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8. Efficacy and safety of 4‐hydroxy 2‐methyl‐N‐(5‐methyl‐2‐thiazolyl)‐2H‐1, 2‐benzothiazin‐3‐carboxamide 1,1‐dioxide, a fast‐acting meloxicam formulation, on moderate‐to‐severe pain following abdominal surgery: A phase III randomized controlled trial

Author

Xiaohua Liu, Yanhua Zhao, Mengchang Yang, Jinghua Ren, Wen Ouyang, Saiying Wang, Yufei Shen, Yuanli Gao, Ling Zhao, Zhong Qin, Jun Cao, Jiangyan Xia, Hongmei Zhou, Haihua Zeng, Jiangang Li, Qiongcan Li, Haitao Jiang, Ruiren Zhou, Kaiming Yuan, Shu’an Jin, Xuanqiang Zhang, Chunhui Wang, Yongquan Chen, Hailong Dong, Jieping Lv, Sen Yu, Yonghui Jiu, Qingsong Wang, Diansan Su, and Weifeng Yu

Subjects
Therapeutics. Pharmacology, RM1-950, Public aspects of medicine, RA1-1270
Abstract

Abstract 4‐hydroxy 2‐methyl‐N‐(5‐methyl‐2‐thiazolyl)‐2H‐1, 2‐benzothiazin‐3‐carboxamide 1,1‐dioxide (QP001), a novel long‐lasting meloxicam formulation, may provide adequate postoperative pain relief with a good safety profile. This study aimed to evaluate the efficacy and safety of QP001 for moderate‐to‐severe pain following abdominal surgery. This multicenter, randomized, double‐blind, placebo‐controlled phase III trial recruited patients undergoing abdominal surgery at 23 centers between October 30, 2022, and July 10, 2023. Patients were randomized to a QP001 or placebo group in a 2:1 ratio. Postoperative pain intensity was evaluated using the Numerical Rating Scale. The primary efficacy outcome was the area under curve (AUC) of pain intensity‐time 0–24 h after awakening from anesthesia (AUC0–24). Adverse events and drug reactions were recorded to evaluate safety. A total of 258 patients underwent randomization, and 255 patients received at least one trial drug, including 170 in the QP001 group and 85 in the placebo group. Among these patients, 250 completed the study. The AUC0–24 was significantly lower in the QP001 group than in the placebo group (50.5 vs. 85.19, difference of 34.69 [40.7%], p

Published
2024
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18. NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

Author

Yuan Ma, Hui-Ping Zhao, Li-Guo Yang, Lu Li, Ai-Lin Wang, Xiao-Juan Zhang, Ke Wang, Bin Yang, Zong-Feng Zhu, Pei-Jun Zhang, Jia-Pu Wang, Rui-Fang Chi, Bao Li, Fu-Zhong Qin, and Zhi-Peng Wang

Subjects
Medicine, Science
Abstract

Abstract Doxorubicin has been used extensively as a potent anticancer agent, but its clinical use is limited by its cardiotoxicity. However, the underlying mechanisms remain to be fully elucidated. In this study, we tested whether NADPH oxidase 2 (Nox2) mediates cardiac sympathetic nerve terminal abnormalities and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced heart failure. Nox2 knockout (KO) and wild-type (WT) mice were randomly assigned to receive a single injection of doxorubicin (15 mg/kg, i.p.) or saline. WT doxorubicin mice exhibited the decreases in survival rate, left ventricular (LV) wall thickness and LV fractional shortening and the increase in the lung wet-to-dry weight ratio 1 week after the injections. These alterations were attenuated in Nox2 KO doxorubicin mice. In WT doxorubicin mice, myocardial oxidative stress was increased, myocardial noradrenergic nerve fibers were reduced, myocardial expression of PGP9.5, GAP43, tyrosine hydroxylase and norepinephrine transporter was decreased, and these changes were prevented in Nox2 KO doxorubicin mice. Myocyte autophagy was increased and myocyte size was decreased in WT doxorubicin mice, but not in Nox2 KO doxorubicin mice. Nox2 mediates cardiac sympathetic nerve terminal abnormalities and myocyte autophagy—both of which contribute to cardiac atrophy and failure after doxorubicin treatment.

