An enhanced EWMA chart with variable sampling interval scheme for monitoring the exponential process with estimated parameter.

Control charts have been used to monitor product manufacturing processes for decades. The exponential distribution is commonly used to fit data in research related to healthcare and product lifetime. This study proposes an exponentially weighted moving average control chart with a variable sampling interval scheme to monitor the exponential process, denoted as a VSIEWMA-exp chart. The performance measures are investigated using the Markov chain method. In addition, an algorithm to obtain the optimal parameters of the model is proposed. We compared the proposed control chart with other competitors, and the results showed that our proposed method outperformed other competitors. Finally, an illustrative example with the data concerning urinary tract infections is presented.

A high-performance long-wave infrared photodetector based on a WSe2/PdSe2 broken-gap heterodiode.

Layered narrow bandgap quasi-two-dimensional (2D) transition metal dichalcogenides (TMDs) demonstrated excellent performance in long-wave infrared (LWIR) detection. However, the low light on/off ratio and specific detectivity (D*) due to the high dark current of the device fabricated using a single narrow bandgap material hindered its wide application. Herein, we report a type-III broken-gap band-alignment WSe2/PdSe2 van der Waals (vdW) heterostructure. The heterodiode device has a prominently low dark current and exhibits a high photoresponsivity (R) of 55.3 A W-1 and a high light on/off ratio >105 in the visible range. Notably, the WSe2/PdSe2 heterodiode shows an excellent uncooled LWIR response, with an R of ∼0.3 A W-1, a low noise equivalence power (NEP) of 4.5 × 10-11 W Hz-1/2, and a high D* of 1.8 × 108 cm Hz1/2 W-1. This work provides a new approach for designing high-performance room-temperature operational LWIR photodetectors.

Lanosterol synthase loss of function decreases the malignant phenotypes of HepG2 cells by deactivating the Src/MAPK signaling pathway.

Cholesterol is critical for tumor cells to maintain their membrane components, cell morphology and activity functions. The inhibition of the cholesterol pathway may be an efficient strategy with which to limit tumor growth and the metastatic process. In the present study, lanosterol synthase (LSS) was knocked down by transfecting LSS short hairpin RNA into HepG2 cells, and cell growth, apoptosis and migratory potential were then detected by Cell Counting Kit-8 cell proliferation assay, flow cytometric analysis and wound healing assay, respectively. In addition, proteins associated with the regulation of the aforementioned cell biological behaviors were analyzed by western blot analysis. The activity of the Src/MAPK signaling pathway was measured by western blotting to elucidate the possible signal transduction mechanisms. LSS knockdown in the HepG2 liver cancer cell line inhibited cell proliferation, with cell cycle arrest at the S phase; it also decreased cell migratory ability and increased apoptosis. The expression proteins involved in the regulation of cell cycle, cell apoptosis and migration was altered by LSS knockdown in HepG2 cells. Furthermore, a decreased Src/MAPK activity was observed in the HepG2 cells subjected to LSS knockdown. LSS loss of function decreased the malignant phenotypes of HepG2 cells by deactivating the Src/MAPK signaling pathway and regulating expression of genes involved in cell cycle regulation, cell apoptosis and migration.

L-asparaginase activity and anti-L-asparaginase antibody as biomarkers in estimating PEG-asp-related anaphylaxis risk in childhood acute lymphoblastic leukemia patients.

