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UV-B irradiation is one of the risk factors in age-related diseases. We have reported that biologically uncommon D-β-Asp residues accumulate in proteins from sun-exposed elderly human skin. A previous study also reported that carboxymethyl lysine (CML; one of the advanced glycation end products (AGEs)) which is produced by the oxidation of glucose and peroxidation of lipid, also increases upon UV B irradiation. The formation of D-β-Asp and CML were reported as the alteration of proteins in UV B irradiated skin, independently. In this study, in order to clarify the relationship between the formation of D-β-Asp and CML, immunohistochemical analysis using anti-D-β-Asp containing peptide antibodies and anti-CML antibodies was performed in UV B irradiated mice. Immunohistochemical analyses clearly indicated that an anti-D-β-Asp containing peptide antibody and anti-CML antibody reacted at a common area in UV B irradiated skin. Western blot analyses of the proteins isolated from UV B irradiated skin demonstrated that proteins of 50-70 kDa were immunoreactive towards antibodies for both D-β-Asp containing peptide and CML. These proteins were identified by proteomic analysis as members of the keratin families including keratin-1, keratin-6B, keratin-10, and keratin-14., (Copyright © 2011 Elsevier B.V. All rights reserved.)

A 65-year-old man was followed up after endoscopic mucosal resection for esophageal cancer in February 2000. Thereafter, he received endoscopic mucosal resection, radiation therapy, and argon plasma coagulation for recurrent and multiple primary esophageal cancers. On follow-up examination, two additional esophageal cancers were detected by endoscopy in September 2003. One lesion was located 16 cm from the incisor close to the entrance to the esophagus. To preserve the larynx, this lesion was removed by mucosal resection using a Weerda distending operating laryngoscope. This report describes this novel use of a Weerda distending operating laryngoscope to remove superficial cervical esophageal cancer.

Experiments were conducted with 159 dogs to investigate the mechanism of persistent dysrhythmias clinically encountered after atrial-level operations. Those found after incisions to the internodal pathways (INPs) of the right atrium were analyzed using cardiac mapping in an anesthetized or extracorporeally perfused state. Longitudinal incisions of the posterior INP often allowed inducible sustained atrial flutter, with circus movement of excitation around the right atrium near the tricuspid orfice. Sustained atrial flutter thus produced was modified in cycle length by coexisting division of the middle INP but inhibited by that of the anterior INP. Its incidence increased at chronic stage, with marked cicatricial changes. The disrupted anterior INP markedly prolonged conduction time to the atrioventricular node and A-H interval compared with the other disruptions. Persistent atrioventricular junctional rhythm developed in about 50% of the animals after disruption of all three INPs or anterior and posterior INPs; division of the anterior INP was the common potent factor, although no single blocked INP produced persistent junctional rhythm. Our results support the "summation theory." The incidence of junctional rhythm and hypoxia of the sinoatrial node (flow rate of less than 10 mL.100 g-1.min-1) were markedly enhanced by coexisting blockade of atrial feeding arteries in addition to division of the anterior INP. In conclusion, massive posterior INP disruption is a potent anatomic substrate in producing sustained atrial flutter, middle INP division a modifier, and anterior INP division an inhibitor. Division of the anterior INP is a potent anatomic substrate in producing junctional rhythm, and hypoxia involving the sinoatrial node reacts as its synergic factor.