Unveiling the driving factors of urban land subsidence in Beijing, China.

Land subsidence, an insidious and gradual geological phenomenon, presents a latent threat to future urban development and socio-economic progress. Beijing City, renowned for its high population density, has encountered significant challenges associated with land subsidence. In this study, we leverage time-series interferometric synthetic aperture radar (time-series InSAR) method to analyze the spatio-temporal patterns of land subsidence in Beijing. Furthermore, we quantify the contributions of natural and anthropogenic factors to land subsidence. Our findings reveal that land subsidence primarily occurs in the plain area of Beijing, exhibiting an average rate of -5.6 mm/year (Positive values indicate uplift, while negative values indicate subsidence.). Notably, several large-scale subsidence centers are identified, with the maximum subsidence rate reaching an alarming -232.7 mm/year. The assessments indicate that geological factors, specifically fault activity, account for 33 % of the observed land subsidence, while human activities contribute to the remaining 67 %, with groundwater overexploitation playing a prominent role. The insights gained from this study provide a foundation for understanding the causative factors behind urban land subsidence and can aid in the formulation of effective intervention policies targeting this critical issue.

Ethanol suppresses rice seed germination through inhibiting ROS signaling.

Ethanol is frequently used not only as priming but also as a solvent to dissolve hardly water-soluble phytohormones gibberellic acid (GA3) and abscisic acid (ABA) in seed germination. However, the molecular and physiological mechanisms of ethanol's impact on seed germination remain elusive. In this report, we investigated how ethanol affected reactive oxygen species (ROS) during rice seed germination. Ethanol at a concentration of 3.5% (v/v) inhibited 90% seed germination, which was almost reversed by H2O2. H2O2 contents in embryos were reduced by ethanol after 18 h imbibition. Antioxidant enzymes assays revealed that only superoxide dismutase (SOD) activities in seed embryos were lowered by ethanol, in line with the suppressed mRNA expression of SOD genes during imbibition. Additionally, compared to the mock condition, ethanol increased ABA contents but decreased GA (GA1 and GA3) in seed embryos, resulting in disharmonizing GA/ABA balance. Conceivably ethanol induced transcription of OsNCEDs, the key genes for ABA biosynthesis, and OsABA8ox3, a key gene for ABA catabolism. Furthermore, ethanol promoted ABA signaling by upregulating ABA receptor genes and ABA-responsive element (ABRE)-binding protein/ABRE-binding factors during imbibition. Overall, our results demonstrate that lowering of H2O2 levels due to suppressed SOD activities in rice germinating seed embryos is the decisive factor for ethanol-induced inhibition of seed germination, and GA/ABA balance and ABA signaling also play important roles in ethanol's inhibitory impact on seed germination.

The role of calcium-sensing receptor in ginsenoside Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon injury.

Calcium-sensing receptor (CaSR) is a G protein-coupled receptor, widely distributed in various tissues, including vascular endothelial cells and smooth muscle cells, which plays an important role in the migration and homing of stem/progenitor cells and the proliferation of tissue cells. Restenosis after Percutaneous coronary intervention (PCI) seriously affects its prognosis and application. Our previous research has found that ginsenoside Rg1 (GS-Rg1) can inhibit the occurrence of restenosis after balloon injury of the common carotid artery in rats, but the mechanism is still unclear. In this study, it was found that GS-Rg1 (4, 8, 16 mg/kg) inhibited vascular restenosis caused by balloon injury, and mobilize endothelial progenitor cells (EPCs) to promote reendothelialization and inhibit intimal hyperplasia, which significantly reduced after administration of CaSR antagonist NPS 2143. Interestingly, CaSR and its downstream JNK, P38 were highly expressed in the proliferative intima and participated in the abnormal proliferation of vascular smooth muscle cells mediated by smooth muscle progenitor cells (SMPCs). GS-Rg1 inhibited intimal hyperplasia, while it decreased the expression of CaSR, JNK, and P38. This might relate to the distribution of CaSR and the facilitation of GS-Rg1 on the vascular endothelial repair. It is concluded that CaSR plays a key role in GS-Rg1 promoting reendothelialization to inhibit intimal hyperplasia after balloon Injury.

