Academic literature on the topic 'Β1-Blockers'

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Journal articles on the topic "Β1-Blockers":

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Bennett, Miriam, Catherina L. Chang, Michael Tatley, Ruth Savage, and Robert J. Hancox. "The safety of cardioselective β1-blockers in asthma: literature review and search of global pharmacovigilance safety reports." ERJ Open Research 7, no. 1 (January 2021): 00801–2020. http://dx.doi.org/10.1183/23120541.00801-2020.

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IntroductionBeta-blockers are key in the management of cardiovascular diseases but blocking airway β2-receptors can cause severe and sometimes fatal bronchoconstriction in people with asthma. Although cardioselective β1-blockers may be safer than non-selective β-blockers, they remain relatively contraindicated and under-prescribed. We review the evidence of the risk associated with cardioselective β1-blocker use in asthma.MethodsWe searched “asthma” AND “beta-blocker” in PubMed and EmbaseOvid from start to May 2020. The World Health Organization (WHO) global database of individual case safety reports (VigiBase) was searched for reports of fatal asthma or bronchospasm and listed cardioselective β1-blocker use (accessed February 2020). Reports were examined for evidence of pre-existing asthma.ResultsPubMed and EmbaseOvid searches identified 304 and 327 publications, respectively. No published reports of severe or fatal asthma associated with cardioselective β1-blockers were found. Three large observational studies reported no increase in asthma exacerbations with cardioselective β1-blocker treatment. The VigiBase search identified five reports of fatalities in patients with pre-existing asthma and reporting asthma or bronchospasm during cardioselective β1-blocker use. Four of these deaths were unrelated to cardioselective β1-blocker use. The circumstances of the fifth death were unclear.ConclusionsThere were no published reports of cardioselective β1-blockers causing asthma death. Observational data suggest that cardioselective β1-blocker use is not associated with increased asthma exacerbations. We found only one report of an asthma death potentially caused by cardioselective β1-blockers in a patient with asthma in a search of VigiBase. The reluctance to use cardioselective β1-blockers in people with asthma is not supported by this evidence.
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do Vale, Gabriel T., Carla S. Ceron, Natália A. Gonzaga, Janaina A. Simplicio, and Júlio C. Padovan. "Three Generations of β-blockers: History, Class Differences and Clinical Applicability." Current Hypertension Reviews 15, no. 1 (January 29, 2019): 22–31. http://dx.doi.org/10.2174/1573402114666180918102735.

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Background: Beta-adrenergic receptors are expressed in cardiomyocytes and activated by either noradrenaline released from sympathetic synapses or circulating catecholamines. Their corresponding receptors have three subtypes, namely, β1, β2 and β3, which are members of the G protein-coupled receptors (GPCRs) family. Activation of β1-adrenergic receptors causes various physiological reactions including cardiac contraction and renin secretion from juxtaglomerular cells of the kidney. Antagonists of β-adrenergic receptors, known as β-blockers, have been used effectively for over four decades and have beneficial effects in the treatment of cardiovascular diseases. There are three generations of β-blockers according to their pharmacological properties. Firstgeneration β-blockers are non-selective, blocking both β1- and β2-receptors; second-generation β- blockers are more cardioselective in that they are more selective for β1-receptors; and thirdgeneration β-blockers are highly selective drugs for β1-receptors. The latter also display vasodilator actions by blocking α1-adrenoreceptors and activating β3-adrenergic receptors. In addition, thirdgeneration β-blockers exhibit angiogenic, antioxidant, anti-proliferative, anti-hypertrophic and antiapoptotic activities among other effects that are still under investigation. Conclusion: The objective of this review is to describe the evolution observed during the development of the three distinctive generations, thereby highlighting the advantages of third-generation β- blockers over the other two drug classes.
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Karoli, N. A., and A. P. Rebrov. "Possibilities and limitations of the use of beta-blockers in patients with cardiovascular disease and chronic obstructive pulmonary disease." Kardiologiia 61, no. 10 (October 30, 2021): 89–98. http://dx.doi.org/10.18087/cardio.2021.10.n1119.

