Infants can breathe and swallow at the same time?

The concept that infants can breathe and swallow simultaneously due to distinct breathing and swallowing channels was propagated primarily by Edmund Crelin and his student, Jeffrey Laitman. Our evaluation of the primary research article that supported this concept found the article to be unconvincing due to numerous misrepresentations of prior data as well as those presented in the article. Despite clear evidence that newborns cannot breathe and swallow simultaneously, Crelin and Laitman continued to support this concept well into the 21st century, which resulted in the concept becoming imbedded in popular literature and the internet, with potentially significant negative clinical consequences.

Newborn anatomy.

Newborn anatomy, despite being distinctly different than adult anatomy, does not constitute a major component of a typical medical school course in gross anatomy. Accordingly, there is a perception that other than the well-known late 20th-century atlas and small textbook by Edmund Crelin on newborn anatomy, there is almost no information available for anatomists and clinicians to refer to on normal infant anatomy. This perception, as verbalized by Crelin in his books, is not correct.

Risk factors for neonatal brachial plexus palsy attributed to anatomy, physiology, and evolution.

The inherent variable anatomy of the neonate and the uniquely-shaped maternal birth canal that is associated with the evolution of human bipedalism constitute risk factors for neonatal brachial plexus palsy (NBPP). For example, those neonates with a prefixed brachial plexus (BP) are at greater risk of trauma due to lateral neck traction during delivery than those with a normal or postfixed BP. Compared to adults, neonates also have extremely large and heavy heads (high head: body ratio) set upon necks with muscles and ligaments that are weak and poorly developed.

Estrogen receptor beta expression and apoptosis of spermatocytes of mice overexpressing a rat androgen-binding protein transgene.

Progression of the first meiotic division in male germ cells is regulated by a variety of factors, including androgens and possibly estrogens. When this regulation fails, meiosis is arrested and primary spermatocytes degenerate by apoptosis. Earlier studies showed that overexpression of rat androgen-binding protein (ABP) in the testis of transgenic mice results in a partial meiotic arrest and apoptosis of pachytene spermatocytes.

Increased expression of estrogen receptor beta in pachytene spermatocytes after short-term methoxyacetic acid administration.

Degeneration of primary spermatocytes by apoptosis occurs during normal spermatogenesis, as well as in several pathological conditions, including exposure to specific testicular toxicants. The mechanisms that regulate the death and survival of primary spermatocytes, however, are still not well understood. The recent localization of estrogen receptor beta (ERbeta) and P450 aromatase in pachytene spermatocytes suggests a role for estrogens in this step of spermatogenesis.

Methoxyacetic acid disregulation of androgen receptor and androgen-binding protein expression in adult rat testis.

Chemical agents can disrupt the balance between survival and apoptosis during spermatogenesis and thus give rise to reduced counts of spermatozoa (oligospermia). One such agent that produces significant germ cell apoptosis at specific stages of the cycle of the seminiferous epithelium is methoxy acetic acid (MAA), the active metabolite of a commonly used solvent, methoxyethanol. Although MAA gives rise to apoptosis of pachytene spermatocytes, it is not known whether MAA exerts a direct effect on germ cells or whether it also affects other testicular cell types such as the Sertoli cells.