Microbial Diversity of the Chinese Tiger Frog (Hoplobatrachus rugulosus) on Healthy versus Ulcerated Skin.

The Chinese tiger frog (Hoplobatrachus rugulosus) is extensively farmed in southern China. Due to cramped living conditions, skin diseases are prevalent among unhealthy tiger frogs which thereby affects their welfare. In this study, the differences in microbiota present on healthy versus ulcerated H. rugulosus skin were examined using 16S rRNA sequences. Proteobacteria were the dominant phylum on H. rugulosus skin, but their abundance was greater on the healthy skin than on the ulcerated skin. Rhodocyclaceae and Comamonadaceae were the most dominant families on the healthy skin, whereas Moraxellaceae was the most dominant family on the ulcerated skin. The abundance of these three families was different between the groups. Acidovorax was the most dominant genus on the healthy skin, whereas Acinetobacter was the most dominant genus on the ulcerated skin, and its abundance was greater on the ulcerated skin than on the healthy skin. Moreover, the genes related to the Kyoto Encyclopedia of Genes and Genomes pathways of levels 2-3, especially those genes that are involved in cell motility, flagellar assembly, and bacterial chemotaxis in the skin microbiota, were found to be greater on the healthy skin than on the ulcerated skin, indicating that the function of skin microbiota was affected by ulceration. Overall, the composition, abundance, and function of skin microbial communities differed between the healthy and ulcerated H. rugulosus skin. Our results may assist in developing measures to combat diseases in H. rugulosus.

HDL-S1P protects endothelial function and reduces lung injury during sepsis in vivo and in vitro.

OBJECTIVE: In sepsis, the protection of the vascular endothelium is essential and the maintenance of its function is critical to prevent further deterioration. High-density lipoprotein (HDL)-associated sphingosine-1-phosphate (S1P) is a bioactive lipid in plasma and its role in sepsis has not been extensively studied. This study aimed to investigate the effects of HDL-S1P on sepsis in cellular and animal models, as well as human plasma samples. MEASUREMENTS: We established an animal model of sepsis with different severities achieved by caecal ligation and puncture (CLP) and lipopolysaccharide (LPS) injection, and then explored the relationship between HDL-S1P and lung endothelial dysfunction in vivo. To determine the effects of HDL-S1P in the pulmonary endothelium of septic rats, we then injected HDL-S1P into septic rats to find out if it can reduce the lung injury caused by sepsis. Further, we explored the mechanism in vitro by studying the role of S1P-specific receptor agonists and inhibitors in LPS-stimulated human umbilical vein endothelial cells. We also explored the relationship between plasma HDL-S1P content and sepsis severity in septic patients by analysing their plasma samples. RESULTS: HDL-S1P concentrations in plasma were negatively correlated with endothelial functional damage in sepsis, both in the animal model and in the septic patients in our study. In vivo, HDL-S1P injection significantly reduced pulmonary oedema and endothelial leakage in septic rats. In vitro, cell experiments showed that HDL-S1P effectively protected the proliferation and migration abilities of endothelial cells, which could be partly explained by its biased activation of the S1P receptor 1. CONCLUSION: Our study preliminary explored the function of HDL-S1P in sepsis in cellular and animal models, as well as human subjects. The results indicate HDL-S1P protected endothelial functions in septic patients. Thus, it has therapeutic potential and can be used for the clinical treatment of sepsis.

A pulmonary source of infection in patients with sepsis-associated acute kidney injury leads to a worse outcome and poor recovery of kidney function.