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In medical literature, increasing attention is paid to comorbidities in patients with chronic obstructive pulmonary disease (COPD). In clinical practice, physicians often hesitate to prescribe beta-blockers (β1-adrenoblockers) to COPD patients. This article summarized new results of using beta-blockers in patients with COPD. According to reports, the selective β1-blocker treatment considerably increases the survival rate of patients with COPD and ischemic heart disease, particularly after myocardial infarction (MI), and with chronic heart failure (CHF). The benefit of administering selective β1-blockers to patients with CHF and/or a history of MI overweighs a potential risk related with the treatment even in patients with severe COPD. Convincing data in favor of the β1-blocker treatment in COPD patients without the above-mentioned comorbidities are not available. At present, the selective β1-blocker treatment is considered safe for patients with cardiovascular diseases and COPD. For this reason, selective β1-blockers, such as bisoprolol, metoprolol or nebivolol can be used in managing this patient cohort. Nonselective β1-blockers may induce bronchospasm and are not recommended for COPD patients. For the treatment with β-blockers with intrinsic sympathomimetic activity, the probability of bronchial obstruction in COPD patients is lower; however, drugs of this pharmaceutical group have not been compared with cardioselective beta-blockers. For safety reasons, the beta-blocker treatment should be started outside exacerbation of COPD and from a small dose. Careful monitoring is recommended for possible new symptoms, such as emergence/increase of shortness of breath, cough or changes in dosing of other drugs (for example, increased frequency of using short-acting bronchodilators).
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Stănciulescu, Maria-Corina, Marius-Călin Popoiu, Anca Maria Cîmpean, Vlad-Laurentiu David, Rodica Heredea, Simona Cerbu, and Eugen-Sorin Boia. "Expression of β1 adrenergic receptor in vascular anomalies in children." Journal of International Medical Research 49, no. 9 (September 2021): 030006052110477. http://dx.doi.org/10.1177/03000605211047713.

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Objective Controversial, heterogeneous, and inconsistent responses to beta-blockers have been reported in some cases of infantile proliferative hemangiomas. On the basis of these clinical observations, we aimed to examine the β1 adrenergic receptor (β1-AR) protein expression distribution among different types of pediatric vascular anomalies. Methods Immunohistochemistry (IHC) was performed for β1-AR on 43 surgical specimens. Results We found positive β1-AR IHC staining in all intramuscular hemangiomas, capillary–lymphatic, lymphatic, venous, and combined malformations, and Masson’s tumor cases, as well as in 7 of 10 cases of proliferative infantile hemangiomas. Conclusions Our research demonstrates, for the first time, the degree of heterogeneous expression of β1-AR among pediatric vascular malformations. Our results support the need for β1-AR assessment in pediatric vascular anomalies to select cases with a robust response to β1-selective blockers. β1-AR assessment may have a strong impact on therapeutic refinement for pediatric vascular anomalies by selecting cases with a stronger response to beta-blockers.
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Barcella, Carlo A., Talip E. Eroglu, Michiel Hulleman, Asger Granfeldt, Patrick C. Souverein, Grimur H. Mohr, Rudolph W. Koster, et al. "Association of beta-blockers and first-registered heart rhythm in out-of-hospital cardiac arrest: real-world data from population-based cohorts across two European countries." EP Europace 22, no. 8 (June 28, 2020): 1206–15. http://dx.doi.org/10.1093/europace/euaa124.

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Abstract Aims Conflicting results have been reported regarding the effect of beta-blockers on first-registered heart rhythm in out-of-hospital cardiac arrest (OHCA). We aimed to establish whether the use of beta-blockers influences first-registered rhythm in OHCA. Methods and results We included patients with OHCA of presumed cardiac cause from two large independent OHCA-registries from Denmark and the Netherlands. Beta-blocker use was defined as exposure to either non-selective beta-blockers, β1-selective beta-blockers, or α-β-dual-receptor blockers within 90 days prior to OHCA. We calculated odds ratios (ORs) for the association of beta-blockers with first-registered heart rhythm using multivariable logistic regression. We identified 23 834 OHCA-patients in Denmark and 1584 in the Netherlands: 7022 (29.5%) and 519 (32.8%) were treated with beta-blockers, respectively. Use of non-selective beta-blockers, but not β1-selective blockers, was more often associated with non-shockable rhythm than no use of beta-blockers [Denmark: OR 1.93, 95% confidence interval (CI) 1.48–2.52; the Netherlands: OR 2.52, 95% CI 1.15–5.49]. Non-selective beta-blocker use was associated with higher proportion of pulseless electrical activity (PEA) than of shockable rhythm (OR 2.38, 95% CI 1.01–5.65); the association with asystole was of similar magnitude, although not statistically significant compared with shockable rhythm (OR 2.34, 95% CI 0.89–6.18; data on PEA and asystole were only available in the Netherlands). Use of α-β-dual-receptor blockers was significantly associated with non-shockable rhythm in Denmark (OR 1.21; 95% CI 1.03–1.42) and not significantly in the Netherlands (OR 1.37; 95% CI 0.61–3.07). Conclusion Non-selective beta-blockers, but not β1-selective beta-blockers, are associated with non-shockable rhythm in OHCA.
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Grande, Fedora, Anna De Bartolo, Maria Antonietta Occhiuzzi, Anna Caruso, Carmine Rocca, Teresa Pasqua, Alessia Carocci, Vittoria Rago, Tommaso Angelone, and Maria Stefania Sinicropi. "Carbazole and Simplified Derivatives: Novel Tools toward β-Adrenergic Receptors Targeting." Applied Sciences 11, no. 12 (June 13, 2021): 5486. http://dx.doi.org/10.3390/app11125486.

