High-quality complete genome sequence of Xanthomonas oryzae pv. oryzicola (Xoc) strain HB8.

Here, we report a high-quality genome of Xanthomonas oryzae pv. oryzicola (Xoc) strain HB8, which causes bacterial leaf streaks in rice. The genome size of HB8 is 4,800,100 bp, with a GC content of 64.03%, which serves as an important resource for the study of the Xanthomonas-rice pathosystem.

Magnetodielectric Properties of Ordered Microstructured Polydimethylsiloxane-Based Magnetorheological Elastomer with Fe3O4@rGO Nanoparticles.

Magnetodielectric properties of prepared ordered microstructured polydimethylsiloxane-based magnetorheological elastomer with the Fe3O4@rGO (Fe3O4@rGO/PDMS-MRE) were investigated to expand the application of magnetorheological elastomer (MRE) in magnetic sensing fields by improving the magnetodielectric effect. Five types of Fe3O4@rGO electromagnetic biphasic composite particles were synthesized by the solvothermal method, and their characterization and magnetic properties were also tested. Microstructurally ordered Fe3O4@rGO/PDMS-MRE samples with different Fe3O4@rGO concentrations were obtained through the magnetic field orientation technique, an experimental platform for magnetodielectric properties was built, and the relative permittivity of the samples was tested under magnetic flux density from 0 to 500 mT. The results show when the ratio of modified Fe3O4 to GO reaches 10:1, the Fe3O4@rGO composite particles exhibit uniform distribution with a flaky structure and strong magnetic properties and have the best bonding effect of composite particles. The relative permittivity of Fe3O4@rGO/PDMS-MRE increases with the rise of Fe3O4@rGO concentration and applied magnetic flux density. The relative permittivity of Fe3O4@rGO/PDMS-MRE with Fe3O4@rGO concentration of 60 wt% reaches 12.934 under the action of 500 mT magnetic flux density, and the magnetodielectric effect is as high as 92.4%. A reasonable mechanism for improving the magnetodielectric effect of ordered microstructured Fe3O4@rGO/PDMS-MRE is proposed.

Local CRF and oxytocin receptors correlate with female experience-driven avoidance change and hippocampal neuronal plasticity.

Understanding how experiences affect females' behaviors and neuronal plasticity is essential for uncovering the mechanism of neurodevelopmental disorders. The study explored how neonatal maternal deprivation (MD) and post-weaning environmental enrichment (EE) impacted the CA1 and DG's neuronal plasticity in the dorsal hippocampus, and its relationships with passive avoidance, local corticotrophin-releasing factor (CRF) levels, and oxytocin receptor (OTR) levels in female BALB/c mice. The results showed that MD damaged passive avoidance induced by foot shock and hotness, and EE restored it partially. In the CA1, MD raised CRF levels and OTR levels. Parallelly, MD increased synaptic connection levels but reduced the branches' numbers of pyramidal neurons. Meanwhile, in the DG, MD increased OTR levels but lowered CRF levels, DNA levels, and spine densities. EE did not change the CA1 and DG's CRF and OTR levels. However, EE added DG's dendrites of granular cells. The additive of MD and EE raised CA1's synaptophysin and DG's postsynaptic density protein-95 and OTR levels, and meanwhile, shaped avoidance behaviors primarily similar to the control. The results suggest that experience-driven avoidance change and hippocampal neuronal plasticity are associated with local CRF and OTR levels in female mice.

Experiences Shape Hippocampal Neuron Morphology and the Local Levels of CRHR1 and OTR.