BACKGROUND: Hospital mortality rates are higher among patients with sepsis-associated acute kidney injury (SA-AKI) than among patients with sepsis. However, the pathogenesis underlying SA-AKI remains unclear. We hypothesized that the source of infection affects development of SA-AKI. We aim to explore the relationship between the anatomical source of infection and outcome in patients with SA-AKI. METHODS: Between January 2013 and January 2018, 113 patients with SA-AKI admitted to our Emergency Center were identified and divided into two groups: those with pulmonary infections and those with other sources of infection. For each patient, we collected data from admission until either discharge or death. We also recorded the clinical outcome after 90 days for the discharged patients. RESULTS: The most common source of infection was the lung (52/113 cases, 46%), followed by gastrointestinal (GI) (25/113 cases, 22.1%) and urinary (22/113, 19.5%) sources. Our analysis showed that patients with SA-AKI had a significantly worse outcome (30/52 cases, P<0.001) and poorer kidney recovery (P=0.015) with pulmonary sources of infection than those infected by another source. Data also showed that patients not infected by a pulmonary source more likely experienced shock (28/61 cases, P=0.037). CONCLUSION: This study demonstrated that the source of infection influenced the outcome of SA-AKI patients in an independent manner. Lung injury may influence renal function in an as-yet undetermined manner as the recovery of kidney function was poorer in SA-AKI patients with a pulmonary source of infection.

Tetramethylpyrazine alleviates LPS-induced inflammatory injury in HUVECs by inhibiting Rho/ROCK pathway.

Endothelial dysfunction plays an important role in the pathogenesis of acute lung injury (ALI). Tetramethylpyrazine (TMP) has been reported to attenuate harmful changes in ALI rats. However, the effects of TMP on endothelial cell injury and its underlying mechanisms remain unknown. In this study, human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS) was used as an inflammatory injury model, also served as LPS group. HUVECs pretreated with TMP for 2 h before induced by LPS was served as LPS + TMP group. Untreated HUVECs was served as control group. After incubation with LPS for 12 h, cell viability and morphology, cell apoptosis rate, CD31-positive endothelial microparticles (EMPs) release, proinflammatory cytokines secretion, and ROCK II expression were evaluated. Compared with LPS group, TMP pretreatment improved cell viability and morphology. Besides, cell apoptosis rate, CD31-positive EMPs amount, TNF-α and IL-1ß concentrates, and ROCK II mRNA and protein levels in LPS + TMP group were significantly decreased when compared with LPS group. To further confirm the mechanism, HUVECs in all the above groups were pretreated with Y27632 (ROCK II inhibitor) for 30 min before grouping, then treated as above. No significant differences in cell apoptosis rate, CD31-positive EMPs amount, and ROCK II expression between Y27632 + LPS group and Y27632 + LPS + TMP group were found. To sum up, our study found that TMP alleviated LPS-induced inflammatory injury in HUVECs by inhibiting Rho/ROCK pathway.

Simvastatin Ameliorates PAK4 Inhibitor-Induced Gut and Lung Injury.

P21 activated kinase 4 (PAK4), a key regulator of cytoskeletal rearrangement and endothelial microparticles (EMPs), is released after lipopolysaccharide (LPS) stimulation. In addition, it participates in LPS-induced lung injury. In this study, forty-eight Sprague Dawley (SD) rats were divided into two groups, including PAK4 inhibitor (P) and PAK4 inhibitor + simvastatin (P + S) treatment groups. All rats were given PAK4 inhibitor (15 mg/kg/d) orally. Immediately after PAK4 inhibitor administration, simvastatin was injected intraperitoneally to P + S group animals at 20 mg/kg/day. Then, treatment effects on the intestinal mucosal barrier and lung injury caused by PAK4 inhibitor and simvastatin were assessed. The results showed that gut Zonula Occludens- (ZO-) 1, PAK4, mitogen-activated protein kinase 4 (MPAK4), and CD11c protein levels were reduced, while plasma endotoxin levels were increased after administration of PAK4 inhibitor. Furthermore, compared with normal rats, wet-to-dry (W/D) values of lung tissues and circulating EMP levels were increased in the treatment group, while PAK4 and CD11c protein amounts were reduced. Therefore, in this lung injury process induced by PAK4 inhibitor, the protective effects of simvastatin were reflected by intestinal mucosal barrier protection, inflammatory response regulation via CD11c+ cells, and cytoskeleton stabilization. In summary, PAK4 is a key regulator in the pathophysiological process of acute lung injury (ALI) and can be a useful target for ALI treatment.