Biotemplate-Assisted Growth of ZnO in Gas Sensors for ppb-Level NO2 Detection.

With the growing concern over the adverse effects of environmental pollution on human health, the combination of environmentally friendly and nontoxic biomaterials with metal oxide semiconductor materials for electronic devices has emerged as a prominent trend in current research. In this study, we utilized 150 mg apple biotemplates to assist in the hydrothermal synthesis of ZnO nanospheres. It successfully achieved high sensitivity for detecting 35 and 350 ppb NO2 at room temperature, with responses of 13.74 and 132.44%, respectively. Simultaneously, the 5-cycle repeatability and multiple-gas selectivity exhibited significant improvements. The ZnO nanospheres demonstrated enhanced sensing performance compared to pure ZnO nanorods, which is attributed to the following mechanisms: reason I, the modified surface morphology increasing the surface-to-volume ratio; reason II, an increase in oxygen vacancies, leading to reduced crystallinity and a higher electron concentration; reason III, incorporation of carbon elements on the nanostructure surface to increase active sites. The novel gas sensor assisted by the apple pectin biotemplate offers a promising solution for NO2 gas detection, featuring low operating temperatures, low concentrations, and high response sensitivity.

Cyclizine-induced proinflammatory responses through Akt-NFκB pathway in macrophages.

Cyclizine exhibits sedation and treatment of nausea, vomiting, and motion sickness due to antihistaminic and antimuscarinic effects. Cyclizine has the potential for abuse due to the hallucinogenic and euphoric effect. The response of overdose and illegal abuse of cyclizine includes confusion, tremors, chest pain, ataxia, seizures, and lead to suicide. Macrophage plays the important role in the innate immunity. However, over activation of macrophages results in pro-inflammatory responses in peripheral tissues. In the present study, cyclizine was found to enhanced the generation of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6. We further found that secretion of nitrogen oxide (NO) induced by cyclizine via expression of inducible nitric oxide synthases (iNOS). Cyclizine exhibited parallel stimulation of phosphorylation of nuclear factor-κB (NFκB) p65, and its up-stream factor Akt. These results indicated that the expression of pro-inflammatory cytokines, pro-inflammatory mediators, and adhesion molecules would be induced by cyclizine via activation of Akt-NFκB pathway in macrophages.

Patient-reported motor chemotherapy-induced peripheral neuropathy impacts function in advanced colorectal cancer survivors receiving chemotherapy: A cross-sectional study.

AIMS: Chemotherapy-induced peripheral neuropathy limits cancer survivors' compliance with chemotherapy and impaired function. This study aimed to examine separate impacts of clinician-assessed, patient-reported sensory and motor chemotherapy-induced peripheral neuropathy on physical/role function and functional interference in advanced colorectal cancer survivors receiving chemotherapy. METHODS: A cross-sectional, correlational design utilizing convenience sampling enrolled 75 stage III or IV colorectal cancer adults undergoing chemotherapy. Participants filled out the Patient Neurotoxicity Questionnaire, Identification Pain Questionnaire, and Peripheral Neuropathy Scale. Then, a trained research nurse conducted a brief neurological assessment using the Total Neuropathy Scale - clinical version. RESULTS: The prevalence of sensory and motor chemotherapy-induced peripheral neuropathy was from 34.7% to 54.7% and from 16.0% to 17.3%, respectively. Further, 20% of participants suffered from neuropathic pain. A low correlation between clinician-assessed and patient-reported chemotherapy-induced peripheral neuropathy was detected. The function was significantly impacted by patient-reported motor chemotherapy-induced peripheral neuropathy. CONCLUSIONS: This study was superior in utilizing the brief and valid patient-reported and clinician-assessed tools to measure sensory and motor chemotherapy-induced peripheral neuropathy. Moreover, the identification of patient-reported motor symptoms has the largest influence on function in advanced colorectal cancer survivors. Nurses may use the brief and easily administered tools in clinical settings for effective screening and early detection of motor and sensory chemotherapy-induced peripheral neuropathy to prevent functional decline in advanced colorectal cancer survivors. However, this study was still limited because of the cross-sectional design, small sample size, sample heterogeneity, and recruiting participants from only one medical center.

