Search

This study primarily analyzed the response of cold tolerance and phenology periods of four pear cultivars to climate differences in central (Gongzhuling) and eastern (Longjing) Jilin, which could provide a theoretical basis for the regional division and cultivation. It showed that there was a significant difference in the cold tolerance of the same cultivars between the two regions. Soluble sugar and soluble starch contents are the most important physiological indicators that determine the cold tolerance of the pear cultivars in Gongzhuling is stronger than that in Longjing. In phenology, only the cessation of terminal shoot extension and growing season length of pear cultivars were significantly related to their contents of soluble sugar and soluble starch. Furthermore, the gray correlation analysis identified the district's effective accumulated temperature as the key meteorological factors affecting the cessation of terminal shoot extension. The precipitation in the growing season was another major meteorological factor affecting the growing season length. Therefore, in this study, the influence of the main district meteorological factors on the key phenology periods of four pear cultivars, which decided the different accumulation of sugar and starch, eventually lead to the difference in cold tolerance of the same pear cultivar in two regions. [ABSTRACT FROM AUTHOR]

Cav1.2 channel phosphorylation plays an important role in regulating neuronal plasticity by action potential-dependent Ca2+ entry. Most studies of Cav1.2 regulation by phosphorylation have been reported in heart and muscles. Here, we identified phosphorylation sites of neuronal Cav1.2 channel protein purified from rat brain using mass spectrometry. The functional characterization of these phosphorylation sites showed altered voltage-dependent biophysical properties of the channel, without affecting current density. These results show that neuronal Cav1.2 channel is regulated by phosphorylation in a complex mechanism involving multiple phosphorylation sites. [ABSTRACT FROM AUTHOR]

Aims: Acyl‐CoA synthetase long chain family member 4 (ACSL4) is closely related to tumor genesis and development in certain tissues. However, the function of ACSL4 in early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) is unclear. In this study, we investigated the expression patterns and role of ACSL4 in SAH and post‐SAH EBI using a rat model of SAH. Methods: The rat model of SAH was induced by autologous blood injection into the prechiasmatic cistern of rats. We also used two specific inhibitors of ferroptosis (Ferrostatin‐1 and Liproxstatin‐1) to investigate the role of ferroptosis in EBI. Results: We found that ACSL4 levels in brain tissue increased significantly in post‐SAH EBI. Inhibiting the expression of ACSL4 using small interfering RNAs alleviated inflammation, blood‐brain barrier (BBB) impairment, oxidative stress, brain edema, and behavioral and cognitive deficits, and increased the number of surviving neurons, after SAH. Similar effects were obtained by suppressing ferroptosis. Conclusions: ACSL4 exacerbated SAH‐induced EBI by mediating ferroptosis. These findings may provide a theoretical basis for potential therapy aimed at alleviating post‐SAH EBI. [ABSTRACT FROM AUTHOR]

Ischemia/reperfusion (I/R) injury is a phenomenon that the reperfusion of ischemic organs or tissues aggravates their damage, which poses a serious health threat and economic burden to the world. I/R gives rise to a series of physiological and pathological world, including inflammatory response, oxidative stress, brain edema, blood-brain barrier destruction, and neuronal death. Therefore, finding effective treatment measures is extremely important to the recovery of I/R patients and the improvement of long-term quality of life. Sevoflurane is an important volatile anesthetic which has been reported to reduce myocardial I/R damage and infarct size. Sevoflurane also has anti-inflammatory and neuroprotective effects. As reported sevoflurane treatment could reduce nerve function injury, cerebral infarction volume and the level of inflammatory factors. At the same time, there is evidence that sevoflurane can reduce neuron apoptosis and antioxidant stress. The protective effect of sevoflurane in brain injury has been proved to be existed in several aspects, so that a comprehensive understanding of its neuroprotective effect is helpful to exploit new treatment paths for I/R, provide clinicians with new clinical treatment decisions, contribute to the effective treatment of I/R patients and the improvement of quality of life after I/R healing. [ABSTRACT FROM AUTHOR]