BACKGROUND: L-Asparaginase (L-asp), the unconjugated form of polyethylene glycol-conjugated L-asparaginase (PEG-asp), regulates T cell stimulation, antibody production, and lysosomal protease activity to mediate PEG-asp-related anaphylaxis. This study aimed to investigate the relation of L-asp activity and anti-L-asp antibody with anaphylaxis risk and non-anaphylaxis adverse reaction risk in childhood acute lymphoblastic leukemia (ALL) patients who underwent PEG-asp contained therapy. METHODS: In total, 170 childhood ALL patients underwent PEG-asp-contained treatment and their L-asp activity and anti-L-asp antibody were detected on the 7th day after treatment initiation. RESULTS: There were 27 (15.9%) patients who had PEG-asp-related adverse reaction: 17 (10.0%) patients experienced PEG-asp-related anaphylaxis and 14 (8.2%) patients experienced PEG- asp-related non-anaphylaxis adverse reaction. Moreover, L-asp activity was negatively related to anti-L-asp antibody in childhood ALL patients (P<0.001). Elevated L-asp activity was associated with the absence of PEG-asp-related anaphylaxis (P<0.001), PEG-asp-related non-anaphylaxis adverse reaction (P=0.004), and PEG-asp-related adverse reaction (P<0.001). However, the anti- L-asp antibody displayed opposite trend similar to L-asp activity. Receiver operating characteristic (ROC) curve analyses exhibited L-asp activity and anti-L-asp antibody exhibited superior predictive values in estimating PEG-asp-related anaphylaxis risk with area under curve (AUC) of 0.955 and 0.905, respectively compared to PEG-asp-related non-anaphylaxis adverse reaction risk with AUC of 0.730 and 0.675, respectively. Besides, patients with de novo disease, higher risk stratification, and allergic history showed trends linked with PEG-asp-related anaphylaxis risk. CONCLUSION: The monitoring of L-asp activity and anti-L-asp antibody maybe useful for early estimation and prevention of PEG-asp-related anaphylaxis in childhood ALL management.

Estimation of process performance index for the two-parameter exponential distribution with measurement error.

Measurement errors are inevitable in practice, but they are not considered in the existing process performance index. Therefore, we propose an estimation method of process performance index for the two-parameter exponential distribution with measurement errors to fill this gap. In this paper, the relationship between the unobservable actual value and measurement value is considered as full error model, and the maximum likelihood estimation method is considered to obtain the unknown parameters. In addition, we also use the Bootstrap method to construct confidence intervals of process performance index. The performance of the proposed estimation is investigated in terms of bias, mean square error (MSE) and average interval length. Simulation results show that the proposed estimator outperforms other estimators. Finally, an example of the mileage data of the military personnel carrier is given to illustrate the implementation of the proposed estimation method.

Ag/Ni-MOF heterostructure with synergistic enrichment and activation properties for electrocatalytic reduction of 4-nitrophenol.

The synchronous optimization of adsorption and activity dominates the practical performance in electrocatalysis, so Ag/Ni-MOF/Ni foam was synthesized for expediting 4-nitrophenol (4-NP) reduction under mild and green conditions. The synergistic combination of selective adsorption (Ni-MOF) and sites (Ag) contributed to the excellent performance of 4-NP reduction. The 4-NP (25 mM) conversion and Faraday efficiency have been achieved up to 98.4% and 99.8%, respectively. Therefore, this work provides a feasible approach for synergistic enrichment and activation to convert pollutants.

Electrocatalytic reduction of 4-nitrophenol over Ni-MOF/NF: understanding the self-enrichment effect of H-bonds.

The chemical adsorption and active sites play a key role in electrocatalysis, so Ni-MOF/nickel foam was fabricated for efficiently reducing 4-nitrophenol (4-NP) without any sacrificial agents. The coordinated water molecules induced the formation of hydrogen bonds (H-bonds) with the nitro group, contributing to the self-enrichment of 4-NP. The reaction rate reached 0.351 µmol min-1 mg-1. Therefore, this work provides a new insight into the H-bond effect in the field of electrocatalysis.

MiR-363 suppresses the tumor growth of natural killer/T-cell lymphoma via the SIRT6/PI3K/AKT axis.