Published
2024
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25. Regulation of FSP1 myristoylation by NADPH: A novel mechanism for ferroptosis inhibition

Author

Na Liu, Wei-Long Wu, Xiao-Rui Wan, Jing Wang, Jia-Ni Huang, Yi-Yue Jiang, Yi-Chao Sheng, Jun-Chao Wu, Zhong-Qin Liang, Zheng-Hong Qin, and Yan Wang

Subjects
Neurodegenerative diseases, Ferroptosis, Excitotoxicity, NADPH, FSP1, Myristoylation, Medicine (General), R5-920, Biology (General), QH301-705.5
Abstract

Excitotoxicity is a prevalent pathological event in neurodegenerative diseases. The involvement of ferroptosis in the pathogenesis of excitotoxicity remains elusive. Transcriptome analysis has revealed that cytoplasmic reduced nicotinamide adenine dinucleotide phosphate (NADPH) levels are associated with susceptibility to ferroptosis-inducing compounds. Here we show that exogenous NADPH, besides being reductant, interacts with N-myristoyltransferase 2 (NMT2) and upregulates the N-myristoylated ferroptosis suppressor protein 1 (FSP1). NADPH increases membrane-localized FSP1 and strengthens resistance to ferroptosis. Arg-291 of NMT2 is critical for the NADPH-NMT2-FSP1 axis-mediated suppression of ferroptosis. This study suggests that NMT2 plays a pivotal role by bridging NADPH levels and neuronal susceptibility to ferroptosis. We propose a mechanism by which the NADPH regulates N-myristoylation, which has important implications for ferroptosis and disease treatment.

Published
2024
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41. Ca2+ addition facilitates the shell repair with eggs production of Pomacea canaliculata through biomineralization and food intaking regulation

Author

Yingtong Chen, Fucheng Yao, Jiaen Zhang, Chunxia Zhang, Zhong Qin, and Jing Guo

Subjects
Medicine, Science
Abstract

Abstract Pomacea canaliculata was by far one of the most harmful invasive organisms in the world, causing serious harm to aquatic crops and ecosystem. Calcium carbonate is a common component of aquatic environment, which is important for the growth of Pomacea canaliculata. Therefore, the objective of this study was to investigate the response characteristics of P. canaliculata suffered shell breakage to the addition of calcium carbonate in water environment. In this experiment, we explored the effects of calcium carbonate addition on the P. canaliculata shell repair rate, food intake, egg production, shell strength, and calcium content through breaking the snails shell and the addition of calcium carbonate treatment. The results showed that snail broken-shell repaired mostly within 21 days. The snails experienced a significant increase in shell repair rates during earlier days of the treatment, especially for female snails. Food intake of snails exhibited different patterns when their shells were broken and calcium carbonate was added. Shell breakage treatment combined with calcium carbonate addition significantly increased the diameter of snail eggs compared with the control and the calcium carbonate addition treatment without shell-broken snail group. There was no significant difference in shell strength or calcium content of male snails between the treatments. The study suggests that P. canaliculata exhibits a sex-dependent response pattern when subjected to shell damage and calcium carbonate addition. The findings can provide some references to better understand the invasion mechanism and survival strategy of the P. canaliculata.

Published
2023
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42. Structural variants involved in high-altitude adaptation detected using single-molecule long-read sequencing

Author

Shi, Jinlong, Jia, Zhilong, Sun, Jinxiu, Wang, Xiaoreng, Zhao, Xiaojing, Zhao, Chenghui, Liang, Fan, Song, Xinyu, Guan, Jiawei, Jia, Xue, Yang, Jing, Chen, Qi, Yu, Kang, Jia, Qian, Wu, Jing, Wang, Depeng, Xiao, Yuhui, Xu, Xiaoman, Liu, Yinzhe, Wu, Shijing, Zhong, Qin, Wu, Jue, Cui, Saijia, Bo, Xiaochen, Wu, Zhenzhou, Park, Minsung, Kellis, Manolis, and He, Kunlun

Published
2023
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