Objectives To investigate the mental status of pregnant women and to determine their obstetric decisions during the COVID‐19 outbreak. Design Cross‐sectional study. Setting Two cities in China––Wuhan (epicentre) and Chongqing (a less affected city). Population A total of 1947 pregnant women. Methods We collected demographic, pregnancy and epidemic information from our pregnant subjects, along with their attitudes towards COVID‐19 (using a self‐constructed five‐point scale). The Self‐Rating Anxiety Scale (SAS) was used to assess anxiety status. Obstetric decision‐making was also evaluated. The differences between cities in all of the above factors were compared and the factors that influenced anxiety levels were identified by multivariable analysis. Main outcome measures Anxiety status and its influencing factors. Obstetric decision‐making. Results Differences were observed between cities in some background characteristics and women's attitudes towards COVID‐19 in Wuhan were more extreme. More women in Wuhan felt anxious (24.5 versus 10.4%). Factors that influenced anxiety also included household income, subjective symptom and attitudes. Overall, obstetric decisions also revealed city‐based differences; these decisions mainly concerned hospital preference, time of prenatal care or delivery, mode of delivery and infant feeding. Conclusions The outbreak aggravated prenatal anxiety and the associated factors could be targets for psychological care. In parallel, key obstetric decision‐making changed, emphasising the need for pertinent professional advice. Special support is essential for pregnant mothers during epidemics. Tweetable abstract The COVID‐19 outbreak increased pregnant women's anxiety and affected their decision‐making.
Mitochondrial iron levels are tightly regulated, as iron is essential for the synthesis of Fe/S clusters and heme in the mitochondria, but high levels can cause oxidative stress. The ATP-binding cassette (ABC) transporter ABCB8 is a mitochondrial inner membrane protein with an unknown function. Here, we show that ABCB8 is involved in mitochondrial iron export and is essential for baseline cardiac function. Induced genetic deletion of ABCB8 in mouse hearts resulted in mitochondrial iron accumulation and cardiomyopathy, as assessed by echocardiography and invasive hemodynamics. Mice with ABCB8 deletion in the heart also displayed mitochondrial damage, and higher levels of reactive oxygen species and cell death. Down-regulation of ABCB8 in vitro resulted in decreased iron export from isolated mitochondria, whereas its overexpression had the opposite effect. Furthermore, ABCB8 is needed for the maturation of the cytosolic Fe/S proteins, as its deletion in vitro and in vivo led to decreased activity of cytosolic, but not mitochondrial, iron–sulfur-containing enzymes. These results indicate that ABCB8 is essential for normal cardiac function, maintenance of mitochondrial iron homeostasis and maturation of cytosolic Fe/S proteins. In summary, this report provides characterization of a protein involved in mitochondrial iron export.
Overexpression of the receptor tyrosine kinase erbB2 (Her2 in humans) is correlated with a poor prognosis in breast and ovarian cancers. Treatment with trastuzumab (a monoclonal antibody against erbB2) improves survival; however, it also causes cardiomyopathy. We hypothesized that blockade of the erbB2 receptor induces cardiomyocyte death through a mitochondrial pathway that is dependent on the production of reactive oxygen species (ROS). We first showed that levels of erbB2 receptor are significantly decreased in an animal model of ischemic heart disease and in human ischemic cardiomyopathy. We treated neonatal rat cardiomyocytes with an inhibitory erbB2 antibody to study the mechanism behind the deleterious effects of erbB2 blockade. These cells displayed a dose-dependent increase in ROS production and cell death compared with control IgGtreated cells; these processes were reversed by the antioxidant, N-acetylcysteine. The effects of erbB2 antibody on both cell death and ROS production were also reversed by cyclosporine A and diazoxide, chemicals that regulate the pro-and anti-apoptotic channels in the mitochondria, respectively. Furthermore, mouse embryonic fibroblasts lacking Bax and Bak (proteins that mediate cell death through a mitochondrial pathway) were resistant to the deleterious effects of erbB2 antibody. These effects of erbB2 blockade appear to occur through a pathway involving AKT and PKC-␣. Our results suggest that erbB2 plays a role in cardiomyocyte survival, and that the deleterious effects of trastuzumab on the heart occur through a mitochondrial pathway and is mediated by ROS production. Manipulation of redox signaling may be beneficial in cancer patients receiving trastuzumab.The Her-2/neu oncogene, also known as erbB2 in nonhuman organisms, is a transmembrane receptor tyrosine kinase that belongs to the epidermal growth factor receptor family (1, 2).Overexpression of Her2 is seen in ϳ30% of breast cancer patients and is associated with poor survival, increased metastasis, and resistance to chemotherapy (3-5). Transgenic mice overexpressing erbB2 develop focal mammary tumors, thus implicating this protein in tumorigenesis (6). Trastuzumab (Herceptin, Genentech, CA) is a monoclonal antibody (Ab) 2 that binds to Her2 with high affinity and improves survival of patients with advanced breast cancer (7). Trastuzumab is clinically efficacious both as a single agent or in combination with standard chemotherapy regimens (4 -6). However, this agent is cardiotoxic on its own, and especially when administered with anthracyclines, where it can cause cardiomyopathy (CM) in up to 27% of patients (8).The importance of erbB2 in normal cardiac development and physiology was demonstrated in mice by cardiac-specific knock-out of erbB2 (9, 10). The mice were initially normal, but developed CM as adults. One study demonstrated no difference between the wild-type and knock-out mice in the degree of cardiac cell death as assessed by TUNEL staining (10). However, in another study that used a more sensitive PCR-base...
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