Effects of hypobaria, hyperoxia, and nitrogen form on the growth and nutritional quality of lettuce.

The objectives of this research were to investigate the impact of hypobaria, hyperoxia, and nitrogen form on the growth and nutritional quality of plants. Pre-culture 20-day-old lettuce (Lactuca sativa L. var. Rome) seedlings grew for 25 days under three levels of total atmospheric pressure (101, 54, and 30 kPa), two levels of oxygen partial pressure (21 and 28 kPa), and two forms of nitrogen (NO3N and NH4N). The ratios of NO3N to NH4N included 3: 1, 4: 0, 2: 2, and 0: 4. The nitrogen quantity included two levels, i.e. N1, 0.1 g N kg-1 dry matrix and N2, 0.2 g N kg-1 dry matrix. The growth status of lettuce plants in different treatments differentiated markedly. Regardless of the nitrogen factor, the growth status of lettuce plants treated with total atmospheric pressure/oxygen partial pressure at 54/21 was equivalent to the treatment of 101/21. Under the hypobaric condition (54 kPa), compared with 21 kPa oxygen partial pressure, hyperoxia (28 kPa) significantly inhibited the growth of lettuce plants and the biomass (fresh weight) decreased by 60.9%-69.9% compared with that under 101/21 treatment. At the N1 level, the sequence of the biomass of lettuce plants supplied with different ratios of NO3N to NH4N was 3: 1 > 4: 0 > 2: 2 > 0: 4, and there were higher concentrations of chlorophyll and carotenoid of lettuce plants supplied with the higher ratio of NO3 to NH4. At the N2 level, the effects of different ratios of NO3N to NH4N on lettuce plants were similar to those at the N1 level. The high nitrogen (N2) promoted the growth of lettuce plants such as 54/21/N2 treatments. Both form and nitrogen level did not affect the stress resistance of lettuce plants. Hypobaria (54 kPa) increased the contents of N, P, and K and hyperoxia (28 kPa) decreased the content of organic carbon in lettuce plants. The high nitrogen (N2) improved the content of total N and the N uptake. The ratios of NO3N to NH4N were 4: 0 and 3: 1, lettuce could absorb and utilize N effectively. This study demonstrated that hyperoxia (28 kPa) inhibited the growth of lettuce plants under the hypobaric condition (54 kPa), and high level of nitrogen (0.2 g N kg-1 dry matrix) and NO3N: NH4N at 3: 1 markedly enhanced the growth, the contents of mineral elements and the nutritional quality of lettuce plants.

The neuroprotective effect of electro-acupuncture on cognitive recovery for patients with mild traumatic brain injury: A randomized controlled clinical trial.

BACKGROUND: Traumatic brain injury (TBI) is a major health and socioeconomic problem that affects all societies. Consciousness disorder is a common complication after TBI while there is still no effective treatment currently. The aim of this study was to investigate the protective effect of electro-acupuncture (EA) on cognitive recovery for patients with mild TBI. METHODS: A total of 83 patients with initial Glasgow coma scale score higher than 12 points were assigned into this study. Then patients were randomly divided into 2 groups: EA group and control group (group C). Patients in group EA received EA treatment at Neiguan and Shuigou for 2 weeks. At 0 minute before EA treatment (T1), 0 minute after EA treatment (T2), and 8 weeks after EA treatment (T3), level of neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), hypoxia inducible factor-1α (HIF-1α), and malondialdehyde were tested by enzyme-linked immunosorbent assay. The score of Montreal Cognitive Function Assessment (MoCA) and mini-mental state examination (MMSE) as well as cerebral oxygen saturation (rSO2) were detected at the same time. RESULTS: Compared with the baseline at T1, the level of NSE, GFAP, HIF-1α, MDA, and rSO2 decreased, and the score of MoCA and MMSE increased in the 2 groups were significantly increased at T2-3 (P < .05). Compared with group C, the level of NSE, GFAP, HIF-1α, MDA, and rSO2 decreased, and the score of MoCA and MMSE increased were significantly increased at T2-3 in group EA; the difference were statistically significant (P < .05). CONCLUSIONS: EA treatment could improve the cognitive recovery for patients with mild TBI and the potential mechanism may be related to improving cerebral hypoxia and alleviating brain injury.

