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The title dinuclear di-μ-oxo-bis­[(1,4,8,11-tetra­aza­cyclo­tetra­decane-κ4 N)­manganese(III,IV)] diperchlorate nitrate complex, [Mn2O2(C10H24N4)2](ClO4)2(NO3) or [(cyclam)Mn­O]2(ClO4)2(NO3), was self-assembled by the reaction of Mn2+ with 1,4,8,11-tetra­aza­cyclo­tetra­decane in aqueous media. The structure of this compound consists of a centrosymmetric binuclear [(cyclam)MnO]3+ unit, two perchlorate anions and one nitrate anion. While the low-temperature electron paramagnetic resonance spectra show a typical 16-line signal for a di-μ-oxo MnIII/MnIV dimer, the magnetic susceptibility studies also confirm a characteristic antiferromagnetic coupling between the electronic spins of the MnIV and MnIII ions. [ABSTRACT FROM AUTHOR]

Objective: To investigate the genotypes and clinical characteristics of thalassemia on children in Wuhan region., Methods: A total of 159 patients diagnosed as thalassemia in Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology from December 2017 to December 2019. The patients were retrospectively analyzed for their types of mutations, detection rates and clinical characteristics., Results: Among the 422 samples, 159 samples were finally diagnosed as thalassemia through genetic testing, the total detection rate was 37.68%. The detection rate of α, β and αβ-thalassemia was 17.30%, 20.14% and 0.24% respectively. Among α-thalassemia, αα/-SEA was the most common one, with a composition ratio of 68.49%(50/73), followed by αα/-α3.7 (19.18%), αα/-α4.2 (6.85%) and αα/ QS (1.37%). 9 types of β-thalassemia gene mutations were detected, and the most common three mutations were IVSII-654(C→T), with a composition ratio of 40.00%, CD41-42(-TTCT) (20.00%) and CD17(A→T)(16.47%). Two novel mutations of β-thalassemia, HBB: c.92-2A＞T and HBB:c.-23A＞G were detected. Among all the positive patients, 134 (84.28%) were 0-3 years old, 19 (11.95%) were 4-6 years old, and 6 (3.77%) were 7 years of age or older. There were 147 patients with mild anemia (92.45%), 11 patients with moderate anemia (6.92%), and 1 patients with severe anemia (0.63%). The MCV of 94(59.12%) patients was lower than 65 fL, and that of 51(32.08%) patients was between 65 fL and 80 fL, while 14(8.81%) patients was higher than 80 fL. MCV in β-thalassemia group was lower than that in α-thalassemia group, and the difference showed statistically significant (P<0.05)., Conclusion: The genotypes of thalassemia in children in Wuhan area are diverse, and most of them are mild thalassemia, and diagnosed under 3 years old. Children with β-thalassemia have smaller red blood cell volumes than those with α-thalassemia.

Atherogenesis is a chronic inflammatory process, closely related to high morbidity and mortality. Circular RNAs (circRNAs) were reported to function in atherosclerosis. However, the functional impact of circRNA ubiquitin-specific Protease 36 (circ&#95;USP36) on atherosclerosis and the possible mechanism are still unclear. Serum specimens were collected from atherosclerosis patients and healthy volunteers. Human umbilical vein smooth muscle cells (HUVSMCs) exposed with 25 μg/mL oxidized low-density lipoprotein (ox-LDL) were utilized to simulate atherosclerosis. Expression of circ&#95;USP36, microRNA (miR)-182-5p and Kruppel-like factor 5 (KLF5) was determined via quantitative real-time polymerase chain reaction or western blot assay. Cell viability and apoptosis were evaluated by Cell Counting Kit-8 and flow cytometry. Cell metastasis, including migration and invasion, was assessed via Transwell assay. Biomarker protein was analyzed by western blot. The relationship among circ&#95;USP36, miR-182-5p and KLF5 was confirmed by dual-luciferase reporter and RNA pull-down assays. Circ&#95;USP36 and KLF5 were up-regulated, while miR-182-5p was down-regulated in atherosclerosis patients and ox-LDL-induced HUVSMCs. Circ&#95;USP36 knockdown inhibited proliferation and metastasis of ox-LDL-induced HUVSMCs by up-regulating miR-182-5p. MiR-182-5p targeted KLF5, and ameliorated ox-LDL-mediated injury of HUVSMCs. Circ&#95;USP36 knockdown down-regulated KLF5 expression by sponging miR-182-5p. Knockdown of circ&#95;USP36 alleviated ox-LDL-mediated injury of HUVSMCs by modulating miR-182-5p/KLF5 axis, potentially providing a treatment target for atherosclerosis., Competing Interests: None., (AJTR Copyright © 2020.)