Effect of pore structure on slippage effect in unsaturated tight formation using pore network model

ACKNOWLEDGMENTS We acknowledge the Beijing Natural Science Foundation of China (No. 2204093), Science Foundation of China University of Petroleum, Beijing (No.2462018YJRC033) and financial support from China Scholarship Council ((No. 201906440134)Peer reviewedPostprin

Serum potassium level in maintenance hemodialysis patients and its effect on outcome

Maintenance hemodialysis is one of the renal replacement therapy that end-stage renal disease patients mainly rely on. Dyskalemia is one of the most common metabolic complications in patients undergoing maintenance hemodialysis. Both pre-dialysis hyperkalemia and hypokalemia during and after dialysis may contribute to a higher risk of all-cause mortality, cardiovascular mortality in hemodialysis patients. The impact of serum potassium fluctuation has attracted widespread attention in recent years. Due to the intermittent nature of maintenance hemodialysis, patients are prone to frequent fluctuations of serum potassium. Potassium variability may be a better indicator to reflect potassium homeostasis, and large variability of potassiun is recognized as a potential risk factor for poor outcomes. In addition, the rapid fluctuation of serum potassium concentration during hemodialysis may increase the risk of malignant arrhythmia, sudden cardiac death and other poor outcomes. The gradient of serum and dialysate potassium is an important factor that influence the removal of potassium, which is also affected by other dialysate components. Therefore, strengthening the monitoring and management of serum potassium, selecting appropriate dialysate potassium concentration and individualizing dialysate prescription may be beneficial to maintain potassium homeostasis, reduce dyskalemia and improve prognosis. This review briefly expounds the feature of serum potassium level and discusses its effect on outcomes in patients with maintenance hemodialysis, emphasizing the relevance of potassium variation and prognosis in patients with maintenance hemodialysis and the impact of dialysate composition on potassium homeostasis

Bacoside-A exerts protective effect against Parkinson’s disease-induced functional damage in mice via inhibition of apoptosis and oxidative response

Purpose: To determine the effect of bacoside-A on Parkinson's disease (PD) in a rat model, and elucidate its mechanism of action.Methods: A rat model of PD was established by administration of 5 µL of 6-hydroxydopamine in ascorbic acid (0.1 %). Measurement of serum levels of inflammatory factors was carried out using enzyme-linked immunosorbent assay (ELISA) kits. Western blotting was used to assay Bax, cytochrome c and Bcl-2 in rat hippocampus.Results: Bacoside-A treatment significantly reduced PD-induced high turning values in rats (p < 0.05). Treatment with bacoside-A reversed PD-mediated suppression of serum activities of CAT and glutathione peroxidase (GPx). In bacoside-A-treated PD rats, dose-dependent suppression of acetylcholinesterase (AChE) and inducible nitric oxide synthase (iNOS) activities were observed (p < 0.05). Bacoside-A-treated PD rats significantly (p < 0.018) reduced interleukin (IL)-1β and IL-6 levels. Treatment of PD rats with bacoside-A effectively reduced levels of tumor necrosis factor (TNF)-α, NF-κB p65, (COX)-2 and p53 protein, and also reversed up-regulations of Bax, cytochrome C, caspase-3 and caspase-9.Conclusion: Bacoside-A exhibits a protective effect against Parkinson disease-induced oxidative damage and neuronal degeneration in rats through downregulation of iNOS, AChE, inflammatory cytokines and pro-apoptotic proteins. Therefore, bacoside-A has potentials for use in the management of Parkinson disease. Keywords: Parkinson disease, Neuroprotective, Pro-apoptotic, Cytokines, Neurotoxicit

Pore network modeling of thin water film and its influence on relative permeability curves in tight formations

Acknowledgments We acknowledge the Beijing Natural Science Foundation of China (No. 2204093), Science Foundation of China University of Petroleum, Beijing (No.2462018YJRC033) and financial support from China Scholarship Council ((No. 201906440134). Dr. Yingfang Zhou would like to acknowledge the support from State Key Laboratory of Oil and Gas Reservoir Geology and Exploitation (Southwest Petroleum University), PLN201602.Peer reviewedPostprin

