The Incidence of Stroke by Socioeconomic Status,Age, Sex,and Stroke Subtype: A Nationwide Study in Korea

Objectives

To date, studies have not comprehensively demonstrated the relationship between stroke incidence and socioeconomic status. This study investigated stroke incidence by household income level in conjunction with age, sex, and stroke subtype in Korea.

Methods

Contributions by the head of household were used as the basis for income levels. Household income levels for 21 766 036 people were classified into 6 groups. The stroke incidences were calculated by household income level, both overall within income categories and further by age group, sex, and stroke subtype. To present the inequalities among the six ranked groups in a single value, the slope index of inequality and relative index of inequality were calculated.

Results

In 2005, 57 690 people were first-time stroke patients. The incidences of total stroke for males and females increased as the income level decreased. The incidences of stroke increased as the income level decreased in those 74 years old and under, whereas there was no difference by income levels in those 75 and over. Intracerebral hemorrhage for the males represented the highest inequality among stroke subtypes. Incidences of subarachnoid hemorrhage did not differ by income levels.

Conclusions

The incidence of stroke increases as the income level decreases, but it differs according to sex, age, and stroke subtype. The difference in the relative incidence is large for male intracerebral hemorrhage, whereas the difference in the absolute incidence is large for male ischemic stroke.     

Naringenin stimulates cholecystokinin secretion in STC-1 cells

BACKGROUND/OBJECTIVES

Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4'',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release.

MATERIALS/METHODS

STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular Ca²⁺ ([Ca²⁺]_i) were measured after incubation of cells with naringenin and naringin for 1 h.

RESULTS

Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in [Ca²⁺]_i, influx of extracellular Ca²⁺, at least in part, and activation of TRP channels, including TRPA1.

CONCLUSION

Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.     

The soluble catalytic ectodomain of ACE2 a biomarker of cardiac remodelling: new insights for heart failure and COVID19

The angiotensin-converting enzyme 2 (ACE2) is a type I integral membrane that was discovered two decades ago. The ACE2 exists as a transmembrane protein and as a soluble catalytic ectodomain of ACE2, also known as the soluble ACE2 that can be found in plasma and other body fluids. ACE2 regulates the local actions of the renin-angiotensin system in cardiovascular tissues, and the ACE2/Angiotensin 1–7 axis exerts protective actions in cardiovascular disease. Increasing soluble ACE2 has been associated with heart failure, cardiovascular disease, and cardiac remodelling. This is a review of the molecular structure and biochemical functions of the ACE2, as well we provided an updated on the evidence, clinical applications, and emerging potential therapies with the ACE2 in heart failure, cardiovascular disease, lung injury, and COVID-19 infection.

     

Platelets activated by collagen through the immunoreceptor tyrosine-based activation motif in the Fc receptor gamma-chain play a pivotal role in the development of myocardial ischemia-reperfusion injury

Platelet activation and the formation of platelet microaggregates in coronary vessels play pivotal roles in myocardial ischemia and reperfusion injury. The Fc receptor gamma-chain (FcR gamma) is coexpressed with glycoprotein (GP) VI, forming a platelet collagen receptor, and the activation of platelets by collagen is closely coupled with tyrosine phosphorylation of the FcRgamma. To examine the functional significance of platelet FcR gamma/GPVI complex in the early phase of myocardial ischemia and reperfusion injury in mice, we performed coronary occlusion and reperfusion experiments using wild type mice and FcRgamma-deficient (FcRgamma(-/-)) mice that lack GPVI. The infarct size was significantly smaller in FcRgamma(-/-) mice subjected to occlusion and reperfusion of the coronary artery than in control FcR gamma(+/+) mice. Twenty-four hours after the reperfusion, electron microscopy of the injured tissue showed substantially more platelet aggregation and occlusive platelet microthrombi in the capillaries of the damaged areas of the wild type mice than in those of the FcR gamma(-/-) mice. Platelet Syk was scarcely activated in the FcR gamma(-/-) mice after myocardial ischemia and reperfusion, but significantly activated in the FcR gamma(+/+) mice. CD11b expression on neutrophils was elevated after myocardial ischemia and reperfusion in both mouse groups, whereas myeloperoxidase activity in the injured areas was significantly lower in the FcRgamma(-/-) mice than in the FcRgamma(+/+) mice. These results suggest that the collagen-induced activation of platelets through the FcR gamma plays a pivotal role in the extension of myocardial ischemia-reperfusion injury. FcRgamma and GPVI may be important therapeutic targets for myocardial ischemia-reperfusion injury.     

