Functional and metabolic impairment in cigarette smoke-exposed macrophages is tied to oxidative stress.

Cigarette smoke inhalation exposes the respiratory system to thousands of potentially toxic substances and causes chronic obstructive pulmonary disease (COPD). COPD is characterized by cycles of inflammation and infection with a dysregulated immune response contributing to disease progression. While smoking cessation can slow the damage in COPD, lung immunity remains impaired.

Identifying aerosolized cyanobacteria in the human respiratory tract: A proposed mechanism for cyanotoxin-associated diseases.

Cyanobacteria produce harmful toxins that have been associated with several acute conditions and chronic human diseases, like gastroenteritis, non-alcoholic liver disease, and amyotrophic lateral sclerosis. Aerosol from waterbodies appears to be a likely mechanism for exposure. We conducted a study of human biospecimens focused on the cyanobacterial aerosilization process by evaluating the extent to which cyanobacteria can invade the human respiratory tract.

A Case of Thyroid Storm Induced by Iodine-Containing Dietary Supplements and Homeopathic Remedies.

: We report the case of a patient who presented to the hospital in thyroid storm following the use of several iodine-containing dietary supplements (DS) and homeopathic remedies (HR). : The patient was a 76-year-old woman with no personal or family history of thyroid or autoimmune disease. On laboratory assessment, a thyroid panel showed that her total T3 and T4 were elevated at 334 ng/dL and 14.

Developing future faculty: a program targeting internal medicine fellows' teaching skills.

Introduction: The increased demand for clinician-educators in academic medicine necessitates additional training in educational skills to prepare potential candidates for these positions. Although many teaching skills training programs for residents exist, there is a lack of reports in the literature evaluating similar programs during fellowship training.

Aim: To describe the implementation and evaluation of a unique program aimed at enhancing educational knowledge and teaching skills for subspecialty medicine fellows and chief residents.

Pulmonary-specific expression of tumor necrosis factor-alpha alters surfactant lipid metabolism.

Tumor necrosis factor (TNF)-alpha is a major cytokine implicated in inducing acute and chronic lung injury, conditions associated with surfactant phosphatidylcholine (PtdCho) deficiency. Acutely, TNF-alpha decreases PtdCho synthesis but stimulates surfactant secretion. To investigate chronic effects of TNF-alpha, we investigated PtdCho metabolism in a murine transgenic model exhibiting lung-specific TNF-alpha overexpression.

Lipid deprivation increases surfactant phosphatidylcholine synthesis via a sterol-sensitive regulatory element within the CTP:phosphocholine cytidylyltransferase promoter.

Lipid-deprived mice increase alveolar surfactant disaturated phosphatidylcholine (DSPtdCho) synthesis compared with mice fed a standard diet by increasing expression of CTP:phosphocholine cytidylyltransferase (CCT), the rate-limiting enzyme for DSPtdCho synthesis. We previously observed that lipid deprivation increases mRNA synthesis for CCT [Ryan, McCoy, Mathur, Field and Mallampalli (2000) J. Lipid Res.