Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

4.1K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
4.1K
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

2.3K
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
2.3K
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

2.7K
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
2.7K
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

3.0K
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
3.0K
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

3.5K
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
3.5K
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

1.9K
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
1.9K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Intravesical mesothelin-based CAR T cells targeting MUC16 effectively control bladder cancer in preclinical models.

The Journal of experimental medicine·2026
Same author

Immune checkpoint blockade augments lymphodepleting chemotherapy-induced antitumor immunity by expanding effector CD8+ T cell clones.

Cancer research·2026
Same author

Reprogramming of TLR-Ferroptosis Signaling and Immunometabolic Pathways Overcomes Myeloid Suppression to Improve Checkpoint Blockade in Prostate Cancer.

Cancer research·2026
Same author

Tumor-intrinsic expression of signal regulatory protein α contributes to the suppression of anti-tumor immune responses.

Cell reports·2026
Same author

Effective PD-1 checkpoint blockade in bladder cancer model requires tumor-draining lymph nodes and lymphocyte trafficking.

Urologic oncology·2026
Same author

Reply to: Blood-Brain Barrier Heterogeneity in NRG BN007: Implications for Immunotherapy Delivery.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology·2026
Same journal

A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions.

Cell·2026
Same journal

Co-option of lysosomal machinery shapes the evolution of the intracellular photosymbiosis supporting coral reefs.

Cell·2026
Same journal

LEF1 and niche factors determine T cell stemness across chronic diseases.

Cell·2026
Same journal

Recurrent patterns of TOP1-mediated neuronal genomic damage shared by major neurodegenerative disorders.

Cell·2026
Same journal

Four-dimensional molecular mapping from a spatial snapshot reveals the dynamics of hair follicle organogenesis.

Cell·2026
Same journal

Whole-cell particle-based digital twin simulations from 4D lattice light-sheet microscopy data.

Cell·2026
查看所有相关文章

相关实验视频

Updated: Apr 4, 2026

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
07:04

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology

Published on: May 2, 2025

1.3K

PD-1 阻塞剂

Jedd D Wolchok1

  • 1Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

Cell
|August 29, 2015
PubMed
概括
此摘要是机器生成的。

尼沃卢马布和潘布罗利祖马布是单克隆抗体,可以阻断编程死亡-1 (PD-1) 受体. 这种免疫治疗方法抑制了抗瘤免疫反应,导致最近获得了黑色素瘤和非小细胞肺癌的批准.

更多相关视频

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates
07:42

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates

Published on: October 18, 2018

6.7K
Monitoring PD-1-Blocking Antibodies Bound to T Cells Derived from a Drop of Peripheral Blood
06:07

Monitoring PD-1-Blocking Antibodies Bound to T Cells Derived from a Drop of Peripheral Blood

Published on: February 5, 2020

6.2K

相关实验视频

Last Updated: Apr 4, 2026

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
07:04

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology

Published on: May 2, 2025

1.3K
Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates
07:42

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates

Published on: October 18, 2018

6.7K
Monitoring PD-1-Blocking Antibodies Bound to T Cells Derived from a Drop of Peripheral Blood
06:07

Monitoring PD-1-Blocking Antibodies Bound to T Cells Derived from a Drop of Peripheral Blood

Published on: February 5, 2020

6.2K

科学领域:

  • 免疫学
  • 癌症学
  • 药理学

背景情况:

  • 单克隆抗体nivolumab和pembrolizumab的目标是编程死亡-1 (PD-1) 受体.
  • 阻断PD-1受体增强了瘤特异性的免疫反应.

研究的目的:

  • 概述PD-1抑制剂的机制和最近的治疗批准.
  • 突出PD-1阻断在癌症治疗中的作用.

主要方法:

  • 对PD-1抑制剂的科学文献的审查.
  • 对nivolumab和pembrolizumab的临床试验数据的分析.

主要成果:

  • 尼沃卢马布和潘布罗利祖马布有效地阻断PD-1受体.
  • 这些药物可以抑制抗瘤免疫反应.

结论:

  • 尼沃卢马布和潘布罗利祖马布在癌症免疫治疗方面取得了重大进展.
  • 最近对转移性黑色素瘤和非小细胞肺癌的批准强调了它们的临床实用性.