Fujio Hara

Pediatric and adult tracheobronchomalacia.

Twelve cases of tracheobronchomalacia (TBM) cases were reviewed: five were pediatric, and seven were adult, two of which were due to relapsing polychondritis (RPC). In pediatric TBM, the malacic segments were short. Resection of the malacic segment in one case and laryngotracheoplasty with autologous costal cartilage in one case were unsuccessful. However, aortopexy gained good results. Two cases managed conservatively experienced gradual improvement of their symptoms. In adult TBM, plication of pars membranacea was not effective in one case. The insertion of a stent was minimally effective in one case, and distinctly in one polychondritic case. The other four cases managed conservatively have deteriorated gradually. From these findings, a new classification system is proposed.

Autocrine regulation of glial proliferation and differentiation: The induction of cytodifferentiation of postmitotic normal glioblast by growth-promoting factor from astrocytoma cell

A growth-promoting factor (GPF) from astrocytoma cells (GA-1) cultured in serum-free medium (N2) exerted on normal glioblasts proliferative and differentiation-promoting effects, which have been observed in glia maturation factor (GMF) stimulation. The serum-free conditioned media of GA-1 provoked DNA synthesis of glioblasts, and subsequently elicited a morphological differentiation characterized by the extrusion of processes as well as biochemical changes including an increased cellular level of glia fibrillary acidic protein (GFA protein), S-100 protein, and alpha-enolase. The transforming growth factor activity was also found in the media. Partially purified GPF had a molecular weight range of 7100-10,000 Mr and acidic isoelectric point (pH 4.6), and showed a susceptibility to heat treatment and denaturation at low and high pHs. The present results and the findings accumulated from our previous studies on gliotrophic growth factors provide a general concept of the growth and differentiation regulations of normal or neoplastic glial cells by growth factors through autocrine systems.

Esophageal tracheoplasty for congenital tracheal stenosis

Two infants with congenital long tracheal stenosis underwent operation by means of an esophageal tracheoplasty. The first patient had previously undergone tracheal reconstruction using the pericardium. Although ventilation improved somewhat following this procedure, the pericardial patch suddenly ruptured 12 days after the operation, requiring an immediate esophageal tracheoplasty. The esophageal portion of the reconstructed trachea epithelialized 1 month later, with the lumen maintaining its proper size. However, the patient died 3 months after the second tracheoplasty. The cause of death was thought to be due to complications arising from prolonged high-pressure use of mechanical ventilation. He had been on a respirator for 6 months before the first tracheoplasty. The second patient has been doing well with no recurring respiratory problems for 25 months now. Her reconstructed trachea has adapted with her growth. This technique should be considered along with other forms of treatment for tracheal reconstruction because it is relatively simple and pliable.

Esophageal tracheobronchoplasty for diseases of the central airway.

Three infants with congenital tracheal stenosis and three adults with various diseases of the central airway underwent esophageal tracheobronchoplasty to repair long-segment stenoses and defects. The primary operative goal was enlargement of the stenosis (n = 4), repair of the defect (n = 1), or both (n = 1). Cardiopulmonary support was required in two cases. All three infants were operated on for generalized congenital tracheal stenoses. There was one postoperative death on the fifth day. Another infant died of pneumonia 3 months after operation. Tracheal patency was excellent in two infants. One infant is well without symptoms 6 years after the operation, although balloon dilation was required three times during the first postoperative year. In the three adult patients, the primary diseases were congenital tracheal stenosis, iatrogenic injury associated with relapsing polychondritis, and malignant mediastinal tumor involving the trachea. All lesions involved both the trachea and main stem bronchi. Postoperative airway patency was excellent in all three adults, although expandable metallic stents had to be inserted in one patient. Postoperative pulmonary function was improved, particularly forced expiratory volume in 1 second and peak expiratory flow rate. Although the postoperative mortality rate was still high, especially among the infants, and prolonged postoperative ventilatory support was required for five of the six patients, long-term patency and postoperative pulmonary functional improvement are encouraging.

Thirty years' experience of open-repair surgery for pectus excavatum: development of a metal-free procedure

OBJECTIVE Throughout the history of surgery for pectus excavatum (PE), the Nuss procedure and open repair have been performed with many modifications, with most of these procedures using a metal bar. However, the use of a metal bar has several drawbacks. Thus, we aimed to develop a procedure that did not require a metal bar. METHODS Through our experience of 426 pediatric cases that underwent various procedures for open repair of PE at Nagoya City University, we arrived at the current procedure that we describe herein. We have evaluated this procedure by review of clinical results and deformity indices (Hallers, steepness, excavation volume, and asymmetry index). RESULTS The latest and current procedure that supports the sternum with a bridge constructed by the 4th or 5th costal cartilages is associated with fewer complications, a lower re-operation rate, and striking improvement in the indices examined. CONCLUSIONS Our current open-repair procedure that does not require a metal bar is recommended for correction of deformities of PE in children.

Detection and partial purification of glial growth inhibitory factor(GGIF) in the conditioned medium of neuroblastoma cells

Glial growth inhibitory factor (GGIF) was detected in the culture medium of mouse neuroblastoma cells. The partial purification and characterization of GGIF revealed that it was an acidic and heat-unstable protein and separated into two molecular weight forms (GGIF1: 33.0 to 40.5 K Mr; and GGIF2: 31.0 to 34.0 K Mr) on DEAE. Sephacel column chromatography. GGIF inhibited the growth of neoplastic glial cells as well as normal glioblasts in monolayer culture. The inhibitory effect of GGIF on proliferation of glioblasts appeared even after the incubation for less than 1 h, and retained thereafter unless the factor was removed. Immobilized GGIF exposed to glioblasts was reusable, suggesting the existence of a certain component or receptor mediating GGIF action in the plasma membrane.