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Background Propofol, a kind of intravenous sedative drug, is certified that exerts anti-inflammation and antitumor functions. However, the influence of propofol in cerebral injury and the corresponding mechanism remains unexplained, that our article focuses on. Methods PC12 cells were treated with propofol and exposed in glutamic acid (Glu) solutions. Cell viability, apoptotic potential, apoptosis-related and autophagy-linked proteins were tested via CCK-8, flow cytometry, and western blot assays. Reverse transcription-quantitative real-time PCR was utilized to test miR-19a expression in Glu-stimulated cells. Next, miR-19a mimic transfection was used to assess the effects of miR-19a on cell apoptosis and autophagy in Glu or propofol treated cells. Finally, western blot was performed to test AMPK and mTOR pathways. Results Glu exposure promoted cell apoptosis and autophagy of PC12 cells, while propofol attenuated cell apoptosis and autophagy triggered by Glu. Additionally, propofol decreased the miR-19a expression in Glu-stimulated PC12 cells. Meanwhile, over-expression of miR-19a reversed the effects of propofol on Glu-induced cell apoptosis and autophagy. Moreover, propofol potentiated AMPK and mTOR pathways in Glu-stimulated PC12 cells via impeding miR-19a expression. Conclusions These finding revealed that propofol relieved Glu-triggered apoptosis and autophagy of PC12, and activated AMPK and mTOR pathways by suppressing miR-19a expression.

Atherosclerosis can result in multiple cardiovascular diseases. Circular RNAs (CircRNAs) have been reported as significant non‐coding RNAs in atherosclerosis progression. Dysfunction of vascular smooth muscle cells (VSMCs) is involved in atherosclerosis. However, up to now, the effect of circ_0002984 in atherosclerosis is still unknown. Currently, we aimed to investigate the function of circ_0002984 in VSMCs incubated by oxidized low‐density lipoprotein (ox‐LDL). Firstly, our findings indicated that the expression levels of circ_0002984 were significantly up‐regulated in the serum of atherosclerosis patients and ox‐LDL‐incubated VSMCs. Loss of circ_0002984 suppressed VSMC viability, cell cycle distribution and migration capacity. Then, we carried out ELISA assay to determine TNF‐α and IL‐6 levels. The data implied that lack of circ_0002984 obviously repressed ox‐LDL–stimulated VSMC inflammation. Meanwhile, miR‐326‐3p, which was predicted as a target of circ_0002984, was obviously down‐regulated in VSMCs treated by ox‐LDL. Additionally, after overexpression circ_0002984 in VSMCs, a decrease in miR‐326‐3p was observed. Subsequently, miR‐326‐3p was demonstrated to target vesicle‐associated membrane protein 3 (VAMP3). Therefore, we hypothesized that circ_0002984 could modulate expression of VAMP3 through sponging miR‐326‐3p. Furthermore, we confirmed that up‐regulation of miR‐326‐3p rescued the circ_0002984 overexpressing‐mediated effects on VMSC viability, migration and inflammation. Additionally, miR‐326‐3p inhibitor‐mediated functions on VSMCs were reversed by knockdown of VAMP3. In conclusion, circ_0002984 mediated cell proliferation, migration and inflammation through modulating miR‐326‐3p and VAMP3 in VSMCs, which suggested that circ_0002984 might hold great promise as a therapeutic strategy for atherosclerosis.

Introduction: The superiority of pulsatile perfusion during cardiopulmonary bypass remains controversial. We analyzed the frequency-domain characteristics and organ protection of pulsatile and nonpulsatile flow in adult patients with valvular disease. Methods: EEP and SHE were used to calculate blood flow energy in 60 patients. The Fast Fourier Transform was employed to analyze the power spectral density and power density ratio (Rvpd) of flow energy. Changes in endothelin-1, nitric oxide, interleukin-6,10, tumor necrotic factor, S100β, NSE, blood and urinary β2-microglobulin levels were investigated to assess the endothelial function, inflammatory reaction, kidney and brain injury during CPB. Results: EEP and SHE in PP group at each time point were 1.52–1.62 times and 2.03–2.22 times higher respectively compared with NP group. Power spectral density analysis demonstrated that the blood flow energy frequencies in each group were all within 40 Hz and the low frequency energy (0–5 Hz) was dominant in physiological perfusion (>90%). The energy ratio of 0–5 Hz at radial artery was significantly decreased compared with that of post arterial filter in PP (81% vs 64%) and NP (63% vs 37%) group. The power density ratio (Rvpd) was higher than that of NP in all frequency ranges at the radial artery (9.51 vs 4.68 vs 3.59) and arterial filter (3.87 vs 2.69 vs 2.38). The S100β, NSE Urinary and plasma β2-microglobulin level were significantly increased at 6 and 24 hours after surgery in two group, and significantly higher in group NP. Conclusion: PP provided more energy than NP. The proportion of low frequency energy in the pulsatile or nonpulsatile flow is significantly reduced. The low-frequency energy is significantly attenuated during conduction to peripheral tissues in nonpulsatile flow. The surplus pulsatile energy influences the secretion of endothelial and inflammatory factors, and demonstrate better cerebral and kidney protective effect at the biological marker level.

