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Tetranychus urticae Koch is a worldwide agricultural pest mite that feeds on more than 1100 kinds of crops. The mite has developed a high level of tolerance to high temperatures, but the physiological mechanism underlying the outstanding adaptability of this pest to high temperatures remains unclear. To clarify the physiological mechanisms of T. urticae in response to short-term heat stress, four temperatures (36, 39, 42, and 45 °C) and three short-term heat durations (2, 4, and 6 h) were conducted to test the effects on protein content, the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), and the total antioxidant capacity (T-AOC). The results showed that protein content, antioxidant enzyme activity, and T-AOC in T. urticae were significantly induced by heat stress. These results suggest that heat stress induces oxidative stress and that antioxidant enzymes play an important role in reducing oxidative damage in T. urticae. The data of this study will provide a basis for further research on the molecular mechanisms of thermostability and ecological adaptability of T. urticae.

Plant fiber/plastic composites (PPCs) have been widely used in food contact materials (FCMs) for many benefits, such as their claimed better environmental footprint compared to conventional plastics. However, their safety is still not fully understood and must be comprehensively evaluated. Non-volatiles extracted from six PPCs with different plant fibers and polymer matrices were characterized by employing ultra-high-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry in combination with various spectral libraries and manual elucidation, taking into account spectral similarity and characteristic product ions. A total of 115 compounds were tentatively identified, 50 of which were oligomers or their derivatives from the sample with polylactic acid (PLA) and polybutylene adipate terephthalate (PBAT) as the polymer matrix, and some of them were Cramer rules class III substances based on the threshold of toxicological concern (TTC). Seven reaction products between PLA and PBAT monomers, as well as four derivatives of melamine, were elucidated and well detailed for the first time. In addition, bisphenol S was detected in all samples even though its origin remains to be further explored. Isoprothiolane, as an insecticide and fungicide used to control a range of rice pests, was identified in the sample with rice husk as fillers, experimentally confirming the presence of agrochemicals in samples containing plant fibers.

Tetranychus urticae Koch is a worldwide pest mite which can cause continuous damage to multiple plants even in hot environment such as greenhouse due to its strong endurance to high temperature. In order to clarify the physiological mechanisms of T. urticae in response to short-term heat stress, four high temperatures (36, 39, 42, and 45°C), three short-term heat durations (2, 4, and 6 h) were conducted to test the effects on the protein content of T. urticae and the activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and total antioxidant capacity (T-AOC), respectively. The results showed that protein content, antioxidant enzymes activity, and T-AOC in T. urticae were significantly affected by both the high temperature and duration after treatment, meanwhile, they showed same trends of increased at 25–39℃, then decreased at 39–42℃ except for CAT activity. The highest values of SOD activity, POD activity and T-AOC were all obtained at 39℃-4h, and that of CAT activity was obtained at 39℃-2h. The higher levels of T-AOC serve an important signal demonstrating that T. urticae has other antioxidant mechanisms except for antioxidant enzymes. Those results suggested that heat stress induces oxidative stress, and antioxidant enzymes played important role in reducing oxidative damage in T. urticae. which provided a basis for further research on the molecular mechanisms of thermostability and ecological adaptability of T. urticae.

Background The lack of effective prognostic models for colorectal cancer (CRC) makes it crucial to establish a reliable prognostic model for colorectal cancer. The aim of this study was to develop a reliable prognostic model in CRC. Using CRC samples from the TCGA database, a multi-gene combination model was screened for prognosis in CRC patients and the prognostic power of the multi-gene combination model was validated. We screened a multi-gene combination model for risk stratification and prognosis of CRC patients, which is important for individualised clinical treatment and long-term management of colorectal cancer patients. Results To solve these questions, we used data from colorectal cancer patients in the TCGA database to uncover differential genes, screened variables using one-way COX analysis and LASSO regression analysis, and then screened for the polygenic combination most associated with colorectal cancer and assessed its significance on survival events using multi-factor COX analysis and ROC curves to assess polygenic combinations. Finally, using gene enrichment analysis, the polygenic combinations were found to be associated with tRNA biosynthesis, homologous recombination, nucleotide excision repair, ribosome biogenesis in eukaryotes and DNA replication. Conclusions The multi-gene combination (FCGBP, GSTM1, IGLV4-69, IGSF9 and PCOLCE2) model screened in this study is capable of prognosticating colorectal cancer, and the findings of this study could shed new light on the prognosis of colorectal cancer in the clinical setting.

