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Background: Anemia caused by left ventricular outflow tract obstruction in patients with hypertrophic obstructive cardiomyopathy (HOCM) has been reported, however, large clinical studies confirming this association are lacking. The objective of the present study was to investigate the relationship between left ventricular outflow tract (LVOT) pressure gradient and hemoglobin in patients with hypertrophic cardiomyopathy (HCM)., Methods: Patient demographics, laboratory and echocardiography data from 310 patients diagnosed with HCM from our hospital who had undergone echocardiography from July 2014 to March 2019 were collected from medical records. Patients were classified into HOCM and non-HOCM groups., Results: Compared to the non-HOCM group, patients in the HOCM group had a lower hemoglobin level (112.2 ± 16.7 vs. 132.9 ± 22.2 g/L, p < 0.001). In addition, significant negative correlations between hemoglobin and LVOT pressure gradient were found in males (r = -0.568, p < 0.001) and females (r = -0.589, p < 0.001). Receiver operating characteristic curve analysis revealed that the best cut-off value for hemoglobin to predict HOCM in male patients was 128 g/L with 74.19% sensitivity and 75.51% specificity (area under the curve: 0.763, p < 0.001). For female patients, the cut-off value was 125 g/L, with a sensitivity and specificity of 89.39% and 48.48%, respectively (area under the curve: 0.718, p < 0.001)., Conclusions: Our results indicate that hemoglobin level is inversely proportional to the LVOT gradient pressure and has value for predicting outflow tract obstruction in patients with HCM.

Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen species (ROS). Amyloid β (Aβ) plays a crucial role in Alzheimer's disease. However, the mechanism of Aβ-induced microglial dysfunction and redox-regulation of microgliosis in aging remains unclear. In this study, we examined Nox2-derived ROS in mediating microglial response to Aβ peptide 1-42 (Aβ 42 ) stimulation in vitro, in aging-associated microgliosis in vivo and in post-mortem human samples. Compared to controls, Aβ 42 markedly induced BV2 cell ROS production, Nox2 expression, p47 phox and ERK1/2 phosphorylation, cell proliferation and IL-1β secretion. All these changes could be inhibited to the control levels in the presence of Nox2 inhibitor or superoxide scavenger. Compared to young (3-4 months) controls, midbrain tissues from wild-type aging mice (20-22 months) had significantly higher levels of Nox2-derived ROS production, Aβ deposition, microgliosis and IL-1β production. However, these aging-related changes were reduced or absent in Nox2 knockout aging mice. Clinical significance of aging-associated Nox2 activation, microgliosis and IL-1β production was investigated using post-mortem midbrain tissues of humans at young (25-38 years) and old age (61-85 years). In conclusion, Nox2-dependent redox-signalling is crucial in microglial response to Aβ 42 stimulation and in aging-associated microgliosis and brain inflammation.

Oxidative stress plays an important role in aging-related neurodegeneration. This study used littermates of WT and Nox2-knockout (Nox2KO) mice plus endothelial cell-specific human Nox2 overexpression-transgenic (HuNox2Tg) mice to investigate Nox2-derived ROS in brain aging. Compared with young WT mice (3-4 months), aging WT mice (20-22 months) had obvious metabolic disorders and loss of locomotor activity. Aging WT brains had high levels of angiotensin II (Ang II) and ROS production; activation of ERK1/2, p53, and γH2AX; and losses of capillaries and neurons. However, these abnormalities were markedly reduced in aging Nox2KO brains. HuNox2Tg brains at middle age (11-12 months) already had high levels of ROS production and activation of stress signaling pathways similar to those found in aging WT brains. The mechanism of Ang II-induced endothelial Nox2 activation in capillary damage was examined using primary brain microvascular endothelial cells. The clinical significance of Nox2-derived ROS in aging-related loss of cerebral capillaries and neurons was investigated using postmortem midbrain tissues of young (25-38 years) and elderly (61-85 years) adults. In conclusion, Nox2 activation is an important mechanism in aging-related cerebral capillary rarefaction and reduced brain function, with the possibility of a key role for endothelial cells.

Mercury contamination in soil and water has become a major concern to environmental quality and human health. Among the existing remediation technologies for mercury pollution control, sorption via iron-based materials has received wide attention as they are environmental friendly and economic, and their reactivity is high and controllable through modulating the morphology and surface properties of particulate materials. This paper aimed to provide a comprehensive overview on environmental application of a variety of iron-based sorbents, namely, zero valent iron, iron oxides, and iron sulfides, for mercury remediation. Techniques to improve the stability of these materials while enhancing mercury sequestration, such as nano-scale size control, surface functionalization, and mechanical support, were summarized. Mechanisms and factors affecting the interaction between mercury and iron-based materials were also discussed. Current knowledge gaps and future research needs are identified to facilitate a better understanding of molecular-level reaction mechanisms between iron-based materials and mercury and the long-term stability of the immobilized mercury.