Objective: Air pollution is one of the most substantial problems globally. Aerodynamic toxic of particulate matter with <10 mm in diameter (PM 10

Objectives Autologous CD133+ bone marrow stem cells may improve cardiac function. This randomized, single‐blind clinical trial inquired whether a combined transepicardial and transseptal implantation of CD133+ stem cells during coronary artery bypass grafting (CABG) improve cardiac function with ejection fraction (EF) changes as a primary endpoint in patients with low EF. Methods Thirty patients with coronary heart disease and EF <35% were randomized to undergo CABG alone or CABG with transseptal and transepicardial implantation of CD133+. Cardiac function was evaluated using cardiac magnetic resonance imaging (MRI) before and 6 months after CABG. Results Preoperative EF was lower in the intervention group (25.88% ± 5.66%) than in the control group (30.18% ± 3.85%; P = .04). The adverse event incidence was similar between both groups. At 6 months, EF changes were significantly higher (8.69% ± 9.49; P = .04) in the CD133+ group than in the CABG‐only group. Compared to the control group, significant improvements were seen in the wall motion score index (P = .003) and scar size proportion (P = .047) in the CD133+ group. The quality of life (QOL), assessed by a 6‐minute walking test, showed considerable improvement in the CD133+ group compared to that in the control group (P = .03). The Minnesota Living with Heart Failure Questionnaire (MLHFQ) scale did not show improvement in the intervention group (P = .09, vs control). Conclusion Combined transepicardial and transseptal autologous CD133+ BMC implantation during bypass grafting improved cardiac function in low EF coronary artery disease patients.

Rheumatic heart disease (RHD) is common in developing countries and poses a big medical challenge and burden. The pathogenesis of RHD is influenced by the triad of host, agent, and environment. Autoantigens generated from Group A Streptococcus (GAS) infection are captured by the resident dendritic cells (DCs) in the heart's valvular endothelium. DCs differentiate into antigen presenting cells (APC) in the valve interstices. APC induces activation of autoreactive T cells, which triggers inflammation and tissue fibrosis. Cardiac fibrosis is promoted through the activation of Mitogen activated protein kinases (MAPKs) and its downstream signaling, including its interaction with transforming growth factor-β (TGF-β) and Smad proteins. TGF-β-induced phosphorylation of Smad2 complexes with Smad3 and Smad4, and translocates into the nucleus. Angiotensin II enhances the migration, maturation, and presentation of DC. In RHD, Angiotensin II induces fibrosis via the stimulation of TGF-β, which further increases the binding of IL-33 to sST2 but not ST2L, resulting in the upregulation of Angiotensin II and progression of cardiac fibrosis. This cascade of inflammation and valvular fibrosis causes calcification and stiffening of the heart valves in RHD. Angiotensin converting enzyme inhibitors (ACEIs) inhibit Angiotensin II production, which in turn decreases TGF-β expression and the onset of overt inflammatory response. This condition leads to a reduction in the sST2 as the decoy receptor to "steal" IL-33, and IL-33 binds to ST2L and results in cardioprotection against cardiac fibrosis in the pathogenesis of RHD.