MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.

MicroRNAs: Target Recognition and Regulatory Functions

Mounting evidence has demonstrated that general anesthetics could induce developmental neurotoxicity, including acute widespread neuronal cell death, followed by long-term memory and learning abnormalities. Propofol is a commonly used intravenous anesthetic agent for the induction and maintenance of anesthesia and procedural and critical care sedation in children. Compared with other anesthetic drugs, little information is available on its potential contributions to neurotoxicity. Growing evidence from multiple experimental models showed a similar neurotoxic effect of propofol as observed in other anesthetic drugs, raising serious concerns regarding pediatric propofol anesthesia. The aim of this review is to summarize the current findings of propofol-induced developmental neurotoxicity. We first present the evidence of neurotoxicity from animal models, animal cell culture, and human stem cell-derived neuron culture studies. We then discuss the mechanism of propofol-induced developmental neurotoxicity, such as increased cell death in neurons and oligodendrocytes, dysregulation of neurogenesis, abnormal dendritic development, and decreases in neurotrophic factor expression. Recent findings of complex mechanisms of propofol action, including alterations in microRNAs and mitochondrial fission, are discussed as well. An understanding of the toxic effect of propofol and the underlying mechanisms may help to develop effective novel protective or therapeutic strategies for avoiding the neurotoxicity in the developing human brain.

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Recent Insights Into Molecular Mechanisms of Propofol-Induced Developmental Neurotoxicity: Implications for the Protective Strategies.

New computer vision solutions combined with artificial intelligence algorithms can help recognize patterns in biological images, reducing subjectivity and optimizing the analysis process. The aim of this study was to propose an approach based on interactive and traditional machine learning methods to classify soybean seeds and seedlings according to their appearance and physiological potential. In addition, we correlated the appearance of seeds to their physiological performance. Images of soybean seeds and seedlings were used to develop models using low-cost approaches and free-access software. The models developed showed high performance, with overall accuracy reaching 0.94 for seeds and seedling classification. The high precision of the models that were developed based on interactive and traditional machine learning demonstrated that the method can easily be used to classify soybean seeds according to their appearance, as well as to classify soybean seedling vigor quickly and non-subjectively. The appearance of soybean seeds is strongly correlated with their physiological performance.

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Interactive machine learning for soybean seed and seedling quality classification

Recently, melatonin has gained significant importance in plant research. The presence of melatonin in the plant kingdom has been known since 1995. It is a molecule that is conserved in a wide array of evolutionary distant organisms. Its functions and characteristics have been found to be similar in both plants and animals. The review focuses on the role of melatonin pertaining to physiological functions in higher plants. Melatonin regulates physiological functions regarding auxin activity, root, shoot, and explant growth, activates germination of seeds, promotes rhizogenesis (growth of adventitious and lateral roots), and holds up impelled leaf senescence. Melatonin is a natural bio-stimulant that creates resistance in field crops against various abiotic stress, including heat, chemical pollutants, cold, drought, salinity, and harmful ultra-violet radiation. The full potential of melatonin in regulating physiological functions in higher plants still needs to be explored by further research.

Phytomelatonin: An overview of the importance and mediating functions of melatonin against environmental stresses

Background:Studies in developing animals have shown that anesthetic agents can lead to neuronal cell death and learning disabilities when administered early in life. Development of human embryonic stem cell–derived neurons has provided a valuable tool for understanding the effects of anesthetics on

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Altered Mitochondrial Dynamics Contributes to Propofol-induced Cell Death in Human Stem Cell-derived Neurons.

Role of miR-34c in ketamine-induced neurotoxicity in neonatal mice hippocampus.

γ oscillations are associated with higher brain functions such as memory, perception and consciousness. Disruption of γ oscillations occur in various neuro-psychological disorders such as schizophrenia. Nicotinic acetylcholine receptors (nAChR) are highly expressed in the hippocampus, however, little is known about the role on hippocampal persistent γ oscillation. This study examined the effects of nicotine and selective nAChR agonists and antagonists on kainate-induced persistent γ oscillation in rat hippocampal slices. Nicotine enhanced γ oscillation at concentrations of 0.1–10 μM, but reduced it at a higher concentration of 100 μM. The enhancement on γ oscillation can be best mimicked by co-application of α4β2- and α7- nAChR agonist and reduced by a combination of nAChR antagonists, DhβE and MLA. However, these nAChR antagonists failed to block the suppressing role of nicotine on γ. Furthermore, we found that the NMDA receptor antagonist D-AP5 completely blocked the effect of nicotine. These results demonstrate that nicotine modulates γ oscillations via α7 and α4β2 nAChR as well as NMDA activation, suggesting that nAChR activation may have a therapeutic role for the clinical disorder such as schizophrenia, which is known to have impaired γ oscillation and hypo-NMDA receptor function.

