predicted and was further verified by CETSA and DARTs assay. In addition, the activation of PI3K is able to rescue the pyroptosis induced by NC in vitro. In xenograft model of LC, NC significantly hindered the transduction of PI3K-AKT pathway, inducing pyroptosis of tumor. CONCLUSION: Our data indicated that NC is a potential therapeutic agent for the treatment of LC via triggering GSDME-dependent pyroptosis.

Hsa_circ_0045932 regulates the progression of colorectal cancer by regulating HK2 through sponging miR-873-5p.

BACKGROUND: Circular RNAs (circRNAs) have been confirmed to be key regulators for colorectal cancer (CRC) progression. The purpose of this research was to explore the biological role and mechanism of hsa_circ_0045932 in CRC. METHODS: RT-qPCR and Western blot (WB) were applied to examine RNA and protein levels, respectively. MTT assay, EdU assay, and transwell assay were used to detect cell proliferative, migration, and invasion. Glucose uptake and lactic acid level were determined to assess cellular glycolysis. Dual-luciferase reporter and RIP assays were carried out to detect the relationship between miR-873-5p and hsa_circ_0045932 or hexokinase 2 (HK2). Xenograft mice model was established to confirm the function of hsa_circ_0045932 in vivo. RESULTS: Hsa_circ_0045932 was overexpressed in CRC tissue samples and cells. Hsa_circ_0045932 knockdown repressed CRC cell proliferation, invasion, migration, and glycolysis abilities in vitro. MiR-873-5p could be sponged by hsa_circ_0045932, and its inhibitor also reversed the inhibitory effect of hsa_circ_0045932 knockdown on CRC cell progression. HK2 was targeted by miR-873-5p, and hsa_circ_0045932 regulated HK2 expression through targeting miR-873-5p. Overexpression of HK2 reversed the repressive effect of hsa_circ_0045932 knockdown on CRC cell malignant behaviors. Furthermore, the pro-tumor role of hsa_circ_0045932 in vivo was also confirmed using animal experiments. CONCLUSION: Hsa_circ_0045932 promoted CRC progression through sponging miR-873-5p to up-regulate HK2, which might offer novel therapeutic target for CRC clinical intervention.

Intelligent Algorithm-Based Electrocardiography to Predict Atrial Fibrillation after Coronary Artery Bypass Grafting in the Elderly.

The objective of this study was to explore the predictive value of electrocardiogram (ECG) based on intelligent analysis algorithm for atrial fibrillation (AF) in elderly patients undergoing coronary artery bypass grafting (CABG). Specifically, 106 elderly patients with coronary heart disease who underwent CABG in the hospital were selected, including 52 patients with postoperative AF (AF group) and 54 patients without arrhythmia (control group). Within 1-3 weeks after operation, the dynamic ECG monitoring system based on Gentle AdaBoost algorithm constructed in this study was adopted. After the measurement of the 12-lead P wave duration, the maximum P wave duration (Pmax) and minimum P wave duration (Pmin) were recorded. As for simulation experiments, the same data was used as the back-propagation algorithm. The results showed that for the detection accuracy of the test samples, the Gentle AdaBoost algorithm showed 93.7% accuracy after the first iteration, and the Gentle AdaBoost algorithm was 16.1% higher than the back-propagation algorithm. Compared with the control group, the detection rate of arrhythmia in patients after CABG was significantly lower (P < 0.05). Bivariate logistic regression analysis on Pmax and Pmin showed as follows: Pmax: 95% confidential interval (CI): 1.024-1.081, P < 0.05; Pmin: 95% CI: 1.036-1.117, P < 0.05. The sensitivity of Pmax and Pmin in predicting paroxysmal AF was 78.2% and 73.4%, respectively; the specificity of them was 80.1% and 85.6%, respectively; the positive predictive value was 81.2% and 83.4%, respectively; and the negative predictive value was 79.5% and 75.3%, respectively. In conclusion, the generalization ability of Gentle AdaBoost algorithm was better than that of back-propagation algorithm, and it can identify arrhythmia better. Pmax and Pmin were important indicators of AF after CABG.

Long Non-coding RNA TMEM220-AS1 Suppressed Hepatocellular Carcinoma by Regulating the miR-484/MAGI1 Axis as a Competing Endogenous RNA.

