The profile of HIV-1 drug resistance in Shanghai, China: a retrospective study from 2017 to 2021.

BACKGROUND: HIV-1 drug resistance is a huge challenge in the era of ART. OBJECTIVES: To investigate the prevalence and characteristics of acquired HIV-1 drug resistance (ADR) in Shanghai, China. METHODS: An epidemiological study was performed among people living with human immunodeficiency virus (PLWH) receiving ART in Shanghai from January 2017 to December 2021. A total of 8669 PLWH were tested for drug resistance by genotypic resistance testing. Drug resistance mutations (DRMs) were identified using the Stanford University HIV Drug Resistance Database program. RESULTS: Ten HIV-1 subtypes/circulating recombinant forms (CRFs) were identified, mainly including CRF01_AE (46.8%), CRF07_BC (35.7%), B (6.4%), CRF55_01B (2.8%) and CRF08_BC (2.4%). The prevalence of ADR was 48% (389/811). Three NRTI-associated mutations (M184V/I/L, S68G/N/R and K65R/N) and four NNRTI-associated mutations (V179D/E/T/L, K103N/R/S/T, V106M/I/A and G190A/S/T/C/D/E/Q) were the most common DRMs. These DRMs caused high-level resistance to lamivudine, emtricitabine, efavirenz and nevirapine. The DRM profiles appeared to be significantly different among different subtypes. CONCLUSIONS: We revealed HIV-1 subtype characteristics and the DRM profile in Shanghai, which provide crucial guidance for clinical treatment and management of PLWH.

Sheathless acoustic based flow cell sorter for enrichment of rare cells.

Cell enrichment is a powerful tool in many kinds of cell research, especially in applications with low abundance cell types. In this work, we developed a microfluidic fluorescence activated cell sorting device that was able to perform on-demand, low loss cell detection, and sorting. The chip utilizes three-dimensional acoustic standing waves to position all cells in the same fluid velocity regime without sheath. When the cells pass through a laser interrogation region, the scattering and fluorescent signals are detected, translated and transported to software. The target cells are then identified by gating on the plots. Short bursts of standing acoustic waves are triggered by order from PC to sort target cells within predefined gating region. For very low abundance and rare labeled lymphocytes mixed with high concentration unlabeled white blood cells (WBCs), (1-100 labeled lymphocytes are diluted in 106 WBCs in 1 ml volume fluid), the device is able to remove more than 98% WBCs and recover labeled lymphocytes with efficiency of 80%. We further demonstrated that this device worked with real clinical samples by successfully isolating fetal nucleated red blood cells (FNRBCs) in the blood samples from pregnant women with male fetus. The obtained cells were sequenced and the expressions of (sex determining region Y) SRY genes were tested to determine fetal cell proportion. In genetic analysis, the proportion of fetal cells in the final picked sample is up to 40.64%. With this ability, the device proposed could be valuable for biomedical applications involving fetal cells, circulating tumor cells, and stem cells.

Sheathless microflow cytometer utilizing two bulk standing acoustic waves.

In recent years, microflow cytometry has become a popular research field because of its potential to provide low-cost and disposable chips for complex cell analyses. Herein, we demonstrate a sheathless microflow cytometer which integrates a bulk standing acoustic wave based microchip capable of three dimensional cell focusing. Flow cytometry was successfully demonstrated using this system with a coefficient of variation (CV) of 2.16% with standard calibration beads. The sensitivities calibrated by rainbow beads are 518 MEFL in fluorescein Isothiocyanate (FITC) channel and 264 MEPE in P-phycoerythrin (PE) channels, respectively. The linearities are more than 99% in both channels. The capability of the proposed microflow cytometer is further demonstrated by immunologically labeled leukocytes differentiation in blood. This acoustic-based microflow cytometer did not require any sheath flows or complex structures and can be mass produced. Because of the simple fluid channel, the chip can be easily made pipeless, disposable for applications requiring no cross contamination. Moreover, with the gentle and bio-compatible acoustic waves used, this technique is expected to maintain the viability of cells and other bioparticles.

