Transplantation of a tooth involved in dentigerous cyst.

CASE REPORT: To salvage an uneruputed tooth within a dentigerous cyst, the retransplantation of the unerupted premolar involved in the dentigerous cyst was performed. In the present case a dentigerous cyst with the impacted maxillary second premolar of a 10-year-old boy was removed, because of the missing eruption after marsupialisation of the premolar 4 months earlier. Covering the crown and the one third of root, the cyst was removed from the tooth, and the premolar was retransplanted into a cavity created between the premolar and first molar in the maxilla. The tooth was fixed with resin and a twisted wire for 1 month. Two years after transplantation, the tooth responded positively to pulp vitality tests but did not move toward the occlusal line, and dental X-ray showed a lamina dura, mineralisation of the pulp cavity, no root resorption and development.

Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma and the effect of angiotensin converting enzyme (ACE) inhibitor.

Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma was developed to evaluate the dynamics of endogenous AT II in various types of hypertension. Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT I and III was 0.037% and 21%, respectively. There were good correlation between the value measured by direct method, and that of extraction method (r = 0.96, P < 0.01) and plasma renin activity (r = 0.80, P < 0.01). By oral administration of ACE inhibitor (captopril 50 mg), AT II levels were suppressed to 10 pg/ml or less in most patients with essential hypertension, renal parenchymal hypertension and renovascular hypertension up to 2 h. However, AT II levels in patients treated with ACE inhibitors chronically were not different from the AT II levels in patients without ACE inhibitor. In primary aldosteronism AT II was extremely low levels. AT II markedly increased by the stimulation test using furosemide (1 mg/kg i.v.). These results suggest that this method may be useful to clarify the pathophysiology of hypertension and the escape of the inhibition by ACE inhibitor.

Changes in peripheral blood levels and pulse frequencies of GnRH in patients with hypopituitarism.

Pituitary dysfunction occasionally results from brain tumors or the surgical resection of brain tumors. The authors examined two patients with hypogonadotropic secondary amenorrhea, who had undergone surgical removal of brain tumors. Changes in immunoreactive gonadotropin-releasing hormone (GnRH) secretion are of interest in patients with a gonadotropin and gonadal steroid deficit, because both steroid and pituitary feedback systems are altered by tumors or tumor resection. The authors thus measured GnRH, luteinizing hormone, and follicle-stimulating hormone levels every 15 minutes for 4 hours by radioimmunoassay and investigated qualitative and quantitative changes in the pulsatile patterns of these hormones in two hypogonadotropic hypogonadism patients. They also performed similar multiple measurements of GnRH in two normal cycle women in follicular phase and two postmenopausal women. The concentration of plasma GnRH in two hypopituitarism patients was compared with that in two normal cycle women and two postmenopausal women. The study showed that the peripheral blood level of GnRH was significantly lower in two hypopituitarism patients than in both normal cycle and postmenopausal women, and that the pulsatile frequency was not different among these three groups. These findings suggest that alteration of feedback systems results in a decrease in the blood level of GnRH, and that pulses of GnRH maintain normal fluctuation despite the alteration of the hormonal circumstances in two hypogonadotropic hypogonadism patients.

Chemotherapy for advanced non-small cell lung cancer.

