Preventing Asthma Emergencies in Schools.

Asthma is a significant public health issue, impacting quality of life, morbidity, and health care costs nationally. Stock asthma rescue medication policies authorize school districts to maintain unassigned albuterol and enable trained staff members to administer the medication in response to asthma symptoms, exercise premedication, and asthma emergencies. Stock asthma rescue (or reliever) medication laws serve as an important fail-safe measure. Such laws provide districts with the ability to respond if a student has an asthma emergency at school but either lacks a diagnosis or does not have access to their own medication. As of September 2019, 13 states have enacted either a law or regulation authorizing the stocking of asthma rescue medication in schools: Arizona, Colorado, Georgia, Illinois, Missouri, New Hampshire, New Jersey, New Mexico, Oklahoma, Ohio, Texas, Utah, and West Virginia. Three additional states provide stock albuterol asthma guidelines but do not have legislation: Indiana, New York, and Nebraska. Some states have found that these policies reduce the need for 911 calls and emergency medical services transports as a result of asthma exacerbations. Initial data also demonstrate that these policies reach populations in need and improve health outcomes. This case study will describe the current state of asthma in Illinois, an innovative policy solution to address asthma emergencies in schools, and the steps taken to advocate for stock asthma rescue medication in Illinois. Legislation for stock albuterol in Illinois was signed into law in August 2018.

A human monoclonal autoantibody to the thyrotropin receptor with thyroid-stimulating blocking activity.

BACKGROUND: Human monoclonal autoantibodies (MAbs) are valuable tools to study autoimmune responses. To date only one human MAb to the thyrotropin (TSH) receptor (TSHR) with stimulating activity has been available. We now describe the detailed characterization of a blocking type human MAb to the TSHR. METHODS: A single heterohybridoma cell line was isolated from the peripheral blood lymphocytes of a patient with severe hypothyroidism (TSH 278 mU/L) using standard techniques. The line stably expresses a TSHR autoantibody (5C9; IgG1/kappa). Ability of 5C9 to bind and compete with 125I-TSH or TSHR antibodies binding to the TSHR was tested using tubes coated with solubilized TSHR. Furthermore, the blocking effects of 5C9 on stimulation of cyclic AMP production was assessed using Chinese hamster ovary (CHO) cells expressing the wild-type human TSHR or TSHRs with amino acid mutations. MAIN OUTCOME: 5C9 IgG bound to the TSHR with high affinity (4 x 10(10) L/mol) and inhibited binding of TSH and a thyroid-stimulating human monoclonal autoantibody (M22) to the receptor. 5C9 IgG preparations inhibited the cyclic AMP-stimulating activities of TSH, M22, serum TSHR autoantibodies and thyroid-stimulating mouse monoclonal antibodies. Furthermore 5C9 reduced the constitutive activity of wild-type TSHR and TSHR with some activating mutations. The effect of different amino acid mutations in the TSHR on 5C9 biological activity was studied and TSHR Lys129Ala or Asp203Ala completely abolished the ability of 5C9 to block TSH-mediated stimulation of cyclic AMP production. CONCLUSIONS: The availability of 5C9 provides new opportunities to investigate the binding and biological activity of TSHR blocking type autoantibodies including studies at the molecular level. Furthermore, monoclonal antibodies such as 5C9 may well provide the basis of new drugs to control TSHR activity including applications in thyroid cancer and Graves' ophthalmopathy.