Advances in the Synthesis of Crystalline Metallosilicate Zeolites via Interlayer Expansion.

Given the numerous industrial applications of zeolites as adsorbents, catalysts, and ion-exchangers, the development of new zeolite structures is highly desired to expand their practical applications. Currently, a general route to develop new zeolite structures is to use interlayer expansion agents to connect layered silicates. In this review, we briefly summarize the novel zeolite structures constructed from the lamellar precursor zeolites MWW, RUB-36, PREFER, Nu-6(1), COK-5, and PLS-1 via interlayer expansion. The contents of the summary contain detailed experiments, physicochemical characterizations, possible expansion mechanisms, and catalytic properties. In addition, the insertion of metal heteroatoms (such as Ti, Fe, Sn) into the layered zeolite precursor through interlayer expansion, which could be helpful to modify the catalytic function, is discussed.

WT1 influences apoptosis and proliferation of immature mice granular cells through regulation of the wnt/ß-catenin signal pathway.

It was to study the influence of Wilms tumor suppressor gene (WT1) on ovarian granular cells (GCs) in mice, and the molecular mechanism involved. LV-WT1 short hairpin ribonucleic acid (shRNA) vector was used to downregulate WT1 expression in granular cells (GCs). The effects of WTI on proliferation and apoptosis of GCs were investigated. Western blot and qRT-PCR were used to assay the mRNA and protein expressions of Bax/bcl-2 in GCs transfected with LV-WT1-RNAi. The expression levels of SUZ12, Wnt5a, Wnt11, Wnt4, Wnt3a, Wnt2 mRNA in GCs were also determined. LV-WT1-RNAi significantly reduced WT1 expression, increased apoptosis and inhibited proliferation of GCs. The inhibition of WT1 had no significant effect on the expression of bcl-2 in GCs. The expressions of Wnt2, Wnt4 and Wnt5a were augmented in WT1-knockdown GCs, relative to non-transfected cells. WT1 activation is necessary for maintaining early survival of GCs in follicles via activation of the Wnt/ß-catenin signal pathway.

Quercetin induces apoptosis and enhances 5-FU therapeutic efficacy in hepatocellular carcinoma.

Quercetin (Q), a flavonoid compound, which is obtained in variety of fruits, seeds, and vegetables, has been reported to possess many pharmacological properties including cancer-preventive and anticancer effects. However, studies on the anticancer effects and underlying mechanisms of Q in human hepatocellular carcinoma (HCC) are still limited. The present study is conducted to investigate the anticancer efficacy and adjuvant chemotherapy action of Q in HCC. HCC cell lines HepG2 and SMCC-7721 were treated with different concentrations of Q. The antiproliferative effects of Q were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and the apoptosis and cell cycle dynamics were assessed by flow cytometry; the expression of apoptosis-associated proteins were evaluated by Western blot and immunohistochemistry staining; the tumor growth in vivo was evaluated in a xenograft mouse model. Our results showed that Q effectively inhibited human HCC cell proliferation and induced apoptosis by upregulating the expression of Bad and Bax and downregulating the expression of Bcl-2 and Survivin in vitro. Furthermore, Q obviously inhibited the tumor growth and enhanced the 5-fluorouracil (5-FU) therapeutic efficacy in vitro and in vivo. Taken together, our findings highlight that Q effectively inhibited the growth of tumor and enhanced the sensitivity to thermotherapy, indicating Q is a potential treatment option for HCC.

ITGB2 fosters the cancerous characteristics of ovarian cancer cells through its role in mitochondrial glycolysis transformation.

