Simple underlay myringoplasty, which was first developed by Yuasa in 1989, is widely performed for repairing a perforation of the tympanic membrane (TM). However, the rate of successful closure of the perforation by Yuasa’s procedure, which has been reported to be 75% to 85%, is inferior to that in standard myringoplasty. The causes of this inferiority include not only displacement/detachment of the underlay tissue graft from TM but also delay in the regeneration of TM. As a wet or moist environment of wounds has been shown to promote re-epithelialization and reduce scar formation in the treatment of bedsores and cutaneous ulcers, compared with treatment in a dry environment, the moist wound healing theory has generally been accepted in the field of wound care. In this study, to reveal whether a moist environment has a favorable effect on the regeneration of TM, which is lined with epithelial tissue, we developed an improved underlay myringoplasty, in which the TM is kept moist.
 The principles of this surgery are as follows: i) The rim of the epithelium at the edge of the perforation is removed by a transcanal approach. ii) A tissue graft is placed medial to underlie the TM, lifted to contact the edge of the perforation tightly, and fixed with fibrin glue. iii) Two pieces of collagen-based artificial dermis (Terudermis^®) are placed over the perforation and tissue graft, and fixed with fibrin glue in order to prevent not only the graft from detaching into the middle ear but also both graft and TM from drying. iv) The external auditory canal is filled with gelatin sponges immersed with antibiotics to keep the operative site moist.
 We applied this improved underlay myringoplasty to five patients, resulting in successful closure of the perforation and improvement of the hearing level in all cases. Since the aim of this report is to present our procedure in detail and since the number of cases is small and the observation period is short, we are planning to report the results of a large-scale study in the near future to confirm the efficacy and long-term effect of our improved underlay myringoplasty.

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 We report here two cases with myelodysplastic syndromes (MDS) carrying tandem triplication of the long arm of chromosome 1. The first case involved a 66-year-old man who presented with thrombocytopenia and monocytosis. Although hematopoietic dysplasia was minimal, cytogenetic analysis of the bone marrow revealed trp(1)(q21q32) in all metaphases analyzed, and the karyotype was determined as 46,XY,trp(1) (q21q32),add(3)(p25)[20]. The second case was a 58-year-old woman who initially presented with bilateral pulmonary infiltration indicative of alveolar proteinosis. Blood tests showed pancytopenia with few blasts, and the bone marrow picture fulfilled the criteria of refractory cytopenia with multilineage dysplasia. The karyotype was 46,XX,trp(1)(q21q32)[20]. Fluorescence in situ hybridization using a probe for the pre-B-cell leukemia homeobox 1 gene localized on 1q23 showed 3 fluorescence signals tandemly aligned on the trp(1) (q21q32) chromosome. Because trp(1)(q21q32) was the sole chromosomal abnormality (case 2) or was accompanied by only a single additional abnormality (case 1), trp(1)(q21q32) may be the primary cytogenetic change in a small fraction of MDS cases.

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 A 9-year-old girl had vomited frequently after norovirus infection and lost 6 kg in weight in 2 months. After admission to our hospital, she underwent an upper gastrointestinal series. The movement of the digestive tract was good and the esophagus was not enlarged, but the passage of barium was delayed from the esophagus to the stomach. Although achalasia was not strongly suspected, we considered the possibility of increased pressure of the lower esophageal sphincter and administered sublingual nitroglycerin, which is the therapeutic medication for achalasia. The patient could eat food without vomiting for 20-30 minutes, during which time the nitroglycerin would be effective, and her body weight gradually increased. However, since her weight gain was limited, we examined her gastrointestinal tract endoscopically. The junction of the esophagus and stomach had stiffened and narrowed, and bled due to the endoscope camera. After the endoscopic examination, the treatment with nitroglycerin was stopped but she could consume food with little vomiting. We thought that reflux esophagitis after norovirus infection had induced lower esophageal stricture, and that the endoscopic examination had exerted a Bougie effect on this stricture.

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