Embedded Immunodetection System for Fecal Occult Blood.

In this paper, a rapid test system with high sensitivity, linearity, and stability is presented for fecal occult blood (FOB) detection. The coloration results of the immune response are used as the basis for the determination of the detection target in combination with an immunochromatographic strip. The rapid test system can be used to detect and calculate the concentration of the sample, so detection of the immune coloration response is more accurate in a quantitative analysis. The system is composed of both hardware and software. The programs used for the analysis and programmed by Python include the main program, polarization calibration, QR Code decoding, Bluetooth transmission, and image processing. After verification of each part of the system, it was found that the rapid test system successfully detects from 0 ng/mL to 400 ng/mL of FOB with coefficients of variation (CV) below 3.7% and 1000 ng/mL with a CV only at 7.41%.

Mg17Al12 phase in magnesium alloy waste facilitating the Ni2+ reduction in nickel plating wastewater.

A process for recycling Ni2+ in Ni-plating wastewater was investigated. This study employed Mg alloy flash waste to reduce the Ni2+ in the wastewater into metallic Ni. Fine second-phase Mg17Al12 in a network is the critical point for promoting the reduction reaction of Ni2+. The microstructures of the Mg alloy flash scrap and the die-cast Mg alloy scrap waste fulfilled the requirement. The Mg17Al12 is like a catalyst for the quick reduction of the Ni2+ ions into pure Ni metal. Contrarily, pure Mg (not containing Mg17Al12 particles) and gravity-cast AZ91D Mg alloy (having coarse Mg17Al12 particles) were not suitable for being used for the Ni2+ wastewater treatment. Based on the above results and discussion, using the Mg alloy flash scrap waste for treating the laboratory-made Ni2+-containing wastewater, the wastewater initially with ∼5600 ppm of Ni2+ ions could be reduced to ∼20 ppm in 2 h. When applying the Mg alloy flash scrap for the Ni plating wastewater from industry, the concentration of Ni2+ was able to be reduced from ∼16,670 ppm to ∼1434 ppm in 10 min for the wastewater at 90 °C.

Systematic review of the potential respiratory carcinogenicity of metallic nickel in humans.

The inhalation of dust containing certain nickel compounds has been associated with an increased risk of lung and nasal cancers in occupational studies of workers who process or refine sulfidic nickel ores and are exposed to relatively high levels of mixtures of water-soluble, sulfidic, oxidic, and/or metallic forms of nickel. We conducted a systematic review of the potential carcinogenicity of metallic nickel, focusing on cancers of the respiratory tract. We evaluated the quality and risk of bias (RoB) of the relevant epidemiology, experimental animal, and in vitro mechanistic studies using the National Toxicology Program's Office of Health Assessment and Translation (OHAT) RoB Rating Tool. We then used a systematic review protocol based on the OHAT approach to critically assess whether metallic nickel should be considered a human respiratory carcinogen. Our evaluation of the epidemiology studies indicates that there is no substantive evidence of increased respiratory cancer risk in workers exposed predominantly to metallic nickel. Animal evidence indicates that metallic nickel does not increase the incidence of respiratory tumors in rodents exposed by inhalation. The in vitro studies are limited in value, as they bypass normal clearance mechanisms. Nevertheless, the mechanistic evidence indicates that metallic nickel is not mutagenic but can induce DNA strand breaks under certain conditions. Based on a standard framework for assessing causality, we conclude that the evidence does not support a causal relationship between metallic nickel exposure and respiratory cancer in humans.

Resistive Switching Behavior of Magnesium Zirconia Nickel Nanorods.

To effectively improve the uniformity of switching behavior in resistive switching devices, this study developed magnesium zirconia nickel (MZN) nanorods grown on ITO electrodes through hydrothermal method. The field emission scanning electron microscope image shows the NR formation. Al/MZN NR/ITO structure exhibits forming-free and bipolar resistive switching behaviors. MZN NRs have relatively higher ON/OFF ratio and better uniformity compared with MZN thin film. The superior properties of MZN NRs can be attributed to its distinct geometry, which leads to the formation of straight and extensible conducting filaments along the direction of MZN NR. The results suggest the possibility of developing sol-gel NR-based resistive memory devices.