Related studies have shown that ITGB2 mediates mitochondrial glycolytic transformation in cancer-associated fibroblasts and participates in tumor occurrence, metastasis and invasion of cancer cells. Based on these studies, we tried to construct a mitochondrial glycolysis regulatory network and explored its effect on mitochondrial homeostasis and ovarian cancer cells' cancerous characteristics. Our research revealed a distinct increase in the expression of ITGB2 and associated signaling pathway elements (PI3K-AKT-mTOR) in cases of ovarian cancer. ITGB2 might control mTOR expression via the PI3K-AKT pathway, thus promote mitochondrial glycolysis transformation and cell energy supply in ovarian cancer. This pathway could also inhibit mitophagy, maintain mitochondrial stability, and enhance the cancerous characteristics in case of ovarian cancer cells by mediating mitochondrial glycolytic transformation. Thus, we concluded that ITGB2-associated signaling route (PI3K-AKT-mTOR) may contribute to the progression of cancerous traits in ovarian cancer via mediating mitochondrial glycolytic transformation.

Quantitative assessment of the influence of PSMA6 variant (rs1048990) on coronary artery disease risk.

The proteasome system is a proteolytic pathway that regulates the expression of genes involved in inflammation. Recently, an association of a functional sequence variation, -8C/G, in the human proteasome subunit a type 6 gene (PSMA6) with the susceptibility to coronary artery disease (CAD) was reported. After that, several validation studies have been conducted among various ethnic populations, but the results have been inconsistent. To investigate this inconsistency and derive a more precise estimation of the relationship, a meta-analysis of 15,991 cases and 16,784 controls from 10 case-control studies was performed. Potential sources of heterogeneity including ethnicity, sample size and HWE status of study were also assessed. In a combined analysis, the summary per-allele OR for CAD of the -8C/G polymorphism was 1.09 (95 % CI: 1.02-1.16; P = 0.006). In the subgroup analysis by ethnicity, significantly increased risks were found in East Asians for the polymorphism; while no significant associations were found among Caucasians and other ethnic population in all genetic models. When restricted to studies concerning myocardial infarction patients, significant associations were detected in all genetic models. Furthermore, significant difference of PSMA6 mRNA expression was found between genotypes. In conclusion, this meta-analysis suggests that G allele of PSMA6-8C/G polymorphism is a risk factor associated with increased CAD susceptibility, but these associations vary in different ethnic populations.

Photocatalytic activity of TiO2 containing anatase nanoparticles and rutile nanoflower structure consisting of nanorods.

A series of TiO2 with different crystal phases and morphologies was synthesized via a facile hydrothermal process using titanium n-butoxide and concentrated hydrochloric acid as raw materials. The photocatalytic activity of the samples was evaluated by degradation of Methyl Orange in aqueous solution under UV-Visible light irradiation. On the basis of detailed analysis of the characterizing results of high-resolution transmission electron microscopy, X-ray powder diffraction measurements, X-ray photoelectron spectroscopy and Brunauer-Emmett-Teller measurement, it was concluded that the photo-activity of the catalyst is related directly to the 3D morphology and the crystal phase composition. An excellent catalyst should have both a rutile 3D flower-like structure and anatase granulous particles. The 3D flower-like structure could enhance light harvesting, as well as the transfer of reactant molecules from bulk solution to the reactive sites on TiO2. In addition, the optimum anatase/rutile phase ratio was found to be 80:20, which is beneficial to the effective separation of the photogenerated electron-hole pairs.

LINC00707 promotes multidrug resistance of ovarian cancer cells by targeting the miR-382-5p/LRRK2 axis.