The dorsal hippocampus is involved in behavioral avoidance regulation. It is unclear how experiences such as the neonatal stress of maternal deprivation (MD) and post-weaning environmental enrichment (EE) affect avoidance behavior and the dorsal hippocampal parameters, including neuronal morphology, corticotrophin-releasing hormone (CRH) signaling, and oxytocin receptor (OTR) level. In male BALB/c mice, we found that MD impaired avoidance behavior in the step-on test compared to non-MD and EE rearing conditions could alleviate that partially. MD increased neuronal branches in the CA1 but decreased synaptic connection levels in the CA2, CA3, and DG. Meanwhile, MD increased the CA1's OTR levels, which negatively correlated with nucleus densities. MD also increased the CA1's and CA2's CRH levels, which positively correlated with CRHR1 levels. However, MD statistically elevated the CA3's CRH receptor 1 (CRHR1) levels, which negatively correlated with nucleus densities and, probably, synaptic connection levels in the CA3. The additive effects of MD and EE maintained similar CRH levels and CRHR1 levels as well as OTR levels in the hippocampal areas as the additive of non-MD and non-EE. However, the presence of MD and EE still decreased the CA1's neuronal branches and the CA2's and DG's synaptic connection levels. The study illustrates how MD and EE affect avoidance behaviors, hippocampal neuron morphology, and CRH and OTR levels. The results indicate that the late-life environmental improvement partially restores the alterations in dorsal hippocampal areas induced by early life stress.

Effects of maternal deprivation and environmental enrichment on anxiety-like and depression-like behaviors correlate with oxytocin system and CRH level in the medial-lateral habenula.

The medial-lateral habenula (LHbM)'s role in anxiety and depression behaviors in female mice remains unclear. Here, we used neonatal maternal deprivation (MD) and post-weaning environmental enrichment (EE) to treat female BALB/c offspring and checked anxiety-like and depression-like behaviors as well as the corticotropin-releasing hormone (CRH), oxytocin receptor (OTR), estrogen receptor-beta (ERß) levels in their LHbM at adulthood. We found that MD enhanced state anxiety-like behaviors in the elevated plus-maze test, and EE caused trait anxiety-like behaviors in the open field test and depression-like behaviors in the tail suspension test. The immunochemistry showed that MD reduced OT immunoreactive neuron numbers in the hypothalamic paraventricular nucleus but increased OTR levels in the LHbM; EE increased CRH levels in the LHbM but decreased OTR levels in the LHbM. The additive effects of EE and MD maintained the behavioral parameters, OT-ir neuronal numbers, CRH levels, and OTR levels similar to the additive of non-MD and non-EE. The correlation analysis showed that CRH levels correlated with synaptic connection levels, OTR levels correlated with nucleus densities, and ERß levels correlated with Nissl body levels and body weights in female mice. Neither MD nor EE affected ERß levels in the LHbM. Together, the study revealed the relationships between behaviors and neuroendocrine and neuronal alterations in female LHbM and the effects of experiences including MD and EE on them.

Oxytocin system driven by experiences modifies social recognition and neuron morphology in female BALB/c mice.

The oxytocin (OT) system, affected by life experiences, modulates neuron morphology in a sex-specific manner, leading to sex differences in social interactions. To date, few studies have focused on the OT system and social interactions of female mice. In this study, we used maternal deprivation (MD) and its possible treatment, environmental enrichment (EE), to affect social recognition in female BALB/c mice. We checked neuron morphology, synaptic connections, oxytocinergic (OTergic) neurons in the hypothalamus paraventricular nucleus (PVH), and OT receptor (OTR) in the basolateral amygdala (BLA) and layer II/III of the prelimbic cortex (PL). Our results showed that MD induced social recognition impairments, increased OTR levels in the BLA, and, meanwhile, reduced OTergic neurons in the magnocellular region of the PVH (mPVH). Decreased Nissl bodies, increased cell nuclei, and increased dendrites of projection neurons paralleled the increased OTR levels in the BLA of MD mice. EE restored MD-induced the impairments of novel object recognition and sociability; this effect paralleled a decrease in cell density in the PL and an increase in OTergic neurons in the parvocellular regions of the PVH and synaptic connections in the BLA and layer II/III of the PL. Our findings indicate that early life stress such as MD impairs social recognition, and meanwhile, remodels neuron morphology region-specifically in the female brain, apparently in the BLA but slightly in the PL; and EE could partially restore the deficits induced by MD. The results provide new insights into sex differences in the prevalence of psychological development disorders.

