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Background Long-term smoking is a risk factor for chronic pain, and chronic nicotine exposure induces pain-like effects in rodents. The anterior cingulate cortex (ACC) has been demonstrated to be associated with pain and substance abuse. This study aims to investigate whether ACC microglia are altered in response to chronic nicotine exposure and their interaction with ACC neurons and subsequent nicotine-induced allodynia in mice. Methods We utilized a mouse model that was fed nicotine water for 28 days. Brain slices of the ACC were collected for morphological analysis to evaluate the impacts of chronic nicotine on microglia. In vivo calcium imaging and whole-cell patch clamp were used to record the excitability of ACC glutamatergic neurons. Results Compared to the vehicle control, the branch endpoints and the length of ACC microglial processes decreased in nicotine-treated mice, coinciding with the hyperactivity of glutamatergic neurons in the ACC. Inhibition of ACC glutamatergic neurons alleviated nicotine-induced allodynia and reduced microglial activation. On the other hand, reactive microglia sustain ACC neuronal excitability in response to chronic nicotine, and pharmacological inhibition of microglia by minocycline or liposome-clodronate reduces nicotine-induced allodynia. The neuron-microglia interaction in chronic nicotine-induced allodynia is mediated by increased expression of neuronal CX3CL1, which activates microglia by acting on CX3CR1 receptors on microglial cells. Conclusion Together, these findings underlie a critical role of ACC microglia in the maintenance of ACC neuronal hyperactivity and resulting nociceptive hypersensitivity in chronic nicotine-treated mice.

Mechanically ventilated patients suffering critical illness are at high risk of developing neurocognitive impairments. Angiotensin type 2 receptor (AGTR2) has been demonstrated to be anti-inflammatory and neuroprotective. The present study thus aimed to investigate whether AGTR2 can alleviate cerebral dysfunction in mice subjected to cochallenge with lipopolysaccharide (LPS) and mechanical ventilation (MV), and to reveal the underlying mechanism. We utilized a mice model that received a single injection of LPS (1 mg/kg, intraperitoneally) followed 2 h later by MV (10 ml/kg, lasting for 2 h). Pretreatment with the AGTR2 pharmacological agonist C21 (0.03, 0.3, and 3 mg/kg, intraperitoneally, once daily, lasting for 10 days). Locomotor activity and behavioral deficits were evaluated 24 h post-MV by open-field and fear-condition tests. Brain hippocampus and prefrontal cortex tissues were collected for immunofluorescence staining and western blotting to evaluate the resulting impacts on microglia, including morphological traits, functional markers, synaptic engulfment, superoxide production, and signaling molecules. Compared with vehicle-control, pre-administrated C21 reduced the branch endpoints and length of microglia processes in a dose-dependent manner in mice subjected to LPS/MV. The neuroprotective effect of AGTR2 was behaviorally confirmed by the improvement of memory decline in LPS/MV-treated mice following C21 pretreatment. In addition to morphological alterations, C21 reduced microglial functional markers and reduced microglial-dendrite contact and microglial engulfment of synaptic protein markers. In terms of the underlying molecular mechanism, AGTR2 stimulation by C21 leads to activation of protein phosphatase 2A, which subsequently mitigates microglial PKCδ and NF-κB activation, and inhibites NOX2-derived ROS production. The AGTR2 agonist C21 alleviates behavioral deficits in those mice subjected to LPS/MV, via mechanisms that involve reactive microglia and abnormal synaptic plasticity in NOX2-derived ROS and the PKCδ-NFκB pathway.

The underwater images suffer from low contrast, low visibility and color deviation which caused by scattering and absorption. In this paper, the method based on color-line model and homomorphic filtering is proposed to enhance the underwater image. First of all, the homomorphic filtering is used to remove the color deviation in the underwater image and the obtained image will be used for subsequent processes. Then, the transmission of the underwater image is estimated through the solution of the offsets that the color lines along the background-light vector from the origin. We develop a non-convex optimization function to obtain the transmission of the underwater image. Finally, the color correction is added in the underwater image which obtained by the color-line method. The simulation experiments results show that the proposed method is superior to the current state-of-the-art methods in the four aspects of quantitative analysis, qualitative analysis, color accuracy analysis, and restoring synthesized underwater images.

