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Upland forests are traditionally thought to be net sinks for atmospheric methane (CH4). In such forests, in situ CH4 fluxes on tree trunks have been neglected relative to soil and canopy fluxes. We measured in situ CH4 fluxes from the trunks of living trees and other surfaces, such as twigs and soils, using a static closed-chamber method, and estimated the CH4 budget in a temperate upland forest in Beijing. We found that the trunks of Populus davidiana emitted large quantities of CH4 during July 2014–July 2015, amounting to mean annual emissions of 85.3 and 103.1 μg m−2 h−1 on a trunk surface area basis on two replicate plots. The emission rates were similar in magnitude to those from tree trunks in wetland forests. The emitted CH4 was derived from the heartwood of trunks. On a plot or ecosystem scale, trunk CH4 emissions were equivalent to c. 30–90% of the amount of CH4 consumed by soils throughout the year, with an annual average of 63%. Our findings suggest that wet heartwoods, regardless of rot or not, occur widely in living trees on various habitats, where CH4 can be produced.

Enhanced external counterpulsation (EECP) is widely utilized in rehabilitating patients after percutaneous coronary intervention (PCI) and has demonstrated efficacy in promoting cardiovascular function recovery. Although the precise mechanisms of the therapeutic effects remain elusive, it is widely postulated that the improvement of biomechanical environment induced by EECP plays a critical role. This study aimed to unravel the underlying mechanism through a numerical investigation of the in-stent biomechanical environment during EECP using an advanced multi-dimensional 0/1D-3D coupled model. Physiological data, including age, height, coronary angiography images, and blood velocity profiles of five different arteries, were clinically collected from eleven volunteers both at rest and during EECP. These data contributed the development of a patient-specific 0/1D model to predict the coronary volumetric flow and a 3D stented coronary artery model to capture the detailed in-stent biomechanical features. Specifically, an immersed solid method was introduced to address the numerical challenges of generating computational cells for the 3D model. Simulations revealed that EECP significantly improved the biomechanical environment within the stented arteries, as evidenced by increased time-averaged wall shear stress (resting vs. 20 kPa vs. 30 kPa: 1.39 ± 0.4773 Pa vs. 1.82 ± 0.6856 Pa vs. 1.96 ± 0.7592 Pa, p = 0.0009) and reduced relative residence time (resting vs. 20 kPa vs. 30 kPa: 1.06 ± 0.3926 Pa−1 vs. 0.89 ± 0.3519 Pa−1 vs. 0.87 ± 0.3764 Pa−1, p < 0.0001). Correspondingly, low-WSS/high-RRT surfaces were obviously reduced under EECP. These findings provide deeper insights into EECP’s therapeutic mechanisms, thereby offering basis to optimize EECP protocols for enhanced clinical outcomes in post-PCI patients.

Enhanced external counterpulsation (EECP) is a treatment and rehabilitation approach for ischemic diseases, including coronary artery disease. Its therapeutic benefits are primarily attributed to the improved blood circulation achieved through sequential mechanical compression of the lower extremities. However, despite the crucial role that hemodynamic effects in the lower extremity arteries play in determining the effectiveness of EECP treatment, most studies have focused on the diastole phase and ignored the systolic phase. In the present study, a novel siphon model (SM) was developed to investigate the interdependence of several hemodynamic parameters, including pulse wave velocity, femoral flow rate, the operation pressure of cuffs, and the mean blood flow changes in the femoral artery throughout EECP therapy. To verify the accuracy of the SM, we coupled the predicted afterload in the lower extremity arteries during deflation using SM with the 0D-1D patient-specific model. Finally, the simulation results were compared with clinical measurements obtained during EECP therapy to verify the applicability and accuracy of the SM, as well as the coupling method. The precision and reliability of the previously developed personalized approach were further affirmed in this study. The average waveform similarity coefficient between the simulation results and the clinical measurements during the rest state exceeded 90%. This work has the potential to enhance our understanding of the hemodynamic mechanisms involved in EECP treatment and provide valuable insights for clinical decision-making.

