Stimulating the expression of sphingosine kinase 1 (SphK1) is beneficial to reduce acrylamide-induced nerve cell damage.

Sphingosine kinase 1 (SphK1) is an important signaling molecule for cell proliferation and survival. However, the role of SphK1 in acrylamide (ACR)-induced nerve injury remains unclear. The purpose of this study was to investigate the role and potential mechanism of SphK1 in ACR-induced nerve injury. Liquid chromatography triple quadrupole tandem mass spectrometry (LC-MS/MS) and reverse transcription-quantitative PCR (RT-qPCR) were used to detect sphingosine 1-phosphate (S1P) content in serum and SphK1 content in whole blood from an occupational work group exposed to ACR compared to a non-exposed group. For in vitro experiments, SphK1 in human SH-SY5Y neuroblastoma cells was activated using SphK1-specific activator phorbol 12-myristate 13-acetate (PMA). Our research also utilized cell viability assays, flow cytometry, western blots, RT-qPCR and related protein detection to assess activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results of the population study showed that the contents of SphK1 and S1P in the ACR-exposed occupational contact group were lower than in the non-exposed group. The results of in vitro experiments showed that expression of SphK1 decreased with the increase in ACR concentration. Activating SphK1 improved the survival rate of SH-SY5Y cells and decreased the apoptosis rate. Activating SphK1 in SH-SY5Y cells also regulated MAPK signaling, including enhancing the phosphorylation of extracellular signal-regulated protein kinases (ERK) and inhibiting the phosphorylation of c-Jun N-terminal kinase (JNK) and p38. These results suggest that activating SphK1 can protect against nerve cell damage caused by ACR.

Fabrication of flavour oil high internal phase emulsions by casein/pectin hybrid particles: 3D printing performance.

In this study, three-dimensional (3D) printable oil/water (O/W) high-internal-phase emulsions (HIPEs) (internal phase fraction = 75%) were fabricated using casein (3% w/v)/pectin (1-5% w/v) hybrid particles with flavour oil. The morphologies of the HIPEs, revealed by confocal laser scanning microscopy (CLSM) and cryo-scanning electron microscopy (cryo-SEM), indicated that the casein/pectin hybrid particles were mainly distributed on the interface of oil droplets. Additionally, the results of rheological and gel-strength measurements indicated that the viscosity (ranging from 1316.51-0.21 to 4301.84-0.79 Pa.s) of HIPEs increased with increasing pectin content (from 0% to 4% w/v), and the gel strength of printed HIPEs increased (from 10.37 to 21.19 g) with increasing pectin (from 1% to 5% w/v). The developed HIPEs were applied for 3D printing and the thus-printed objects could adequately maintain the designed shape and structure. The developed 3D printable HIPEs have excellent potential applications in the food, medical, and cosmetic industries.

A urinary metabolomic study from subjects after long-term occupational exposure to low concentration acrylamide using UPLC-QTOF/MS.

Because long-term occupational exposure to low concentrations of acrylamide (ACR) has the potential to cause neurological damage, it is important to identify biomarkers that can be used to evaluate this risk. In the present study, urine metabolomics of the ACR-exposed and non-exposed groups to identify potential metabolites was carried out using ultra high performance liquid chromatography coupled with quadrupole time of flight mass spectrometry. Serum biochemical indexes of the exposed and non-exposed groups were also determined. Principal component analysis showed a differential separation between exposed group and non-exposed group and a total of 7 metabolites were identified in positive and negative ionization modes; Area under curve of anthranilic acid, ß-guanidinopropionic acid and mesobilirubinogen were 0.980, 0.843 and 0.801 respectively and these metabolites showed high sensitivity and specificity. The 13 biochemical indexes were divided into three classes based on physiological functions. Only biomarkers of dysregulated liver function including alanine aminotransferase, aspartic transaminase, total bilirubin, direct bilirubin and triglyceride were significantly higher in the exposed group than in the non-exposed group. This study identifies important related metabolic changes in the bodies of workers after long-term occupational exposure to low concentration ACR and suggests new biomarkers of nervous system injury caused by ACR. The study also provides a sound basis for exploring the biochemical mechanisms and metabolic pathways of nervous system toxicity caused by ACR.

Nickel-smelting fumes induce mitochondrial damage and apoptosis, accompanied by decreases in viability, in NIH/3T3 cells.

