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Taken together, the results demonstrated that BBG contributed to the suppression of the inflammatory effects in LPS-induced BV2 cells via the inhibition of NF-κB and MAPKs signaling pathways.The aim of the present study was to explore the role of toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling in the contrast-induced injury of renal tubular epithelial cells, and to investigate the potential mechanisms. HK-2 cells cultured in vitro were randomly divided into six groups as follows i) The blank group; ii) the iohexol group; iii) the NF-κB RNAi group (NF-κB siRNA + iohexol); iv) the TLR4 RNAi group (TLR4 siRNA + iohexol); v) the NF-κB blocker group (PDTC + iohexol); and vi) the TLR4 blocker group (CLI-095 + iohexol). The expression of the TLR4/MyD88/NF-κB signaling pathway proteins was detected by reverse transcription-quantitative (RT-q)PCR and western blot analysis, and the cellular proliferation rate was determined using the Cell Counting Kit-8 assay. The mRNA expression levels of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were also detected using RT-qPCR, and apoptosis was assessed by flow cytometry and western blotting to detect apoptosis-associated proteins (caspase-3, caspase-9 and cleaved caspase-9). Compared with the blank group, the apoptotic rates and the expression levels of TLR4, MyD88, NF-κB, caspase-3, cleaved caspase-9, TNF-α, IL-1β and IL-6 were upregulated in the iohexol group (P less then 0.001). However, when TLR4 or NF-κB were blocked or silenced, these effects were reversed (P less then 0.001). Collectively, the results of the present study indicated that TLR4/MyD88/NF-κB signaling is involved in the contrast-induced injury of renal tubular epithelial cells by inducing inflammation and apoptosis.Aldehyde dehydrogenase 2 (aldh2) serves an important role in the development of organ injury. Therefore, the present study investigated the effects of aldh2 on the oxidative stress response in a mouse model of ketamine-induced cystitis (KIC). A total of 60 8-week-old male Institute of Cancer Research wild-type (WT) mice and 45 aldh2 knock-out (KO) mice were randomized to receive low-dose ketamine (30 mg/kg), high-dose ketamine (60 mg/kg) or normal saline (controls). At 4, 8 and 12 weeks post-injection, bladder tissues were harvested and used to investigate the protective mechanisms of aldh2 on bladder function. The results demonstrated that aldh2 KO mice exhibited significant weight loss following chronic ketamine injection compared with that in WT mice. Furthermore, ketamine treatment increased the urination rate (P less then 0.05), pathological score (P less then 0.05), levels of the oxidative stress product malondialdehyde (P less then 0.05) in addition to reducing the expression of the anti-oxidative stress enzyme superoxide dismutase (P less then 0.05) and glutathione-SH (P less then 0.05). Oxidative stress in aldh2 KO mice was also found to significantly enhance the expression of proteins associated with the NF-κB signaling pathway, which promoted the expression of inducible nitric oxide synthase (P less then 0.05) and cyclooxygenase-2 (P less then 0.05) further. Finally, aldh2 KO mice demonstrated higher severity of fibrosis in the submucosal and muscular layers of the bladder. In conclusion, the present study suggests that aldh2 serves a protective role in preventing inflammation and fibrosis in KIC.
Insulin resistance can occur in all metabolic organs including the liver, adipose tissue, and skeletal muscles. Circulating soluble epidermal growth factor receptor (soluble EGFR) and adipsin levels are altered in obese diabetic mice and are possibly correlated with insulin resistance in both mice and humans. Here, we investigated the significance of soluble EGFR and adipsin as biomarkers for insulin resistance in Japanese subjects with type 2 diabetes.
We measured the soluble EGFR and adipsin levels in sera from 47 non-diabetic subjects and 106 subjects with type 2 diabetes using enzyme-linked immunosorbent assays (ELISAs) and analyzed the correlations between the soluble EGFR or adipsin levels and metabolic parameters in type 2 diabetes subjects. We also measured the gene expression levels of
and
(adipsin) in the liver, adipose tissue, and skeletal muscle in mice with/without obesity or diabetes.
The soluble EGFR levels were correlated with the fasting blood glucose level (
= 0.010), HOMA-IR (, while adipsin, an adipokine, is associated with adipose insulin resistance.Trial registration UMIN Clinical Trials Registry (www.umin.ac.jp), UMIN000020474. Registered 8 January 2016.Fusobacterium nucleatum (Fn) is frequently found in colorectal cancers (CRCs). High loads of Fn DNA are detected in CRC tissues with microsatellite instability-high (MSI-H), or with the CpG island hypermethylation phenotype (CIMP). Fn infection is also associated with the inflammatory tumor microenvironment of CRC. A subtype of CRC exhibits inflammation-associated microsatellite alterations (IAMA), which are characterized by microsatellite instability-low (MSI-L) and/or an elevated level of microsatellite alterations at selected tetra-nucleotide repeats (EMAST). Here we describe two independent CRC cohorts in which heavy or moderate loads of Fn DNA are associated with MSI-H and L/E CRC respectively. We also show evidence that Fn produces factors that induce γ-H2AX, a hallmark of DNA double strand breaks (DSBs), in the infected cells.Marine phytoplankton produce essential fatty acids (FA), which are key component of a healthy diet in humans and marine food webs. Increased temperatures can reduce lipid and FA content in phytoplankton; thus, ocean warming poses a risk for the global production of these essential FA. However, responses to warming may differ between phytoplankton species especially after long-term exposure because phenotypic plasticity, de novo mutations, or genetic evolution may occur. Here, we examine the content of FA and lipids in phytoplankton following long-term selection (~2 years) to warming conditions (+4°C), and we observe that FA and lipids content were partly or entirely recovered following long-term exposure to warming conditions. Furthermore, this observed long-term response also offset the predicted losses of some essential polyunsaturated fatty acids (PUFA) in three of the four species tested. Our study suggests that long-term exposure of phytoplankton to warming may help to maintain marine food quality in a moderately warming ocean. The responses of FA to increasing temperatures may vary among species, and the level of this idiosyncrasy remains to be further studied.