Utilizing Experimental Mouse Model to Identify Effectors of Hepatocellular Carcinoma Induced by HBx Antigen.

Hepatocellular carcinoma (HCC) is among the ten most commonly diagnosed cancers and the fourth leading cause of cancer-related death. Patients with hepatitis B virus (HBV) infection are prone to developing chronic liver diseases (i.e., fibrosis and cirrhosis), and the HBV X antigen plays an important role in the development of HCC. The difficulty in detecting HCC at the early stages is one of the main reasons that the death rate approximates the incidence rate. The regulators controlling the downstream liver protein expression from HBV infection are unclear. Mass spectrometric techniques and customized programs were used to identify differentially expressed proteins which may be involved in the development of liver fibrosis and HCC progression in hepatitis B virus X protein transgenic mice (HBx mice). FSTL1, CTSB, and TGF-ß enhanced the signaling pathway proteins during the pathogenesis of HBx. Missing proteins can be essential in cell growth, differentiation, apoptosis, migration, metastasis or angiogenesis. We found that LHX2, BMP-5 and GDF11 had complex interactions with other missing proteins and BMP-5 had both tumor suppressing and tumorigenic roles. BMP-5 may be involved in fibrosis and tumorigenic processes in the liver. These results provide us an understanding of the mechanism of HBx-induced disorders, and may serve as molecular targets for liver treatment.

Prenatal and early life diesel exhaust exposure disrupts cortical lamina organization: Evidence for a reelin-related pathogenic pathway induced by interleukin-6.

Several epidemiological studies have shown associations between developmental exposure to traffic-related air pollution and increased risk for autism spectrum disorders (ASD), a spectrum of neurodevelopmental disorders with increasing prevalence rate in the United States. Though animal studies have provided support for these associations, little is known regarding possible underlying mechanisms. In a previous study we found that exposure of C57BL/6J mice of both sexes to environmentally relevant levels (250-300 µg/m3) of diesel exhaust (DE) from embryonic day 0 to postnatal day 21 (E0 to PND21) caused significant changes in all three characteristic behavioral domains of ASD in the offspring. In the present study we investigated a potential mechanistic pathway that may be of relevance for ASD-like changes associated with developmental DE exposure. Using the same DE exposure protocol (250-300 µg/m3 DE from E0 to PND21) several molecular markers were examined in the brains of male and female mice at PND3, 21, and 60. Exposure to DE as above increased levels of interleukin-6 (IL-6) in placenta and in neonatal brain. The JAK2/STAT3 pathway, a target for IL-6, was activated by STAT3 phosphorylation, and the expression of DNA methyltransferase 1 (DNMT1), a STAT3 target gene, was increased in DE-exposed neonatal brain. DNMT1 has been reported to down-regulate expression of reelin (RELN), an extracellular matrix glycoprotein important in regulating the processes of neuronal migration. RELN is considered an important modulator for ASD, since there are several polymorphisms in this gene linked to the disease, and since lower levels of RELN have been reported in brains of ASD patients. We observed decreased RELN expression in brains of the DE-exposed mice at PND3. Since disorganized patches in the prefrontal cortex have been reported in ASD patients and disrupted cortical organization has been found in RELN-deficient mice, we also assessed cortical organization, by labeling cells expressing the lamina-specific-markers RELN and calretinin. In DE-exposed mice we found increased cell density in deeper cortex (lamina layers VI-IV) for cells expressing either RELN or calretinin. These findings demonstrate that developmental DE exposure is associated with subtle disorganization of the cerebral cortex at PND60, and suggest a pathway involving IL-6, STAT3, and DNMT1 leading to downregulation of RELN expression that could be contributing to this long-lasting disruption in cortical laminar organization.

Sex and genetic differences in the effects of acute diesel exhaust exposure on inflammation and oxidative stress in mouse brain.