Nickel (Ni) is widely present in the occupational environment and causes various adverse effects on the human body. Apoptosis induced by Ni2+ may be a key mechanism underlying its toxic effect. In the present study, we investigated the effect of Ni-smelting fumes on cell viability, mitochondrial damage, and apoptosis-related proteins in NIH/3T3 cells. The effects of Ni-smelting fumes at concentrations of 0, 25, 50, and 100 µg/mL were tested. Treatment with Ni-smelting fumes for 24 h and 48 h significantly decreased cell viability and lactate dehydrogenase activity in a dose- and time-dependent manner compared with the blank control group. Exposure to Ni-smelting fumes increased mitochondrial permeability transition pore opening in a dose-dependent manner and decreased mitochondrial membrane potential and the activity of the mitochondrial respiratory chain complexes I, II, and IV. The fumes significantly downregulated Bcl-2, procaspase-9, and procaspase-3 and upregulated Bax, caspase-9, and caspase-3 (P < 0.05). Ni-smelting fumes caused significant cytotoxicity, oxidative stress, mitochondrial damage, and apoptosis through the intrinsic pathway in mammalian cells. The present paper provides hypotheses and experimental support for these hypotheses that Ni-smelting fumes cause cytotoxicity through the mechanism of inducing mitochondrial damage and apoptosis in NIH/3T3 cells.

One-pot synthesis of nickel-cobalt hydroxyfluorides nanowires with ultrahigh energy density for an asymmetric supercapacitor.

A novel and unique nickel-cobalt hydroxyfluorides (NiCo-HF) nanowires material is fabricated by one-pot solvothermal synthesis method for asymmetric supercapacitor. The synthesis mechanism and factors that influence the formation of the NiCo-HF nanowires have been further discussed. The as-prepared NiCo-HF electrode exhibits a high specific capacitance of 3,372.6 F g-1, and the capacitance retention of 94.3% can be achieved at a high current density of 20 A g-1 after 10,000 cycles. The outstanding electrochemical performance of the electrode can be attributed to the synergistic effect of the nanowires morphology and complicated redox process of active material. Furthermore, an asymmetric supercapacitor assembled with NiCo-HF nanowires as positive electrode and activated carbon as the negative electrode shows an ultrahigh energy density of 83.6 Wh kg-1 at a power density of 379.4 W kg-1 and an excellent cycling stability with 86.3% capacitance retention after 10,000 cycles, indicating that this novel material has great promise for potential application in energy storage device.

Metabolomics analysis of serum from subjects after occupational exposure to acrylamide using UPLC-MS.

Since occupational exposure to acrylamide (ACR) may cause nerve damage, sensitive biomarkers to evaluate the early effects of ACR on human health are needed. In the present study, we have compared a group of individuals with occupational exposure to ACR (contact group, n = 65) with a group of individuals with no exposure (non-contact group, n = 60). Serum metabolomics analysis of the contact and non-contact groups was carried out using ultra performance liquid chromatograph/time of flight mass spectrometry, combined with multivariate analysis, to identify potential metabolites. Serum biochemical indexes of the contact and non-contact groups were also determined using an automatic biochemistry analyzer. There was a clear separation between the contact group and the non-contact group; receiver operator characteristic curve analysis suggested that phytosphingosine, 4E,15Z-bilirubin IXa and tryptophan were the best metabolites to use as biomarkers. Liver function was also found to be abnormal in the contact group. Important, ACR-related, metabolic changes were seen in the contact group and new biomarkers for assessing the toxicity of ACR on the central nervous system have been proposed. This study will provide a sound basis for exploring the toxic mechanisms and metabolic pathways of ACR.

Tea polyphenols dominate the short-term tea (Camellia sinensis) leaf litter decomposition.

Polyphenols are one of the most important secondary metabolites, and affect the decomposition of litter and soil organic matter. This study aims to monitor the mass loss rate of tea leaf litter and nutrient release pattern, and investigate the role of tea polyphenols played in this process. High-performance liquid chromatography (HPLC) and classical litter bag method were used to simulate the decomposition process of tea leaf litter and track the changes occurring in major polyphenols over eight months. The release patterns of nitrogen, potassium, calcium, and magnesium were also determined. The decomposition pattern of tea leaf litter could be described by a two-phase decomposition model, and the polyphenol/N ratio effectively regulated the degradation process. Most of the catechins decreased dramatically within two months; gallic acid (GA), catechin gallate (CG), and gallocatechin (GC) were faintly detected, while others were outside the detection limits by the end of the experiment. These results demonstrated that tea polyphenols transformed quickly and catechins had an effect on the individual conversion rate. The nutrient release pattern was different from other plants which might be due to the existence of tea polyphenols.

Nickel-Refining Fumes Induced DNA Damage and Apoptosis of NIH/3T3 Cells via Oxidative Stress.

