Varied responses to copper for plant regeneration from calli of different rice varieties

Enrichment of copper to the culture mediumcould enhance the plant regeneration from cal-lus of indica rice variety Qiugui’ai 11. Westudied the effect of copper on plant regenera-tion of other rice varieties.Calli of 14 indica and 2 japonica varietieswere induced from disinfected mature embryoson an agar-gelled medium containing Nbasal

Edaravone protects against oxygen-glucose-serum deprivation/restoration-induced apoptosis in spinal cord astrocytes by inhibiting integrated stress response

We previously found that oxygen-glucose-serum deprivation/restoration（OGSD/R） induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase（PERK）, eukaryotic initiation factor 2-alpha（eIF2α） and activating transcription factor 4（ATF4）. We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes. To test this, we established primary cultures of rat astrocytes, and exposed them to 8 hours/6 hours of OGSD/R with or without edaravone（0.1, 1, 10, 100 μM） treatment. We found that 100 μM of edaravone significantly suppressed astrocyte apoptosis and inhibited the release of reactive oxygen species. It also inhibited the activation of caspase-12 and caspase-3, and reduced the expression of homologous CCAAT/enhancer binding protein, phosphorylated（p）-PERK, p-eIF2α, and ATF4. These results point to a new use of an established drug in the prevention of OGSD/R-mediated spinal cord astrocyte apoptosis via the integrated stress response.

The HMGB1 signaling pathway activates the inflammatory response in Schwann cells

Schwann cells are not only myelinating cells, but also function as immune cells and express numerous innate pattern recognition receptors, including the Toll-like receptors. Injury to peripheral nerves activates an inflammatory response in Schwann cells. However, it is unclear whether specific endogenous damage-associated molecular pattern molecules are involved in the inflammatory response following nerve injury. In the present study, we demonstrate that a key damage-associated molecular pattern molecule, high mobility group box 1（HMGB1）, is upregulated following rat sciatic nerve axotomy, and we show colocalization of the protein with Schwann cells. HMGB1 alone could not enhance expression of Toll-like receptors or the receptor for advanced glycation end products（RAGE）, but was able to facilitate migration of Schwann cells. When Schwann cells were treated with HMGB1 together with lipopolysaccharide, the expression levels of Toll-like receptors and RAGE, as well as inflammatory cytokines were upregulated. Our novel findings demonstrate that the HMGB1 pathway activates the inflammatory response in Schwann cells following peripheral nerve injury.

Anti-inflammatory properties of lipoxin A4 protect against diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury

Lipoxin A4 can alleviate cerebral ischemia/reperfusion injury by reducing the inflammatory reaction,but it is currently unclear whether it has a protective effect on diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury.In this study,we established rat models of diabetes mellitus using an intraperitoneal injection of streptozotocin.We then induced focal cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery for 2 hours and reperfusion for 24 hours.After administration of lipoxin A4 via the lateral ventricle,infarction volume was reduced,the expression levels of pro-inflammatory factors tumor necrosis factor alpha and nuclear factor-kappa B in the cerebral cortex were decreased,and neurological functioning was improved.These findings suggest that lipoxin A4 has strong neuroprotective effects in diabetes mellitus complicated by focal cerebral ischemia/reperfusion injury and that the underlying mechanism is related to the anti-inflammatory action of lipoxin A4.

Neuroprotective effect of Cerebralcare Granule after cerebral ischemia/reperfusion injury

Cerebralcare Granule（CG） improves cerebral microcirculation and relieves vasospasm,but studies investigating its therapeutic effect on cerebral ischemia/reperfusion injury are lacking.In the present study,we administered CG（0.3,0.1 and 0.03 g/m L intragastrically） to rats for 7 consecutive days.We then performed transient occlusion of the middle cerebral artery,followed by reperfusion,and administered CG daily for a further 3 or 7 days.Compared with no treatment,high-dose CG markedly improved neurological function assessed using the Bederson and Garcia scales.At 3 days,animals in the high-dose CG group had smaller infarct volumes,greater interleukin-10 expression,and fewer interleukin-1β-immunoreactive cells than those in the untreated model group.Furthermore,at 7 days,high-dose CG-treated rats had more vascular endothelial growth factor-immunoreactive cells,elevated angiopoietin-1 and vascular endothelial growth factor expression,and improved blood coagulation and flow indices compared with untreated model animals.These results suggest that CG exerts specific neuroprotective effects against cerebral ischemia/reperfusion injury.

In vivo field recordings effectively monitor the mouse cortex and hippocampus under isoflurane anesthesia

Isoflurane is a widely used inhaled anesthetic in the clinical setting. However, the mechanism underlying its effect on consciousness is under discussion. Therefore, we investigated the effect of isoflurane on the hippocampus and cortex using an in vivo field recording approach. Our results showed that 1.3%, 0.8%, and 0.4% isoflurane exerted an inhibitory influence on the mouse hippocampus and cortex. Further, high frequency bands in the cortex and hippocampus showed greater suppression with increasing isoflurane concentration. Our findings suggest that in vivo field recordings can monitor the effect of isoflurane anesthesia on the mouse cortex and hippocampus.

Regulation of chromatin organization during animal regeneration

Activation of regeneration upon tissue damages requires the activation of many developmental genes responsible for cell proliferation,migration,differentiation,and tissue patterning.Ample evidence revealed that the regulation of chromatin organization functions as a crucial mechanism for establishing and maintaining cellular identity through precise control of gene transcription.The alteration of chromatin organization can lead to changes in chromatin accessibility and/or enhancer-promoter interactions.Like embryogenesis,each stage of tissue regeneration is accompanied by dynamic changes of chromatin organization in regeneration-responsive cells.In the past decade,many studies have been conducted to investigate the contribution of chromatin organization during regeneration in various tissues,organs,and organisms.A collection of chromatin regulators were demonstrated to play critical roles in regeneration.In this review,we will summarize the progress in the understanding of chromatin organization during regeneration in different research organisms and discuss potential common mechanisms responsible for the activation of regeneration response program.