In addition to increased morbidity and mortality caused by respiratory and cardiovascular diseases, air pollution may also contribute to central nervous system (CNS) diseases. Traffic-related air pollution is a major contributor to global air pollution, and diesel exhaust (DE) is its most important component. DE contains more than 40 toxic air pollutants and is a major constituent of ambient particulate matter (PM), particularly of ultrafine-PM. Limited information suggests that exposure to DE may cause oxidative stress and neuroinflammation in the CNS. We hypothesized that males may be more susceptible than females to DE neurotoxicity, because of a lower level of expression of paraoxonase 2 (PON2), an intracellular anti-oxidant and anti-inflammatory enzyme. Acute exposure of C57BL/6 mice to DE (250-300µg/m3 for 6h) caused significant increases in lipid peroxidation and of pro-inflammatory cytokines (IL-1α, IL-1ß, IL-3, IL-6, TNF-α) in various brain regions (particularly olfactory bulb and hippocampus). In a number of cases the observed effects were more pronounced in male than in female mice. DE exposure also caused microglia activation, as measured by increased Iba1 (ionized calcium-binding adapter molecule 1) expression, and of TSPO (translocator protein) binding. Mice heterozygotes for the modifier subunit of glutamate cysteine ligase (the limiting enzyme in glutathione biosynthesis; Gclm+/- mice) appeared to be significantly more susceptible to DE-induced neuroinflammation than wild type mice. These findings indicate that acute exposure to DE causes neuroinflammation and oxidative stress in brain, and suggest that sex and genetic background may play important roles in modulating susceptibility to DE neurotoxicity.

Alleviation of Dermatophagoides microceras-induced allergy by an immunomodulatory protein, FIP-fve, from Flammulina velutipes in mice.

Asthma is a major public health concern. Its greatest risk factor is house dust mite (HDM). Dermatophagoides microceras (Der m) is a type of HDM, and in central Taiwan, there is approximately 80% prevalence of sensitization to Der m. FIP-fve is a fungal immunomodulatory protein (FIP) isolated from the fungus Flammulina velutipes, and exhibits anti-inflammatory properties. To investigate whether FIP-fve affects Der m-induced asthma and inflammation, we evaluated hyper-responsiveness (AHR), pathological changes, and cytokines in mice. We demonstrated that oral FIP-fve decreased Der m-induced airway AHR, airway inflammation, cell infiltration, and expression of cytokines in the bronchoalveolar lavage fluid of Balb/c mice. The results of this study suggest that FIP-fve suppresses asthma, inflammation, and respiratory pathogenesis stimulated by Der m. FIP-fve is able to maintain immunomodulatory activity even in simulated gastric fluid and intestinal fluid. FIP-fve could be a safe and stable agent for suppression of allergic asthma.

Alleviation of respiratory syncytial virus replication and inflammation by fungal immunomodulatory protein FIP-fve from Flammulina velutipes.

Respiratory syncytial virus (RSV) causes bronchiolitis in children followed by inflammation and asthma-like symptoms. The development of preventive therapy for this virus continues to pose a challenge. Fungal immunomodulatory proteins (FIPs) exhibit anti-inflammatory function. FIP-fve is an immunomodulatory protein isolated from Flammulina velutipes. To determine whether FIP-fve affects the infection or consequence of immunity of RSV, we investigated viral titers of RSV and inflammatory cytokine levels in vivo and in vitro. Oral FIP-fve decreased RSV-induced airway hyperresponsiveness (AHR), airway inflammation, and IL-6 expression in bronchoalveolar lavage fluid (BALF) of BALB/c mice. RSV replication and interleukin 6 (IL-6) levels in RSV-infected HEp-2 cells were compared before and after FIP-fve treatment. FIP-fve inhibited viral titers on plaque assay and Western blot, as well as inhibited RSV-stimulated expression of IL-6 on ELISA and RT-PCR. The results of this study suggested that FIP-fve decreases RSV replication, RSV-induced inflammation and respiratory pathogenesis. FIP-fve is a widely used, natural compound from F.velutipes that may be a safe agent for viral prevention and even therapy.

