The Clockmaker, c. 1735, color engraving, Engelbrecht, Martin (1684--1756). Engelbrecht, a noted print-seller and engraver, was best known for his miniature theater dioramas. Eight scenery-like cards are inserted into a peep-box, aligned one behind the other, creating a three-dimensional view. These popular home-theaters have been cited by photographers and cinematographers for their dramatic optical effects. Some even suggest that they are forerunners of cable television. Our grandmother
clock, an 18th-century Rococo extravaganza of ormolu scrolls and miniature dragons, stands stage center against a backdrop of cedar trees. Her body consists of two timepieces: one resting on her bosomy mantel and the other, a longcase model resting on curlicued paws. In her right hand, she dangles a pendulum—perhaps a reference to Galileo's discovery. The theatrical image may also be a tribute to Engelbrecht's hometown of Augsburg, the chief supplier of highly ornamental clocks to all of Europe. In this issue, we learn how tobacco smoke disrupts the circadian rhythm of clock gene expression, increasing lung inflammation to produce emphysema in mice via sirtuin 1 (SIRT1)-dependent acetylation of the core clock gene, brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1). Image courtesy of Bibliothèque des Arts décoratifs, Paris, France/Archives Charmet/Bridgeman Art Library; Ann Weissmann, fine arts editor.
Environmental Medicine professor, Irfan Rahman's current article has been featured on the cover of the Journal of The Federation of American Societies for Experimental Biology. The article, entitled Circadian clock function is disrupted by environmental tobacco/cigarette smoke, leading to lung inflammation and injury via a SIRT1-BMAL1 pathway, deals with patients with obstructive lung diseases display abnormal circadian rhythms in lung function. The Rahman lab determined the mechanism whereby environmental tobacco/cigarette smoke (CS) modulates expression of the core clock gene BMAL1, through Sirtuin1 (SIRT1) deacetylase during lung inflammatory and injurious responses.