Background Treatment based on syndrome differentiation under the traditional Chinese medicine (TCM) framework has been shown to be helpful in patients with coronary artery disease. We hypothesized that syndrome types could predict the risk of type 2 myocardial infarction (T2MI) caused by imbalance between myocardial oxygen supply and demand in critically ill patients with pulmonary disease. Methods This retrospective study included consecutive critically ill patients with pulmonary disease admitted to the ICU at Jiading District Central Hospital Affiliated Shanghai University of Medicine & Health Sciences from January 1, 2017, to July 1, 2019. Diagnosis of T2MI was based on the fourth universal definition of myocardial infarction. Risk factors associated with T2MI were identified using multivariate regression analysis. Results A total of 244 patients were included in the study: 78 who developed T2MI and the remaining 166 who did not develop T2MI during hospitalization. The incidence of phlegm syndrome and deficiency syndrome was 61.9% and 38.1%, respectively. In comparison with the patients with phlegm syndrome, the incidence of T2MI in patients with deficiency syndrome is significantly higher (40.9% vs. 26.5%, P=0.019). In multivariate logistic regression, T2MI was independently associated with the baseline troponin level (OR 12.682, 95% CI 1.397∼115.121; P=0.024), hemoglobin < 55 g/L (OR 12.76, 95% CI 2.359∼69.021; P=0.003), mechanical ventilation (OR 2.244, 95% CI 1.029∼4.892; P=0.042), and TCM deficiency syndrome (OR 2.214, 95% CI 1.032∼4.749; P=0.041). After adjusting for confounding factors in Cox regression models, the hazard ratio (95% confidence interval) of qi deficiency syndrome groups was 1.183 (95% CI 1.053∼3.123, P=0.032). Conclusions Patients with deficiency syndrome are at high risk of T2MI, especially those combined with qi deficiency syndrome.

Correlation between Traditional Chinese Medicine Syndromes and Type 2 Myocardial Infarction in Critically Ill Patients with Pulmonary Disease

Three major functional roles for the two ubiquitous G protein–coupled receptor (GPCR) adapter proteins, βarrestin1 and -2 (also known as Arrestin-2 and -3, respectively), are known: a) functional desensitization of the receptor, b) GPCR internalization via clathrin-coated pits resulting in resensitization or receptor downregulation (lysosomal degradation), and c) G protein–independent signal transduction. Both βarrestin1 and -2 can scaffold a variety of cellular effectors (or other signal transducers) to elicit signaling in their own right. βarrestin signaling usually follows the heterotrimeric G protein activation and signal transduction induced by the receptor, which appears mandatory for full activation of the agonist-GPCR-G protein ternary complex and of the receptor itself. A large portion of cardiac function is regulated by GPCRs and thus, cardiac βarrestins play important roles in the functional regulation of not only the normal healthy but also failing heart, via their actions on cardiac GPCRs. One important aspect in the study of βarrestin signaling that oftentimes gets overlooked is that signaling mediated by the two βarrestin isoforms can result in vast, even diametrically opposite, functions in various tissues and organs of the human body, including the myocardium. This needs to be accounted for in the design and development of novel biased agonist drugs for heart failure and other heart diseases. In this chapter, we provide an update on the physiology and pharmacology of the two βarrestins specifically in the myocardium. We also highlight some of the functional differences between βarrestin1 and βarrestin2 in the heart that have already been uncovered, as well as what their impact might be for the translational potential of agents targeting these two versatile proteins for heart failure treatment. 

Arrestins in cardiac function

Alzheimer's disease (AD) is a progressive neurological disorder characterized by a wide range of cognitive and non-cognitive impairments. The present study was designed to investigate the potential effects of cacao on cognitive and non-cognitive performance and to identify the role of oxidative stress in an AD animal model induced by unilateral intracerebroventricular (U-ICV) injection of amyloid beta 

Cacao Ameliorates Amyloid Beta-Induced Cognitive and Non-Cognitive Disturbances

Heart failure (HF) is a complicated clinical syndrome that is considered an increasingly frequent reason for hospitalization, characterized by a complex therapeutic regimen, reduced quality of life, and high morbidity. Long-standing hypertension ultimately paves the way for HF. Recently, there have been improvements in the treatment of hypertension and overall management not limited to only conventional medications, but several novel pathways and their pharmacological alteration are also conducive to the treatment of hypertension. Beta-arrestin (β-arrestin), a protein responsible for beta-adrenergic receptors’ (β-AR) functioning and trafficking, has recently been discovered as a potential regulator in hypertension. β-arrestin isoforms, namely β-arrestin1 and β-arrestin2, mainly regulate cardiac function. However, there have been some controversies regarding the function of the two β-arrestins in hypertension regarding HF. In the present review, we try to figure out the paradox between the roles of two isoforms of β-arrestin in the treatment of HF.

/pdf/beta-arrestins-in-the-treatment-of-heart-failure-related-to-141rhwcw0h.pdf

Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review.

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Beta-Arrestins in the Treatment of Heart Failure Related to Hypertension: A Comprehensive Review.