Effectiveness of Super-selective Embolization for Parasagittal Meningiomas and Its Effect on the Level of Inflammatory Factors.

Objective: To evaluate the effectiveness of super-selective embolization for parasagittal meningiomas and its effect on the level of inflammatory factors. Methods: A total of 48 patients with parasagittal meningiomas diagnosed and treated in our hospital from September 2018 to March 2020 were randomly included and assigned to receive meningioma resection (control group) or meningioma resection plus super-selective embolization (study group), with 24 patients in each group. Outcome measures included clinical indices, tumor resection outcome, inflammatory factor levels, and follow-up results. Results: Patients in the study group had shorter operative time and less intraoperative bleeding volume than those in the control group (P < 0.05). The study group had more patients with Simpson I resection (87.50%) than the control group (62.50%) (P < 0.05). There was no statistically significant difference in the levels of inflammatory factors between the two groups of patients before treatment (P > 0.05). After treatment, the levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, and hypersensitive C-reactive protein (hs-CRP) in patients in the study group were significantly lower than those of the control group. The results of the three-month follow-up showed that one patient in the study group was reoperated for tumor recurrence and there was no death record, while three patients in the control group were reoperated for tumor recurrence and one patient died. The difference in the recurrence and mortality between the two groups did not come up to the statistical standard (P > 0.05). Conclusion: Super-selective embolization for parasagittal meningiomas contributes to reducing intraoperative bleeding, effectively improving tumor resection and surgical safety, and lowering inflammatory factor levels. Further trials are, however, required before clinical promotion.

LINC01087 inhibits glioma cell proliferation and migration, and increases cell apoptosis via miR-384/Bcl-2 axis.

BACKGROUND: Long non-coding RNA (LncRNA) is associated with disease progression. It is reported that LINC01087 is highly expressed in cancer and participates in tumorigenesis. However, whether it regulates the development of glioma has not been studied. So, the goal of this research is to determine the role of LINC01087 in gliomas and to provide potential targets for clinical treatment. METHODS: The gene expression was detected by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blotting (WB). Cell proliferation was analyzed by CCK8 and colony formation test, and apoptosis was detected by flow cytometry. Luciferase report experiment and RNA Binding Protein Immunoprecipitation confirmed the interaction between LINC01087, miR-384 and Bcl-2. The effect of regulating LINC01087 on the growth of glioma was confirmed in vitro. RESULTS: The LINC01087 expression was up-regulated in clinical glioma samples (n = 35). Furthermore, LINC01087 silencing can obviously suppress the proliferation of glioma cells and induce apoptosis. Mechanically, we found that LINC01087 was the molecular sponge of miR-384. LINC01087 could inhibit the miR-384 expression and boost the Bcl-2 expression through sponge expression of miR-384. The repair of Bcl-2 effectively saved the proliferation and apoptosis of glioma cells lacking LINC01087. CONCLUSION: LINC01087 is highly expressed in glioma and can participate in the growth of glioma through miR-384/Bcl-2 axis. So, it is a potential therapeutic target.

The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/ß-Catenin pathway.