Transcriptomic divergence drives plant ecological adaptation. Upland rice is differentiated in drought tolerance from lowland rice during its adaptation to the drought-prone environment. They provide a good system to learn the evolution of drought tolerance in rice.
We estimate morphological differences between the two rice ecotypes under well-watered and drought conditions, as well as their genetic and transcriptomic divergences by the high-throughput sequencing. Upland rice possesses higher expression diversity than lowland rice does. Thousands of genes exhibit expression divergences between the two rice ecotypes, which contributes to their morphological differences in drought tolerance. These transcriptomic divergences contribute to drought adaptation of upland rice during its domestication. Mutations in transcriptional regulatory regions, which cause presence and absence of
-elements, are the cause of expression divergence. About 15.3% transcriptionally selected genes also receive sequence-based selection in upland or lowland ecotype. Some highly differentiated genes promote the transcriptomic divergence between rice ecotypes
gene co-expression network. In addition, we also detected transcriptomic trade-offs between drought tolerance and productivity.
Many key genes, which promote transcriptomic adaptation to drought in upland rice, have great prospective in breeding water-saving and drought-resistant rice. Meanwhile, appropriate strategies are required in breeding to overcome the potential transcriptomic trade-off.
Many key genes, which promote transcriptomic adaptation to drought in upland rice, have great prospective in breeding water-saving and drought-resistant rice. Meanwhile, appropriate strategies are required in breeding to overcome the potential transcriptomic trade-off.Biological control is a popular tool for invasive species management, but its success in nature is difficult to predict. One risk is that invasive plants, which may have adapted to lower herbivore pressure in the introduced range, could rapidly evolve defences upon re-association with their biocontrol agent(s). Previous studies have demonstrated that populations of the invasive plant purple loosestrife (Lythrum salicaria) exposed to biocontrol exhibit traits consistent with the rapid evolution of defence. However, to date, no one has tested this hypothesis under field-natural levels of herbivory. Using seed from 17 populations of purple loosestrife growing in eastern Canada, that varied in their history of exposure to their biocontrol agent, the leaf beetle Neogalerucella spp., we transplanted 1,088 seedlings from 136 maternal families into a common garden under ambient herbivory. Over the following three and half years, we assessed plant performance in the face of biocontrol by measuring early-season plant sxistence of refuges of large, reproductive individuals.Some microbes have a fascinating ability to degrade compounds that are toxic for humans in a process called bioremediation. Although these traits help microbes survive the toxins, carrying them can be costly if the benefit of detoxification is shared by all surrounding microbes, whether they detoxify or not. Detoxification can thereby be seen as a public goods game, where nondegrading mutants can sweep through the population and collapse bioremediation. Here, we constructed an evolutionary game theoretical model to optimize bioremediation in a chemostat initially containing "cooperating" (detoxifying) microbes. We consider two types of mutants "cheaters" that do not detoxify, and mutants that become resistant to the toxin through private mechanisms that do not benefit others. By manipulating the concentration and flow rate of a toxin into the chemostat, we identified conditions where cooperators can exclude cheaters that differ in their private resistance. However, eventually, cheaters are bound to invade. To overcome this inevitable outcome and maximize detoxification efficiency, cooperators can be periodically reinoculated into the population. Our study investigates the outcome of an evolutionary game combining both public and private goods and demonstrates how environmental parameters can be used to control evolutionary dynamics in practical applications.
Brown planthoppers (
) are the most serious insect pests of rice, one of the world's most important staple crops. They reproduce year-round in the tropical parts of their distribution, but cannot overwinter in the temperate areas where they occur, and invade seasonally from elsewhere. Decades of research have not revealed their source unambiguously.
We sequenced the genomes of brown planthopper populations from across temperate and tropical parts of their distribution and show that the Indochinese peninsula is the major source of migration into temperate China. The Philippines, once considered a key source, is not significant, with little evidence for their migration into China. https://www.selleckchem.com/products/Gefitinib.html We find support for immigration from the west of China contributing to these regional dynamics.
The lack of connectivity between the Philippine population and the mainland Chinese populations explains the different evolution of Imidacloprid resistance in these populations. This study highlights the promise of whole-genome sequence data to understand migration when gene flow is high-a situation that has been difficult to resolve using traditional genetic markers.
