Baccalaureate, Liceo Classico, "Istituto Zaccaria" (Milan, Italy), 1956
University of Milan, Milan, Italy, Doctor in Medicine and Surgery (M.D.), 1962
Istituto Provinçial de Obstetricia y Gynecologia, Madrid, Spain, Obstetrics and Gynecology, July 1961
University of Milan, Italy , Surgical Resident, Surgery, 1962-1964
University of Milan, Italy, Postdoctoral Fellow, Pharmacology, 1962-1966
Hopital Broussais, Paris, France, Visiting Surgeon, Cardiac Surgery, July 1965
McLean Hospital, (Harvard), Boston, MA, Research Fellow, Biophysics, 1966-1967
Harvard Medical School, Research Fellow, Neuropathology, 1966-1967
Duke University, Durham, NC, Research Associate, Anatomy, 1967-1970
Educational Council for Medical Graduates (ECFMG) Certificate Number 098-006, 1967
Our research has focused for several decades on the molecular mechanisms that regulate the permeability of gap junction channels. These channels mediate direct cell-to-cell exchange of small cytosolic molecules. Cell communication via gap junction channels is becoming an area of research increasingly relevant to clinical medicine. Altered cell-cell communication resulting from mutations of gap junction channel proteins (connexins), plays a key role in the X-linked Charcot-Marie-Tooth demyelinating peripheral neuropathy, hereditary non-syndromic deafness, hereditary skin disorders, and certain forms of hereditary cataract, and may be involved in the pathogenesis of cardiac arrhythmias and cancer.
Recently, we have demonstrated a functional interplay between the cystic fibrosis transmembrane conductance regulator chloride channel (CFTR) and various connexin channels. The mechanism of channel regulation and gating has been studied in paired Xenopus oocytes by dual voltage-clamp electrophysiology. The molecular domains that participate in channel gating have been studied by combining molecular genetics and biophysics. The participation of calmodulin in channel gating has been suggested by data generated in oocyte pairs expressing calmodulin and connexin mutants.