主要研究目的：按有关生物等效性试验的规定，选择Sanofi Aventis U.S.,LLC为持证商的盐酸决奈达隆片（商品名：迈达龙，规格：400mg）为参比制剂，对石家庄四药有限公司生产的受试制剂盐酸决奈达隆片（规格：400mg）进行餐后给药人体生物等效性试验，比较受试制剂中药物的吸收速度和吸收程度与参比制剂的差异是否在可接受的范围内，评价两种制剂在餐后给药条件下的生物等效性。次要研究目的：观察健康志愿受试者口服受试制剂盐酸决奈达隆片（规格：400mg）和参比制剂盐酸决奈达隆片（商品名：迈达龙，规格：400mg）的安全性。

开始日期2023-11-19

申办/合作机构

石家庄四药有限公司

CTR20233468 / CompletedN/A

盐酸决奈达隆片的人体生物等效性研究

研究空腹/餐后状态下单次口服受试制剂盐酸决奈达隆片与参比制剂盐酸决奈达隆片（迈达龙®）在健康成年男性受试者体内的药代动力学，评价空腹/餐后状态下口服两种制剂的生物等效性和安全性。

开始日期2023-10-25

申办/合作机构

齐鲁制药有限公司

CTR20233080 / CompletedN/A

在中国健康受试者空腹及餐后状态下单次口服盐酸决奈达隆片（规格：400 mg）的人体生物等效性试验

主要目的：评价中国健康受试者空腹及餐后条件下单次口服盐酸决奈达隆片受试制剂（规格：400 mg，生产厂家：江西科睿药业有限公司）和参比制剂（商品名：迈达龙®，规格：400 mg，生产厂家：Sanofi Winthrop Industrie）后的药代动力学特征，考察两制剂在空腹及餐后条件下是否具有生物等效性。次要目的：评价盐酸决奈达隆片受试制剂（规格：400 mg）和参比制剂（商品名：迈达龙®，规格：400 mg）在健康受试者中的安全性。

开始日期2023-10-17

申办/合作机构

江西科睿药业有限公司

100 项与 ADRA1 x L-type calcium channel 相关的临床结果

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100 项与 ADRA1 x L-type calcium channel 相关的转化医学

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0 项与 ADRA1 x L-type calcium channel 相关的专利（医药）

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项与 ADRA1 x L-type calcium channel 相关的文献（医药）

2023-10-01·Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

Mechanism of Lingbao Huxin Dan in the treatment of bradyarrhythmia complicated with coronary heart disease: a network pharmacology analysis.

Article

作者: Huagang, Han ; Junling, Cao ; Tianquan, Wang ; Lingyan, Dong ; Ziqiang, L I ; Jingfeng, Ouyang

OBJECTIVETo investigate the mechanism of action of the Lingbao Huxin Dan in treating bradycardia arrhythmia with coronary heart disease (BA-CHD) by network pharmacology.METHODSThe active ingredients of the Lingbao Huxin Dan were screened on the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and Bioinformatics tools designed for the analysis of molecular mechanisms of Chinese medicine platform; target prediction was conducted with the SwissTargetPrediction database, and Cytoscape 3.8 was used to construct a drug ingredient-target network. The Genecards, Online Mendelian Inheritance in Man, and DrugBank databases were searched for disease targets. Venn plots were used to display the common targets of BA-CHD and active ingredients. The STRING platform was used to construct a protein-protein interaction network. The Metascape data platform was used for Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to construct a signaling pathway network of the active ingredients of the Lingbao Huxin Dan.RESULTSThere were 121 active ingredients, 899 related targets, 39 targets important in BA-CHD and 14 targets which intersected between the active ingredients and BA-CHD. There were 27 core therapeutic ingredients, 153 biological processes, 18 cell ingredients and 20 molecular functions obtained by GO enrichment analysis. The KEGG pathway analysis yielded 19 signaling pathways.CONCLUSIONRBA-CHD may treat BA-CHD by regulating adrenergic receptor beta-1, alpha 1-α adrenergic receptor, calcium voltage-gated channel subunit alpha1 C, alpha-1β-adrenergic receptor, nitric oxide synthase 2, beta-2 adrenergic receptor, voltage-dependent calcium channel subunit alpha-2/delta-1, an- giotensin-converting enzyme, Raf-1 proto-oncogene serine/threonine-protein kinase, and other targets, potentially by affecting adrenergic receptor binding and calcium channel opening, to regulate the activity of cardiomyocytes.

