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Early synchronized spontaneous network activity is a hallmark of the brain growth spurt period, during which general anesthetics cause widespread neuronal apoptosis and subsequent cognitive dysfunction. However, the relationship of such activity to anesthetic-induced neuronal apoptosis remains to be determined. In this study, we utilized patch-clamp electrophysiological recording, immunohistochemistry, and TUNEL assays to investigate the potential roles of spontaneous network activity in ketamine-induced neuronal apoptosis during early development. All experiments were performed using acutely dissected whole-mount Sprague-Dawley rat retinas (0-14 postnatal days [P0-P14]). Ketamine reversibly blocked spontaneous network activity in the rat retina from P0 to P9 and irreversibly blocked such activity from P10 to P12. The peak of physiological and ketamine-induced neuronal apoptosis mainly occurred from P7 to P9. Blockade of nicotinic acetylcholine receptors (nAChRs) also induced reversible inhibition of spontaneous network activity from P0 to P7 and extensive neuronal apoptosis in the P7 rat retina, while activation of nAChRs or increases in endogenous ACh levels attenuated ketamine-induced apoptotic responses. Furthermore, blockade of α7-nAChR and ß2-nAChR subtypes induced neuronal apoptosis in the developing retina, while activation of the α7-nAChR subtype attenuated ketamine-induced apoptotic responses. These results demonstrate that ketamine may inhibit early synchronized spontaneous network activity by blocking nAChRs, and that such inhibition may contribute to ketamine-induced neuronal apoptosis in the developing rat retina.

Apoptosis has been identified as the primary cause of fetal alcohol spectrum disorder (FASD), and the development of methods to prevent and treat FASD have been based on the mechanisms of alcohol-induced apoptosis. The present study aimed to explore the effects of dopamine on alcohol‑induced neuronal apoptosis using whole‑mount cultures of rat retinas (postnatal day 7). Retinas were initially incubated with ethanol (100, 200 or 500 mM), and in subsequent analyses retinas were co‑incubated with ethanol (200 mM) and dopamine (10 µM). In addition, several antagonists and inhibitors were used, including a D1 dopamine receptor (D1R) antagonist (SCH23390; 10 µM), a D2R antagonist (raclopride; 40 µM), an adenosine A2A receptor (AA2AR) antagonist (SCH58261; 100 nM), an adenylyl cyclase (AC) inhibitor (SQ22536; 100 µM) and a PKA inhibitor (H‑89; 1 µM). The results demonstrated that exposure increased neuroapoptosis in the retinal ganglion cell layer (GCL) in a dose‑dependent manner. Dopamine treatment significantly attenuated ethanol‑induced neuronal apoptosis. D1R, D2R and AA2AR antagonists partially inhibited the protective effects of dopamine against ethanol‑induced apoptosis; similar results were observed with AC and PKA inhibitor treatments. In summary, the present study demonstrated that dopamine treatment may be able to attenuate alcohol‑induced neuroapoptosis in the developing rat retina by activating D1R, D2R and AA2AR, and by upregulating cyclic AMP/protein kinase A signaling.

With the IoT technology as the entry point, this paper designs the general plan for the IoT-based forest fire warning & monitoring system of Jizhou District, through the analysis of the application of IoT technology in the forest fire prevention of Tianjin; builds the workflow of the IoT-based forest fire warning system; and put forward the suggestions and countermeasures for the development of forest fire warning system in Jizhou District, thus providing theoretical basis and realistic foundation for improving the efficiency of Tianjin forest disaster prevention and mitigation.

Background A range of strategies including physical interventions, intravenous fluids and vasopressor drugs have been used to minimize or prevent spinal anesthesia-induced hypotension. Recent studies suggest that ondansetron, a commonly used antiemetic, also affects hypotension. This systematic review investigated the effects of prophylactic ondansetron on hemodynamic changes following spinal anesthesia. Methods Medline, Embase, Cochrane Library databases and www.clinicaltrials.gov were searched for randomized controlled trials studying the effects of ondansetron on hemodynamic changes induced by spinal anesthesia. The primary outcome was hypotension. Relative risk (RR) or mean difference, with 95% confidence intervals (CI), were used to analyze outcomes. Results Ten randomized controlled trials with 863 patients were included in the analysis. Prophylactic ondansetron reduced the incidence of spinal anesthesia-induced hypotension in both obstetric and non-obstetric patients. The RR of spinal anesthesia-induced hypotension after ondansetron administration was 0.53 (95% CI 0.32 to 0.86) in obstetric patients and 0.16 (95% CI 0.05 to 0.51) in non-obstetric patients. There was significant heterogeneity among obstetric studies (I 2 = 71%). Ondansetron also reduced the incidence of bradycardia, nausea and vomiting after spinal anesthesia with RRs of 0.27 (95% CI 0.16 to 0.47), 0.24 (95% CI 0.14 to 0.42) and 0.48 (95% CI 0.08 to 3.08), respectively. The doses of ephedrine and phenylephrine required to treat hypotension were reduced by ondansetron with mean differences of −2.35mg (95% CI −4.14 to −0.55mg) and −31.16μg (95% CI −57.46 to −4.87μg), respectively. Conclusion This review suggests that prophylactic ondansetron reduces the incidence of spinal anesthesia-induced hypotension and vasopressor consumption in both obstetric and non-obstetric patients. In addition, ondansetron can also reduce related adverse outcomes such as bradycardia, nausea and vomiting. However, given the relatively large heterogeneity and small sample sizes in current studies, further large and strict randomized clinical trials investigating the effects of ondansetron on spinal anesthesia-induced hemodynamic changes and side effects are still needed, especially among obstetric patients.

Deprivation of spontaneous rhythmic electrical activity in early development by anesthesia administration, among other interventions, induces neuronal apoptosis. However, it is unclear whether enhancement of neuronal electrical activity attenuates neuronal apoptosis in either normal development or after anesthesia exposure. The present study investigated the effects of dopamine, an enhancer of spontaneous rhythmic electrical activity, on ketamine-induced neuronal apoptosis in the developing rat retina. TUNEL and immunohistochemical assays indicated that ketamine time- and dose-dependently aggravated physiological and ketamine-induced apoptosis and inhibited early-synchronized spontaneous network activity. Dopamine administration reversed ketamine-induced neuronal apoptosis, but did not reverse the inhibitory effects of ketamine on early synchronized spontaneous network activity despite enhancing it in controls. Blockade of D1, D2, and A2A receptors and inhibition of cAMP/PKA signaling partially antagonized the protective effect of dopamine against ketamine-induced apoptosis. Together, these data indicate that dopamine attenuates ketamine-induced neuronal apoptosis in the developing rat retina by activating the D1, D2, and A2A receptors, and upregulating cAMP/PKA signaling, rather than through modulation of early synchronized spontaneous network activity.

With the constant progress and expansion of agricultural products, the trade volume of agricultural products has increased gradually and market demand has been expanded. However, the fast and safe circulation of agricultural products is hindered seriously by the concept of attaching importance to production while neglecting circulation. This paper starts from the current status and features of logistics supply chain of agricultural products, analyzes risk factors influencing logistics supply chain of agricultural products, puts forward reasonable countermeasures and guarantees that they can improve the growth rate of agricultural products and promote agricultural development.