Less than 20% of all cases of non-small cell lung cancer are operable. The treatment option available for such patients is either radiotherapy or chemotherapy. Various combinations of chemotherapeutic agents have been tried. The combination of cisplatin and 5-fluorouracil (5-FU) has been proved to have a synergistic antitumour effect in many experimental and clinical studies. In this paper the authors report the results of a trial using tegafur (which is a prodrug of 5-FU; 1-[2-tetrahydrofuryl]-5-FU) and uracil along with cisplatin in inoperable non-small cell lung cancer. Thirty-one patients were entered into the study, all of whom were less than 75 years old (mean age 61 years). The patients (except for 2) had either stage IIIB (12) or stage IV (17) disease with adenocarcinoma and squamous cell carcinoma in equal proportions (15 each). A combination of uracil and tegafur (400 mg/m2) in 100 mg capsules (100 mg tegafur and 224 mg of uracil), was given orally for 21 days. Most of the patients received 300 mg of the combination tablets twice a day. Cisplatin (80 mg/m2) was given as an infusion over 90 minutes on day 8 after adequately hydrating the patients. This cycle was repeated every 4 weeks. At least 2 treatment cycles were given, unless there was disease progression or toxicity. The response and survival rates were assessed after a follow up period which ranged between 9 and 30 months. The patients received 1 to 4 cycles of therapy and the response rates were: complete response--nil,partial response--11, no change--11 and disease progression--9. The overall response rate was 35% (95% CI: range 19-52%). Five patients achieved at least 50% tumour reduction after 2 cycles. Of the 11 patients who showed partial response, 5 (35%) had stage IV disease and 6 (36%) had other stages; 6 (40%) had squamous cell carcinomas and 5 (31%) had tumours of other histological types. The median duration of response was 6 months (3-13 months). In stage III disease, the 1-year survival rate was 31%, with a median survival time of 11 months, while in stage IV disease it was 29% with a median survival time of 8 months. There was a low incidence of toxicity, with anaemia (10%), leukopenia (6%) and thrombocytopenia (6%) being the most common side-effects. There were also no treatment-related deaths. The authors concluded that oral uracil and tegafur were as effective as other combinations with cisplatin. They also caused very few side-effects. They suggest that a larger trial needs to be carried out.

The diagnostic accuracy of a solitary pulmonary nodule, using thin-section high resolution CT: a solitary pulmonary nodule by HRCT.

A solitary pulmonary nodule (SPN) less than 2 cm in diameter of 60 patients was evaluated with thin-section, high-resolution computed tomography (HRCT). The presence of an irregular margin, speculation, convergence of the surrounding structure, an air bronchogram and the involvement of more than 3 vessels was observed more frequently in malignant nodules than in benign nodules. When one point was given for each finding, the mean total scores of each histologic type were as follows; adenocarcinoma; 2.7, squamous cell carcinoma; 2.5, benign tumor; 0.3, tuberculosis; 1.3, pneumonia; 2.0. When SPNs were classified by the total scores, the SPNs with higher scores (> or = 3) included 18 of 33 (56%) malignant lesions and only 2 of 28 (7%) benign lesions. This means that sensitivity and specificity in the diagnosis of malignancy in the SPNs with high scores were 56% and 93%, respectively. These observations suggest that SPNs with a score higher than 3 points would be highly suspicious for malignancy but the number of such SPNs is rather limited. Therefore, more sophisticated methods may be necessary to better differentiate between malignant and benign SPNs.

A phase II trial of oral tegafur and uracil plus cisplatin in patients with inoperable nonsmall cell lung cancer.

BACKGROUND: The combination of uracil and tegafur in a 4:1 molar concentration (UFT) has a greater antitumor activity than 5-fluorouracil (5-FU) and tegafur. Because the combination of 5-FU and cisplatin has been proven to have a synergistic antitumor effect in many experimental and clinical studies, a Phase II study was conducted using the combination of UFT and cisplatin in patients with inoperable nonsmall cell lung cancer. METHODS: Thirty-one patients with measurable disease were entered into the study; all were evaluable for toxicity and response. Their median age was 61 years (range, 36-75 years). There were 13 patients with Stage III and 17 with Stage IV disease. Twenty-two (71%) patients had received no prior treatment. UFT (400 mg/m2) was administered orally on days 1 through 21 and cisplatin (80 mg/m2) was injected intravenously on day 8. This treatment was repeated every 4 weeks. RESULTS: The median number of treatment cycles was two (range, 1-4 cycles). There were 11 partial responses (35%; 95% confidence interval, 19%-52%). The median response time was 6 months (range, 3-13 months). The median survival time was 11 months (range, 4-27+ months) for Stage III and 8 months (range, 2-22 months) for Stage IV. This chemotherapy regimen was well tolerated. The hematologic toxicities, such as leukopenia and thrombocytopenia of grades 3 and 4, occurred in only 2 of 31 (6%) patients. Nonhematologic toxicities of grades 3 or 4 were not observed. CONCLUSIONS: Oral UFT plus cisplatin administration demonstrated an activity comparable with that of other combinations based on cisplatin and an extremely low incidence of side effects. These observations suggest that this chemotherapy regimen is worthy of further investigation in a multi-institutional trial to determine the antitumor effect and the quality of life of patients.