2023-04-01·Poultry Science

Serum bone remodeling parameters and transcriptome profiling reveal abnormal bone metabolism associated with keel bone fractures in laying hens

Article

作者: Wei, Haidong ; Li, Jianhong ; Wang, Yulai ; Bao, Jun ; Bi, Yanju ; Zhang, Runxiang ; Zhao, Qian

Keel bone fractures affect welfare, health, and production performance in laying hens. A total of one hundred and twenty 35-wk-old Hy-line Brown laying hens with normal keel (NK) bone were housed in furnished cages and studied for ten weeks to investigate the underlying mechanism of keel bone fractures. At 45 wk of age, the keel bone state of birds was assessed by palpation and X-ray, and laying hens were recognized as NK and fractured keel (FK) birds according to the presence or absence of fractures in keel bone. The serum samples of 10 NK and 10 FK birds were collected to determine bone metabolism-related indexes and slaughtered to collect keel bones for RNA-sequencing (RNA-seq), Micro-CT, and histopathological staining analyses. The results showed that the concentrations of Ca, phosphorus, calcitonin, 25-hydroxyvitamin D₃, and osteocalcin and activities of alkaline phosphatase and tartrate-resistant acid phosphatase (TRAP) in serum samples of FK birds were lower than those of NK birds (P < 0.05), but the concentrations of parathyroid hormone, osteoprotegerin, and corticosterone in serum samples of FK birds were higher than those of NK birds (P < 0.05). TRAP staining displayed that FK bone increased the number of osteoclasts (P < 0.05). Micro-CT analysis indicated that FK bone decreased bone mineral density (P < 0.05). Transcriptome sequencing analysis of NK and FK bones identified 214 differentially expressed genes (DEGs) (|log2FoldChange| > 1, P < 0.05), among which 88 were upregulated and 126 downregulated. Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) analysis indicated that 14 DEGs related to skeletal muscle movement and bone Ca transport (COL6A1, COL6A2, COL6A3, PDGFA, MYLK2, EGF, CAV3, ADRA1D, BDKRB1, CACNA1S, TNN, TNNC1, TNNC2, and RYR3) were enriched in focal adhesion and Ca signaling pathway, regulating bone quality. This study suggests that abnormal bone metabolism related to keel bone fractures is possibly responded to fracture healing in laying hens.

2021-06-01·Molecular Genetics and Metabolism Reports4区 · 医学

Molecular basis of ventricular arrhythmogenicity in a Pgc-1α deficient murine model

4区 · 医学

ArticleOA

作者: Edling, Charlotte E ; Jeevaratnam, Kamalan ; Chadda, Karan R ; Valli, Haseeb ; Ahmad, Shiraz ; Saadeh, Khalil ; Huang, Christopher L-H ; Fazmin, Ibrahim T ; Nanthakumar, Nakulan

Mitochondrial dysfunction underlying metabolic disorders such as obesity and diabetes mellitus is strongly associated with cardiac arrhythmias. Murine Pgc-1α^-/- hearts replicate disrupted mitochondrial function and model the associated pro-arrhythmic electrophysiological abnormalities. Quantitative PCR, western blotting and histological analysis were used to investigate the molecular basis of the electrophysiological changes associated with mitochondrial dysfunction. qPCR analysis implicated downregulation of genes related to Na⁺-K⁺ ATPase activity (Atp1b1), surface Ca²⁺ entry (Cacna1c), action potential repolarisation (Kcnn1), autonomic function (Adra1d, Adcy4, Pde4d, Prkar2a), and morphological properties (Myh6, Tbx3) in murine Pgc-1α^-/- ventricles. Western blotting revealed reduced Na_V1.5 but normal Cx43 expression. Histological analysis revealed increased tissue fibrosis in the Pgc-1α^-/- ventricles. These present findings identify altered transcription amongst a strategically selected set of genes established as encoding proteins involved in cardiac electrophysiological activation and therefore potentially involved in alterations in ventricular activation and Ca²⁺ homeostasis in arrhythmic substrate associated with Pgc-1α deficiency. They complement and complete previous studies examining such expression characteristics in the atria and ventricles of Pgc-1 deficient murine hearts.