Experiences affect social behaviors via altering neuronal morphology and oxytocin system.

Life experiences, such as maternal deprivation (MD) and environment enrichment (EE), affect social behaviors in the adult. But, the underlying mechanism remains unclear. In the present study, we determined whether neonatal MD induces social deficits, whether postweaning EE restores the deficits, and their effects on neuron morphology and oxytocin (OT)-oxytocin receptor (OTR) system. We found that MD induced repetitive behavior and deficits in novel object recognition and sociability, and EE alleviated these deficits. MD decreased oxytocinergic neurons in the magnocellular hypothalamic paraventricular nucleus (mPVH), which was parallel to the increased OTR levels and dendritic branches of projection neurons in the basolateral amygdala (BLA). EE increased the OTR levels in the prelimbic cortex (PL) and the oxytocinergic neurons in the parvocellular PVH (vPVH), which were parallel to the increased dendritic branches of small pyramidal neurons in the PL and synaptic connections marked with synaptophysin and postsynaptic density protein 95 in the BLA and PL. Together, the results suggest that postweaning EE alleviates the social impairments induced by neonatal MD and OT-OTR system are experience-dependent and associated with social behaviors and neuron morphology.

Mechanisms underlying dimethyl sulfoxide-induced cellular migration in human normal hepatic cells.

Numerous studies have reported that low-dose dimethyl sulfoxide (DMSO, <1.5%, v/v) can interfere with various cellular processes, such as cell proliferation, differentiation, apoptosis, and cycle. By contrast, minimal information is available about the effect of low-dose DMSO on cell migration. Here, we report the effect of DMSO (0.0005%-0.5%, v/v) on cellular migration in human normal hepatic L02 cells. We used the Cell Counting Kit-8 assay to measure cell viability, scratch wound healing assay to observe cellular migration, flow cytometry to analyze cell cycle and death pattern, reverse transcription quantitative polymerase chain reaction to evaluate mRNA expression, and Western blot to detect protein levels. After treatment with 0.0005% (v/v) DMSO, more cells entered S phase arrest, the MMP1/TIMP1 ratio increased, and HSP27 expression was elevated. After treatment with 0.1% (v/v) DMSO, more cells entered G0/G1 phase arrest, the MMP2/TIMP2 ratio increased, the p-p38 and p-Smad3 signaling pathways were activated, and neuropilin-1 expression was elevated. These results showed that cells migrate when their MMP1/TIMP1 and MMP2/TIMP2 ratios are imbalanced. Such migration is modulated by the p38/HSP27 signaling pathway and TGF-ß/Smad3 dependent signaling pathway.

Hemoglobin-derived peptides and mood regulation.

Evidence accumulated over the past decades has revealed that red blood cells and hemoglobin (Hb) in the blood play important roles in modulating moods and emotions. The number of red blood cells affects the mood. Hb is the principal content in the red blood cells besides water. Denatured Hb is hydrolyzed to produce bioactive peptides. RVD-hemopressin α (RVD-Hpα), which is a fragment of α-chain (95-103) in Hb, functions as a negative allosteric modulator of cannabinoid receptor 1 and a positive allosteric modulator of cannabinoid receptor 2. Hemorphins, which are fragments of ß-chain in Hb, exert their effects on opioid receptors. Two hemorphins, namely, LVV-hemorphin-6 and LVV-hemorphin-7, could induce anxiolytic-like effects. The use of Hb-derived bioactive peptides for the treatment of mood disorders is desirable due to cannabinoid-opioid cross modulation and the critical roles of the two systems in physiological processes, such as memory, mood and emotion.

Signaling molecules targeting cannabinoid receptors: Hemopressin and related peptides.