Although there have been numerous studies examining the toxicity and carcinogenicity of nickel compounds in humans and animals, its molecular mechanisms of action are not fully elucidated. In our research, NIH/3T3 cells were exposed to nickel-refining fumes at the concentrations of 0, 6.25, 12.50, 25, 50 and 100 µg/mL for 24 h. Cell viability, cell apoptosis, reactive oxygen species (ROS) level, lactate dehydrogenase (LDH) assay, the level of glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) level were detected. The exposure of NIH/3T3 cells to nickel-refining fumes significantly reduced cell viability and induced cell apoptotic death in a dose-dependent manner. Nickel-refining fumes significantly increased ROS levels and induced DNA damage. Nickel-refining fumes may induce the changes in the state of ROS, which may eventually initiate oxidative stress, DNA damage and apoptosis of NIH/3T3 cells.

Characterization of proteolysis in muscle tissues of sea cucumber Stichopus japonicus.

The proteolysis in muscle tissues of sea cucumber Stichopus japonicus (sjMTs) was characterized. The proteins from sjMTs were primarily myosin heavy chains (MHCs), paramyosin (Pm), and actin (Ac) having a molecular mass of approximately 200, 98, and 42 kDa, respectively. Based on SDS-PAGE analysis and quantification of trichloroacetic acid (TCA)-soluble peptides released, degradation of muscle proteins from sjMTs was favorable at pH 5 and 50°C. Proteolysis of MHCs was mostly inhibited by cysteine protease inhibitors, including trans-epoxysuccinyl-L-leucyl-amido (4-guanidino) butane (E-64) and antipain (AP). E-64 and AP completely inhibited the degradation of Pm and Ac, while iodoacetic acid showed a partially inhibitory effect. These results indicated that the proteolysis of sjMTs was mainly attributed to cysteine proteases. Avoidance of setting the tissues at 40-50°C and slightly acidic condition and inhibition of cysteine proteases are helpful for decreasing sea cucumber autolysis.

Effects of nickel-smelting fumes on the regulation of NIH/3T3 cell viability, necrosis, and expression of hMLH1 and RASSF1A.

Nickel is widely used and distributed in various industries. This study investigated the effect of nickel-smelting fumes on the regulation of NIH/3T3 cell viability, apoptosis, and necrosis and the expression of the tumor suppressor genes hMLH1 and RASSF1A. Cell viability was determined using a methylthiazolyl tetrazolium colorimetric assay. NIH/3T3 cell viability was reduced after exposure to different concentrations of nickel-smelting fumes, but cell apoptosis and necrosis were induced. Moreover, cell morphology changed significantly after exposure to different concentrations of nickel-smelting fumes, as determined using an inverted microscope or transmission electron microscope. Real-time RT-PCR and Western blot analyses showed that exposure of cells to concentrations of ≥100 µg/mL of nickel-smelting fumes upregulated the expression of hMLH1 and RASSF1A compared to the negative controls. These data suggest that nickel-smelting fumes could be toxic to cells, upregulating the expression of hMLH1 and RASSF1A and in turn inducing cell apoptosis and necrosis.

Placebo analgesia, acupuncture and sham surgery.

Invasive procedures, such as surgery and acupuncture, are likely better than the others in terms of eliciting placebo analgesia. Understanding how invasive procedures can elicit enhanced placebo responses may provide new insights into mechanisms underlying placebo analgesia. In this essay, it is argued that sensory, cognitive and emotional factors are major determinants of the magnitude of placebo analgesia. Sham surgery and acupuncture are good examples of placebo interventions, which generate robust placebo responses through simultaneously manipulating such three factors.

[Genetic damage of mammalian cells induced by nickel-refining fumes].

OBJECTIVE: To study the effects of two kinds of nickel-refining fumes on DNA damage of NIH/3T3 cell and the difference. METHODS: NIH/3T3 cells were treated by two kinds of nickel fumes collected from smelting furnace and refining workshop of a nickel-smeltery, and PBS taken the place of nickel-smelting fumes was used as negative control. Several hours later, the cytotoxicity of on NIH/3T3 cells was detected with MTT colorimetric assay, and the DNA damage was also measured by comet assay (single cell gel electrophoresis). RESULT: With the extension of exposure time and increasing of concentration, the living rate of NIH/3T3 cells was decreased; the tail rate, tail extent moment and tail DNA percent of NIH/3T3 cell induced by these two refining fumes were increased. After cells were treated with 100.00 microg/ml of nickel-smelting fume for 48 h, the living rate of NIH/3T3 cells was 24.5% and 26.5% respectively. The tail length of NIH/3T3 cell induced by these two refining fumes was not significant difference. Tail DNA percent of NIH/3T3 cell induced by smelting furnace fume was higher than negative control group (P < 0.05). The tail rate, and tail DNA percent (except 12.5 microg/ml and 50.0 microg/ml treated 2 h group) of NIH/3T3 cell induced by refining workshop fume was higher than negative control group (P < 0.05). CONCLUSION: Nickel-smelting fume could depress the survival rate of NIH/3T3 cells, and induce different degree DNA damage of NIH/3T3 cell.