Long non-coding RNAs (lncRNAs) have a considerable regulatory influence on multiple biological processes. Nevertheless, the role of TMEM220-AS1 in hepatocellular carcinoma (HCC) remains unclear. We used The Cancer Genome Atlas (TCGA) database to analyze the differentially expressed lncRNAs. qRT-PCR was used to verify the results for a large population. The in vitro effects of TMEM220-AS1 on HCC cells were determined using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and Transwell assays in HCC cells. We used qRT-PCR and western blotting to identify the epithelial-mesenchymal transition (EMT). Moreover, we performed bioinformatics analysis, western blotting, dual luciferase reporter gene assay, RNA pull-down, and RNA binding protein immunoprecipitation (RIP) to investigate the underlying molecular mechanisms of TMEM220-AS1 function. Finally, the function of TMEM220-AS1 was verified in vivo. The results showed that TMEM220-AS1 was expressed at considerably low levels in HCC. It was demonstrated that malignant phenotypes and EMT of HCC cells were promoted by the knock down of TMEM220-AS1 both in vivo and in vitro. TMEM220-AS1, which was detected primarily in the cytoplasm, functioned as an miRNA sponge to bind miR-484 and promote the level of membrane-associated guanylate kinase, WW, and PDZ domain containing 1 (MAGI1), thereby curbing the malignant phenotypes of HCC cells. In conclusion, low levels of TMEM220-AS1 promote proliferation and metastasis through the miR-484/MAGI1 axis in HCC.

lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/ß-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12.

Hepatocellular carcinoma (HCC) belongs to the most frequent cancer with a high death rate worldwide. Thousands of long non-coding RNAs (lncRNAs) have been confirmed to influence the development of human cancers, including HCC. Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR) that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in vitro and facilitated tumor growth in vivo. In addition, western blot analysis and TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/ß-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/ß-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.

Total and bioaccessible heavy metals in cabbage from major producing cities in Southwest China: health risk assessment and cytotoxicity.

Green leafy vegetables are economical and nutritious, but they may be contaminated with heavy metals. In this study, we assessed the total and bioaccessible concentrations of As, Cd, Pb and Cr in a popular vegetable cabbage (Brassica oleracea) from four major producing cities in Yunnan, Southwest China. With the mean concentrations of As, Cd, Pb and Cr being 0.24, 0.20, 0.32 and 1.28 mg kg-1, the As, Cd and Pb concentrations were within the limits of 0.2-0.5 mg kg-1 based on Chinese National Standards and the WHO/FAO, but Cr concentration was 2.6-times greater than the limit of 0.5 mg kg-1. Based on an in vitro bioaccessibility assay of the Solubility Bioaccessibility Research Consortium (SBRC), As bioaccessibility was the lowest at 11% while those of Cd, Pb and Cr were much greater at 68-87%. The estimated daily intake (EDI) of metals through cabbage ingestion was similar for children and adults. Among the four metals, only Cr's EDI at 2.29-1.87 exceeded 1 based on total and bioaccessible concentrations. The high Cr concentration at 1.28 mg kg-1 coupled with its high bioaccessibility at 67.5% makes Cr of concern in cabbage. However, human gastrointestinal cells exposed to the gastric digesta with high bioaccessible heavy metals and risky EDI, showed no obvious cytotoxicity, indicating that existing models based on total or bioaccessible heavy metals may overestimate their human health risk. Taken together, to accurately assess the human health risk of heavy metals in cabbage, both total/bioaccessible concentrations and the gastrointestinal cell responses should be considered.

Effects of matrine in combination with cisplatin on liver cancer.