Multidrug resistance severely limits the efficacy of ovarian cancer (OC) treatment. Recent studies have revealed the carcinogenic role of LINC00707 RNA. However, the role of LINC00707 in the development of multidrug resistance in OC has not been clarified. Therefore, the aim of this study was to investigate the relationship between LINC00707 and multidrug resistance in OC, which can facilitate the development of new therapeutic agents for effectively addressing this issue. The RNA expression of LINC00707, miR-382-5p and leucine-rich repeat kinase 2 (LRRK2) in SKOV3 (a human OC cell line) cells was detected by qRT-PCR. The effects of LINC00707 on the proliferation and viability of SKOV3 cells were determined by MTT assay and colony formation assay. The interaction of LINC00707, miR-382-5p, and LRRK2 was bioinformatically predicted and verified with dual-luciferase reporter assay. In addition, the effect of LINC00707 on drug resistance in SKOV3 cells through targeting the miR-382-5p/LRRK2 axis was explored. The expression of LINC00707 and LRRK2 was significantly increased in SKOV3 cells, while miR-382-5p expression was significantly decreased. The results of bioinformatic prediction and colony formation assay demonstrated that LINC00707 could regulate LRRK2 expression in SKOV3 cells by targeting miR-382-5p. Additionally, knockdown of LINC00707 markedly increased expression of miR-382-5p and decreased that of LRRK2, increased cell proliferation and viability, as well as sensitivity to chemotherapeutic agents in SKOV3 cells. Notably, these manifestations were more obvious with simultaneous knockdown of LINC00707 and miR-382-5p compared with knockdown of LINC00707 alone. LINC00707 is overexpressed in SKOV3 cells and promotes SKOV3 cell proliferation and resistance to chemotherapeutic drugs via targeting the miR-382-5p/LRRK2 axis.

LncRNA CACNA1G-AS1 up-regulates FTH1 to inhibit ferroptosis and promote malignant phenotypes in ovarian cancer cells.

Previous study revealed that ferritin heavy chain-1 (FTH1) could regulate ferritinophagy and affect intracellular Fe2+ content in various tumors, while its N6-methyladenosine (m6A) RNA methylation was closely related the prognosis of ovarian cancer patients. However, little is known about the role of FTH1 m6A methylation in ovarian cancer (OC) and its possible action mechanisms. In this study we constructed FTH1 m6A methylation regulatory pathway (LncRNA CACNA1G-AS1/IGF2BP1) according to related bioinformatics analysis and research, through clinical sample detections we found that these pathway regulatory factors were significantly up-regulated in ovarian cancer tissues, and their expression levels were closely related to the malignant phenotype of ovarian cancer. In vitro cell experiments showed that LncRNA CACNA1G-AS1 could up-regulate FTH1 expression through IGF2BP1 axis, thus inhibited ferroptosis by regulating ferritinophagy, and finally promoted proliferation and migration in ovarian cancer cells. Tumor-bearing mice studies showed that the knock-down of LncRNA CACNA1G-AS1 could inhibited the tumorigenesis of ovarian cancer cells in vivo condition. Our results demonstrated that LncRNA CACNA1G-AS1 could promote the malignant phenotypes of ovarian cancer cells through FTH1-IGF2BP1 regulated ferroptosis.

ZFP57 promotes ovarian cancer progression by transcriptionally regulating BRCA1 and managing G1 checkpoint.

Ovarian cancer (OC) which is one of the frequently-occurring gynecologic malignant tumors, endangers the health of women. The zinc finger protein 57 (ZFP57) plays crucial functions during the progression of cancer and is reported as a prognostic and therapeutic candidate in a variety of cancer. However, the biological function as well as the underlying mechanism of ZFP57 during OC progression remains unknown. Here, ZFP57 expression was found prominently increased in OC tissues and correlated with the prognosis of OC patients. Knock down of ZFP57 in OC cells inhibited the cell proliferation and migration, and also arrested the cells at G1 phase as well as accelerated the apoptosis. Additionally, ZFP57 transcriptionally regulated BRCA1 expression in OC, indicating that ZFP57 may affect BRCA1 mediated G1 checkpoint to regulate the cell cycle of OC cells and further influence the progression of OC. Taken together, our present study discovered a novel function of ZFP57 in OC, suggesting that ZFP57 could be potentially treated as a prognostic biomarker and therapeutic target for OC patients.

C-MYC Inhibited Ferroptosis and Promoted Immune Evasion in Ovarian Cancer Cells through NCOA4 Mediated Ferritin Autophagy.

