Honglei Li

Background: Exposure to atmospheric pollutants is closely associated with the occurrence of allergic rhinitis (AR). However, the role of sulfur dioxide (SO₂) in promoting allergic inflammation in AR is poorly understood. Our study aims to investigate the effect of SO₂ on allergic inflammation in house dust mite (HDM)-sensitized mice. Methods: Thirty mice were randomly divided into five groups: the control, AR model, AR model exposed to SO₂, AR model with long-term SO₂ exposure, and SO₂-treated control groups. Nasal symptom score was recorded. The serum HDM specific IgE (sIgE) was measured by enzyme-linked immunosorbent assay. Expression of Th1/Th2/Th17 cytokines in nasal mucosa was detected by immunohistochemistry and quantitative PCR. Expression of a low-affinity sIgE receptor (CD23) on B lymphocytes in nasal mucosa was assessed by immunofluorescence. Results: SO₂ increased not only nasal symptom score but also the number of infiltrating eosinophils and expression of Th1/Th2/Th17 cytokines in nasal mucosa of HDM-sensitized AR mice. Furthermore, SO₂ increased the serum sIgE level in AR mice. However, long-term SO₂ exposure decreased the serum sIgE level in AR mice. Moreover, long-term SO₂ exposure decreased CD23⁺ B lymphocytes in the nasal mucosa. Conclusion: SO₂ exposure aggravated nasal symptom, serum sIgE level, eosinophil infiltration, and Th1/Th2/Th17 inflammation in AR mice. However, the serum sIgE level could be lowered by long-term SO₂ exposure. This inhibitory effect of SO₂ on IgE production may be suppressed by CD23⁺ B lymphocytes.

Angiogenesis is positively correlated with the survival rate of stroke patients. Therefore, studying factors that initiate and promote angiogenesis after ischemic stroke is crucial for finding novel and effective treatment targets that improve the prognosis of stroke. X‐box binding protein l splicing (XBP1s) plays a positive regulatory role in cell proliferation and angiogenesis. However, the role and mechanism of XBP1s on the proliferation of brain microvascular endothelial cells (BMECs) and angiogenesis after cerebral ischemia remains unclear. In the current study, we investigated the role XBP1s plays in BMEC proliferation and angiogenesis following cerebral ischemia. In this study, the roles of XBP1s on cell survival, apoptosis, cycle migration, and angiogenesis were determined in oxygen‐glucose deprivation (OGD) treated BMECs. The expression of XBP1s in BMECs, which were exposed to OGD at 0, 2, 4, and 6 hr, increased in a time‐dependent manner. The overexpression of XBP1s promoted cell survival, cell cycle, migration, and angiogenesis of BMECs, and inhibited the apoptosis in OGD‐treated BMECs. In addition, the overexpression of XBP1s promoted the expression of cyclin D1, matrix metalloproteinase (MMP‐2), and MMP‐9, but inhibited cleaved Caspase‐3 and cleaved Caspase‐9 expression in OGD‐treated BMECs. The overexpression of XBP1s also promoted the expression of hypoxia‐inducible factor 1‐alpha, vascular endothelial growth factor, phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, p‐AKT, p‐mTOR, p‐GSK3β, and p‐extracellular signal‐regulated kinase1/2 in OGD‐treated BMECs. The effect of XBP1s silencing was opposite to that of XBP1s overexpression. In conclusion, using an in vitro OGD model, we demonstrated that XBP1s may be a promising target for ischemic stroke therapy to maintain BMECs survival and induce angiogenesis.

As the most active plateau on the Earth, the Qinghai-Tibet Plateau (TP) has a complex crust–mantle structure. Knowledge of the distribution of such a structure provides information for understanding the underlying geodynamic processes. We obtain a three-dimensional model of the density of the crust and the upper mantle beneath the TP and surrounding areas from height anomalies using the Earth Gravitational Model 2008 (EGM2008). We refine the estimated density in the model iteratively using an initial density contrast model. We confirm that the EGM2008 products can be used to constrain the crust–mantle density structures. Our major findings are: (1) At a depth of 300–400 km, high-D(ensity) anomalies terminate around the Jinsha River Suture (JRS) in the central TP, which suggests that the Indian Plate has reached across the Bangong Nujiang Suture (BNS) and almost reaches the JRS. (2) On the eastern TP, low-D(ensity) anomalies at a depth of 0–300 km and with high-D anomalies at 400–670 km further verified the current eastward subduction of the Indian Plate. The ongoing subduction process provides force that results in frequent earthquakes and volcanoes. (3) At a depth of 600 km, low-D anomalies inside the TP illustrate the presence of hot weak material beneath it, which contribute to the inward thrusting of external material.

As the most active plateau on the Earth, the Qinghai-Tibet Plateau has a complex crust-mantle structure. Knowledge of the distribution of such a structure provides information for understanding the underlying geodynamic processes. We obtains a three-dimensional density model of crustal and upper mantle beneath Qinghai-Tibet plateau and its surrounding areas from the residual geoid anomalies using the Earth Gravitational Model (EGM) 2008. We estimate a refined density model by iterations, using an initial density contrast model. We confirm that the EGM2008 mission products can be used to constrain the crust-mantle density structures. Our major findings are: (1). At 300-400 km depth, high-D anomalies terminate around Jinsha River Suture (JRS) in the central TP, suggesting that the Indian plate has been reached over the Bangong Nujiang Suture (BNS) and almost reach to the JRS. (2). On the eastern TP, low-D anomalies at the depth of 0-300 km together with high-D anomalies at 400-670 km further verified the current eastward subduction of Indian plate. The ongoing subduction provides forces to the occurrences of frequent earthquakes and volcano. (3). At 600 km depth, low-D anomalies inside the TP illustrate the existence of hot weak material beneath there, contributing to the external material inward-thrusting.