Matrine, an alkaloid isolated from Sophora flavescens, promotes tumor cell apoptosis and strengthens the anticancer capacity of chemotherapeutic drugs. The present study aimed to investigate the inhibitory effect and underlying mechanism of matrine in combination with cisplatin on liver cancer progression. Tumor progression was studied in nude mice. The human liver cancer cell line HepG2 was injected into BALB/c nude mice subcutaneously to establish a tumor model. Mice were subsequently treated with matrine, cisplatin, matrine + cisplatin or normal saline. Nude mice and tumor growth were monitored. Tumors were excised and the expression of survivin, caspase-3, caspase-7 and caspase-9 was detected by immunohistochemistry. Western blotting was used to determine the expression of survivin, caspase-3, caspase-7, caspase-9 and X-linked inhibitor of apoptosis protein (XIAP) in tumor tissues. The results demonstrated that matrine exerted anticancer effects in liver cancer-transplanted tumors, as evidenced by decrease in tumor weight and volume. Furthermore, the tumor inhibition rate in mice treated with matrine + cisplatin was 83.3%, whereas it was of 37.5 and 75% in mice treated with matrine or cisplatin alone, respectively. In addition, the expression of survivin and XIAP was significantly downregulated, whereas the expression of caspase-3, caspase-7 and caspase-9 was significantly upregulated in tumor tissues from nude mice treated with matrine + cisplatin, compared with those treated with cisplatin, matrine or normal saline. These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9.

Adoptive transfer of regulatory T cells stimulated by Allogeneic Hepatic Stellate Cells mitigates liver injury in mice with concanavalin A-induced autoimmune hepatitis.

Regulatory T cell (Treg)-based therapy can effectively control autoimmune hepatitis (AIH). Hepatic stellate cells (HSC) can selectively stimulate allogeneic Treg proliferation following liver transplantation. This study tested the therapeutic effect and potential mechanisms underlying the action of HSC-stimulated Tregs on AIH in a mouse model of Concanavalin A (ConA)-induced AIH. HSC were isolated from BALB/c mice and characterized. Splenic CD4+CD25+ Tregs were isolated from C57BL/6 mice by immunomagnetic beads. The cells were co-cultured with primary (HSC-0), the second generation of HSC (HSC-2) for 72 h. The proliferation of Tregs was determined by flow cytometry. Similarly, the Tregs were co-cultured with HSC in transwell plates to determine the potential cell-cell contact dependent. The CD4+CD25- effector T cells (CFSE-Teffs) were co-cultured with Teff or Tregs in the presence or absence of HSC to determine the suppressive capacity of Tregs. The effects of Tregs or HSC-stimulated Tregs on AIH severity and the frequency of splenic Tregs and Th17 cells were examined in mice. Co-culture with HSC-2 significantly promoted Treg proliferation in a dose- and cell-cell contact-dependent manner, and allogeneic HSC enhanced the suppressive activity of Tregs to inhibit the proliferation of Teff in vitro. Adoptive transfer of Tregs, particularly of HSC-stimulated Tregs, significantly reduced liver injury, inflammation and Ishak modified histology activity index in AIH mice, which were associated with improving the balance of Treg and Th17 cell responses. Our data indicated that mature HSC stimulated allogeneic Treg proliferation in a dose and cell-cell contact-dependent manner, and HSC enhanced the suppressive activity of Tregs to inhibit the proliferation of Teff. Adoptive transfer of HSC-stimulated Tregs significantly reduced liver injury in AIH mice by modulating the balance of Treg and Th17 cell responses.

Regulating structural dimensionality and emission colors by organic conjugation between SmIII at a fixed distance.

The conjugation of bridging bis(diphenylphosphine oxide) alkane or arene ligands was found to control the structural dimensionality and the emission color of complexes from reactions with SmIII(hfac)3(H2O)2 (hfac- = hexafluoroacetylacetonato) while retaining the SmSm distances. Bis(diphenylphosphine oxide)-1,4-butane (L1) affords a one-dimensional (1D) ribbon {Sm(hfac)3(L1)}∞ (1) that emits red color, while bis(diphenyl-phosphinoyl)-1,4-benzene (L2) results in a two-dimensional (2D) network {Sm(hfac)2(CF3COO)(L2)3}∞ (2) and near-white emission, but bis(diphenyl-phosphinoyl)-9,10-anthracene (L3) forms a zero-dimensional (0D) cyclic structure {Sm(hfac)3(L3)}2 (3) with strong ππ interactions that emit green color. Noticeably, the conjugation change is accompanied by a configurational change of coordination from trans for 1 and 2 to cis for 3. The color change is associated with the superposition of ligand and Sm based electronic band energies and their intensities. Such white light emission by a single compound having contributions from different building components is quite rare.

Sensitized near infrared emission through supramolecular d → f energy transfer within an ionic Ru(ii)-Er(iii) pair.