OBJECTIVE: We aimed to construct the ferritin autophagy regulatory network and illustrate its mechanism in ferroptosis, TME immunity and malignant phenotypes of ovarian cancer. METHODS: First, we used Western blot assays and immunohistochemistry to detect the pathway expression in ovarian cancer samples (C-MYC, NCOA4). Then, we performed RIP and FISH analysis to verify the targeted binding of these factors after which we constructed ovarian cancer cell models and detected pathway regulator expression (NCOA4). Co-localization and Western blot assays were used to detect ferritin autophagy in different experimental groups. We selected corresponding kits to assess ROS contents in ovarian cancer cells. MMP was measured using flow cytometry and mitochondrial morphology was observed through TEM. Then, we chose Clone, EdU and Transwell to evaluate the proliferation and invasion abilities of ovarian cancer cells. We used Western blot assays to measure the DAMP content in ovarian cancer cell supernatants. Finally, we constructed tumor bearing models to study the effect of the C-MYC pathway on ovarian cancer tumorigenesis and TME immune infiltration in in vivo conditions. RESULTS: Through pathway expression detection, we confirmed that C-MYC was obviously up-regulated and NCOA4 was obviously down-regulated in ovarian cancer samples, while their expression levels were closely related to the malignancy degree of ovarian cancer. RIP, FISH and cell model detection revealed that C-MYC could down-regulate NCOA4 expression through directly targeted binding with its mRNA. Ferritin autophagy and ferroptosis detection showed that C-MYC could inhibit ferroptosis through NCOA4-mediated ferritin autophagy, thus reducing ROS and inhibiting mitophagy in ovarian cancer cells. Cell function tests showed that C-MYC could promote the proliferation and invasion of ovarian cancer cells through the NCOA4 axis. The Western blot assay revealed that C-MYC could reduce HMGB1 release in ovarian cancer cells through the NCOA4 axis. In vivo experiments showed that C-MYC could promote tumorigenesis and immune evasion in ovarian cancer cells through inhibiting HMGB1 release induced by NCOA4-mediated ferroptosis. CONCLUSION: According to these results, we concluded that C-MYC could down-regulate NCOA4 expression through directly targeted binding, thus inhibiting ferroptosis and promoting malignant phenotype/immune evasion in ovarian cancer cells through inhibiting ferritin autophagy.

[Retracted] Aberrant expression of B7­H3 in gastric adenocarcinoma promotes cancer cell metastasis.

Following the publication of the above paper, an interested reader drew to the authors' attention that the scratch­wound assay data featured in Fig. 5A on p. 2090 appeared to contain some overlapping data comparing between the panels, such that these data, which were intended to show the results from differently performed experiments, may have been derived from the same original source. After having re­examined their original data, the authors conceded that the figure had been assembled incorrectly (specifically, four of the images selected out of the nine data panels included in this figure part had been chosen erroneously). Furthermore, the first author on the paper (Wei Dai) also acknowledged that several of the named authors had not given their prior consent to be included as such as authors on the paper, and therefore a request was made that the paper be retracted from the publication. In view of these admissions, the Editor of Oncology Reports has accepted the authors' request that the paper be retracted from the journal. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 32: 2086­2092, 2014; DOI: 10.3892/or.2014.3405].

Corrigendum: Modifying SnS2 with carbon quantum dots to improve photocatalytic performance for Cr(VI) reduction.

[This corrects the article DOI: 10.3389/fchem.2022.911291.].

Comprehensive Molecular Analyses of a TNF Family-Based Gene Signature as a Potentially Novel Prognostic Biomarker for Cervical Cancer.