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β-Adrenergic receptors (β-ARs) are G protein-coupled receptors involved in important physiological and pathological processes related to blood pressure and cardiac activity. The inhibition of cardiac β1-ARs could be beneficial in myocardial hypertrophy, ischemia and failure. Several carbazole-based compounds have been described as promising β-blockers. Herein, we investigate the capability of a carbazole derivative and three simplified indole analogs to interact with the active binding site of β1-AR by molecular docking studies. In the light of the obtained results, our compounds were tested by biological assays in H9c2 cardiomyocytes exposed to isoproterenol (ISO) to confirm their potential as β1-blockers agents, and two of them (8 and 10) showed interesting and promising properties. In particular, these compounds were effective against ISO-dependent in vitro cardiac hypertrophy, even at concentrations lower than the known β-AR antagonist propranolol. Overall, the data suggest that the indole derivatives 8 and 10 could act as potent β1-blockers and, active at low doses, could elicit limited side effects.
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Artym, Vira V., and Howard R. Petty. "Molecular Proximity of Kv1.3 Voltage-gated Potassium Channels and β1-Integrins on the Plasma Membrane of Melanoma Cells." Journal of General Physiology 120, no. 1 (June 10, 2002): 29–37. http://dx.doi.org/10.1085/jgp.20028607.

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Tumor cell membranes have multiple components that participate in the process of metastasis. The present study investigates the physical association of β1-integrins and Kv1.3 voltage-gated potassium channels in melanoma cell membranes using resonance energy transfer (RET) techniques. RET between donor-labeled anti–β1-integrin and acceptor-labeled anti-Kv1.3 channels was detected on LOX cells adherent to glass and fibronectin-coated coverslips. However, RET was not observed on LOX cells in suspension, indicating that molecular proximity of these membrane molecules is adherence-related. Several K+ channel blockers, including tetraethylammonium, 4-aminopyridine, and verapamil, inhibited RET between β1-integrins and Kv1.3 channels. However, the irrelevant K+ channel blocker apamin had no effect on RET between β1-integrins and Kv1.3 channels. Based on these findings, we speculate that the lateral association of Kv1.3 channels with β1-integrins contributes to the regulation of integrin function and that channel blockers might affect tumor cell behavior by influencing the assembly of supramolecular structures containing integrins.
8

Singh, Bramah N. "β-Adrenergic Blockers as Antiarrhythmic and Antifibrillatory Compounds: An Overview." Journal of Cardiovascular Pharmacology and Therapeutics 10, no. 4_suppl (October 2005): S3—S14. http://dx.doi.org/10.1177/10742484050100i402.

