Enhancing antioxidant levels and mitochondrial function in porcine oocyte maturation and embryonic development through notoginsenoside R1 supplementation.

This study examines the impact of Notoginsenoside R1 (NGR1), a compound from Panax notoginseng, on the maturation of porcine oocytes and their embryonic development, focusing on its effects on antioxidant levels and mitochondrial function. This study demonstrates that supplementing in vitro maturation (IVM) medium with NGR1 significantly enhances several biochemical parameters. These include elevated levels of glutathione (GSH), nuclear factor erythrocyte 2-related factor 2 (NRF2) and mRNA expression of catalase (CAT) and GPX. Concurrently, we observed a decrease in reactive oxygen species (ROS) levels and an increase in JC-1 immunofluorescence, mitochondrial distribution, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) and nuclear NRF2 mRNA levels. Additionally, there was an increase in ATP production and lipid droplets (LDs) immunofluorescence. These biochemical improvements correlate with enhanced embryonic outcomes, including a higher blastocyst rate, increased total cell count, enhanced proliferative capacity and elevated octamer-binding transcription factor 4 (Oct4) and superoxide dismutase 2 (Sod2) gene expression. Furthermore, NGR1 supplementation resulted in decreased apoptosis, reduced caspase 3 (Cas3) and BCL2-Associated X (Bax) mRNA levels and decreased glucose-regulated protein 78 kD (GRP78) immunofluorescence in porcine oocytes undergoing in vitro maturation. These findings suggest that NGR1 plays a crucial role in promoting porcine oocyte maturation and subsequent embryonic development by providing antioxidant levels and mitochondrial protection.

CDC Like Kinase 2 plays an oncogenic role in colorectal cancer via modulating the Wnt/ß-catenin signaling.

Colorectal cancer (CRC) is a common malignant tumor with high morbidity and mortality, and significant heterogeneity among patients. In this study, we aimed to explore the role and mechanism of CLK2 in CRC, a kinase that phosphorylates SR proteins involved in splicing. Based on the analysis from The Cancer Genome Atlas (TCGA) dataset and tissue microarray, we found that CLK2 was upregulated in CRC tissues and associated with a higher tumor stage and poorer overall survival. Consistent with the bioinformatics analysis, the functional experiments validated that CLK2 acted as a tumor-promoting factor in CRC progression. CLK2 knockdown suppressed aggressive cell proliferation, migration, and invasion in vitro, as well as restrained tumor growth in vivo. In terms of mechanism, we found that the Wnt/ß-catenin signaling pathway was responsible for the CLK2-induced CRC progression, based on the results of pathway enrichment analysis and subsequent experimental validation. Thus, our study, for the first time, identified the role of CLK2 in CRC development and provided a compelling biomarker for targeted therapy in CRC treatment.

[The role of histone acetylation in the basolateral amygdala in morphine-associated memory in rats].

To examine the regulatory effect of histone acetylation on memory related molecules, 34 healthy male SD rats were randomly divided into control and basolateral amygdala (BLA) intracranial positioning operation groups. In the process of conditioned place preference (CPP) training, Trichostafin A (TSA) was administrated by the route of BLA and morphine was injected into enterocoelia with dimethyl sulfoxide or saline as control. Expression levels of H3K14 acetylation and brain-derived neurotrophic factor (BDNF) in BLA were evaluated by Western blotting.The results showed that CPP could be established by intraperitoneal injection of morphine. Compared with control groups, a stronger place preference was established and expression of H3K14 acetylation and BDNF was significantly increased in the group treated with TSA and morphine. In addition, there was a synergistic effect between morphine and TSA. Our results suggested that the level of histone acetylation in BLA is associated with the formation of morphine memory in rats. Inhibition of the activity of histone deacetylases in BLA can promote the formation of cue-associated memory induced by morphine and the involvement of BDNF in BLA maybe was regulated by histone acetylation.

[Optimization of dry granulating technique of Qibai Pingfei granule through response surface methodology].

