Syntax Tree Constrained Graph Network for Visual Question Answering

Visual Question Answering (VQA) aims to automatically answer natural language questions related to given image content. Existing VQA methods integrate vision modeling and language understanding to explore the deep semantics of the question. However, these methods ignore the significant syntax information of the question, which plays a vital role in understanding the essential semantics of the question and guiding the visual feature refinement. To fill the gap, we suggested a novel Syntax Tree Constrained Graph Network (STCGN) for VQA based on entity message passing and syntax tree. This model is able to extract a syntax tree from questions and obtain more precise syntax information. Specifically, we parse questions and obtain the question syntax tree using the Stanford syntax parsing tool. From the word level and phrase level, syntactic phrase features and question features are extracted using a hierarchical tree convolutional network. We then design a message-passing mechanism for phrase-aware visual entities and capture entity features according to a given visual context. Extensive experiments on VQA2.0 datasets demonstrate the superiority of our proposed model

miR-21 Protects Against Ischemia/Reperfusion-Induced Acute Kidney Injury by Preventing Epithelial Cell Apoptosis and Inhibiting Dendritic Cell Maturation

Renal tubular injury and innate immune responses induced by hypoxia contribute to acute kidney injury. Accumulating evidence suggests that miR-21 overexpression protects against kidney ischemia injury. Additionally, miR-21 emerges as a key inhibitor in dendritic cell maturation. Thus, we hypothesized that miR-21 protects the kidney from IR injury by suppressing epithelial cell damage and inflammatory reaction. In this study, we investigated effects of miR-21 and its signaling pathways (PTEN/AKT/mTOR/HIF, PDCD4/NFκ-B) on kidney ischemia/reperfusion (IR) injury in vitro and in vivo. The results revealed that IR increased miR-21, HIF1α, and 2α expression in vivo and in vitro. MiR-21 interacted with HIF1α and 2α through the PTEN/AKT/mTOR pathway. Moreover, inhibition of miR-21 activated PDCD4/NFκ-B pathways, which are critical for dendritic cell maturation. Renal IR triggers local inflammation by inducing the dendritic cell maturation and promoting the secretion of IL-12, IL-6, and TNF-α cytokines. Knockdown of miR-21 intensified the effect of IR on tubular epithelial cell apoptosis and dendritic cell maturation. Our results suggested that IR-inducible miR-21 protects epithelial cells from IR injury via a feedback interaction with HIF (PTEN/AKT/mTOR/HIF/miR-21) and by inhibiting maturation of DCs through the PDCD4/NF-κB pathway. These findings highlight new therapeutic opportunities in AKI

Hydrogen-Rich Saline Alleviates Kidney Fibrosis Following AKI and Retains Klotho Expression

Purpose: Acute kidney injury (AKI) is a prominent risk factor for the development of chronic kidney disease (CKD). To date, the related mechanism and effective therapy have not been rigorously explored. The present study aims to investigate the reno-protection of hydrogen-rich saline (HRS) against ischemia/reperfusion (IR)-induced AKI.Methods: Adult male C57 mice were randomly allocated into three groups: Sham, IR, IR+HRS. Renal IR injury model was generated via 35 min occlusion of bilateral kidney pedicles, and then, mice were administered with different treatments intraperitoneally in various groups. After 14- or 28-day treatment, mice were perfused and the kidneys were collected following reperfusion. Many proteins were detected by western blots, including renal fibrotic proteins [a-smooth muscle actin (a-SMA), collagen I (Col I)], Klotho, the methylation of Klotho, damage-regulated autophagy modulator (Beclin-1), and microtubule-associated protein light 3-II (LC3-II). Finally, the levels of serum blood urea nitrogen (BUN) and creatinine (Cr) were measured to investigate the renal function.Results: Histological data showed that the HRS treatment significantly decreased the fibrosis in renal tissues when compared with the IR group, and both of BUN and Cr were lower in the HRS group than IR group (8.9 ± 0.6 vs. 9.9 ± 0.1 mmol/l, 51 ± 6.5 vs. 60 ± 5.8 μmol/l) (P < 0.05). The expression of fibrotic markers, a-SMA and Col I, showed a robust increase in IR injury models than the Sham group, which was consistent with the result of Trichrome staining. However, the levels of a-SMA and Col I expression were sharply decreased in the IR+HRS group (P < 0.05). IR injury also enhanced LC3-II and Beclin-1 expression, but decreased Klotho level. The Klotho level was alleviated by HRS, but LC3-II and Beclin-1 were starkly enhanced in HRS group (P < 0.05).Conclusion: HRS showed a protective effect in the prevention of renal injury and could inhibit renal fibrosis after IR injury in mice. This role of HRS might be exerted via retaining Klotho expression and activating autophagy in the kidney

Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway

Pb2+ biosorption from aqueous solutions by live and dead biosorbents of the hydrocarbon-degrading strain Rhodococcus sp. HX-2.

In this study, the Pb2+ biosorption potential of live and dead biosorbents of the hydrocarbon-degrading strain Rhodococcus sp. HX-2 was analyzed. Optimal biosorption conditions were determined via single factor optimization, which were as follows: temperature, 25°C; pH, 5.0, and biosorbent dose, 0.75 g L-1. A response surface software (Design Expert 10.0) was used to analyze optimal biosorption conditions. The biosorption data for live and dead biosorbents were suitable for the Freundlich model at a Pb2+ concentration of 200 mg L-1. At this same concentration, the maximum biosorption capacity was 88.74 mg g-1 (0.428 mmol g-1) for live biosorbents and 125.5 mg g-1 (0.606 mmol g-1) for dead biosorbents. Moreover, in comparison with the pseudo-first-order model, the pseudo-second-order model seemed better to depict the biosorption process. Dead biosorbents seemed to have lower binding strength than live biosorbents, showing a higher desorption capacity at pH 1.0. The order of influence of competitive metal ions on Pb2+ adsorption was Cu2+ > Cd2+ > Ni+. Fourier-transform infrared spectroscopy analyses revealed that several functional groups were involved in the biosorption process of dead biosorbents. Scanning electron microscopy showed that Pb2+ attached to the surface of dead biosorbents more readily than on the surface of live biosorbents, whereas transmission electron microscopy confirmed the transfer of biosorbed Pb2+ into the cells in the case of both live and dead biosorbents. It can thus be concluded that dead biosorbents are better than live biosorbents for Pb2+ biosorption, and they can accordingly be used for wastewater treatment