Background Whether supplemental oxygen worsens long-term mortality remains unclear, with contradictory trial results. The authors therefore tested the hypothesis that supplemental oxygen (80% vs. 30%) increases the hazard for long-term mortality. Methods The authors conducted a post hoc analysis of a large multiple crossover cluster trial in which more than 5,000 colorectal surgeries on 4,088 adults were allocated to receive either 30% or 80% inspired oxygen during general anesthesia. The authors assessed the effect of 80% versus 30% target-inspired oxygen on long-term mortality and calculated Kaplan–Meier survival estimates. Analysis was restricted to patients with a home address in Ohio because the authors could obtain reliable vital status information from the Ohio Department of Health (Columbus, Ohio) for them. Results A total of 3,471 qualifying colorectal surgeries performed in 2,801 patients were analyzed, including 1,753 (51%) surgeries in 1,577 patients given 80% oxygen and 1,718 surgeries in 1,551 patients given 30% oxygen. The observed incidence of death after a median of 3 yr was 13% (234 of 1,753) in the 80% oxygen group and 14% (245 of 1,718) in the 30% oxygen group. The estimated hazard ratio for mortality was 0.94 (95% CI, 0.78 to 1.13; P = 0.493). Conclusions In this post hoc analysis of a large, controlled trial, supplemental oxygen did not increase postoperative mortality. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Supplemental material, sj-pdf-1-prf-10.1177_02676591211012216 for Frequency domain analysis and clinical outcomes of pulsatile and non-pulsatile blood flow energy during cardiopulmonary bypass by Qiliang Jiang, Jian Sun, Lingfeng Xu, Xin Chang, Lin Sun, Yue Zhen and Zhen Guo in Perfusion

Propofol, a kind of intravenous sedative drug, is certified that exerts anti-inflammation and antitumor functions. However, the influence of propofol in cerebral injury and the corresponding mechanism remains unexplained, that our article focuses on.PC12 cells were treated with propofol and exposed in glutamic acid (Glu) solutions. Cell viability, apoptotic potential, apoptosis-related and autophagy-linked proteins were tested via CCK-8, flow cytometry, and western blot assays. Reverse transcription-quantitative real-time PCR was utilized to test miR-19a expression in Glu-stimulated cells. Next, miR-19a mimic transfection was used to assess the effects of miR-19a on cell apoptosis and autophagy in Glu or propofol treated cells. Finally, western blot was performed to test AMPK and mTOR pathways.Glu exposure promoted cell apoptosis and autophagy of PC12 cells, while propofol attenuated cell apoptosis and autophagy triggered by Glu. Additionally, propofol decreased the miR-19a expression in Glu-stimulated PC12 cells. Meanwhile, over-expression of miR-19a reversed the effects of propofol on Glu-induced cell apoptosis and autophagy. Moreover, propofol potentiated AMPK and mTOR pathways in Glu-stimulated PC12 cells via impeding miR-19a expression.These finding revealed that propofol relieved Glu-triggered apoptosis and autophagy of PC12, and activated AMPK and mTOR pathways by suppressing miR-19a expression.

Prolonged or high-dose exposure to anesthetics, such as propofol, can cause brain cell degeneration and subsequent long-term learning or memory deficits, particularly in the developing brain. However, the cellular and molecular mechanisms underlying the deleterious effects of propofol at certain stages of development remain unclear. In this study we found that propofol inhibited the proliferation, neuronal differentiation, and migration of neural stem cells (NSCs) while upregulating miR-141-3p. Silencing of miR-141-3p abrogated the effects of propofol on NSC neurogenesis. Propofol treatment downregulated IGF2BP2, a direct target of miR-141-3p, whereas overexpression of IGF2BP2 attenuated the effects of propofol and miR-141-3p on NSC neurogenesis. In short, propofol inhibits NSC neurogenesis through a mechanism involving the miR-141-3p/IGF2BP2 axis. Our results may provide a potential approach for preventing the neurodegenerative effects of propofol in the developing brain.