Background: Natural killer/T cell lymphoma (NKTCL) is a rare and aggressive tumor of non-Hodgkin's lymphoma. The role of micro ribonucleic acid (RNA) (miR)-363 in NKTCL has not yet been elucidated. The present study aimed to investigate the potential role of miR-363 in NKTCL. Methods: The expression of the top five differentially expressed microRNAs (miRNAs) as well as sirtuin 6 (SIRT6) in NK normal cells and its tumor cell lines were explored. The clinical tissues of NKTCL patients were collected and analyzed for expression of miR-363 and SIRT6. In addition, human NK/T-cell lymphoma cells (SNK-6) were transfected into different groups to detect cell proliferation and apoptosis abilities through cell counting kit 8 (CCK-8) experiment and flow cytometry analysis. Western blot assay was employed to examine protein expression. NKTCL nude mice models were constructed by subcutaneous injection of stably transfected SNK-6 cells to validate the mechanism of miR-363 in NKTCL via SIRT6 in vivo. Results: MiR-363 was down-regulated in NKTCL tissues and cell lines. Overexpression of miR-363 inhibited cell proliferation and promoted cell apoptosis. In contrast, SIRT6 was up-regulated in NKTCL and proved to be a downstream target of miR-363. SIRT6 could activate the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Also, miR-363 mimic could suppress the proliferation and induce the apoptosis of NKTCL via the SIRT6/PI3K/AKT axis both in vitro and in vivo. Conclusions: MiR-363 suppresses the SIRT6/PI3K/AKT pathway to restrain cell proliferation and accelerate cell apoptosis during NKTCL progression.

Understanding the Z-scheme heterojunction of BiVO4/PANI for photoelectrochemical nitrogen reduction.

Based on the idea that a heterojunction can significantly promote photoelectrochemical (PEC) efficiency, BiVO4/PANI (polyaniline), as a Z-scheme heterojunction, was designed in this work. BiVO4/PANI achieved a desirable NH3 yield rate (rNH3 = 0.93 µg h-1 cm-2) and faradaic efficiency (FE = 26.43%). This study presents novel insight into PEC NRR research, and it could be extended to the modification of other catalysts for boosting PEC N2 reduction reaction performance.

Charge-transfer dynamics at a Ag/Ni-MOF/Cu2O heterostructure in photoelectrochemical NH3 production.

Ag-decorated ultrathin Ni-MOF on Cu2O was fabricated for the first time. The charge-transfer dynamics at the heterostructure was studied by ultrafast transient absorption spectroscopy in depth. An NH3 yield rate of 4.63 µg h-1 cm-2 with a faradaic efficiency of 24.3% has been achieved. DFT calculations further supported to further comprehend the nitrogen reduction reaction mechanism.

Amorphous MnCO3/C Double Layers Decorated on BiVO4 Photoelectrodes to Boost Nitrogen Reduction.

NH3 is mainly obtained by the Haber-Bosch method in the process of industrial production, which is not only accompanied by huge energy consumption but also environmental pollution. The reduction of N2 to NH3 under mild conditions is an important breakthrough to solve the current energy and environmental problems, so the preparation of catalysts that can effectively promote the reduction of N2 is a crucial step. In this work, BiVO4 decorated with amorphous MnCO3/C double layers has been successfully synthesized by a one-step method for the first time. The C and MnCO3 have been formed as ultrathin film, which enables the establishment of a uniform and tight interface with BiVO4. The temperature-programmed desorption of N2 (N2-TPD) spectra confirmed that the MnCO3/C could endow BiVO4 with a drastic enhancement of the chemical absorption ability of a N2 molecule compared with the pristine BiVO4. Meanwhile, the method of isotope labeling proved that the catalyst exhibited excellent selectivity for the photocatalytic nitrogen reduction reaction (NRR). The production rate of NH3 up to 2.426 mmol m-2 h-1 has been achieved over the BiVO4/MnCO3/C, which is almost 8 times that of pristine BiVO4. The promoted production rate of NH3 over BiVO4/MnCO3/C could be mainly attributed to the cooperative process between MnCO3 and C amorphous layers. Therefore, this work could provide an alternative insight to understand the NRR process based on the model of a hierarchical amorphous structure.

Atractylenolide III reduces NLRP3 inflammasome activation and Th1/Th2 imbalances in both in vitro and in vivo models of asthma.