INTRODUCTION: Temozolomide (TMZ) is commonly used for glioma chemotherapy. However, TMZ resistance limits the therapeutic effect of TMZ in glioma treatment. LncRNA-H19 acts as an oncogenic LncRNA in some types of cancers and has been reported to be up-regulated in glioma. MATERIALS AND METHODS: In our present study, we established TMZ-resistant glioma cells (U-251TMZ and M059JTMZ) to explore the effect of H19 on the chemoresistance of glioma cells. RESULTS: We observed that the expression of H19 was significantly increased in U-251TMZ and M059JTMZ cells. Knockdown of H19 expression using specific shRNA in U-251TMZ and M059JTMZ led to decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis rates, indicating that the silencing of H19 decreased chemoresistance of glioma cells to TMZ. In addition, silencing of H19 suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin and decreasing the expression of mesenchymal marker Vimentin and ZEB1. Moreover, inducing EMT by TGF-ß1 treatment led to increased IC50 values for TMZ and decreased cell apoptosis rates compared with TMZ+H19 shRNA group, suggesting that the induction of EMT counteracted the inhibitory effect of H19 shRNA on chemoresistance of glioma cells to TMZ. Furthermore, the reduced expression of H19 down-regulated the expression of ß-Catenin and its downstream targets c-myc and Survivin in TMZ-treated glioma cells. Activation of Wnt/ß-Catenin pathway by Licl treatment promoted EMT and enhanced chemoresistance to TMZ compared with TMZ+H19 shRNA group. CONCLUSION: Taken together, our data suggest that H19 decreased chemoresistance of glioma cells to TMZ by suppressing EMT via the inhibition of Wnt/ß-Catenin pathway. Our study might represent a novel therapeutic target for TMZ-resistant glioma.

MAPK pathway mediates the anti-oxidative effect of chicoric acid against cerebral ischemia-reperfusion injury in vivo.

The aim of the present study was to investigate the protective effect of chicoric acid on oxidative stress and inflammation in rats with cerebral ischemia-reperfusion injury. A cerebral ischemia-reperfusion injury rat model was created via transient middle cerebral artery occlusion (MCAO) and rats were treated with various doses of chicoric acid (0, 1, 10 and 100 mg/kg). Neurological deficits and infarct volume were used to estimate the protective effects of chicoric acid treatment. Levels of reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, nitric oxide (NO) and prostaglandin E2 (PGE2) were assessed. Western blot analysis was also used to measure the expression of cyclooxygenase (COX)-2, p38-mitogen activated protein kinase (MAPK), c-Jun, phosphorylated protein kinase B (p-AKT) and AKT. Chicoric acid exposure was observed to reduce neurological deficits and infarct volume in rats with cerebral ischemia-reperfusion injury. In addition, ROS production and inflammation were significantly suppressed following treatment with chicoric acid. Chicoric acid was demonstrated to significantly inhibit the upregulation of NO and PGE2 levels in rats following MCAO. Furthermore, chicoric acid significantly suppressed the MCAO-induced promotion of COX-2, p38-MAPK and c-Jun protein expression and enhanced the inhibition of p-AKT/AKT. These results suggest that chicoric acid has a protective effect, preventing oxidative stress and inflammation in rats with cerebral ischemia-reperfusion injury via the p38-MAPK, c-Jun and AKT signaling pathways.

Capsaicin ameliorates stress-induced Alzheimer's disease-like pathological and cognitive impairments in rats.

Hyperphosphorylated tau aggregated into neurofibrillary tangles is a hallmark lesion of Alzheimer's disease (AD) and is linked to synaptic and cognitive impairments. In animal models, cold water stress (CWS) can cause cognitive disorder and tau hyperphosphorylation. Capsaicin (CAP), a specific TRPV1 agonist, is neuroprotective against stress-induced impairment, but the detailed mechanisms are still elusive. Here, we investigated whether CAP mitigates CWS-induced cognitive and AD-like pathological alterations in rats. The animals were administered CAP (10 mg/kg in 0.2 ml, 0.1% ethanol) or a control (0.2 ml normal saline, 0.1% ethanol) by intragastric infusion 1 h before CWS treatment. Our results showed that CAP significantly attenuated CWS-induced spatial memory impairment and suppression of PP-DG long-term potentiation; CAP abolished CWS-induced dendritic regression and enhanced several memory-associated proteins decreased by CWS, such as synapsin I and PSD93; CAP also prevented CWS-induced tau hyperphosphorylation by abolishing inhibition of protein phosphatase 2A. Taken together, this study demonstrated that activation of TRPV1 can mitigate CWS-induced AD-like neuropathological alterations and cognitive impairment and may be a promising target for therapeutic intervention in AD.