Cross-sectional study of hepatitis B antibody status in health care workers immunized as children at an academic medical center in Wisconsin.

Individuals who received the hepatitis B vaccine series as young children are entering the healthcare workforce. Our study measured the persistence of antibody to the hepatitis B surface antigen (anti-HBs) at time of employment. Among 986 individuals born in 1991 or more recently with documentation of completion of the hepatitis B vaccine series, 51% had anti-HBs < 10mIU/ml. Of these 507 healthcare workers, 446 (88%) received documented fourth dose of hepatitis B vaccine followed by another anti-HBs ≥ 28 days post vaccination; 11% (50/446 or 5% of the total population) did not mount an anamnestic response. The non-responders were more likely to be male or complete the vaccine series prior to age 7 months. Measuring anti-HBs at the time of hire in this population of healthcare workers who had documentation of hepatitis B series completion as young children may be unnecessary because of the high rate of hepatitis B vaccine protection.

Global deletion of lipocalin 2 does not reverse high-fat diet-induced obesity resistance in stearoyl-CoA desaturase-1 skin-specific knockout mice.

Over the past century, obesity has developed into a paramount health issue that affects millions of people worldwide. Obese individuals have an increased risk to develop other metabolic disorders, such as insulin resistance and atherosclerosis, among others. Previously we determined that mice lacking stearoyl-CoA desaturase-1 (SCD1) enzyme specifically in the skin (SKO) were lean and protected from high-fat diet induced adiposity. Additionally, lipocalin 2 (Lcn2) mRNA was found to be 27-fold higher in the skin of SKO mice compared to control mice. Given reports suggesting that Lcn2 plays a role in protection against diet-induced weight gain, adiposity and insulin resistance, we hypothesized that deletion of Lcn2 alongside the skin-specific SCD1 deficiency would diminish the obesity resistance observed in SKO mice. To test this, we developed mice lacking SCD1 expression in the skin and also lacking Lcn2 expression globally and surprisingly, these mice did not gain significantly more weight than the SKO mice under high-fat diet conditions. Therefore, we conclude that Lcn2 does not mediate the protection against high-fat diet-induced adiposity observed in SKO mice.