Comparative analysis of characteristics and physical mechanisms for typical summer extreme precipitation in Pakistan

The 2022 floods in Pakistan resulted in severe losses and garnered global attention. This study aims to enhance the understanding of extreme precipitation (EP) events in Pakistan by examining the characteristics and mechanisms behind the persistent EP during summer, utilizing daily precipitation data from the Climate Prediction Center (CPC). Results showed that the monsoon precipitation in 2010, 2020 and 2022 are the highest three years on record. Notably, these peak events in 2010 (concentrating in the north) and 2022 (concentrating in the south) spanned from July through August. Conversely, the extreme precipitation in August 2020 was concentrated in northern Pakistan. For the circulation patterns, the intensification of the South Asian High and the western Pacific subtropical high with a strong Indian monsoon is a unifying feature, but the Iranian high and monsoon low-pressure system on the south of Pakistan was different. Additionally, the EP in July 2010 and August 2022 were also influenced by the teleconnection associated with European Blocking. La Niña events and the negative-phase Indian Ocean Dipole (IOD) also played a role in affecting summer EP, with the strongest La Niña occurring in 2010 and a notable triple-dip La Niña coinciding with a significant negative IOD phase in 2022. La Niña contributed to the formation of an anomalously strong anticyclone over the northwest Pacific and easterly winds along the southern Himalayas, impacting moisture transport to Pakistan. Conversely, the negative IOD phase amplified EP in Pakistan by enhancing the northward movement of convective systems and westerly winds over the Indian Ocean. Furthermore, reduced snow cover on the Tibetan Plateau in the springs of 2010 and 2022 likely induced a stronger thermal dynamical effect, acting as a heat source in summer and increasing precipitation in Pakistan

ZIF-derived in situ nitrogen decorated porous carbons for CO 2 capture

Accessed by 10/2016International audienc

Three-Dimensional Covalent Organic Frameworks with Dual Linkages for Bifunctional Cascade Catalysis

Accessed by 12/2016International audienc

A Three-Dimensional Tetraphenylethylene-Based Fluorescence Covalent Organic Framework for Molecular Recognition

The development of highly-sensitive recognition of hazardous chemicals, such as volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs), is of significant importance because of their widespread social concerns related to environment and human health. Here, we report a three-dimensional (3D) covalent organic framework (COF, termed JUC-555) bearing tetraphenylethylene (TPE) side chains as an aggregation-induced emission (AIE) fluorescence probe for sensitive molecular recognition. Due to the rotational restriction of TPE rotors in highly interpenetrated framework after inclusion of dimethylformamide (DMF), JUC-555 shows impressive AIE-based strong fluorescence. Meanwhile, owing to the large pore size (11.4 Å) and suitable intermolecular distance of aligned TPE (7.2 Å) in JUC-555, the obtained material demonstrates an excellent performance in the molecular recognition of hazardous chemicals, e.g., nitroaromatic explosives, PAHs, and even thiophene compounds, via a fluorescent quenching mechanism. The quenching constant (KSV) is two orders of magnitude better than those of other fluorescence-based porous materials reported to date. This research thus opens 3D functionalized COFs as a promising identification tool for environmentally hazardous substances.</p

Tenovin 3 induces apoptosis and ferroptosis in EGFR 19del non small cell lung cancer cells

Abstract Epidermal growth factor receptor (EGFR) exon 19 deletion is a major driver for the drug resistance of non-small cell lung cancer (NSCLC). Identification small inhibitor capable of selectively inhibiting EGFR-19del NSCLC is a desirable strategy to overcome drug resistance in NSCLC. This study aims to screen an inhibitor for EGFR exon 19 deletion cells and explore its underlying mechanism. High through-put screen was conducted to identify an inhibitor for EGFR-19del NSCLC cells. And tenovin-3 was identified as a selective inhibitor of PC9 cells, an EGFR-19del NSCLC cells. Tenovin-3 showed particular inhibition effect on PC9 cells proliferation through inducing apoptosis and ferroptosis. Mechanistically, tenovin-3 might induce the apoptosis and ferroptosis of PC9 cells through mitochondrial pathway, as indicated by the change of VDAC1 and cytochrome c (cyt c). And bioinformatics analyses showed that the expression levels of SLC7A11 and CPX4 were correlated with NSCLC patient’s survival. Our findings provide evidences for tenovin-3 to be developed into a novel candidate agent for NSCLC with EGFR exon 19 deletion. Our study also suggests that inducing ferroptosis may be a therapeutic strategy for NSCLC with EGFR exon 19 deletion

NAD Supplement Alleviates Intestinal Barrier Injury Induced by Ethanol Via Protecting Epithelial Mitochondrial Function

Background: The epithelial tight junction is an important intestinal barrier whose disruption can lead to the release of harmful intestinal substances into the circulation and cause damage to systemic injury. The maintenance of intestinal epithelial tight junctions is closely related to energy homeostasis and mitochondrial function. Nicotinamide riboside (NR) is a NAD booster that can enhance mitochondrial biogenesis in liver. However, whether NR can prevent ethanol-induced intestinal barrier dysfunction and the underlying mechanisms remain unclear. Methods: We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms. NAD homeostasis and mitochondrial function were measured. In addition, knockdown of SirT1 in Caco-2 cells was further applied to explore the role of SirT1 in the protection of NR. Results: We found that ethanol increased intestinal permeability, increased the release of LPS into the circulation and destroyed the intestinal epithelial barrier structure in mice. NR supplementation attenuated intestinal barrier injury. Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis. In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis. These effects were diminished with the knockdown of SirT1 in Caco-2 cells. Conclusion: Boosting NAD by NR alleviates ethanol-induced intestinal epithelial barrier damage via protecting mitochondrial function in a SirT1-dependent manner