Background: Increasing evidence suggests that tumour necrosis factor (TNF) family genes play important roles in cervical cancer (CC). However, whether TNF family genes can be used as prognostic biomarkers of CC and the molecular mechanisms of TNF family genes remain unclear. Methods: A total of 306 CC and 13 normal samples were obtained from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. We identified differentially expressed TNF family genes between CC and normal samples and subjected them to univariate Cox regression analysis for selecting prognostic TNF family genes. Least absolute shrinkage and selection operator (LASSO) regression and multivariate Cox regression analyses were performed to screen genes to establish a TNF family gene signature. Gene set enrichment analysis (GSEA) was performed to investigate the biological functions of the TNF family gene signature. Finally, methylation and copy number variation data of CC were used to analyse the potential molecular mechanisms of TNF family genes. Results: A total of 26 differentially expressed TNF family genes were identified between the CC and normal samples. Next, a TNF family gene signature, including CD27, EDA, TNF, TNFRSF12A, TNFRSF13C, and TNFRSF9 was constructed based on univariate Cox, LASSO, and multivariate Cox regression analyses. The TNF family gene signature was related to age, pathological stages M and N, and could predict patient survival independently of clinical factors. Moreover, KEGG enrichment analysis suggested that the TNF family gene signature was mainly involved in the TGF-ß signaling pathway, and the TNF family gene signature could affect the immunotherapy response. Finally, we confirmed that the mRNA expressions of CD27, TNF, TNFRSF12A, TNFRSF13C, and TNFRSF9 were upregulated in CC, while that of EDA was downregulated. The mRNA expressions of CD27, EDA, TNF, TNFRSF12A, TNFRSF13C, and TNFRSF9 might be influenced by gene methylation and copy number variation. Conclusion: Our study is the first to demonstrate that CD27, EDA, TNF, TNFRSF12A, TNFRSF13C, and TNFRSF9 might be used as prognostic biomarkers of CC and are associated with the immunotherapy response of CC.

Outbreak of occupational Brucella infection caused by live attenuated Brucella vaccine in a biological products company in Chongqing, China, 2020.

The northern areas of China are traditional endemic regions for brucellosis in both animals and humans, while occasional outbreaks of brucellosis have been observed in neglected southern provinces. On 16 December 2020, Chongqing Center for Disease Control and Prevention (CQCDC) received a report of 15 Brucella seropositive employees in a biological products company. The CQCDC and the local health administrative department launched an investigation that included identification of cases, laboratory testing of samples, and employees' interview to identify the cause of this incident. A case-control study was implemented to compare high-risk factors between cases and serology-negative personals. Human and animal serum samples and environmental swabs were collected for testing. A total of 61 recessive infectors were found with an infection rate of 43.57% (61/140). Fisher's exact test showed that there were significant differences in Brucella infection rates among different post classifications (p = 0.02), working places (p = 0.007), and buildings (p < 0.0001). Case-control study showed that working in vaccine production workshop was independently associated with an increased risk of infection (odds ratio (OR): 2.60; 95% confidence interval (CI): 1.31-5.19). The positive detection rate was 88.06% (59/67) for production environment and 16.67% (2/12) for external environment. The investigation indicated that close contact with biological products and aerosol were the potential transmission routes of this outbreak under the condition of insufficient personal protection and disinfection. Our study provides new epidemiological evidence for a more detailed understanding of occupational infections with live attenuated Brucella vaccine.

Modifying SnS2 With Carbon Quantum Dots to Improve Photocatalytic Performance for Cr(VI) Reduction.

The photoreduction for hazardous Cr(VI) in industrial wastewater has been considered a "green" approach with low-cost and easy-to-go operation. SnS2 is a promising narrow bandgap photocatalyst, but its low charge carrier separation efficiency should be solved first. In this work, N-doped carbon quantum dots (CQDs) were prepared and loaded onto SnS2 nanoparticles via an in situ method. The resulting composite samples (NC@SnS2) were characterized, and their photocatalytic performance was discussed. SnS2 nanoparticles were obtained as hexagonal ones with a bandgap of 2.19 eV. The optimal doping level for NC@SnS2 was citric acid: urea:SnS2 = 1.2 mmol:1.8 mmol:3.0 mmol. It showed an average diameter of 40 nm and improved photocatalytic performance, compared to pure SnS2, following a pseudo-first-order reaction with a kinetic rate constant of 0.1144 min-1. Over 97% of Cr(VI) was photo-reduced after 30 min. It was confirmed that modification of SnS2 with CQDs can not only improve the light-harvesting ability but also stimulate the charge separation, which therefore can enhance the photoreactivity of SnS2 toward Cr(VI) reduction. The excellent stability of NC@SnS2 indicates that it is promising to be practically used in industrial wastewater purification.