The newly synthesized ionic triple salt Ru-Er, {[RuII(bpy)2(dbim)][ErIII(hfac)4][CF3COO]·H2O} (bpy = 2,2'-bipyridine; hfac- = hexafluoroacetylacetonate; dbim = 2,2'-dibenzimidazole) exhibits near-infrared (NIR) emission at 1535 nm by intermolecular Ru → Er (d → f) energy transfer across supramolecular interactions when pumped within the Ru(ii) 3MLCT band. It is the first such observation for a transition metal-lanthanide ionic pair.

Decorin-loaded poly lactic-co-glycolic acid nanoparticles modified by anti-alpha fetoprotein antibody: preparation, proliferation inhibition and induced apoptosis effects on HepG2 cells in vitro.

OBJECTIVES: Decorin (DCN) is a negative regulatory factor for the growth of cancer cells and can inhibit the proliferation, metastasis of cancer cells and angiogenesis in cancer tissues. The aims of this study were to prepare the nanoparticles consisting of DCN and poly lactic-co-glycolic acid (PLGA) modified by anti-alpha fetoprotein (AFP) monoclonal antibody (mAb) and to examine the conventional physical properties, the in-vitro release of DCN and the targeting effect of these nanoparticles on HepG2 cells. KEY FINDINGS: The encapsulated plasmid was slowly and steadily released from the nanoparticles. The targeted PLGA nanoparticles were initiatively taken in HepG2 cells high-efficiently. According to the results of RT-PCR, DCN gene in AFPmAb-PLGA-rhDCN nanoparticles can be expressed in HepG2 cells successfully. These nanoparticles significantly inhibited the proliferation of HepG2 cells and induced apoptosis. The mRNA expression of Bcl-2 gene in the AFPmAb-PLGA-rhDCN-treated groups appeared significantly to decrease and the caspase-3 gene had the opposite trend as compared with that of control group (P < 0.01). CONCLUSION: These studies revealed that these nanoparticles were capable of specifically targeting the HepG2 cells and inhibiting the proliferation and they induce apoptosis of HepG2 cells in vitro, which was in a dose- and time-dependent manner.

The efficacy of topical tranexamic acid in total hip arthroplasty: a meta-analysis.

BACKGROUND: Topical tranexamic acid (TXA) has been shown to be effective in reducing blood loss and the need for transfusion after total knee arthroplasty. However, the effectiveness of topical TXA use in total hip arthroplasty (THA) still remains unclear. The purpose of this meta-analysis is to examine the safety and efficacy of topical use of TXA following THA. HYPOTHESIS: Topical TXA reduces blood loss and transfusion rates without increasing risk of deep vein thrombosis in patients with THA. METHODS: An electronic literature search of PubMed, Embase, the Cochrane Library, Web of Science and Chinese Biomedical Database was performed, to identify studies published before February 2015. All randomized controlled trials and cohort studies evaluating the efficacy of topical TXA during THA were included. Two independent authors identified the eligible studies, assessed their methodological quality, and extracted data. The data were using fixed-effects or random-effects models with (standard) mean differences and risk ratios for continuous and dichotomous variables, respectively. Data were analysed using RevMan 5.3 software. RESULTS: Fourteen studies encompassing 2594 patients met the inclusion criteria for our meta-analysis. Our meta-analysis indicated that when compared with the placebo group, topical use of TXA significantly reduced total blood loss (MD = -297.65 ml, 95 % CI -371.68 ml, 116.08 ml; P < 0.01), drainage loss (MD = -164.68 ml, 95 % CI -236.63 ml, -92.73 ml; P < 0.01), transfusion rate (RR = 0.26, 95 % CI 0.17, 0.40; P < 0.01) and with less of a drop in haemoglobin level (SMD = -0.66, 95 % CI -0.91, -0.41; P < 0.01) after primary THA. No significant difference in length of hospital stay (MD = -0.40, 95 % CI -0.91, 0.11; P = 0.14), deep vein thrombosis (RR = 1.19, 95 % CI 0.40, 3.57; P = 0.16) and pulmonary embolism (RR = 1.11, 95 % CI 0.11, 10.81; P = 0.21) among the study groups. CONCLUSIONS: Topical TXA could significantly reduce total blood loss, drainage loss, transfusion rates and decrease haemoglobin level following THA, without increasing risk of venous thromboembolisms.