To determine the optimum process conditions for dry granulating technique of Qibai Pingfei granule, granule excipient type, rolling wheel speed and pressure and feeding speed were studied. Taking shaping rate at a time, moisture absorption and dissolubility as index, the type and amount of granule excipient were determined. In addition, taking shaping rate at a time as index, parameters of rolling wheel speed and pressure and feeding speed were researched through single factor test and response surface methodology. The optimum parameters were as follows: lactose as excipient, dry extract powder to excipient at 1:2, rolling wheel speed and pressure at 10.9 Hz and 6.4 MPa and feeding speed at 7.2 Hz. After validation of three batches pilot-scale production, the optimum processing parameters for dry granulating technique of Qibai Pingfei granule is reasonable and feasible, which can provide reliable basis for production.

Laparoscopic vs open surgery for gastric cancer: Assessing time, recovery, complications, and markers.

BACKGROUND: Gastric cancer (GC) is one of the most common cancers worldwide. Morbidity and mortality have increased in recent years, making it an urgent issue to address. Laparoscopic radical surgery (LRS) is a crucial method for treating patients with GC; However, its influence on tumor markers is still under investigation. AIM: To determine the effects of LRS on patients with GC and their serum tumor markers. METHODS: The data of 194 patients treated at Chongqing University Cancer Hospital between January 2018 and January 2019 were retrospectively analyzed. Patients who underwent traditional open surgery and LRS were assigned to the control (n = 90) and observation groups (n = 104), respectively. Independent sample t-tests and χ2 tests were used to compare the two groups based on clinical efficacy, changes in tumor marker levels after treatment, clinical data, and the incidence of postoperative complications. To investigate the association between tumor marker levels and clinical efficacy in patients with GC, three-year recurrence rates in the two groups were compared. RESULTS: Patients in the observation group had a shorter duration of operation, less intraoperative blood loss, an earlier postoperative eating time, and a shorter hospital stay than those in the control group (P < 0.05). No significant difference was observed between the two groups regarding the number of lymph node dissections (P > 0.05). After treatment, the overall response rate in the control group was significantly lower than that in the observation group (P = 0.001). Furthermore, after treatment, the levels of carbohydrate antigen 19-9, cancer antigen 72-4, carcinoembryonic antigen, and cancer antigen 125 decreased significantly. The observation group also exhibited a significantly lower incidence rate of postoperative complications compared to the control group (P < 0.001). Additionally, the two groups did not significantly differ in terms of three-year survival and recurrence rates (P > 0.05). CONCLUSION: LRS effectively treats early gastric cancer by reducing intraoperative bleeding, length of hospital stays, and postoperative complications. It also significantly lowers tumor marker levels, thus improving the short-term prognosis of the disease.

Superconductivity and density-wave fluctuations in an extended triangular Hubbard model: an application to SnSe2.

We employ the fluctuation-exchange approximation to study the relation of superconducting pairing symmetries and density-wave fluctuations based on the extended triangular Hubbard model upon electron doping and interactions, with an possible application to the layered metal dichalcogenide SnSe2. For the case where the interactions between electrons contain only the on-site Hubbard term, the superconducting pairings are mainly mediated by spin fluctuations, and the spin-singlet pairing with thed-wave symmetry robustly dominates in the low and moderate doping levels, and ad-wave to extendeds-wave transition is observed as the electron doping reachesn = 1. When the near-neighbor site Coulomb interactions are also included, the charge fluctuations are enhanced, and the spin-triplet pairings with thep-wave andf-wave symmetries can be realized in the high and low doping levels, respectively.

Effect of Maximal Oxygen Pulse on Patients with Chronic Obstructive Pulmonary Disease.

