Termination of Pregnancy as a Means to Reduce Maternal Mortality in Pregnant Women With Medical Comorbidities.

The United States is the world's only developed country with a rising maternal mortality rate, with an increase of 26% between 2000 and 2014. Of the approximately 700 pregnancy-related deaths per year in the United States, nearly 30% are attributable to preexisting disease. Maternal-fetal medicine physicians are in a unique position-they are tasked with counseling patients regarding the risks of pregnancy in the context of their medical comorbidities. Individual physicians' opinions regarding the level of risk of death at which a termination of pregnancy would be considered "medically indicated" are highly variable and are influenced by where physicians are from, where they trained, and their knowledge regarding the safety of termination of pregnancy. Additionally, 43 states have legislated restrictions to abortion access that contain exceptions to protect women's life or health, but what constitutes a risk to a woman's life or health is not well-defined and appropriates medical terminology for political purposes. The current statements from the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine advocate for safe, legal, and unobstructed access to pregnancy termination services. These statements attempt to remove health care providers' own biases regarding the exact risk level at which they would consider an abortion to be medically indicated. Because the risk of death from a first- or second-trimester termination is less than that of a traditional delivery, any medical problem that increases that risk of death could be considered an indication for counseling patients regarding the option of termination of pregnancy as a means to reduce mortality or morbidity.

Requirement of male-specific dosage compensation in Drosophila females--implications of early X chromosome gene expression.

Dosage compensation equates between the sexes the gene dose of sex chromosomes that carry substantially different gene content. In Drosophila, the single male X chromosome is hypertranscribed by approximately two-fold to effect this correction. The key genes are male lethal and appear not to be required in females, or affect their viability. Here, we show these male lethals do in fact have a role in females, and they participate in the very process which will eventually shut down their function--female determination. We find the male dosage compensation complex is required for upregulating transcription of the sex determination master switch, Sex-lethal, an X-linked gene which is specifically activated in females in response to their two X chromosomes. The levels of some X-linked genes are also affected, and some of these genes are used in the process of counting the number of X chromosomes early in development. Our data suggest that before the female state is set, the ground state is male and female X chromosome expression is elevated. Females thus utilize the male dosage compensation process to amplify the signal which determines their fate.