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BackgroundThe coronavirus disease (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in the self-quarantine of countless people due to possible infection. This situation makes telemedicine necessary as it can overcome geographical barriers, increase the number of people served, and provide online clinical support for patients. However, the outcomes of telemedicine have not yet been evaluated. ObjectiveThe aim of our study is to describe the epidemiological features and clinical symptoms of patients receiving remote diagnosis and treatment at the online outpatient clinic of our hospital, as well as to analyze the outcomes and advantages of telemedicine, during the COVID-19 pandemic. MethodsData from patients receiving remote diagnosis and treatment via consultation services for COVID-19 concerns at the online outpatient clinic of Henan Provincial People's Hospital from January 24 to February 17, 2020, were collected. A retrospective analysis was performed on epidemiological features, clinical symptoms, and preliminary outcomes. ResultsOnline inquiry, consultation, and suggestions were provided for patient concerns related to COVID-19. Our hospital also offered offline noncontact drug delivery services following online ordering and payment. A total of 4589 patients receiving remote diagnosis and treatment were recruited. The daily number of online outpatient visits initially increased and then decreased, reaching its peak on January 28 when the daily number of online outpatient visits totaled 612. Of 4589 patients, 1940 (42.3%) were males and 2649 (57.7%) were females (age range: 78 days to 85 years). Most patients were aged 20-39 years (n=3714, 80.9%) and came from Henan Province (n=3898, 84.9%). The number of patients from other provinces was 691 (15.1%). During the online consultations, patients discussed the following symptoms: fever (n=2383), cough (n=1740), nasal obstruction (n=794), fatigue (n=503), and diarrhea (n=276). A total of 873 orders of noncontact drug delivery following online payment was completed. The daily number of such orders gradually stabilized after the initial, steady increase. For offline drug delivery orders, the median (IQR) was 36 (58). An online satisfaction survey was filled out postconsultation by patients; of the 985 responses received, 98.1% (n=966) of respondents were satisfied with the service they received. ConclusionsRemote diagnosis and treatment offered via online outpatient consultations effectively reduced the burden on hospitals, prevented overcrowding, reduced the risk of cross-infection, and relieved patients' anxiety during the COVID-19 outbreak. This plays an essential role in pandemic management.

The Concise Guide to PHARMACOLOGY 2021/22 is the fifth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of nearly 1900 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes over 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/bph.15539. Ion channels are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2021, and supersedes data presented in the 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14749. Ion channels are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

As the leading cause of mortality worldwide, cardiovascular disease (CVD) represents a variety of heart diseases and vascular disorders, including atherosclerosis, aneurysm, ischemic injury in the heart and brain, arrythmias, and heart failure. Macrophages, a diverse population of immune cells that can promote or suppress inflammation, have been increasingly recognized as a key regulator in various processes in both healthy and disease states. In healthy conditions, these cells promote the proper clearance of cellular debris, dead and dying cells, and provide a strong innate immune barrier to foreign pathogens. However, macrophages can play a detrimental role in the progression of disease as well, particularly those inflammatory in nature. This review will focus on the current knowledge regarding the role of macrophages in cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Aims Damage of the blood–brain barrier (BBB) is a hallmark of brain injury during the early stages of ischemic stroke. The subsequent endothelial hyperpermeability drives the initial pathological changes and aggravates neuronal death. Transient receptor potential melastatin 2 (TRPM2) is a Ca2+-permeable nonselective cation channel activated by oxidative stress. However, whether TRPM2 is involved in BBB degradation during ischemic stroke remains unknown. We aimed to investigate the role of TRPM2 in BBB degradation during ischemic stroke and the underlying molecular mechanisms. Methods and results Specific deletion of Trpm2 in endothelial cells using Cdh5 Cre produces a potent protective effect against brain injury in mice subjected to middle cerebral artery occlusion (MCAO), which is characterized by reduced infarction size, mitigated plasma extravasation, suppressed immune cell invasion, and inhibited oxidative stress. In vitro experiments using cultured cerebral endothelial cells (CECs) demonstrated that either Trpm2 deletion or inhibition of TRPM2 activation attenuates oxidative stress, Ca2+ overload, and endothelial hyperpermeability induced by oxygen–glucose deprivation (OGD) and CD36 ligand thrombospondin-1 (TSP1). In transfected HEK293T cells, OGD and TSP1 activate TRPM2 in a CD36-dependent manner. Noticeably, in cultured CECs, deleting Trpm2 or inhibiting TRPM2 activation also suppresses the activation of CD36 and cellular dysfunction induced by OGD or TSP1. Conclusions In conclusion, our data reveal a novel molecular mechanism in which TRPM2 and CD36 promote the activation of each other, which exacerbates endothelial dysfunction during ischemic stroke. Our study suggests that TRPM2 in endothelial cells is a promising target for developing more effective and safer therapies for ischemic stroke. [ABSTRACT FROM AUTHOR]