Objective: This study evaluated the effect of maximal oxygen pulse (O 2P max) on patients with chronic obstructive pulmonary disease (COPD) and confirmed the predictive effect on acute exacerbations of COPD (AECOPD). Methods: This retrospective study included 91 participants who underwent cardiopulmonary exercise testing (CPET), lung function testing, a dyspnea scale assessment, and a 3-year follow-up. The participants were divided into two groups according to the O 2P max value. Exercise capacity, ventilatory conditions, gas exchange efficiency, and dyspnea symptoms were compared, and the correlations between O 2P max and these indices were evaluated. The ability of O 2P max to predict AECOPD was examined. Results: Exercise capacity, ventilatory conditions, and gas exchange efficiency were lower, and dyspnea symptom scores were higher in the impaired O 2P max group ( P < 0.05). O 2P max was positively correlated with forced vital capacity (FVC)%, forced expiratory volume in 1 sec (FEV 1)%, FEV 1/FVC%, anaerobic threshold (AT), work rate (WR)%, aximal oxygen uptake (V̇O 2max)%, V̇O 2/kg max, V̇O 2/kg max%, WR AT, WR max, V̇O 2AT, V̇O 2max, and V̇ Emax, and was negatively correlated with EqCO 2AT, and EqCO 2max ( P < 0.05). Most importantly, O 2P max could be used to predict AECOPD, and the best cut-off value was 89.5% (area under the curve, 0.739; 95% CI, 0.609-0.869). Conclusion: O 2P max reflected exercise capacity, ventilation capacity, gas exchange capacity, and dyspnea symptoms in patients with COPD and may be an independent predictor of AECOPD.

LncRNA BACE1-AS Promotes Autophagy-Mediated Neuronal Damage Through The miR-214-3p/ATG5 Signalling Axis In Alzheimer's Disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease and is characterized by progressive memory loss and cognitive dysfunction. Long non-coding RNAs (lncRNAs) have been shown to be among the most promising biomarkers and therapeutic targets of AD. Here, we aimed to investigate whether lncRNA BACE1-AS plays a role in the potential mechanisms of AD. The expression of BACE1-AS, miR-214-3p and ATG5 mRNA was detected using qRT-PCR. The expression of the LC3, P62, ATG5, Bcl-2, p-Tau and cleaved-caspase 3 proteins was examined using western blot analysis. Cell apoptosis, cytotoxicity and ROS levels were estimated using flow cytometry, an LDH kit and a DCFH-DA assay, respectively. The interaction between BACE1-AS or ATG5 and miR-214-3p was validated using a dual-luciferase reporter assay. HE staining and a TUNEL assay were employed to evaluate hippocampal neuronal injury. The BACE1-AS level was found to be upregulated in serum samples of AD patients, brain tissues of AD transgenic (Tg) mice and Aß1-42-treated SH-SY5Y cells. Autophagy activity was increased in both Tg mice and Aß1-42-treated cells. BACE1-AS knockdown alleviated Aß1-42-induced cell injury. Rapamycin abolished the protective effects of sh BACE1-AS against Aß1-42 induced cell injury. BACE1-AS indirectly regulated ATG5 expression by binding miR-214-3p. The miR-214-3p inhibitor reversed the protective effects of sh BACE1-AS and sh ATG5 against Aß1-42-induced cell injury. Knockdown of BACE1-AS alleviated neuronal injury by repressing autophagy in vivo. Our findings demonstrate that silencing of BACE1-AS alleviated neuronal injury by regulating autophagy through the miR-214-3p/ATG5 signalling axis in AD.

Sea surface pCO2 in an urbanized coastal system (Jiaozhou Bay, China) during summer.

Various biogeochemical processes complicate carbon dioxide (CO2) behaviour in coastal oceans. Through eight summer surveys, detailed variations in CO2 mechanisms in the urbanized Jiaozhou Bay, China, were analysed. During the rainless period, respiration and dissolved inorganic carbon input from treated wastewater made the northeastern region a strong CO2 source, while the western region with cleaner seawater was a weak source because calcium carbonate (CaCO3) precipitation exceeded primary production. Rainfall events with different intensities and locations caused significantly different effects. When rainfall occurred over the sea, enhanced primary production caused a CO2 sink; when rainfall induced little terrestrial pollutant input, CaCO3 precipitation exceeded net primary production, leading to a CO2 source. When heavy rain caused bulk runoff, the northeastern region was a strong CO2 source because rivers flowing through downtown regions inputted considerable organic matter, while in the western region, runoff through suburbs and wetlands led to a strong sink.

Variations in dissolved inorganic carbon species in effluents from large-scale municipal wastewater treatment plants (Qingdao, China) and their potential impacts on coastal acidification.