Interruption of lung cancer cell migration and proliferation by fungal immunomodulatory protein FIP-fve from Flammulina velutipes.

FIP-fve is an immunomodulatory protein isolated from Flammulina velutipes that possesses anti-inflammatory and immunomodulatory activities. However, little is known about its anticancer effects. It is suppressed cell proliferation of A549 lung cancer cells on MTT assay following 48 h treatment of FIP-fve. FIP-fve treatment also resulted in cell cycle arrest but not apoptosis on flow cytometry. This immunomodulatory protein was observed to increase p53 expression, as well as the expression of its downstream gene p21, on Western blot. FIP-fve inhibited migration of A549 cells on wound healing assay and decreased filopodia fiber formation on labeling with Texas Red-X phalloidin. To confirm the effect of FIP-fve on the role of Rac1 in filopodia formation, we investigated the activity of Rac1 in A549 cells following FIP-fve treatment. FIP-fve inhibited EGF-induced activation of Rac1. We demonstrated that FIP-fve decreases RACGAP1 mRNA and protein levels on RT-PCR and Western blot. In addition, the reporter activity of RACGAP1 was reduced by FIP-fve on RacGAP1 promoter assay. Silencing of RacGAP1 decreased cell migration, and overexpression of RacGAP1 increased cell migration in A549 cells. In conclusion, FIP-fve inhibits lung cancer cell migration via RacGAP1 and suppresses the proliferation of A549 via p53 activation pathway.

In utero and early life exposure to diesel exhaust air pollution increases adult susceptibility to heart failure in mice.

BACKGROUND: Fine particulate air pollution (PM2.5) is a global health concern, as exposure to PM2.5 has consistently been found to be associated with increased cardiovascular morbidity and mortality. Although adult exposure to traffic related PM2.5, which is largely derived from diesel exhaust (DE), has been associated with increased cardiac hypertrophy, there are limited investigations into the potential effect of in utero and early life exposure on adult susceptibility to heart disease. In this study, we investigate the effect of in utero and early life exposure to DE on adult susceptibility to heart failure. METHODS: Female C57BL/6 J mice were exposed to either filtered air (FA) or DE for 3 weeks (≈ 300 µg/m3 PM2.5 for 6 hours/day, 5 days/week) and then introduced to male breeders for timed matings. Female mice were exposed to either FA or DE throughout pregnancy and until offspring were 3 weeks of age. Offspring were then transferred to either FA or DE for an additional 8 weeks of exposure. At 12 weeks of age, male offspring underwent a baseline echocardiographic assessment, followed by a sham or transverse aortic constriction (TAC) surgery to induce pressure overload. Following sacrifice three weeks post surgery, ventricles were processed for histology to assess myocardial fibrosis and individual cardiomyocyte hypertrophy. mRNA from lung tissue was isolated to measure expression of inflammatory cytokines IL6 and TNFα. RESULTS: We observed that mice exposed to DE during in utero and early life development have significantly increased susceptibility to cardiac hypertrophy, systolic failure, myocardial fibrosis, and pulmonary congestion following TAC surgery compared to FA control, or adult DE exposed mice. In utero and early life DE exposure also strongly modified the inflammatory cytokine response in the adult lung. CONCLUSIONS: We conclude that exposure to diesel exhaust air pollution during in utero and early life development in mice increases adult susceptibility to heart failure. The results of this study may imply that the effects of air pollution on cardiovascular disease in human populations may be strongly mediated through a 'fetal origins' of adult disease pathway. Further investigations on this potential pathway of disease are warranted.

Arsenic trioxide modulates the central snail neuron action potential.