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β-Adrenergic blockers have a wide spectrum of action for controlling cardiac arrhythmias that is larger than initially thought. Data from the past several decades indicate that, as an antiarrhythmic class, β-blockers remain among the very few pharmacologic agents that reduce the incidence of sudden cardiac death, prolong survival, and ameliorate symptoms caused by arrhythmias in patients with cardiac disease. As a class of compounds, β-blockers have a fundamental pharmacologic property that attenuates the effects of competitive adrenergic receptors. However, the net clinical effects of the different β-receptor blockers may vary quantitatively because of variations in associated intrinsic sympathomimetic agonism and in their intrinsic potency for binding to β-receptors. These individual compounds also differ in their selectivity for β1- and β2-receptors. Metoprolol is a β1-selective blocker, whereas carvedilol is a nonselective β1- and β2-blocker, an antioxidant, and has a propensity to inhibit α1-receptors and endothelin. Evolving data from controlled and uncontrolled clinical trials suggest that there are clinically significant differences among this class of drugs. Recent evidence also suggests that the antiarrhythmic actions of certain β-receptor blockers such as carvedilol and metoprolol extend beyond the ventricular tissue to encompass atrial cells and help maintain sinus rhythm in patients with atrial fibrillation, especially in combination with potent antifibrillatory agents such as amiodarone. This introduction provides a current perspective on these newer developments in the understanding of the antiarrhythmic and antifibrillatory actions of β-blockers.
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Winther, K., and C. Hedman. "Beta-Adrenoceptor Blockade, Platelets, and Rheologic Factors." Cephalalgia 6, no. 5_suppl (May 1986): 33–40. http://dx.doi.org/10.1177/03331024860060s504.

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Alterations in platelet function and other hemorheologic factors have been reported to occur in patients with migraine. The prophylactic treatment of migraine with beta blockers is at present well established, and non-selective as well as β1-selective beta blockers exert an effect. The aim of this presentation is to summarize how beta blockers, depending on their receptor selectivity, modulate platelet function and hemorheologic factors. We conclude that nonselective beta blockade increases factors, such as platelet aggregability, and decreases fibrinolytic activity compared with β1-selective blockade with metoprolol. These differences do not reflect on their migraine prophylactic effect and indicate that alterations in platelet function are not a primary cause of migraine: rather, they are epiphenomena.
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Diniz, Gabriela Placoná, Marcela Sorelli Carneiro-Ramos, and Maria Luiza Morais Barreto-Chaves. "Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors." International Journal of Endocrinology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/384890.

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TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

Dissertations / Theses on the topic "Β1-Blockers":

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Bourcier, Camille. "Implication des pièges extracellulaires dans la neuro-inflammation induite par infection ou par traumatisme médullaire." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ005.

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Qu'il soit déclenché par une infection ou par un traumatisme, un dérèglement de la réponse immunitaire peut avoir de graves conséquences. Généralement étudiés indépendamment, ces origines différentes peuvent toutefois mettre en jeu des mécanismes communs. Au cours de ma thèse, j'ai donc cherché à étudier plusieurs de ces mécanismes. L'un d'entre eux a plus particulièrement retenu mon attention : la production de pièges extracellulaires (ETs). Pour évaluer ces possibles interactions, j'ai travaillé sur deux pathologies : le sepsis, en tant que facteur infectieux, et la lésion de la moelle épinière, en tant que facteur d'origine traumatique. Les études menées après lésion de la moelle épinière ont permis de caractériser les types cellulaires produisant les ETs dans ce modèle. Celles menées sur deux modèles précliniques de sepsis ont permis de caractériser et explorer les effets des ETs sur les troubles neuromusculaires au cours de cette pathologie. Ces troubles peuvent être atténués par l'administration d'un inhibiteur spécifique de la production de ETs ou par une modulation spécifique du système adrénergique, ce qui a également permis de réduire les dysfonctions d'organes et d'améliorer la survie. Cette piste thérapeutique semble prometteuse et pourrait être envisagée afin d'améliorer la prise en charge des patients atteints d'une neuro-inflammation excessive
Whether triggered by infection or trauma, immune dysfunction can have serious consequences. Usually studied independently, these different origins may nevertheless involve common mechanisms. In the course of my thesis, I set out to study several of these mechanisms. One in particular caught my attention: the production of extracellular traps (ETs). To assess these possible interactions, I worked on two pathologies: sepsis, as an infectious factor, and spinal cord injury, as a factor of traumatic origin. Studies carried out after spinal cord injury enabled us to characterize the cell types producing ETs in this model. Studies carried out on two preclinical models of sepsis have enabled us to characterize and explore the effects of ETs on neuromuscular disorders in this pathology. These disorders can be alleviated by the administration of a specific inhibitor of ETs production, or by specific modulation of the adrenergic system, which has also been shown to reduce organ dysfunction and improve survival. This appears to be a promising therapeutic avenue which could be considered to improve the management of patients with excessive neuroinflammation
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Hu, Hsin, and 胡馨. "β1-Adrenoceptor Genetic Polymorphisms and Other Predictors of the Tolerability and Response to β-Blockers in Patients with Heart Failure in Taiwan." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/89650008662264541624.