Neuropathic pain is among the most debilitating forms of chronic pain. Studies have suggested that chronic pain pathogenesis involves neuroimmune interactions and blood-spinal cord barrier (BSCB) disruption. However, the underlying mechanisms are poorly understood. We modeled neuropathic pain in rats by inducing chronic constriction injury (CCI) of the sciatic nerve and analyzed the effects on C-X-C motif chemokine 10 (CXCL10)/CXCR3 activation, BSCB permeability, and immune cell migration from the circulation into the spinal cord. We detected CXCR3 expression in spinal neurons and observed that CCI induced CXCL10/CXCR3 activation, BSCB disruption, and mechanical hyperalgesia. CCI-induced BSCB disruption enabled circulating T cells to migrate into the spinal parenchyma. Intrathecal administration of an anti-CXCL10 antibody not only attenuated CCI-induced hyperalgesia, but also reduced BSCB permeability, suggesting that CXCL10 acts as a key regulator of BSCB integrity. Moreover, T cell migration may play a critical role in the neuroimmune interactions involved in the pathogenesis of CCI-induced neuropathic pain. Our results highlight CXCL10 as a new potential drug target for the treatment of nerve injury-induced neuropathic pain.

Background The relationship between obstructive sleep apnea (OSA) and the occurrence of arrhythmias and heart rate variability (HRV) in hypertensive patients is not elucidated. Our study investigates the association between OSA, arrhythmias, and HRV in hypertensive patients. Methods We conducted a cross-sectional analysis involving hypertensive patients divided based on their apnea-hypopnea index (AHI) into two groups: the AHI ≤ 15 and the AHI > 15. All participants underwent polysomnography (PSG), 24-hour dynamic electrocardiography (DCG), cardiac Doppler ultrasound, and other relevant evaluations. Results The AHI > 15 group showed a significantly higher prevalence of frequent atrial premature beats and atrial tachycardia ( P  = 0.030 and P  = 0.035, respectively) than the AHI ≤ 15 group. Time-domain analysis indicated that the standard deviation of normal-to-normal R-R intervals (SDNN) and the standard deviation of every 5-minute normal-to-normal R-R intervals (SDANN) were significantly higher in the AHI > 15 group ( P  = 0.020 and P  = 0.033, respectively). Frequency domain analysis revealed that the low-frequency (LF), high-frequency (HF) components, and the LF/HF ratio were also significantly elevated in the AHI > 15 group ( P  < 0.001, P  = 0.031, and P  = 0.028, respectively). Furthermore, left atrial diameter (LAD) was significantly larger in the AHI > 15 group ( P  < 0.001). Both univariate and multivariable linear regression analyses confirmed a significant association between PSG-derived independent variables and the dependent HRV parameters SDNN, LF, and LF/HF ratio ( F  = 8.929, P  < 0.001; F  = 14.832, P  < 0.001; F  = 5.917, P  = 0.016, respectively). Conclusions Hypertensive patients with AHI > 15 are at an increased risk for atrial arrhythmias and left atrial dilation, with HRV significantly correlating with OSA severity.

How oxidative stress contributes to neuro-inflammation and chronic pain is documented, and methane is reported to protect against ischemia–reperfusion injury in the nervous system via anti-inflammatory and antioxidant properties. We studied whether methane in the form of methane rich saline (MS) has analgesic effects in a monoarthritis (MA) rat model of chronic inflammatory pain. Single and repeated injections of MS (i.p.) reduced MA-induced mechanical allodynia and multiple methane treatments blocked activation of glial cells, decreased IL-1β and TNF-α production and MMP-2 activity, and upregulated IL-10 expression in the spinal cord on day 10 post-MA. Furthermore, MS reduced infiltrating T cells and expression of IFN-γ and suppressed MA-induced oxidative stress (MDA and 8-OHDG), and increased superoxide dismutase and catalase activity. Thus, MS may offer anti-inflammatory and antioxidant effects to reduce chronic inflammatory pain.

Increasing evidence suggests that T cells and glia participate in the process of neuropathic pain. However, little is known about the involvement of T cells or the interaction between glia and T cells at the molecular level. Here we investigated the phenotype of T cell infiltration into the spinal cord in inflammatory pain and explored potential crosstalk between glia and T cells. The establishment of monoarthritis produced T cell infiltration and astrocyte activation, exhibiting similar kinetics in the spinal cord. T-cell-deficient (Rag1 −/− ) mice significantly attenuated MA-induced mechanical allodynia and GFAP upregulation. Double immunofluorescence staining showed that CD3 mainly colocalized with interferon-gamma (IFN-γ). Western blot and flow cytometry showed that multiple intrathecal administrations of astrocytic inhibitor fluorocitrate decreased IFN-γ-production without decreasing T cell number in the spinal cord. Spinal IFN-γ blockade reduced MA-induced mechanical allodynia and astroglial activation. In contrast, treatment with rIFN-γ directly elicited persistent mechanical allodynia and upregulation of GFAP and pJNK1/2 in naïve rats. Furthermore, rIFN-γ upregulated the phosphorylation of NF-κB p65 in cultured astrocytes vitro and spinal dorsal horn vivo . The results suggest that Th1 cells and astrocytes maintain inflammatory pain and imply that there may be a positive feedback loop between these cells via IFN-γ.

