Influence of Stratification and Wind Forcing on the Dynamics of Lagrangian Residual Velocity in a Periodically Stratified Estuary

<p>Deng_OS</p&gt

An Analysis of the 8.85- and 4.42-Year Cycles in the Gulf of Maine

In the background of global warming and climate change, nuisance flooding is only caused by astronomical tides, which could be modulated by the nodal cycle. Therefore, much attention should be paid to the variation in the amplitude of the nodal cycle. In this paper, we utilize the enhanced harmonic analysis method and the independent point scheme to obtain the time-dependent amplitudes of the 8.85-year cycle of N2 tide and the 4.42-year cycle of 2N2 tide based on water level records of four tide gauges in the Gulf of Maine. Results indicate that the long-term trends of N2 and 2N2 tides vary spatially, which may be affected by the sea-level rise, coastal defenses, and other possible climate-related mechanisms. The comparison between Halifax and Eastport reveals that the topography greatly influences the amplitudes of those cycles. Moreover, a quasi 20-year oscillation is obvious in the 8.85-year cycle of N2 tide. This oscillation probably relates to a 20-year mode in the North Atlantic Ocean

Scale Factor Calibration for a Rotating Accelerometer Gravity Gradiometer

Rotating Accelerometer Gravity Gradiometers (RAGGs) play a significant role in applications such as resource exploration and gravity aided navigation. Scale factor calibration is an essential procedure for RAGG instruments before being used. In this paper, we propose a calibration system for a gravity gradiometer to obtain the scale factor effectively, even when there are mass disturbance surroundings. In this system, four metal spring-based accelerometers with a good consistency are orthogonally assembled onto a rotary table to measure the spatial variation of the gravity gradient. By changing the approaching pattern of the reference gravity gradient excitation object, the calibration results are generated. Experimental results show that the proposed method can efficiently and repetitively detect a gravity gradient excitation mass weighing 260 kg within a range of 1.6 m and the scale factor of RAGG can be obtained as (5.4 ± 0.2) E/μV, which is consistent with the theoretical simulation. Error analyses reveal that the performance of the proposed calibration scheme is mainly limited by positioning error of the excitation and can be improved by applying higher accuracy position rails. Furthermore, the RAGG is expected to perform more efficiently and reliably in field tests in the future

HDAC6 Inhibition Alleviates Ischemia- and Cisplatin-Induced Acute Kidney Injury by Promoting Autophagy

Histone deacetylase (HDAC) 6 exists exclusively in cytoplasm and deacetylates cytoplasmic proteins such as α-tubulin. HDAC6 dysfunction is associated with several pathological conditions in renal disorders, including UUO-induced fibrotic kidneys and rhabdomyolysis-induced nephropathy. However, the role of HDAC6 in ischemic acute kidney injury (AKI) and the mechanism by which HDAC6 inhibition protects tubular cells after AKI remain unclear. In the present study, we observed that HDAC6 was markedly activated in kidneys subjected to ischemia- and cisplatin (cis)-induced AKI treatment. Pharmacological inhibition of HDAC6 alleviated renal impairment and renal tubular damage after ischemia and cisplatin treatment. HDAC6 dysfunction was associated with decreased acetylation of α-tubulin at the residue of lysine 40 and autophagy. HDAC6 inhibition preserved acetyl-α-tubulin-enhanced autophagy flux in AKI and cultured tubular cells. Genetic ablation of the renal tubular (RT) Atg7 gene or pharmacological inhibition of autophagy suppressed the protective effects of HDAC6. Taken together, our study indicates that HDAC6 contributes to ischemia- and cisplatin-induced AKI by inhibiting autophagy and the acetylation of α-tubulin. These results suggest that HDAC6 could be a potential target for ischemic and nephrotoxic AKI

Oxygen enhances antiviral innate immunity through maintenance of EGLN1-catalyzed proline hydroxylation of IRF3

Abstract Oxygen is essential for aerobic organisms, but little is known about its role in antiviral immunity. Here, we report that during responses to viral infection, hypoxic conditions repress antiviral-responsive genes independently of HIF signaling. EGLN1 is identified as a key mediator of the oxygen enhancement of antiviral innate immune responses. Under sufficient oxygen conditions, EGLN1 retains its prolyl hydroxylase activity to catalyze the hydroxylation of IRF3 at proline 10. This modification enhances IRF3 phosphorylation, dimerization and nuclear translocation, leading to subsequent IRF3 activation. Furthermore, mice and zebrafish with Egln1 deletion, treatment with the EGLN inhibitor FG4592, or mice carrying an Irf3 P10A mutation are more susceptible to viral infections. These findings not only reveal a direct link between oxygen and antiviral responses, but also provide insight into the mechanisms by which oxygen regulates innate immunity