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碩士
國立臺灣大學
臨床藥學研究所
94
Background: The tolerated doses of β-blockers in Chinese heart failure (HF) patients were substantially lower than those wildly used in the Western countries, and the therapeutic response was heterogeneous. Although the mechanism responsible for the various tolerability and response was often attributed to β1-adrenoceptor (β1-AR) genetic polymorphisms at codon 49 and 389, their allele distribution was similar between Chinese and Caucasian, and β1-AR genetic full length sequencing has not been performed in Asian population. Objective: This study aimed to examine whether there are novel polymorphic loci in the β1-AR gene responsible for the difference in tolerability to β-blockers between Chinese and Caucasian HF patients, and to assess for other clinical predictors of tolerability and therapeutic response to β-blockers in Chinese population. Methods: We performed full length sequencing for β1-AR in 69 patients who had the diagnosis of chronic HF and were using, or have used, one of the three β-blockers carvedilol, metoprolol succinate, and bisoprolol. Clinical parameters including comorbidities, HF etiology, concurrent medication, left ventricular ejection fraction (LVEF) before the initiation and at the stable dose of β-blocker were retrieved from the medical records or inquiries into the patients. Results: Tolerated carvedilol stable dose was significantly different by HF etiology (p = 0.047). The stable dose of carvedilol for patients with dilated cardiomyopathy (DCMP) as the etiology of HF was higher than that of valvular heart disease (VHD) patients (14.589 ± 8.882 and 5.357 ± 7.594 mg/day, respectively, p = 0.018), and also tended to be higher than that of coronary artery disease (CAD) patients (9.544 ± 5.558 mg/day for CAD, p = 0.054). Multiple stepwise regression revealed that DCMP (B = 4.852, p = 0.007) was the only significant predictor of stable carvedilol dose; DCMP (B = 9.015, p = 0.011) and baseline LVEF (B = - 0.503, p < 0.001) appeared to be the significant predictors of LVEF improvement. In a subgroup analysis of 26 patients with CAD or DCMP (baseline LVEF≦35%), low-dose carvedilol (12.464 ± 7.977 mg / day) produced a significant improvement in LVEF (13.49 ± 16.66 %, p < 0.001). Neither novel variants other than the reported codon 49 and codon 389 within the coding region, nor correlation between β1-AR gene diplotypes and tolerability or response was found. The allele distributions of codon 49 and 389 were similar to those reported previously in the Chinese and Caucasian populations. Conclusion: Low-dose β-blocker therapy improved left ventricular function in Chinese patients with HF. Moreover, DCMP patients tolerated better to β-blocker, and those with DCMP as the etiology of HF or those had lower LVEF at baseline gained a greater improvement. For the β1-AR gene polymorphism, neither novel variant within the coding region, nor a different distribution pattern of alleles at codon 49 and codon 389 was noted.

Book chapters on the topic "Β1-Blockers":

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Wang, Ting, Cai’e Wang, Hongyu Li, and Ran Wang. "Non-Selective Beta-Blockers in Patients with Cirrhosis: Current Evidence and Controversy." In Liver Cirrhosis - Advances in Diagnosis and Management [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005683.

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Non-selective beta-blockers (NSBBs) are the cornerstone of management of liver cirrhosis and its complications. They decrease portal vein blood flow and portal vein pressure via antagonism of β1 and β2 receptors, thereby improving the hyperdynamic circulatory status and reducing the risk of decompensated events in cirrhotic patients with portal hypertension (PH). Currently, NSBBs have been recommended for the primary and secondary prevention of variceal bleeding in patients with cirrhosis. Nevertheless, it has been noted that the clinical risk-benefit ratio appears to deteriorate for NSBBs in patients with advanced liver cirrhosis. Considering that the use of NSBBs in the clinical practice of cirrhotic patients remains controversial, this chapter aims to summarize the evidence of current recommendations and controversies regarding the use of NSBBs in patients with cirrhosis.

Conference papers on the topic "Β1-Blockers":

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Kim, M., N. Baumlin, N. Silswal, J. S. Dennis, and M. A. Salathe. "Comparison of the Effectiveness of Angiotensin Receptor Blockers in Reversing TGF-β1-Induced CFTR and Mucociliary Dysfunction in Cystic Fibrosis Airway Epithelial Cells." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6356.

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