A simple approach for the synthesis of Lidocaine-Ibuprofen ionic liquid stabilized silver nanoparticles (IL-AgNPs) was reported in this work. The shape, size and surface morphology of the Lidocaine-Ibuprofen ionic liquid stabilized AgNPs were characterized by using spectroscopic and microscopic techniques such as Ultraviolet-visible spectroscopy (UV-Visible), X-ray diffraction (XRD) analysis, Selected area electron diffraction (SAED), Transmission electron microscopy (TEM). TEM analysis showed the formation of 20-30nm size of IL-AgNPs with very clear lattice fringes. SAED pattern confirmed the highly crystalline nature of fabricated IL stabilized AgNPs. EDS results confirmed the formation of nanosilver. The fabricated IL-AgNPs were studied for their local anesthetic effect in rats. The results of local anesthetic effect showed that the time for onset of action by IL-AgNPs is 10min, which is significantly higher than that for EMLA. Further, tactile test results confirmed the stronger and faster local anesthetic effect of IL-AgNPs when compared to that of EMLA.

Our daily life is more convenient than ever before because of the great progress of science and technology. However, the body building or fitness are always ignored in modern daily life. In this paper, we propose a Virtual Personal Trainer to provide real time visually action guide and action assessment during the fitness time of users via the Microsoft Kinect Sensor. The user actions are captured by Kinect and compared to standard actions so as to give a fitness score representing how well users perform actions in real time. Users can see the skeletons of his/her own action and standard action in the screen together with videos. An action correctness guide will be displayed to guide the user to correct his/her actions. Users correct his/her actions to match the standard action in our pre-collected fitness action library. Thus our system can provide interpretable feedback on how people can improve their action. The whole system gives a new definition of the family gym in the future with the power of human-machine interactive.

Many literatures have proven that postoperative cognitive dysfunction (POCD) was very common in old patients after the injury of acute myocardial ischemia-reperfusion (AMIR) clinically such as the off-pump coronary artery bypass surgery (OPCAB) without definite mechanism; however, reports on the animal experiments were rarely seen. We hypothesized that AMIR could contribute to cognitive dysfunction, and this severe injury might be impeded by EA via hindering neuroinflammation and oxidative stress response as well as modulating the balance of the autonomic nervous system. The aged male Sprague Dawley rats were randomly assigned into three experimental groups: sham (sham operation), AMIR, and EA (electroacupunture treatment, acupoints GV20 and ST36+AMIR) groups. The survival rate, heart rate variability analysis, examination of pathology within the hippocampal CA1, oxidative stress, systemic inflammation and the behavior testing were evaluated by their corresponding methods. The results showed that the rats subjected to AMIR had lower survival rates, higher malondialdehyde (MDA), decreased superoxide dismutase (SOD) activity, more microglial activation, and presented evidence of severe brain injury and cognitive dysfunction on the 1st, 3rd, 7th days after reperfusion compared to sham-operated controls. Most important of all, the above damages induced by the AMIR were significantly improved by the EA treatment. Our findings indicated that EA treatment could be a neuroprotective therapy for the cognitive dysfunction induced by the AMIR event, which might be attributablefor balancing the autonomic nervous system, inhibiting the neuronic apoptosis, hindering microglial activation, attenuating oxidative stress and restraining the central and peripheral inflammation reactions.

In this study, we aimed to compare the effects of low- and high-quality cardiopulmonary resuscitation (CPR) on cardioprotection by induced hypothermia (IH) at 34 °C and examine whether extracellular signal-regulated kinase or endothelial nitric oxide synthase mediates this cardioprotection. Left ventricle infarct sizes were evaluated in six groups of rat hearts (n = 6) following Langendorff perfusion and triphenyltetrazolium chloride staining. Controls underwent 30 min of global ischemia at 37 °C, followed by 10 min of simulated low- or high-quality CPR reperfusion and 90 min of reperfusion at 75 mmHg. The IH groups underwent IH at 34 °C during reperfusion. The U0126 group received U0126 (60 μM)-an extracellular signal-regulated kinase inhibitor-during reperfusion at 34 °C. The L-NIO (N-(1-iminoethyl)-L-ornithine dihydrochloride) group received L-NIO (2 μM)-an endothelial nitric oxide synthase inhibitor-5 min before global ischemia at 37 °C to the end of reperfusion at 34 °C. Infarct size did not significantly differ between the control and IH groups receiving low-quality CPR. However, IH with high-quality CPR reduced the infarct size from 47.2% ± 10.2% to 26.0% ± 9.4% (P = 0.005). U0126 reversed the IH-induced cardioprotection (45.9% ± 9.4%, P = 0.010), whereas L-NIO had no significant effect. Cardiopulmonary resuscitation quality affects IH-induced cardioprotection. Extracellular signal-regulated kinase may mediate IH-induced cardioprotection.