Inferior Vena Cava as a Trigger for Paroxysmal Atrial Fibrillation: Incidence, Characteristics, and Implications.

BACKGROUND: Identifying nonpulmonary vein triggers during atrial fibrillation (AF) ablation is of great importance. Currently, there are limited data on AF triggered by the inferior vena cava (IVC). OBJECTIVES: This study was performed to investigate the incidence, characteristics, and implications of IVC triggers for AF. METHODS: A total of 661 patients who underwent initial paroxysmal AF ablation were included. After pulmonary vein isolation, ectopic beats that triggered AF were further studied. Activation mapping and angiography were performed to confirm the location of ectopic origin. Electrocardiographic analysis of the ectopic P-wave (P'-wave) was performed. RESULTS: Six patients (0.91%) with AF triggered by the IVC were confirmed. The mean distance from the earliest activation site to the IVC ostium was 6.8 ± 2.5 mm (5.2 to 11.2 mm). Furthermore, the arrhythmogenic foci within the IVC were all located at the apical hemisphere of the IVC (3 at the septal side and 3 at the anterior side). A total of 2.3 ± 0.5 applications of radiofrequency energy were delivered to eliminate IVC triggers. The mean duration of the P' wave was 91.2 ± 11.2 milliseconds (81 to 108 milliseconds), which was narrower than that of the sinus P-wave (115.2 ± 19.3 milliseconds [87 to 139 milliseconds]; P = 0.002). Moreover, the configuration of all P' waves in the inferior leads was negative. During a mean follow-up period of 25.5 ± 7.3 months, all 6 patients remained arrhythmia free without antiarrhythmic drugs. CONCLUSIONS: IVC trigger, a rare but latent source of paroxysmal AF, could be identified and safely eliminated by focal radiofrequency ablation. Ectopic beats originating from the IVC presented with narrow P'-wave duration and negative P' waves in all inferior leads.

Dispersive solid phase microextraction based on magnesium oxide nanoparticles for preconcentration of auramine O and methylene blue from water samples.

In this study, we investigated the process of preconcentrate and determine trace amounts of Auramine O (AO) and methylene blue (MB) dyes in environmental water samples. For this purpose, the ultrasound-assisted dispersive-magnetic nanocomposites-solid-phase microextraction (UA-DMNSPME) method was performed to extract AO and MB from aqueous samples by applying magnesium oxide nanoparticles (MgO-NPs). The proposed technique is low-cost, facile, fast, and compatible with many existing instrumental methods. Parameters affecting the extraction of AO and MB were optimized using response surface methodology (RSM). Short extraction time, low experimental tests, low consumption of organic solvent, low limits of detection (LOD), and high preconcentration factor (PF) was the advantages of method. The PF was 44.5, and LOD for AO and MB was 0.33 ng mL-1 and 1.66 ng mL-1, respectively. The linear range of this method for AO and MB were 1-1000 ng mL-1 and 5-2000 ng mL-1, respectively. In addition, the relative standard deviation (RSD; n = 5) of the mentioned analytes was between 2.9% and 3.1%. The adsorption-desorption studies showed that the efficiency of adsorbent extraction had not declined significantly up to 6 recycling runs, and the adsorbent could be used several times. The interference studies revealed that the presence of different ions did not interfere substantially with the extraction and determination of AO and MB. Therefore, UA-DMNSPME-UV/Vis method can be proposed as an efficient method for preconcentration and extraction of AO and MB from water and wastewater samples.