[Measurement of anti-acetylcholine receptor antibody using human rhabdomyosarcoma cell line].

We developed a radioimmunoassay for AChR Ab using AChR solubilized from membrane extracts of human rhabdomyosarcoma cell line (RD cell). The binding affinity of this AChR to the alpha-Bungarotoxin (alpha-BTX) was similar to that of AChR from cell surface. Lyophilized AChR was stable within two months at -20 degrees C. In our assay system, sera from patients with Myasthenia Gravis (MG) showed markedly high titers and frequency (94%) of anti-AChR Ab. On the other hand, almost all sera from normal and non-myasthenic patients such as rheumatoid arthritis and thyroid disease were negative (< 0.2nmol/l). Our assay using AChR from RD cells shows sufficient results in the intra- and inter-CV values, and recovery and dilution tests. AChR Ab titers of our assay showed good correlations with those measured by AChRs from both human ischemic muscles and TE671 cells (commercial kit). The radioimmunoassay for AChR Ab using the membrane extracts of RD cells has high sensitivity, specificity and stability. Therefore, the assay is valuable as the routine assay for the diagnosis of MG.

A simple technique to manage malignant pericardial effusion with a local instillation of bleomycin in non-small cell carcinoma of the lung.

To examine the efficacy of bleomycin on the local control of malignant pericardial effusion, we prospectively conducted a clinical trial consisting of continuous pericardial drainage and a local instillation of bleomycin. In the current study, we treated 7 patients, who suffered from malignant pericardial effusion with cardiac tamponade due to advanced-stage non-small cell carcinoma of the lung. The pericardial effusions were continuously drained through an echo-guided inserted catheter. After the effusions were drained as completely as possible, 5 mg of bleomycin were instilled locally via the catheter. In all patients but one, the draining catheter could be successfully removed. The duration of drainage ranged from 4 to 13 days (mean: 9.2 days). Five of the 7 patients achieved a complete remission of pericardial effusions, which was maintained until death or the last day of follow-up. Intrapericardial bleomycin treatment was thus found to be effective on malignant pericardial effusions without any adverse effects. However, a further study comparing the effect of pericardial instillation of bleomycin versus drainage alone would be needed for the determination of the usefulness of bleomycin.

Postrecurrent survival of patients with non-small-cell lung cancer undergoing a complete resection.

The postrecurrent survival of 215 patients who had undergone a complete resection of non-small-cell lung cancer was examined on the basis of various factors, which included gender (female, male), age (< 65, > or = 65), the pathologic stage of disease at the time of operation (I, II, III), histologic type (squamous cell, nonsquamous cell carcinoma), type of operation (pneumonectomy, other), the selection of adjuvant treatment before recurrence (no treatment, mild chemotherapy, intensive chemotherapy and/or radiotherapy), recurrent site (local, distant), and the disease-free interval (< or = 365, > or = 365 days). A univariate analysis of the postrecurrent survival showed that the significant factors influencing the survival consisted of gender, pathologic stage, recurrent site, selection of adjuvant treatment, and the disease-free interval. Namely, female patients or patients who had pathologic stage I disease, local recurrence, no adjuvant treatment, or a disease-free interval of more than 365 days would be expected to have a prolonged survival after recurrence. Of the five significant factors, only two factors (gender and the selection of the adjuvant treatment) were found to be predominant postrecurrent prognostic factors by multivariate analysis. These observations suggest that the biologic behavior of a recurrent tumor may therefore be influenced by gender and adjuvant treatment before recurrence.

Platelet-derived growth factor is released into the coronary circulation after coronary spasm.

BACKGROUND: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells and is implicated in the vascular response to injury and the pathogenesis of atherosclerosis. It is also a potent vasoconstrictor. METHODS: To examine whether acute myocardial ischemia increases the level of PDGF in the coronary circulation, we measured plasma levels of PDGF in the coronary sinus and the aortic root simultaneously in 14 patients with coronary spastic angina. These measurements were performed before and after the left coronary artery spasm induced by intracoronary injection of acetylcholine, and measurements were also taken in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Eleven patients with chest pain but normal coronary arteries and no coronary spasm served as controls. RESULTS: Plasma PDGF levels increased significantly (P < 0.01) from 274 +/- 28 pg/mL to 364 +/- 27 pg/mL only in coronary sinus after anginal attacks in the patients with coronary spastic angina. However, plasma PDGF levels in coronary sinus remained unchanged after these attacks in the patients with stable exertional angina (from 230 +/- 27 pg/ml to 247 +/- 28 pg/mL) and after intracoronary injection of acetylcholine in the control subjects. Plasma PDGF levels in aortic root remained unchanged in all three patient groups. CONCLUSIONS: PDGF is released into the coronary circulation after coronary artery spasm, and this may exacerbate coronary artery spasm.