Paediatric asthma is a common inflammatory disease in children. Atractylenolide III is an active component of the Atractylodes rhizome, an herbal medicine that has been used as an asthma treatment. This study aimed to explore the effects and underlying mechanisms of atractylenolide III in IL-4-induced 16HBE cells and ovalbumin-induced asthmatic mice. The results showed that IL-4 stimulation significantly decreased, and atractylenolide III treatment increased, growth and apoptosis of 16HBE cells. In 16HBE cells, administration of atractylenolide III also significantly suppressed the IL-4-induced increases in the expression of cleaved caspase-1; apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC); and nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3). Moreover, the numbers of total leukocytes, neutrophils, eosinophils, and macrophages significantly increased in ovalbumin-induced mice, and then decreased after atractylenolide III treatment. In ovalbumin-induced asthmatic mice, atractylenolide III treatment also significantly inhibited NLRP3 inflammasome activation and restored the Th1/Th2 balance. These results indicate that atractylenolide III reduced NLRP3 inflammasome activation and regulated the Th1/Th2 balance in IL-4 induced 16HBE cells and ovalbumin-induced asthmatic mice, suggesting it has a protective effect that may be useful in the treatment of paediatric asthma.

Serum levels of vitamin A and 25-hydroxyvitamin D3 (25OHD3) as reflectors of pulmonary function and quality of life (QOL) in children with stable asthma: A case-control study.

BACKGROUND: This study aims to explore the relationship between serum vitamin A and 25-hydroxyvitamin D3 (25OHD3) levels with pulmonary function and quality of life (QOL) in children with stable asthma. METHODS: A total of 117 cases of children with stable asthma were assigned into the case group and 129 healthy children underwent physical examination during the same period into the control group. Electrochemiluminescence was employed to determine serum vitamin A and 25OHD3 levels. The children with stable asthma were further divided into the mild, moderate, and severe groups according to their degree of asthma. A pulmonary function meter was used to assess the pulmonary function indexes: percentage of forced expiratory volume in 1 sec/predictive value (FEV1%pred), forced vital capacity (FVC), forced expiratory volume in 1 sec/forced vital capacity (FEV1/FVC), peak expiratory flow (PEF), and maximal voluntary ventilation (MVV). The children's quality (QOL) of life with asthma was evaluated by their activities of daily living (ADLs) and Medical Research Council (MRC) scores. Pearson correlation analysis was applied to analyze the correlations of serum vitamin A and 25OHD3 levels with FEV1%pred, FVC, FEV1/FVC, PEF, MVV, ADL, and MRC. RESULTS: Serum vitamin A and 25OHD3 levels were lower in children with stable asthma than those who were in the control group (P < .05). The severe group showed the lowest FEV1%pred, FVC, FEV1/FVC, PEF, MVV, and ADL scores, and the highest MRC score compared to the mild and moderate groups (all P < .05). Serum vitamin A and 25OHD3 levels were positively correlated with pulmonary function and ADL score in children with stable asthma, while serum vitamin A and 25OHD3 levels were negatively correlated with MRC score (all P < .05). In the case group, serum vitamin A and 25OHD3 levels were positively correlated with serum calcium and phosphorus levels (all P < .05). CONCLUSION: These findings indicate that increased serum vitamin A and 25OHD3 levels reflect good pulmonary function and good QOL in children with stable asthma.

TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-κB pathway.

Asthma, an increasingly common chronic disease among children, are characterized by airway remodeling, which is partly attributed to the proliferation and migration of airway smooth muscle cell (ASMC). The purpose of the present study was to investigate potential roles and mechanisms of the tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible molecule 14 (Fn14) axis on cell proliferation and migration in HASMCs. Compared to HASMCs from non-asthmatic patients, those from asthmatic patients showed elevated expression levels of both Fn14 and TWEAK. Additionally, similar to the response triggered by platelet-derived growth factor-BB, stimulation with recombinant TWEAK strongly induced cell proliferation and migration in HASMCs. However, depletion of Fn14 remarkably abrogated the enhancement of TWEAK on the cell proliferation and migration of HASMCs. Furthermore, treatment with TWEAK led to the activation of NF-κB. This effect was eliminated by silencing Fn14, indicating that TWEAK-induced NF-κB signaling was mediated via Fn14. Moreover, the TWEAK/Fn14 interaction promoted cell proliferation and migration. These effects were blocked by NF-κB inhibitor SN50, which suggest that the TWEAK/Fn14 signaling system partially depends on NF-κB activity. Collectively, we demonstrated that the TWEAK/Fn14 axis accelerated HASMC cell proliferation and migration by activating the NF-κB pathway, thereby exacerbating airway remodeling in asthma. Altogether, these findings indicate a novel role for the TWEAK/Fn14/NF-κB pathway as a potent option for limiting airway remodeling in asthma.