Seeing that the light in the water is affected by absorption and scattering, underwater image will suffer degradation including low contrast, low visibility and color deviation. Therefore, the key issue of underwater image enhancement is to improve the visibility and the contrast of underwater images. In this paper, we proposed an underwater image dehazing algorithm combining three main steps of homomorphic filtering, double transmission map and dual-image wavelet fusion. First at all, we removed the color deviation in the underwater image by homomorphic filtering. Then, we obtained the enhanced image by depth map which calculate the difference between the light and dark channels. Finally, the dual-image wavelet fusion technique is used to combine the enhanced image obtained by the depth map with the enhanced image obtained by the dark channel. In addition, we obtained the contrast enhanced image which use Contrast-Limited Adaptive Histogram Equalization (CLAHE) method. Through simulation experiments, the proposed method has better visual effects and better effect on entropy, average gradient and underwater color image quality evaluation (UCIQE) compared with other popular methods.

Flower-specific promoters can enable transgenic enhancement of valuable ornamental traits, including flower shape and color. However, the identification of strong, tissue-specific promoters remains a limiting factor. To obtain enhanced flower-specific promoters, we constructed four chimeric promoters (p35S-PCHS-Ω, p35S-LCHS-Ω, pOCS-PCHS-Ω and pOCS-LCHS-Ω) combining the 35S or OCS enhancer fused to a 302 bp CHSA core promoter fragment from petunia (PCHS) or a 307 bp CHS core promoter fragment from lily (LCHS), and also containing an omega element (Ω). Each promoter was fused to the β-glucuronidase (GUS) reporter gene, and we examined the levels and tissue specificity of GUS expression in transgenic Torenia fournieri. p35S-PCHS-Ω and p35S-LCHS-Ω drove strong, constitutive GUS expression in all tissues, especially in colored corollas (p35S-PCHS-Ω) or in colored corollas and roots (p35S-LCHS-Ω). pOCS-PCHS-Ω drove stronger GUS expression in colored corollas than in other tissues but expression was weaker than that of p35S-PCHS-Ω. pOCS-LCHS-Ω drove GUS in colored corollas but also in roots. Among the four chimeric promoters, pOCS-PCHS-Ω exhibited stronger activity only in colored corollas, making it useful for transgenic enhancement of floral traits, such as expressing ‘blue genes’ in lily to produce new lines with blue flowers.

Flavonoid 3′, 5′-hydoxylase (F3′5′H) is a key enzyme for biosynthesis of the blue anthocyanin pigment delphinidin. A number of F3′5′H genes from dicots have been tested for their effects on flower pigmentation; here F3′5′H from a monocot was tested for its effect on delphinidin accumulation in petals. To this end, F3′5′H (PhF3′5′H) from the orchid Phalaenopsis was expressed under the control of the chalcone synthase promoter in petunia flowers. Quantitative RT-PCR showed that PhF3′5′H was expressed mainly in the petal limb; this expression produced an increase in dihydromyricetin and delphinidin and a change in petal color from pink to deeper pink. To increase the accumulation of delphinidin, Hyacinth HyDFR, which encodes dihydroflavonol 4-reductase, and petunia DifF, which encodes a cytochrome b 5 that is required for full activity of F3′5′H were overexpressed. The HyDFR petunia transformants had a deeper color petal limb, increased dihydromyricetin and delphinidin contents and adaxial petals with a number of blue cells. The flowers of the DifF petunia transformants also showed a slight color change. We also tested PhF3′5′H in Lilium oriental ‘Sorbonne’, where transient PhF3′5′H expression by particle bombardment resulted in purple cells in the petals. Production of blue flowers by Phalaenopsis F3′5′H and hyacinth DFR potentially enables manipulation of flower color in ornamental plants, including production of blue flowers.

The inflorescence of the broad-leafed grape hyacinth, Muscari latifolium, shows an interesting, two-tone appearance with the upper flowers being pale blue and the lower ones purple. To elucidate the mechanism of the differential color development, anatomical research was carried out and a cytological study of the colored protoplasts in which the shapes of the cells accumulating anthocyanin were observed by scanning electron microscopy. Next, vacuolar pH was recorded using a pH meter with a micro combination pH electrode, and the sap's metal-ion content was measured by inductively coupled plasma mass spectrometry. The anthocyanin and co-pigment composition was determined by high-performance liquid chromatography (HPLC). Chemical analyses reveal that the difference in metal-ion content of the two parts was not great. The vacuolar pHs of the upper and lower flowers were 5.91 and 5.84, respectively, with the difference being nonsignificant. HPLC results indicate that the dihydroflavonol and flavonol contents are also very similar in the two sorts of flower. However, the upper flowers contained only delphinidin, whereas the lower flowers also contained cyanidin. The total anthocyanin content in the lower flowers was 4.36 mg g(-1), which is approximately seven times higher than in the upper flowers, while the delphinidin content is four times higher. Quantitative real-time PCR analysis established that the two-tone flower was a result of different expressions of the F3'5'H, F3'H and DFR genes, and these lead to different amounts of anthocyanin.