Screening of differentially expressed genes in the hypothalamus of a rat neuropathic pain model following sciatic nerve injury.

BACKGROUND: Neuropathic pain is induced by injury or disease of the nervous system. Most studies have so far focused only on a few known molecules and signaling pathways among neurons. However, all signal transmissions involved in neuropathic pain appear to be an integral system at different molecular levels. This study was designed to screen the differentially expressed genes of the hypothalamus in chronic constriction injury (CCI) rats and analyze their functions in developing neuropathic pain. METHODS: Ten adult female Sprague-Dawley rats ((200 +/- 10) g) were used in experimental group and sham group (n = 5 in each group). Mechanical allodynia tests were performed to ensure that the CCI rat model was constructed successfully. Total hypothalamus RNAs were isolated from each group. Forward suppression subtractive hybridization (SSH) library of rat hypothalamus was constructed and up-regulated cDNA clones at neuropathic pain states were obtained via suppressed subtractive hybridization technique and the functions of these genes were analyzed bioinformatically. RESULTS: Mechanical allodynia tests showed that the experimental rats had a significantly reduced mechanical allodynia threshold 3 to 13 days after CCI vs sham surgery rats (P < 0.01), indicating that the model was successful. Forward SSH library of the rat hypothalamus was constructed successfully and 26 over-expressed expression sequence tags (ESTs) were obtained from these up-regulated cDNA clones. CONCLUSION: Twenty-six up-regulated genes, involved in the regulation of cell cycle and apoptosis, signal transduction, and neuroprotection, may play key roles in decreasing mechanical withdraw thresholds in CCI rats, which implicates a multidimensional and integrated molecular mechanism at gene level in developing neuropathic pain with the supraspinal contributions.

[The cytotoxicity of nickel-refining dusts for chinese hamster lung cells and effects on gap junctional intercellular communication].

OBJECTIVE: To investigate the cytotoxicity of the nickel-refining dusts for Chinese hamster lung (CHL) cells and the effects of nickel-refining dusts on the gap junctional intercellular communication (GJIC) of CHL cells. METHODS: The cytotoxicity of the nickel-refining dusts for the CHL cells was determined in two nickel-refining dusts samples with the CHL cells as the target cells by MTT method while the effects of nickel-refining dusts on the CJIC of the CHL cells were investigated using the scrape-loading and dye transfer (SLDT) technique. RESULTS: There were no significant difference in the CHL proliferation between all dosage groups in the two samples and the control group at 6 and 12 hours (P > 0.05). The survival rate of cells in all dosage groups were all decreased at 36 hours (P < 0.05), presenting the dosage-reaction relationship and the time-reaction relationship. IC(50) was 21.36 and 23.07 micro/ml for the two samples respectively at 36 hours. Compared with the control group, the transport of Lucifer Yellow (LY) from the injury line to the adjacent cells was decreased when the CHL cells were treated with nickel-refining dusts of 25.00, 50.00 and 100.00 microg/ml (P < 0.01). CONCLUSION: The nickel-refining dusts have cytotoxicity for the CHL cells cultivated in vitro, can inhibit the growth of the cells and at a certain concentration can inhibit the GJIC function of CHL cells.

[Experimental study on the DNA damage of NIH/3T3 cells induced by nickel-refining dusts].

OBJECTIVE: To study the effects of nickel-refining dusts on DNA damage in mouse NIH/3T3 cell. METHOD: DNA damage of mouse NIH/3T3 cell induced by two nickel-refining dust samples was determined with single cell gel electrophoresis (SCGE) technique. RESULTS: (1) Under the condition of the same treatment time, the tailed cell (%) of NIH/3T3 cells increased with the increase in doses of nickel-refining dusts (35.5%, 69.7%, 85.2%, 41.3%, 75.7%, 89.2% respectively except for sample 2, 50 microg/ml, 24 h group), and DNA strand breaks reached the peak value at 4 h of exposure; (2) When we treated the NIH/3T3 cells with the same dose of nickel-refining dusts, the tail rate at 4 h was higher than those at 2 h and 24 h of exposure; (3) Both sample 1 and sample 2 with different doses of nickel-refining dusts could induce higher comet tail, DNA%, tail length (except for 12.5 microg/ml), extent of TM (except for sample 1, 12.5 microg/ml) than in control group (P < 0.05). The DNA damage range was significantly increased in different tested doses of nickel-refining dusts and the damage range reached the peak value when the cells were treated for 4 h. CONCLUSION: Nickel-refining dusts could induce different degree DNA damage in NIH/3T3 cells.