BACKGROUND/PURPOSE: The electropharmacological effect of arsenic trioxide (As2O3) is unknown. The present study investigated the effects of As2O3 on spontaneous neuronal impulse activity. METHODS: Intracellular recordings and the two-electrode voltage clamp method were used to study the effect of As2O3 on the RP4 neuron, the number 4 neuron in the right partial ganglion of the giant African snail (Achatina fulica Ferussac). RESULTS: The RP4 neuron generated spontaneous action potentials, which were affected by As2O3 in a concentration-dependent manner. Extracellular application of 1 or 3 mM As2O3 decreased the frequency of spontaneously generated action potentials. At 10 mM, As2O3 first depolarized and then elicited irreversible bursts of potential (BoPs) at 60 minutes after administration. At 30 mM, As2O3 depolarized the resting membrane potential and abolished the spontaneous action potentials. The BoPs elicited by 10mM As2O3 were blocked when neurons were pretreated with phospholipase C (PLC) inhibitors (10 microM U73122 or 3mM neomycin). The BoPs elicited by As2O3 remained unchanged in the presence of KT5720, verapamil, or calcium replacement solution. Voltage-clamp studies revealed that 10mM As2O3 decreased the fast inward current and had no effect on the steady-state outward current of the neuron. CONCLUSION: As2O3 at 10 mM elicits BoPs in central snail neurons and this effect may relate to the PLC activity of the neuron, rather than protein kinase A activity, or calcium influxes of the neuron. As2O3 at higher concentration irreversibly abolishes the spontaneous action potentials of the neuron.

Bursts of potential elicited by d-amphetamine in central snail neuron: effect of sodium azide.

Effects of sodium azide (NaN(3)) on spontaneously generated action potential and bursts of potential elicited by d-amphetamine (d-amphetamine-elicited BoP) were studied on the right parietal 4 (RP4) neuron of the snail Achatina fulica Ferussac in vitro. Sodium azide altered the spontaneous action potential of RP4 neuron in a concentration-dependent manner. In lower concentrations, neither NaN(3) (30, 100, 300 microM; 1 and 3 mM) nor d-amphetamine (135 microM) affect the resting membrane potential, amplitude and frequency of RP4 neurons, while in the higher concentrations NaN(3) (30 mM) did abolish the spontaneous action potential on RP4 neurons and depolarized the RP4 neurons reversibly. At lower concentration, NaN(3) (30 microM) facilitated the d-amphetamine-elicited BoP. The BoP elicited by NaN(3) (30 microM) and d-amphetamine (135 microM) were decreased following treatment with KT5720 (protein kinase A inhibitor), or intracellular injection of EGTA [ethylene glycol-bis(2-aminoethyl ether)-N,N,N',N'-tetraacetic acid]. However, the BoP was not affected by applying U73122 (1-[6-[((17beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione) or neomycin (phospholipase inhibitors). Voltage clamp studies revealed that NaN(3) (30 microM) did not alter the total fast inwards currents (70 msec.) and the steady-state outwards currents (5 sec.). It appeared that the BoP elicited by NaN(3) (30 microM) and d-amphetamine (135 microM) was mainly due to protein kinase A-related messenger system and intracellular calcium. It is concluded that d-amphetamine-elicited BoP was not mainly due to inhibition of the function of mitochondria in the neuron while the function of mitochondria did alter the BoP elicited by amphetamine.

Effects of rolipram on induction of action potential bursts in central snail neurons.

Effects of rolipram, a selective inhibitor of phosphodiesterases (PDE) IV, on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of the giant African snail (Achatina fulica Ferussac). Oscillations of membrane potential bursts were elicited by rolipram and forskolin. The bursts of potential elicited by rolipram were not inhibited after administration with (a) calcium-free solution, (b) high-magnesium solution (30 mM) or (c) U73122. However, the bursts of potential elicited by rolipram were inhibited by pretreatment with KT-5720 (10 microM). Voltage-clamp studies revealed that rolipram decreased the total inward current and steady-state outward currents of the RP4 neuron. The negative slope resistance (NSR) was not detectable in control or rolipram treated RP4 neurons. TEA elicited action potential bursts and an NSR at membrane potential between -50 mV and -30 mV. It is suggested that the bursts of potential elicited by rolipram were not due to (1) synaptic effects of neurotransmitters; (2) NSR of steady-state I-V curve; (3) phospholipase activity of the neuron. The rolipram-elicited bursts of potential were dependent on the phosphodiesterases inhibitory activity and the cAMP signaling pathway in the neuron.