[Chemotherapy with cisplatin and daily administration of UFT for unresectable non-small cell lung cancer].

A combination chemotherapy of cisplatin and UFT was administered to fourteen patients with unresectable non-small cell lung cancer. To determine the maximum safety dose of UFT combined with CDDP (80 mg/m2), patients were assigned to three groups as follows: step 1: UFT (400 mg/m2) from day 1 to day 14; step 2: from day 1 to day 21; step 3: from day 1 to day 28. Cisplatin was administered on day 8 in each group. Myelosuppression with grade 3-4 and gastrointestinal toxicity of grade 3 were observed in one and two patients, respectively. The other toxicity was mild. There was no difference in the degree of toxicity among the three groups. The response rate of twelve evaluable patients was 50%; CR 0, PR 6, NC 4 and PD 2. Thus, chemotherapy using cisplatin 80 mg/m2 with daily administration of UFT 400 mg/m2 was considered to be well tolerated and effective in the treatment of non-small cell lung cancer.

Plasma platelet-derived growth factor levels in coronary circulation in unstable angina pectoris.

To examine whether plasma platelet-derived growth factor (PDGF) levels are elevated in the coronary circulation of patients with unstable angina, the plasma PDGF levels in the coronary sinus and aortic root were simultaneously examined in 14 patients with unstable angina, 15 with stable exertional angina, and 15 control subjects. The mean plasma PDGF level (pg/ml) in the coronary sinus was significantly higher (p less than 0.01) in patients with unstable angina than in those with stable exertional angina and in control subjects (502.1 +/- 98.7 vs 301.3 +/- 62.5, and 312.7 +/- 62.6). However, there were no significant differences in mean plasma PDGF levels in the aortic root among the 3 groups. It is concluded that PDGF release is increased in the coronary circulation in patients with unstable angina.

Production of chromogranin A and B derived peptides in human small cell lung carcinoma cell lines.

Production of chromogranin (Cg)A and B derived peptides [pancreastatin (PST), GAWK, CCB] was studied using human lung carcinoma derived cell lines. PST-like immunoreactivity (LI) was detected in the culture medium in 3 of 6 small cell lung carcinoma (SCLC) cell lines, while GAWK- and CCB-LIs were detected in 5 of 6 and all the 6 SCLC cell lines, respectively. CCB-LI was produced in large amounts in SCLC cell lines as compared to PST- and GAWK-LIs. In non-SCLC cell lines, on the other hand, PST- and GAWK-LIs were not detected. CCB-LI was detected in 1 of 7 non-SCLC cell lines, but not detected in the remainder. PST, GAWK and CCB-LIs, secreted by these cell lines, consisted of several peaks, and these peaks were different among cell lines. This suggests that processing of CgA and B is different in the cell lines. Production of CgA and B derived peptides seems to be a characteristic feature of SCLC, and among them, CCB LI may be a useful marker for SCLC.

Establishment of a sensitive radioimmunoassay for serum thymic factor with a special reference to extraction procedures.

A radioimmunoassay (RIA) for serum thymic factor (facteur thymique serique) was established. This assay could detect less than 0.5 pg of serum thymic factor without the interference by other thymic hormones, including thymopoietin II and thymosin alpha 1. Both zinc-free and zinc-bound serum thymic factor showed a similar standard curve, indicating that this RIA could detect both forms of serum thymic factor in the same way. We observed that two procedures were required prior to the measurement in order to measure serum thymic factor content in plasmas; the first, the extraction procedure to remove substances interfering with the assay nonspecifically; the second, the storage of the sample with ethylenediamine tetraacetic acid disodium salt to inhibit the proteases in the plasma to degrade serum thymic factor. By employing this assay system, we observed that cord blood plasmas contained significantly higher level of serum thymic factor than did adult blood plasmas.