The predatory mite Neoseiulus barkeri (Acari: Phytoseiidae), which is one of the best natural enemies, has been used as a biological control agent against multiple insect pests, such as spider mite, Tetranychus urticae and thrips. Its growth and development were affected by the environmental temperature changes. This study was conducted to evaluate the hatching rate of the eggs and the immature developmental times of N. barkeri after incubation of the eggs under heat stress at 38, 40 and 42℃, 85% ± 5% RH and a 16h:8h light: dark (L:D) photoperiod for 2, 4 and 6h. After adult females emerged, they were treated under the same conditions again, and the parameters such as oviposition period, fecundity and female longevity were observed. The results showed that with the increase of the temperature and the extension of the duration of the heat stress, the hatching rate was lower. The eggs treated at 42℃ for 2h or more could not hatch, and the developmental duration of each immature stage showed a trend of decreasing at first and then increasing. The fastest development was observed after incubation of eggs at 40℃ for 2h, and the shortest developmental duration was 4.60d. Under the condition of 38℃, the oviposition period and life span of adult females were shortened with the extension of treatment time, and the fecundity decreased at first and then increased. At 40℃, the fecundity, oviposition period and longevity of adult females showed a trend of gradual increase with the extension of treatment time. The shortest oviposition period, the lowest fecundity and the shortest life span of adult females were 12.14d, 18.92 eggs and 16.65d, respectively after incubation of eggs at 40℃, for 2h. Therefore, the short-term heat stress had a significant effect on the hatching rate and the duration of the immature stage, and also had a negative effect on the fecundity, oviposition period and longevity of adult females. In rearing and field release, heat stress should be avoided as much as possible to achieve the best predation and control effect of N. barkeri.

To study the physiological mechanisms of Neoseiulus barkeri in response to short-term heat stress, the eggs and the emerged adults were exposed to 38, 40, and 42°C, 85% ± 5%RH,16 h:8 h (L:D) for 2, 4, and 6 h. The activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) as well as the protein content of N. barkeri were examined. All treatments caused significant different changes compared to the untreated control. The protein content increased as the temperature increased, while it showed different changing trends with the prolongation of exposure duration. The enzymatic activity of SOD, CAT, and POD was significantly affected by the temperature treatment. Both the maximum and minimum level of the three enzymes after a short-term heat stress differed significantly to the control group (p < 0.05). The highest values of three enzymatic activities were all obtained at 40°C-4 h. Person correlation analysis indicates that the high temperature was the primary factor affecting the enzymatic activity, while the exposure duration of the heat stress was the secondary factor. In general, the short-term heat stress increased the protein content of Neoseiulus barkeri and up-regulated the expression of SOD, CAT, and POD activities as well.

The spider mite Tetranychus urticae is one of the most economically key mite pests of fields and greenhouse crops over the world. In order to clarify the control efficacy of Neoseiulus barkeri on T. urticae in the presence of entomopathogenic fungus Acremonium hansfodii. This study was conducted to evaluate the control of combining N. barkeri with A. hansfodii against T. urticae. The results showed that the functional response of N. barkeri treated with Ahy1 strain to T. urticae was Holling type II equation. Among these, the highest predation number and the shortest attack time were obtained for the predator feeding on eggs, then followed by feeding on nymphs, female adults ranked as the lowest. That of N. barkeri to T. urticae treated with Ahy1 strain was also Holling type II equation. The predation capacity of N. barkeri on nymphs and female adults of T. urticae treated by Ahy1 strain increased with the increase of the concentration of Ahy1 strain, but that when feeding eggs had no significant difference. Therefore, the combination of EPF with N. barkeri on control of TSSM had synergistic effects, which will provide the guidance to carry out combined utilization of entomogenous fungi with predatory mites.

Chemotherapy resistance is the dominant challenge in the treatment of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) exerts a vital function in drug resistance of many tumors. Nevertheless, the potential molecular mechanism of Nrf2 regulating the base excision repair pathway that mediates AML chemotherapy resistance remains unclear. Here, in clinical samples, we found that the high expression of Nrf2 and base excision repair pathway gene encoding 8-hydroxyguanine DNA glycosidase (OGG1) was associated with AML disease progression. In vitro, Nrf2 and OGG1 were highly expressed in drug-resistant leukemia cells. Upregulation of Nrf2 in leukemia cells by lentivirus transfection could decrease the sensitivity of leukemia cells to cytarabine, whereas downregulation of Nrf2 in drug-resistant cells could enhance leukemia cell chemosensitivity. Meanwhile, we found that Nrf2 could positively regulate OGG1 expression in leukemia cells. Our chromatin immunoprecipitation assay revealed that Nrf2 could bind to the promoter of OGG1. Furthermore, the use of OGG1 inhibitor TH5487 could partially reverse the inhibitory effect of upregulated Nrf2 on leukemia cell apoptosis. In vivo, downregulation of Nrf2 could increase the sensitivity of leukemia cell to cytarabine and decrease OGG1 expression. Mechanistically, Nrf2-OGG1 axis-mediated AML resistance might be achieved by activating the AKT signaling pathway to regulate downstream apoptotic proteins. Thus, this study reveals a novel mechanism of Nrf2-promoting drug resistance in leukemia, which may provide a potential therapeutic target for the treatment of drug-resistant/refractory leukemia.