Targeting human mast cells expressing g-protein-coupled receptors in allergic diseases

The G-protein-coupled receptors (GPCRs) are the largest known group of integral membrane receptor proteins and are the most common targets of pharmacotherapy. Mast cells (MCs) have been reported to play an important role in allergic diseases, such as urticaria and bronchial asthma. There is an increasing body of clinical evidence that MCs are recruited into allergic reactions by non-IgE-dependent mechanisms. Human MCs are activated and secrete histamine in response to neuropeptides, such as substance P and somatostatin, mediated by a GPCR, MRGX2. The microenvironment surrounding MCs in their resident tissues is likely to contain multiple factors that modify antigen-dependent MC activation. MCs express various GPCRs, and since the function of human MCs is modulated by various GPCR ligands, such as adenosine and sphingosine-1-phosphate, which are present in high levels in the bronchial alveolar lavage fluid of asthmatic patients, the GPCRs expressed on MCs may play an important role in human allergic diseases. The GPCRs expressed on MCs may serve as drug targets for the treatment of allergic diseases.     

Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: a urocortin1-independent mechanism

A common expression of neuroadaptations induced by repeated exposure to addictive drugs is a persistent sensitized behavioral response to their stimulant properties. Neuroplasticity underlying drug-induced sensitization has been proposed to explain compulsive drug pursuit and consumption characteristic of addiction. The hypothalamic-pituitary-adrenal (HPA) axis-activating neuropeptide, corticotropin-releasing factor (CRF), may be the keystone in drug-induced neuroadaptation. Corticosterone-activated glucocorticoid receptors (GRs) mediate the development of sensitization to ethanol (EtOH), implicating the HPA axis in this process. EtOH-induced increases in corticosterone require CRF activation of CRF1 receptors. We posited that CRF1 signaling pathways are crucial for EtOH-induced sensitization. We demonstrate that mice lacking CRF1 receptors do not show psychomotor sensitization to EtOH, a phenomenon that was also absent in CRF1 + 2 receptor double-knockout mice. Deletion of CRF2 receptors alone did not prevent sensitization. A blunted endocrine response to EtOH was found only in the genotypes showing no sensitization. The CRF1 receptor antagonist CP-154,526 attenuated the acquisition and prevented the expression of EtOH-induced psychomotor sensitization. Because CRF1 receptors are also activated by urocortin-1 (Ucn1), we tested Ucn1 knockout mice for EtOH sensitization and found normal sensitization in this genotype. Finally, we show that the GR antagonist mifepristone does not block the expression of EtOH sensitization. CRF and CRF1 receptors, therefore, are involved in the neurobiological adaptations that underlie the development and expression of psychomotor sensitization to EtOH. A CRF/CRF1-mediated mechanism involving the HPA axis is proposed for acquisition, whereas an extrahypothalamic CRF/CRF1 participation is suggested for expression of sensitization to EtOH.     

Value of gated-SPECT in defining the post-revascularization prognosis of patients with ischemic cardiomyopathy

INTRODUCTION AND OBJECTIVES: Gated-SPECT simultaneously evaluates perfusion and ventricular function and could provide important prognostic information in ischemic cardiomyopathy. Our aim was to study the value of gated-SPECT performed before revascularization in a cardioischemic population to predict the outcome of revascularization. METHODS: One hundred and ten patients who had undergone percutaneous (n = 100) or surgical revascularization were included. Patients underwent sestamibi gated-SPECT before revascularization. After revascularization, they were followed-up for at least 12 months (mean 23.7 months, maximum 44 months). We recorded deaths and a combined clinical event of death, non-fatal infarction, and hospital re-admission for cardiac reasons. We analyzed the prognostic value of clinical, angiographic, and gated-SPECT variables. RESULTS: During follow-up, there were 14 deaths (6.4%/ year) and 36 cases of combined events (16.5%/year). Multivariate analysis showed that depressed gated-SPECT ejection fraction (threshold 0.30) was the only variable independently related to death (OR = 4.8; 95%CI, 1.6-14.6) and combined event (OR = 2.5; 95%CI, 1.2-4.8). Survival analysis showed that patients with ejection fraction < or = 0.30% had a significantly shorter period of time free of death (33 months [28-38] versus 42 months [40-44]; p = 0.002) and combined events (28 months [23-32] versus 36 months [33-39]; p = 0.007). CONCLUSIONS: Gated-SPECT, due to the information it provides about left ventricular function, predicts the prognosis of patients after coronary revascularization.