Cannabinoid receptors (CBRs) are part of the endocannabinoid system, which is involved in various physiological processes such as nociception, inflammation, appetite, stress, and emotion regulation. Many studies have linked the endocannabinoid system to neuroinflammatory and neurodegenerative disorders such as Parkinson's disease, Huntington's chorea, Alzheimer's disease, and multiple sclerosis. Hemopressin [Hp; a fragment of the hemoglobin α1 chain (95-103 amino acids)] and related peptides [VD-Hpα and RVD-Hpα] are peptides that bind to CBRs. Hp acts as an inverse agonist to CB1 receptor (CB1R), VD-Hpα acts as an agonist to CB1R, and RVD-Hpα acts as a negative allosteric modulator of CB1R and a positive allosteric modulator of CB2R. Because of the critical roles of CBRs in numerous physiological processes, it is appealing to use Hp and related peptides for therapeutic purposes. This review discusses their discovery, structure, metabolism, brain exposure, self-assembly characteristics, pharmacological characterization, and pharmacological activities.

Long noncoding RNA DLGAP1-AS1 promotes cell proliferation in hepatocellular carcinoma via sequestering miR-486-5p.

Hepatocellular carcinoma (HCC) is most prevalent tumor in liver and one of the most fatal cancers in the world. Long noncoding RNAs (lncRNAs) have been accepted as important regulators in carcinomas. But there are still many lncRNAs including DLGAP1-AS1 unannotated in HCC. First of all, GEPIA suggested that DLGAP1-AS1 presented high expression in HCC tissue samples relative to the normal tissues. Besides, overexpression of DLGAP1-AS1 was also proved in HCC cell lines. Moreover, DLGAP1-AS1 knockdown efficiently suppressed cell proliferation in HCC. Interestingly, miR-486-5p was predicted and validated to interact with DLGAP1-AS1, while the level of miR-486-5p was significantly increased In HCC after DLGAP1-AS1 knockdown. Moreover, we uncovered that ectopic expression of miR-486-5p induced suppression on HCC cell proliferation and that miR-486-5p inhibition offset the effect of DLGAP1-AS1 silence on HCC cell proliferation and apoptosis. Furthermore, H3F3B was identified as target of miR-486-5p and was therefore positively regulated by DLGAP1-AS1 in HCC. Of note, H3F3B upregulation partly revived the declined cell proliferative capacity in response to DLGAP1-AS1 knockdown. To conclude, DLGAP1-AS1 exerted its oncogenic role in HCC via miR-486-5p/H3F3B axis. Our new findings provided novel theoretical basis for discovery of therapeutic targets of HCC.

Hyperoside protects rat ovarian granulosa cells against hydrogen peroxide-induced injury by sonic hedgehog signaling pathway.

Sustained exogenous stimuli induce oxidative stress in granulosa cells and cause cell apoptosis, thereby resulting in follicular atresia. Hyperoside is a natural flavonoid that possesses anti-oxidant activity. The present study aimed to evaluate the effect of hyperoside on hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in granulosa cells. Cell viability was measured using MTT assay. The malondialdehyde (MDA) level and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were detected to reflect the oxidative stress. Flow cytometry was performed to measure the apoptotic rate. Western blot was carried out to determine the expression of Bcl-2, Bax, Sonic hedgehog (SHH), Gli1, and smoothened (SMO). The mRNA levels of SHH, Gli1, and SMO were analyzed using qRT-PCR. We found that hyperoside improved cell viability in H2O2-stimulated granulosa cells. The increased MDA level and decreased activities of SOD, GSH-Px, and CAT caused by H2O2 stimulation were reversed by hyperoside treatment. The apoptotic rate of H2O2-stimulated granulosa cells was reduced after treatment with hyperoside. Hyperoside treatment caused a decrease in Bax expression and an increase in Bcl-2 expression in H2O2-stimulated granulosa cells. The mRNA and protein levels of SHH, Gli1, and SMO in H2O2-stimulated granulosa cells were elevated by hyperoside treatment. Suppression of SHH pathway by cyclopamine attenuated the protective effects of hyperoside on H2O2-induced injury. In short, hyperoside protected granulosa cells from H2O2-induced cell apoptosis and oxidative stress via activation of the SHH signaling pathway.