To better help resolve the dilemma of more demand for bank lending and increasing defaulted bank loans, this paper develops a pricing model on SMEs’ group lending practice using a gaming me...

Flies of the Colocasiomyia toshiokai species group depend exclusively on inflorescences/infructescences of the aroid tribe Homalomeneae. The taxonomy and reproductive biology of this group is reviewed on the basis of data and samples collected from Southeast Asia. The species boundaries are determined by combining morphological analyses and molecular species delimitation based on sequences of the mitochondrial COI (cytochrome c oxidase subunit I) gene. For the phylogenetic classification within this species group, a cladistic analysis of all the member species is conducted based on 29 parsimony-informative, morphological characters. As a result, six species are recognised within the toshiokai group, including one new species, viz. C. toshiokai, C. xanthogaster, C. nigricauda, C. erythrocephala, C. heterodonta and C. rostrata sp. n. Various host plants are utilised by these species in different combinations at different localities: Some host plants are monopolized by a single species, while others are shared by two or three species. C. xanthogaster and C. heterodonta cohabit on the same host plant in West Java, breeding on spatially different parts of the spadix. There is a close synchrony between flower-visiting behaviour of flies and flowering events of host plants, which indicate an intimate pollination mutualism.

Drug resistance remains a major challenge in the current treatment of acute myeloid leukemia (AML). Finding specific molecules responsible for mediating drug resistance in AML contributes to the effective reversal of drug resistance. Recent studies have found that mitogen- and stress-activated protein kinase 1 (MSK1) is of great significance in the occurrence and development of tumors. In the current study, MSK1 was found highly expressed in drug-resistant AML patients. Heme oxygenase-1 (HO-1) has been previously validated to be associated with drug resistance in AML. Our study revealed a positive correlation between MSK1 and HO-1 in patient samples. In vitro experiments revealed that the sensitivity of AML cell lines THP-1 and U937 to cytarabine (Ara-C) significantly decreased after overexpression of MSK1. Meanwhile, downregulation of MSK1 by siRNA transfection or treatment of pharmacological inhibitor SB-747651A in AML cell lines and primary AML cells enhanced the sensitivity to Ara-C. Flow cytometry analysis showed that downregulation of MSK1 in AML cells accelerated apoptosis and arrested cell cycle progression in G0/G1 phase. However, the increased cell sensitivity induced by MSK1 downregulation was reversed by the induction of HO-1 inducer Hemin. Through further mechanism exploration, real-time PCR, immunofluorescence and Western blot analysis demonstrated that brahma related gene 1 (BRG1) was involved in the regulatory effect of MSK1 on HO-1. High expression of MSK1 could promote the resistance of AML through BRG1-mediated upregulation of HO-1. Downregulation of MSK1 enhanced the sensitivity of AML cells to Ara-C. Our findings provide novel ideas for developing effective anti-AML targets.

Background/Aims: Parkinson’s disease (PD) is a prevalent disease that leads to motor and cognitive disabilities, and oxidative stress (OS) injury was found to be related to the etiology of PD. Increasing evidence has shown that SHC3 is aberrantly expressed in neurons. The current study examines the involvement of SHC3 silencing in OS injury in the nigral dopamine neurons in rats with PD via the PI3K-AKT-FoxO signaling pathway. Methods: To study the mechanisms and functions of SHC3 silencing in PD at the tissue level, 170 rats were selected, and a lentivirus-based packaging system was designed to silence SHC3 expression in rats. Furthermore, PC12 cells were selected for in vitro experimentation. To evaluate the effect of SHC3 silencing in nigral dopamine neuronal growth, an MTT assay, propidium iodide (PI) single staining and Annexin V-PI double staining were performed to detect cell viability, cell cycle progression and cell apoptosis, respectively. Results: SHC3 shRNA led to decreased SOD and MDA levels and enhanced GSH activity, indicating that SHC3 silencing leads to motor retardation. SHC3 silencing repressed the extent of Akt and FoxO phosphorylation, thereby inhibiting the PI3K-AKT-FoxO signaling pathway. Furthermore, in cell experiments, SHC3 silencing suppressed PC12 cell proliferation and cell cycle progression, whereas it enhanced cell apoptosis. Conclusion: The current study provides evidence suggesting that SHC3 silencing may aggravate OS injury in nigral dopamine neurons via downregulation of the PI3K-AKT-FoxO signaling pathway in PD rats.