The association between declining lung function and stroke risk: insights from an observational study and Mendelian randomization

BackgroundStroke, prevalent globally, particularly impacts low- and middle-income countries. Decreased lung function is one of the risk factors for stroke, and there is a lack of sufficient research on the association between the two, especially based on evidence from representative large samples. We aimed to explore the association between lung function and stroke incidence.MethodsWe collected data from 13,371 participants from the 2007–2012 U.S. national cross-sectional study and 11,192 participants from the Chinese national cohort study during the 2011–2018 follow-up period. Multivariate logistic regression and Cox proportional hazards regression were used to assess cross-sectional and longitudinal associations of peak expiratory flow with stroke risks. Additionally, we used publicly available GWAS data from a European population to conduct Mendelian randomization analysis, further exploring the potential causal relationship.ResultsThe results of the cross-sectional study suggest that a decline in peak expiratory flow may be associated with an increased risk of stroke. The cohort study revealed that, compared to the first tertile group, the risk of stroke incidence in the second and third tertile groups of PEF decreased by 19% (hazard ratio (HR) = 0.810, 95%CI = 0.684–0.960) and 21.4% (HR = 0.786, 95%CI = 0.647–0.956), respectively. Mendelian randomization analysis clarified that higher PEF levels are significantly associated with a reduced risk of stroke (OR = 0.852, 95%CI = 0.727–0.997).ConclusionDecreased lung function is a risk factor for stroke. As a simple and accurate indicator of lung function, PEF can be used to monitor lung function in community populations and patients for primary stroke prevention

Considerable effects of lateralization and aging in intracortical excitation and inhibition

IntroductionFindings based on the use of transcranial magnetic stimulation and electromyography (TMS-EMG) to determine the effects of motor lateralization and aging on intracortical excitation and inhibition in the primary motor cortex (M1) are inconsistent in the literature. TMS and electroencephalography (TMS-EEG) measures the excitability of excitatory and inhibitory circuits in the brain cortex without contamination from the spine and muscles. This study aimed to investigate the effects of motor lateralization (dominant and non-dominant hemispheres) and aging (young and older) and their interaction effects on intracortical excitation and inhibition within the M1 in healthy adults, measured using TMS-EMG and TMS-EEG.MethodsThis study included 21 young (mean age = 28.1 ± 3.2 years) and 21 older healthy adults (mean age = 62.8 ± 4.2 years). A battery of TMS-EMG measurements and single-pulse TMS-EEG were recorded for the bilateral M1.ResultsTwo-way repeated-measures analysis of variance was used to investigate lateralization and aging and the lateralization-by-aging interaction effect on neurophysiological outcomes. The non-dominant M1 presented a longer cortical silent period and larger amplitudes of P60, N100, and P180. Corticospinal excitability in older participants was significantly reduced, as supported by a larger resting motor threshold and lower motor-evoked potential amplitudes. N100 amplitudes were significantly reduced in older participants, and the N100 and P180 latencies were significantly later than those in young participants. There was no significant lateralization-by-aging interaction effect in any outcome.ConclusionLateralization and aging have independent and significant effects on intracortical excitation and inhibition in healthy adults. The functional decline of excitatory and inhibitory circuits in the M1 is associated with aging

Bmi-1 Absence Causes Premature Brain Degeneration

Bmi-1, a polycomb transcriptional repressor, is implicated in cell cycle regulation and cell senescence. Its absence results in generalized astrogliosis and epilepsy during the postnatal development, but the underlying mechanisms are poorly understood. Here, we demonstrate the occurrence of oxidative stress in the brain of four-week-old Bmi-1 null mice. The mice showed various hallmarks of neurodegeneration including synaptic loss, axonal demyelination, reactive gliosis and brain mitochondrial damage. Moreover, astroglial glutamate transporters and glutamine synthetase decreased in the Bmi-1 null hippocampus, which might contribute to the sporadic epileptic-like seizures in these mice. These results indicate that Bmi-1 is required for maintaining endogenous antioxidant defenses in the brain, and its absence subsequently causes premature brain degeneration