Serum levels of inhibin in maternal and umbilical blood during pregnancy.

Inhibin levels were measured by a double antibody heterologous radioimmunoassay in the peripheral serum of 75 pregnant women throughout gestation and in serum from the umbilical vein and artery, which was obtained at the time of delivery. For reference, samples were obtained from 20 nonpregnant women in the early (days 0 to 3), mid (days 4 to 8), and late (days 9 to 14) luteal or follicular phase. Maternal serum levels of inhibin (mean +/- SEM) in early (6 to 12 weeks) gestation (36.4 +/- 2.6 U/ml, n = 36) were significantly (p less than 0.01) higher than those in serum from nonpregnant women in the mid (23.9 +/- 2.5 U/ml, n = 19) or late (11.3 +/- 0.6 U/ml, n = 19) luteal phase. Inhibin levels in maternal serum fell to 15.9 +/- 1.4 U/ml (n = 24) in mid (14 to 20 weeks) gestation and then gradually increased during late (21 to 40 weeks) gestation to peak levels of 49.4 +/- 5.1 U/ml (n = 9) at 36 to 37 weeks. Inhibin levels declined in parallel with human chorionic gonadotropin concentrations during the first trimester (r = 0.587 at p less than 0.01). Significant positive correlations (p less than 0.001) were observed between serum levels of inhibin and 17 beta-estradiol (r = 0.560), progesterone (r = 0.648), and human placental lactogen (r = 0.715) during mid and late (20 to 40 weeks) gestation. Inhibin levels in umbilical vein serum (38.5 +/- 1.3 U/ml, n = 5) were not different from those in umbilical artery serum (39.4 +/- 3.6 U/ml) but were significantly (p less than 0.01) lower than those in maternal serum (50.9 +/- 5.3 U/ml), which was obtained at the time of delivery. By day 5 of puerperium, serum levels of inhibin in the maternal vein were extremely low (2.3 +/- 0.1 U/ml, n = 7); these levels were nearly one fifth lower than follicular phase levels of 10.9 +/- 3.4 U/ml (n = 38). We propose that maternal inhibin in early gestation is secreted from the corpus luteum of pregnancy but that increasing inhibin levels during mid and late gestation result from inhibin that is produced by the placenta. The lack of an umbilical arterial-venous gradient for inhibin and the higher levels of inhibin in maternal serum argue against a fetal source of inhibin in the maternal circulation. The physiologic function of inhibin that is produced by the corpus luteum and by the placenta remains to be determined.

Uremic serum contains humoral factor(s) larger than fifty kilodaltons which suppresses endothelin production in cultured endothelial cells.

Direct effects of human uremic serum on the production of endothelin-1 in cultured porcine endothelial cells were examined in this study. Uremic serum decreased the level of monomeric endothelin-1 secreted into the culture medium by endothelial cells. This effect occurred at a transcriptional step because uremic serum decreased the endothelin-1 mRNA level in those cells. For the partial characterization of this inhibitory activity, uremic serum was fractionated with a centricut column. Uremic serum contains humoral factor(s) larger than 50 kD which suppress the endothelin-1 mRNA level in cultured endothelial cells.

In vivo activation of human neutrophil functions by administration of recombinant human granulocyte colony-stimulating factor in patients with malignant lymphoma.

Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was administered (50 to 800 micrograms/m2) once daily as a half-hour intravenous (IV) infusion for 14 days to seven patients with malignant lymphoma. In all patients, administration of rhG-CSF not only ameliorated the decrease in absolute neutrophil count after the cytotoxic chemotherapy but also enhanced superoxide (O2-) release in neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP). The priming effect of rhG-CSF on neutrophil O2- release was rapid (evident within 6.5 hours) and sustained at least for 24 hours after a single IV administration of rhG-CSF. The responsiveness to further in vitro challenge of rhG-CSF was lost or reduced in neutrophils isolated after rhG-CSF treatment, indicating that neutrophils already primed in vivo by rhG-CSF are desensitized to this factor. In contrast to the results obtained with FMLP, when phorbol myristate acetate (PMA) was used as stimulus, no consistent enhancement of O2- release was observed, suggesting that rhG-CSF modulates the signal transduction pathways linked to FMLP receptors rather than increases the components of the O2- producing enzyme complexes. Administration of rhG-CSF also rapidly (evident within 15 minutes) caused an increase in expression of neutrophil C3bi-receptors that was sustained for at least 24 hours after a single IV administration of rhG-CSF. Pharmacokinetic study of rhG-CSF showed a half-life (t1/2) of 114 min. These findings show that rhG-CSF is a potent activator for neutrophil functions both in vivo and in vitro.