Predicted future shifts in the magnitude and frequency (larger but fewer) of precipitation events and enhanced nitrogen (N) deposition may interact to affect grassland productivity, but the effects of N enrichment on the productivity response to individual precipitation events remain unclear. In this study, we quantified the effects of N addition on the response patterns of gross primary productivity (GPP) to individual precipitation events of different sizes ( P size ) in a temperate grassland in China. The results showed that N enrichment significantly increased the time-integrated amount of GPP in response to an individual precipitation event (GPP total ) and the N-induced stimulation of GPP increased with increasing P size . N enrichment rarely affected the duration of the GPP response, but it significantly stimulated the maximum absolute GPP response. Higher foliar N content might play an important role in the N-induced stimulation of GPP. GPP total in both the N-addition and control treatments increased linearly with P size with similar P size intercepts (approximately 5 mm, indicating a similar lower P size threshold to stimulate the GPP response) but had a steeper slope under N addition. Our work indicates that the projected larger precipitation events will stimulate grassland productivity and this stimulation might be amplified by increasing N deposition.

BACKGROUND AND AIMS: Root growth and development are closely dependent upon nitrate supply in the growth medium. To unravel the mechanism underlying dependence of root growth on nitrate, an examination was made of whether endogenous nitric oxide (NO) is involved in nitrate-dependent growth of primary roots in maize. METHODS: Maize seedlings grown in varying concentrations of nitrate for 7 d were used to evaluate the effects on root elongation of a nitric oxide (NO) donor (sodium nitroprusside, SNP), a NO scavenger (methylene blue, MB), a nitric oxide synthase inhibitor (Nω-nitro-L-arginine, L-NNA), H₂O₂, indole-3-acetic acid (IAA) and a nitric reducatse inhibitor (tungstate). The effects of these treatments on endogenous NO levels in maize root apical cells were investigated using a NO-specific fluorescent probe, 4, 5-diaminofluorescein diacetate (DAF-2DA) in association with a confocal microscopy. KEY RESULTS: Elongation of primary roots was negatively dependent on external concentrations of nitrate, and inhibition by high external nitrate was diminished when roots were treated with SNP and IAA. MB and L-NNA inhibited root elongation of plants grown in low-nitrate solution, but they had no effect on elongation of roots grown in high-nitrate solution. Tungstate inhibited root elongation grown in both low- and high-nitrate solutions. Endogenous NO levels in root apices grown in high-nitrate solution were lower than those grown in low-nitrate solution. IAA and SNP markedly enhanced endogenous NO levels in root apices grown in high nitrate, but they had no effect on endogenous NO levels in root apical cells grown in low-nitrate solution. Tungstate induced a greater increase in the endogenous NO levels in root apical cells grown in low-nitrate solution than those grown in high-nitrate solution. CONCLUSIONS: Inhibition of root elongation in maize by high external nitrate is likely to result from a reduction of nitric oxide synthase-dependent endogenous NO levels in maize root apical cells.

Nitrogen (N) resorption from senescing leaves is an important mechanism of N conservation for terrestrial plant species, but changes in N-resorption traits over wide-range and multi-level N addition gradients have not been well characterized. Here, a 3-year N addition experiment was conducted to determine the effects of N addition on N resorption of six temperate grassland species belonging to three different life-forms: Stipa krylovii Roshev. (grass), Cleistogenes squarrosa (T.) Keng (grass), Artemisia frigida Willd. (semishrub), Melissitus ruthenica C.W.Wang (semishrub and N-fixer), Potentilla acaulis L. (forb) and Allium bidentatum Fisch.ex Prokh. (forb). Generally, N concentrations in green leaves increased asymptotically for all species. N concentrations in senescent leaves for most species (5/6) also increased asymptotically, except that the N concentration in senescent leaves of A. bidentatum was independent of N addition. N-resorption efficiency decreased with increasing N addition level only for S. krylovii and A. frigida, while no clear responses were found for other species. These results suggest that long-term N fertilization increased N uptake and decreased N-resorption proficiency, but the effects on N-resorption efficiency were species-specific for different temperate grassland species in northern China. These inter-specific differences in N resorption may influence the positive feedback between species dominance and N availability and thus soil N cycling in the grassland ecosystem in this region.