Oral direct factor Xa inhibitor versus enoxaparin for thromboprophylaxis after hip or knee arthroplasty: Systemic review, traditional meta-analysis, dose-response meta-analysis and network meta-analysis.

OBJECTIVES: To analyze the efficacy and safety of direct factor Xa inhibitors for thromboprophylaxis after total hip or knee replacement. To delineate the dose response effect of direct factor Xa inhibitors. To compare the efficacy between any two direct factor Xa inhibitors. DESIGN: Systemic review, traditional meta-analysis, dose-response meta-analysis and network meta-analysis. DATA SOURCE: PubMed, EMBASE and Cochrane Library. STUDY SELECTION: Randomized controlled trials of rivaroxaban, apixaban, betrixaban, darexaban and edoxaban were compared with enoxaparin for thromboprophylaxis after total hip or knee replacement. Two reviewers independently checked the quality of RCTs. Another two investigators independently extracted data. The primary efficacy outcomes (composite of deep venous thrombosis, non-fatal pulmonary embolism and death of all causes) and the primary bleeding outcomes (major bleeding and non-major but clinically relevant bleeding) were summarized for meta-analysis. Stata software was used for traditional meta-analysis and dose-response meta-analysis, and Winbugs software was used for network meta-analysis. RESULTS: Twenty trials with 38,507 subjects in the intention-to-treat population were included. Compared with enoxaparin, the risk of total venous thromboembolism was lower with rivaroxaban (relative risk 0.70, 95% confidence interval 0.60 to 0.81), apixaban (0.62, 0.47 to 0.81), and edoxaban (0.62, 0.39 to 0.97) and similar to darexaban (0.96, 0.84 to 1.11) and betrixaban (1.28, 0.97 to 1.68). Compared with enoxaparin, the risk of major or clinically relevant non-major bleeding was higher with rivaroxaban (1.52, 1.14 to 2.02), lower with betrixaban (0.34, 0.14 to 0.84) and similar to apixaban (0.88, 0.73 to 1.05), darexaban (0.85, 0.66 to 1.09) or edoxaban (1.30, 0.72 to 2.33). The risk of major and clinically relevant non-major bleeding of rivaroxaban had a linear relationship with its treatment doses; the risk of total venous thromboembolism of betrixaban and darexaban had linear relationships with their respective treatment doses. There was no linear nor non-liner relationships between the effect of apixaban and its treatment dose. The ranking of total venous thromboembolism risk from low to high was: rivaroxaban, apixaban, edoxaban, enoxaparin, darexaban, and betrixaban. The ranking of major and clinically relevant non-major bleeding from low to high was: betrixaban, enoxaparin, darexaban, edoxaban, apixaban, and rivaroxaban. CONCLUSIONS: Direct oral factor Xa inhibitors are more effective to prevent venous thromboembolism after total hip or knee replacement. Their anticoagulant effect was not necessarily compromised with a higher bleeding risk. Rivaroxaban, apixaban and edoxaban showed a better anticoagulant effect, as compared with enoxaparin. Rivaroxaban had a higher bleeding rate, while apixaban and edoxaban did not show significantly higher bleeding risks.

Strong expression of paired-like homeodomain transcription factor 1 (PITX1) is associated with a favorable outcome in human osteosarcoma.

Paired-like homeodomain transcription factor 1 (PITX1) has been implicated as a tumor suppressor in various cancers. However, the biological and clinical significance of PITX1 in osteosarcoma has not been fully elucidated. Here, we studied the expression and clinical significance of PITX1 in 6 normal lower limb bone tissue specimens and 35 osteosarcoma tissue samples by immunohistochemistry. PITX1 was expressed in all normal tissues (6/6, 100 %) and in 85.7 % (30/35) of tumor tissues (P > 0.05). In addition, all normal tissue specimens showed high PITX1 expression (6/6, 100 %) while only 23.3 % (7/30) osteosarcoma tissue specimens had high PITX1 expression (P < 0.05). Patients with median overall survival (OS) >12 months had significantly higher PITX1 levels compared with those whose median OS was less than or equal to 12 months (P < 0.05 or 0.001). Furthermore, patients with lung metastasis had significantly lower PITX1 levels than patients without lung metastasis. In conclusion, PITX1 expression is downregulated in osteosarcoma and correlates with patient survival and lung metastasis.