Lymphatic Circulation Disseminates Bartonella Infection Into Bloodstream.

The hallmark of Bartonella infection is long-lasting intraerythrocytic parasitism. However, the process of Bartonella bacteremia is still enigmatic. In the current study, we used Bartonella tribocorum to determine how Bartonella invasion into the bloodstream from dermal inoculation might occur. Bartonella was poorly phagocytized by peritoneal macrophages in vitro. Intracellular Bartonella survived and replicated in macrophages at an early stage of infection. Intracellular Bartonella inhibited spontaneous cell death of macrophages. They also inhibited Salmonella-induced pyroptosis and mildly reduced inflammasome activation through an unidentified mechanism. A rat model confirmed that Bartonella was also inadequately phagocytized in vivo, because numerous free-floating bacilli were observed in lymph collected from thoracic duct drainage as early as 2 hours after inoculation. Lymphatic fluid drainage in the bloodstream significantly reduced the bacterial load in the bloodstream. These findings illustrated a potential route by which Bartonella invade bloodstream from dermal inoculation before they are competent to infect erythrocytes.

Depolymerization of cytokeratin intermediate filaments facilitates intracellular infection of HeLa cells by Bartonella henselae.

Bartonella henselae is capable of invading epithelial and endothelial cells by modulating the function of actin-dependent cytoskeleton proteins. Although understanding of the pathogenesis has been increased by the development of an in vitro infection model involving endothelial cells, little is known about the mechanism of interaction between B. henselae and epithelial cells. This study aims to identify the binding candidates of B. henselae in epithelial cells and explores their effect on B. henselae infection. Pull-down assays and mass spectrometry analysis confirmed that some of the binding proteins (keratin 14, keratin 6, and F-actin) are cytoskeleton associated. B. henselae infection significantly induces the expression of the cytokeratin genes. Chemical disruption of the keratin network by using ethylene glycol tetraacetic acid promotes the intracellular persistence of B. henselae in HeLa cells. However, cytochalasin B and phalloidin treatment inhibits B. henselae invasion. Immunofluorescent staining demonstrates that B. henselae infection induces an F-actin-dependent rearrangement of the cytoskeleton. However, we demonstrated via immunofluorescent staining and whole-mount cell electron microscopy that keratin intermediate filaments are depolymerized by B. henselae. The results indicate that B. henselae achieves an intracellular persistence in epithelial cells through the depolymerization of cytokeratin intermediate filaments that are protective against B. henselae invasion.

Staining of Bartonella henselae with carboxyfluorescein diacetate succinimidyl ester for tracking infection in erythrocytes and epithelial cells.

Bartonella infection (Bartonella henselae in particular) is responsible for a widening spectrum of human diseases. The persistent colonization of erythrocytes is a feature of Bartonella infection. Endothelial and epithelial cells are also widely used to study the pathogenesis of bartonellosis in vitro. Exploring a convenient method for visualizing the bacillus without affecting infectivity would be very interesting. Carboxyfluorescein diacetate succinimidyl ester (CFSE) has been previously used for staining several bacterial species to study their adhesion to host cells. The present study demonstrated the efficiency and safety of using CFSE in staining B. henselae. The staining of bacillus-invaded erythrocytes and epithelial cells in vitro successfully allowed for flow cytometry and confocol microscopy analyses. Parallel tests using untreated bacteria confirmed that CFSE staining did not result in side effects on the infectivity of B. henselae. Labeling Bartonella with CFSE is a valuable method for studying the bacteria-host interaction.