With rapid development of global wastewater treatment plants (WWTPs), acidification and enhanced CO2 release in receiving waters caused by high-CO2 treated wastewater input have raised concerns. Insights into the variations in dissolved inorganic carbon (DIC) species in treated wastewater contribute to understanding the mechanisms of the acidification process. Here, we investigated three large-scale municipal WWTPs that discharged into the coast of Qingdao, China, for variations in effluent DIC species and their control mechanisms. The results showed that the effluent DIC concentrations, with a range of 2554-5718 µmol/L, significantly exceeded the concentration in seawater and mainly increased from winter to spring and decreased from summer to autumn. The effluent DIC and its δ13CDIC showed a good negative correlation. The ratios of effluent DIC to total alkalinity (DIC/TAlk) ranged from 1.00 to 1.24, and the proportions of CO2 in DIC ranged from 0.9 to 19.7%; both sets of values significantly exceeded those in seawater. The proportions of CO32- in DIC were only ~ 0.4%. These features determined that the CO2 concentrations in effluents fluctuated from 3 to 80 times the concentration in seawater, whereas the CO32- concentrations were less than 1/15 of those in seawater. Organic matter degradation and nitrogen removal processes made important contributions to the high effluent CO2 concentrations. The increase in solubility induced by decreased temperature may be the main cause for the higher effluent CO2 concentrations during winter as well as spring months with low effluent temperatures. Correspondingly, the effluent pH values were significantly lower than the seawater pH values and showed a good negative logarithmic correlation with the DIC/TAlk values, reflecting the control of DIC species on the pH values in treated wastewater. Variations in DIC species in treated wastewater can cause changes in the affected region and the degree of the induced acidification in receiving waters.

Overexpression of suppressor of IKBKE 1 is associated with vincristine resistance in colon cancer cells.

In a previous study, the suppressor of IKBKE 1 expression level was confirmed to be higher in vincristine (VCR)-resistant HCT-8 (HCT-8/V) colon cancer cells than in non-VCR-resistant HCT-8 cells. In the current study, IKBKE 1 expression in VCR-resistant colon cancer cells was investigated further. HCT-8 and HCT-8/V human colon cancer cells were used, and polymerase chain reaction (PCR) primers were designed to amplify the IKBKE 1 gene. Fluorescence reverse transcription-quantitative PCR (RT-qPCR) was performed to detect differences in IKBKE 1 expression between sensitive and drug-resistant colon cancer cell lines. Western blotting was performed to further observe IKBKE 1 expression. Based on the RT-qPCR and western blot results, IKBKE 1 expression was observed to be markedly higher in the HCT-8/V cells, and this difference was significant (P<0.05). Thus, IKBKE 1 expression was identified to be associated with the resistance of colon cancer cells to VCR.

Th17/Treg Imbalance Induced by Dietary Salt Variation Indicates Inflammation of Target Organs in Humans.

The functions of T helper 17 (Th17) and regulatory T (Treg) cells are tightly orchestrated through independent differentiation pathways that are involved in the secretion of pro- and anti-inflammatory cytokines induced by high-salt dietary. However, the role of imbalanced Th17/Treg ratio implicated in inflammation and target organ damage remains elusive. Here, by flow cytometry analysis, we demonstrated that switching to a high-salt diet resulted in decreased Th17 cells and reciprocally increased Treg cells, leading to a decreased Th17/Treg ratio. Meanwhile, Th17-related pathway was down-regulated after one day of high salt loading, with the increase in high salt loading as shown by microarray and RT-PCR. Subsequently, blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) observed hypoxia in the renal medulla (increased R2(*) signal) during high-salt loading, which was regressed to its baseline level in a step-down fashion during low-salt feeding. The flow-mediated vasodilatation (FMD) of the branchial artery was significantly higher on the first day of high salt loading. Collectively, these observations indicate that a short-term increase in dietary salt intake could induce reciprocal switches in Th17/Treg ratio and related cytokines, which might be the underlying cellular mechanism of high-salt dietary induced end organ inflammation and potential atherosclerotic risk.