Detection of a novel antigen (1G12) on the surface of peripheral blood mononuclear cells from cancer patients by a sensitive radioimmunoassay. A possible marker for the early diagnosis of cancer.

A murine monoclonal antibody designated 1G12 has been produced by immunizing mice with A549 human lung adenocarcinoma. Using radiolabeled monoclonal antibody 1G12, a sensitive radioimmunoassay to detect 1G12 antigen has been developed. The antigen was detected on the surface of peripheral blood mononuclear cells (PBMC). A study was performed to examine the frequency of distribution of this antigen on the surface of PBMC from healthy donors and patients with cancer. An antigen level of above 30 units per 1 x 10(6) PBMC was considered positive. None of 41 healthy donors (0%) and 16 of 96 patients (16.7%) with benign diseases of the lung, ovary, and uterus were positive. In contrast, 27 of 41 patients (65.8%) with lung cancer, 14 of 18 patients (77.8%) with ovarian cancer, and 16 of 27 patients (59.2%) with uterine cervical cancer had elevated levels of 1G12 antigen. When patients were grouped by stages of cancer, PBMC from patients in relatively early stages (stages I and II) also gave positive results, i.e., 9 of 17 patients (59.2%) with lung cancer, 6 of 10 patients (60%) with ovarian cancer, and 11 of 22 patients (50%) with uterine cervical cancer of these stages were positive. These results suggest that the detection of 1G12 antigen on PBMC of patients may be useful for early diagnosis of cancers.

The major pectic arabinogalactan having activity on the reticuloendothelial system from the roots and rhizomes of Saposhnikovia divaricata.

The major acidic polysaccharide, named saposhnikovan A, was isolated from the roots and rhizomes of Saposhnikovia divaricata. It showed remarkable reticuloendothelial system-potentiating activity in a carbon clearance test. It is composed of L-arabinose: D-galactose: D-galacturonic acid in the molar ratio of 6:15:10, and its molecular weight was estimated to be 54000. About 35% of the D-galacturonic acid residues exist as the methyl esters. Methylation analysis, 13C-nuclear magnetic resonance, and controlled Smith degradation studies indicated that the polysaccharide has the alpha-1----4-linked D-galacturonan backbone bearing alpha-1----5-linked L-arabino-beta-3,6-branched D-galactan side chains.

[Survey on nutrition of infants in the Tokyo metropolitan area. 1. Carious dentitions, anomalies of occlusion and ways of eating].

In September, 1987, a survey on the nutrition of infants was conducted with 1,235 children from 3 to 6 years of age selected from six nurseries and six kindergartens in the metropolis of Tokyo. We compared the survey results with other similar survey reports with respect to three areas; 1, caries attack on primary teeth, 2, anomalies of dentition and occlusion and 3, how foods are eaten, to observe the difference by age and also between children in nurseries and in kindergartens. The following are the results of this comparative investigation. 1) The ratio of caries attacks on the 4-year-old in this survey was 69.6%, which was lower than the 83.4% of the nationwide survey of 1987 conducted by the Ministry of Health and Welfare, while the average value of the df index per person was 4.7, which was lower than the 6.1 of 1981. 2) The caries incidence rate was higher with children in kindergarten than those in nurseries and many kindergarten children had had more than one caries attack. 3) The frequency rate of anomalies of dentition and occlusion in the entire survey sample was 12.9% for deep overbite, 11.4% for open bite and 10.7% for edge-to-edge bite. 4) In the survey of how foods were eaten, the question, "Does your child like to eat things that are hard to bite on?" was asked, and 10.4% of the group answered "My child prefers eating soft food," which was quite high. To the question, "Does your child often eat things that are difficult to eat?", 17.1% of the entire group answered, "My child refuses to." This tendency was greater among the children in kindergaretens.