The classical and non-classical axes of renin-angiotensin system in Parkinson disease: The bright and dark side of the moon.

Parkinson disease (PD) is a common brain neurodegenerative disease due to progressive degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). Of note, the cardio-metabolic disorders such as hypertension are adversely affect PD neuropathology through exaggeration of renin-angiotensin system (RAS). The RAS affects the stability of dopaminergic neurons in the SNpc, and exaggeration of angiotensin II (AngII) is implicated in the development and progression of PD. RAS has two axes classical including angiotensin converting enzyme (ACE)/AngII/AT1R, and the non-classical axis which include ACE2/Ang1-7/Mas receptor, AngIII, AngIV, AT2R, and AT4R. It has been shown that brain RAS is differs from that of systemic RAS that produce specific neuronal effects. As well, there is an association between brain RAS and PD. Therefore, this review aims to revise from published articles the role of brain RAS in the pathogenesis of PD focusing on the non-classical pathway, and how targeting of this axis can modulate PD neuropathology.

SARS-CoV-2 induced HDL dysfunction may affect the host's response to and recovery from COVID-19.

INTRODUCTION: Covid-19 is linked with the development of cardio-metabolic disorders, including dyslipidemia, dysregulation of high-density lipoprotein (HDL), and low-density lipoprotein (LDL). Furthermore, SARS-Co-2 infection is associated with noteworthy changes in lipid profile, which is suggested as a possible biomarker to support the diagnosis and management of Covid-19. METHODS: This paper adopts the literature review method to obtain information about how Covid-19 affects high-risk group patients and may cause severe and critical effects due to the development of acute lung injury and acute respiratory distress syndrome. A narrative and comprehensive review is presented. RESULTS: Reducing HDL in Covid-19 is connected to the disease severity and poor clinical outcomes, suggesting that high HDL serum levels could benefit Covid-19. SARS-CoV-2 binds HDL, and this complex is attached to the co-localized receptors, facilitating viral entry. Therefore, SARS-CoV-2 infection may induce the development of dysfunctional HDL through different mechanisms, including induction of inflammatory and oxidative stress with activation of inflammatory signaling pathways. In turn, the induction of dysfunctional HDL induces the activation of inflammatory signaling pathways and oxidative stress, increasing Covid-19 severity. CONCLUSIONS: Covid-19 is linked with the development of cardio-metabolic disorders, including dyslipidemia in general and dysregulation of high-density lipoprotein and low-density lipoprotein. Therefore, the present study aimed to overview the causal relationship between dysfunctional high-density lipoprotein and Covid-19.

Montelukast and Acute Coronary Syndrome: The Endowed Drug.

Acute coronary syndrome (ACS) is a set of signs and symptoms caused by a reduction of coronary blood flow with subsequent myocardial ischemia. ACS is associated with activation of the leukotriene (LT) pathway with subsequent releases of various LTs, including LTB4, LTC4, and LTD4, which cause inflammatory changes and induction of immunothrombosis. LTs through cysteine leukotriene (CysLT) induce activation of platelets and clotting factors with succeeding coronary thrombosis. CysLT receptor (CysLTR) antagonists such as montelukast (MK) may reduce the risk of the development of ACS and associated complications through suppression of the activation of platelet and clotting factors. Thus, this critical review aimed to elucidate the possible protective role of MK in the management of ACS. The LT pathway is implicated in the pathogenesis of atherosclerosis, cardiac hypertrophy, and heart failure. Inhibition of the LT pathway and CysL1TR by MK might be effective in preventing cardiovascular complications. MK could be an effective novel therapy in the management of ACS through inhibition of pro-inflammatory CysLT1R and modulation of inflammatory signaling pathways. MK can attenuate thrombotic events by inhibiting platelet activation and clotting factors that are activated during the development of ACS. In conclusion, MK could be an effective agent in reducing the severity of ACS and associated complications. Experimental, preclinical, and clinical studies are recommended to confirm the potential therapeutic of MK in the management of ACS.

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection.

Coronavirus disease 2019 (COVID-19) is caused by a novel virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2-induced hyperinflammation together with alteration of plasma proteins, erythrocyte deformability, and platelet activation, may affect blood viscosity. Thus, this review aimed to study the link between SARS-CoV-2 infection and alteration of blood viscosity in COVID-19 patients. In order to review findings related to hyperviscosity in COVID-19, we suggested a protocol for narrative review of related published COVID-19 articles. Hyperviscosity syndrome is developed in different hematological disorders including multiple myeloma, sickle cell anemia, Waldenstorm macroglobulinemia, polycythemia, and leukemia. In COVID-19, SARS-CoV-2 may affect erythrocyte morphology via binding of membrane cluster of differentiation 147 (CD147) receptors, and B and 3 proteins on the erythrocyte membrane. Variations in erythrocyte fragility and deformability with endothelial dysfunction and oxidative stress in SARS-CoV-2 infection may cause hyperviscosity syndrome in COVID-19. Of interest, hyperviscosity syndrome in COVID-19 may cause poor tissue perfusion, peripheral vascular resistance, and thrombosis. Most of the COVID-19 patients with a blood viscosity more than 3.5 cp may develop coagulation disorders. Of interest, hyperviscosity syndrome is more commonly developed in vaccine recipients who had formerly received the COVID-19 vaccine due to higher underlying immunoglobulin concentrations, and only infrequently in those who have not received the COVID-19 vaccine. Taken together, these observations are untimely too early to give a final connotation between COVID-19 vaccination and the risk for development of hyperviscosity syndrome, consequently prospective and retrospective studies are necessary in this regard.

Transcatheter closure of patent ductus arteriosus using ado device: retrospective study of 149 patients.

BACKGROUND: Patent ductus arteriosus (PDA) is a common form of congenital heart disease and forms about 5-10% of congenital heart diseases. Surgical closure is safe and effective; however, certain patients may experience some morbidity. Recently, transcatheter closure of PDA using the Amplatzer duct occluder has been shown to be safe and efficacious. OBJECTIVES: To evaluate whether transcatheter closure with this device offers an alternative to surgical closure of PDA. PATIENTS AND METHODS: Between July 2006 to July 2008, 149 patients (98 females and 51 males) with PDA underwent cardiac catheterization in an attempt to close their PDA by transcatheter approach using Amplatzer duct occluder device. RESULTS: The patient's age ranged from 4 months to 45 years (median 5 years). Successful PDA closure was achieved in 136 patients (91.2%) with 100% complete closure rate within 24 hours after the procedure. Thirteen patients (8.7%) had unsuccessful attempts, 11 (7.3%) of them had failure of deployment of the device, while embolization of the device occurred in two of the patients (1.3%). CONCLUSIONS: Amplatzer duct occluder device is safe and effective for closure of different types and sizes of PDA with low rate of complication.