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The modulation of nicotinic acetylcholine receptors on the neuronal network oscillations in rat hippocampal CA3 area

Acute lung injury (ALI) is a critical syndrome that is associated with a high morbidity and mortality in patients. Sevoflurane has a lung protective effect in ALI as it reportedly has anti‑inflammatory and apoptotic‑regulating activity. However, the mechanism is still not entirely understood. The aim of the present study was to explore the effects of sevoflurane on lipopolysaccharide (LPS)‑induced ALI in mice and the possible mechanisms involved. The results revealed that sevoflurane treatment improved LPS‑induced lung injury, as evidenced by the reduction in mortality, lung permeability, lung wet/dry ratio and lung histopathological changes in mice. Total cell counts and the production of pro‑inflammatory cytokines [tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6] in bronchoalveolar fluid were also decreased following treatment with sevoflurane. Additionally, LPS‑triggered apoptosis in lung tissues, which was eliminated by sevoflurane. Furthermore, a miRCURY™ LNA array was employed to screen for differentially expressed microRNAs (miRs/miRNAs). Among these miRNAs, 6 were differentially expressed and were involved in the inflammatory response, but only miR‑27a‑3p (miR‑27a) was regulated by sevoflurane. Subsequently, the present study investigated whether sevoflurane exerts its function through the modulation of miR‑27a. The results demonstrated that the overexpression of miR‑27a via an injection with agomiR‑27a produced similar protections as sevoflurane, while the inhibition of miR‑27a suppressed the lung protective effects of sevoflurane in ALI mice. In addition, the present study identified that miR‑27a inhibited Toll‑like receptor 4 (TLR4) by binding to its 3'‑untranslated region. Western blot analysis demonstrated that sevoflurane may ameliorate the inflammatory response by blocking the miR‑27a/TLR4/MyD88/NF‑κB signaling pathway. The present results indicate that sevoflurane may be a viable therapeutic option in the treatment of patients with ALI.

/pdf/sevoflurane-alleviates-lps-induced-acute-lung-injury-via-the-8bcaa6k98m.pdf

Sevoflurane alleviates LPS‑induced acute lung injury via the microRNA‑27a‑3p/TLR4/MyD88/NF‑κB signaling pathway.

Common chemotherapeutic agents such as vincristine often cause neuropathic pain during cancer treatment in patients. Such neuropathic pain is refractory to common analgesics and represents a challenging clinical issue. Angelicae dahuricae radix is an old traditional Chinese medicine with demonstrated analgesic efficacy in humans. However, the active component(s) that attribute to the analgesic action have not been identified. This work described the anti-hyperalgesic effect of one coumarin component, auraptenol, in a mouse model of chemotherapeutic agent vincristine-induced neuropathic pain. We reported that auraptenol dose-dependently reverted the mechanical hyperalgesia in mice within the dose range of 0.05–0.8 mg/kg. In addition, the anti-hyperalgesic effect of auraptenol was significantly blocked by a selective serotonin 5-HT1A receptor antagonist WAY100635 (1 mg/kg). Within the dose range studied, auraptenol did not significantly alter the general locomotor activity in mice. Taken together, this study for the first time identified an active component from the herbal medicine angelicae dahuricae radix that possesses robust analgesic efficacy in mice. These data support further studies to assess the potential of auraptenol as a novel analgesic for the management of neuropathic pain.

/pdf/auraptenol-attenuates-vincristine-induced-mechanical-41qi1qu8uy.pdf

Auraptenol attenuates vincristine-induced mechanical hyperalgesia through serotonin 5-HT1A receptors

Common chemotherapeutic agents such as vincristine often cause neuropathic pain during cancer treatment in patients. Such neuropathic pain is refractory to common analgesics and represents a challenging clinical issue. Angelicae dahuricae radix is an old traditional Chinese medicine with demonstrated analgesic efficacy in humans. However, the active component(s) that attribute to the analgesic action have not been identified. This work described the anti-hyperalgesic effect of one coumarin component, auraptenol, in a mouse model of chemotherapeutic agent vincristine-induced neuropathic pain. We reported that auraptenol dose-dependently reverted the mechanical hyperalgesia in mice within the dose range of 0.05–0.8 mg/kg. In addition, the anti-hyperalgesic effect of auraptenol was significantly blocked by a selective serotonin 5-HT1A receptor antagonist WAY100635 (1 mg/kg). Within the dose range studied, auraptenol did not significantly alter the general locomotor activity in mice. Taken together, this study for the first time identified an active component from the herbal medicine angelicae dahuricae radix that possesses robust analgesic efficacy in mice. These data support further studies to assess the potential of auraptenol as a novel analgesic for the management of neuropathic pain.

/pdf/retraction-note-auraptenol-attenuates-vincristine-induced-4ol09zd13d.pdf

Xiaoran Zhang

Papers

Role of miR-34c in ketamine-induced neurotoxicity in neonatal mice hippocampus.

The modulation of nicotinic acetylcholine receptors on the neuronal network oscillations in rat hippocampal CA3 area

Sevoflurane alleviates LPS‑induced acute lung injury via the microRNA‑27a‑3p/TLR4/MyD88/NF‑κB signaling pathway.

Auraptenol attenuates vincristine-induced mechanical hyperalgesia through serotonin 5-HT1A receptors

Retraction Note: Auraptenol attenuates vincristine-induced mechanical hyperalgesia through serotonin 5-HT 1A receptors