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We aimed to identify the relationship between thyroid transcription factor-1 (TTF-1) expression of lung adenocarcinoma and the efficacy of immune-checkpoint inhibitor (ICI) therapy.This retrospective multicenter study comprised patients with advanced lung adenocarcinoma treated with ICI monotherapy. We collected clinical medical records including data on TTF-1 expression and analyzed the relationship between TTF-1 expression and programmed death-ligand 1 tumor proportion score (PD-L1 TPS), objective response rate (ORR), progression-free survival (PFS), and overall survival (OS).In total, 108 patients with lung adenocarcinoma were analyzed. The rate of TPS ≥1% and ≥50% in patients with positive TTF-1 expression was significantly higher than that in patients with negative TTF-1 expression (88% vs. 60%, p 0.001; 65% vs. 24%, p 0.001). The ORR was significantly higher in TTF-1 positive patients than in TTF-1-negative patients (38% vs. 8%, p = 0.003). Among patients with TPS ≥50% and 1%-49%, the ORR in TTF-1 positive and negative patients was 48% (26/54) versus 17% (1/6) (p = 0.21), and 32% (6/19) versus 11% (1/9) (p = 0.37), respectively. The ORR for patients with TPS1% was 0% in both the TTF-1 negative and positive cases. The median PFS and OS was significantly longer in TTF-1-positive patients than in TTF-1-negative patients (5.4 vs. 1.6 months, p 0.001; 18.2 vs. 8.0 months, p = 0.041). Multivariate analysis revealed that TTF-1-negative status was an independent unfavorable prognostic factor for PFS.Patients with TTF-1-positive status receiving ICI monotherapy showed better outcomes than those with TTF-1-negative lung adenocarcinoma.

Immune checkpoint inhibitors (ICIs) are currently a standard treatment tool for non-small cell lung cancer (NSCLC). RNA-binding motif protein 17 (RBM17), a splicing factor,is frequently overexpressed in NSCLC, but little is known about the role of RBM17 in the efficacy of ICIs for NSCLC. Thus, we investigated the correlations between RBM17 expression and ICI efficacy in NSCLC. We collected biopsy or surgical specimens from patients with advanced or recurrent NSCLC who received ICI monotherapy or chemo-immunotherapy in a first-line setting. RBM17 expression was examined by immunohistochemistry. We evaluated the correlation between the efficacy of ICI monotherapy or chemo-immunotherapy and RBM17 expression. Among the 218 cases, 115 (52.8%) cases were positive for RBM17 expression. RBM17 expression was not associated with the objective response rate (ORR) or progression-free survival (PFS) in either of the ICI monotherapy or chemo-immunotherapy groups. However, among those with a low PD-L1 expression level (PD-L1 < 50%; n = 86), RBM17 expression was significantly associated with a better ORR (p = 0.045) and a better PFS (p < 0.001) in the ICI monotherapy group, and was significantly associated with a poor ORR in the chemo-immunotherapy group (p = 0.041). In conclusion, RBM17 might be a useful predictive marker for a higher efficacy of ICI monotherapy in NSCLC patients with a low PD-L1 expression level.

Lay abstract This case report describes a 72-year-old man with non-small-cell lung cancer who received four cycles of pembrolizumab-containing chemotherapy. He developed multiple immune-related adverse events (irAEs), which are significant side effects of immune checkpoint inhibitors (ICIs). Despite the discontinuation of pembrolizumab due to multiple irAEs, he developed immune-related hepatitis and neutropenia at 92 days and 118 days, respectively, after the final pembrolizumab dose. He received supportive care and immunosuppressive therapy and recovered from neutropenia. Recently, delayed development of irAEs was reported even in patients that discontinued ICIs; this is referred to as a delayed immune-related event (DIRE). This case developed strikingly delayed immune-related neutropenia as a DIRE. Clinicians should pay close attention to neutropenia as a possible life-threatening DIRE after ICI treatment.

Objectives: The study was designed to investigate the safety and tolerability of ramucirumab administered in combination with erlotinib or osimertinib for patients with untreated EGFR-mutated non–small cell lung cancer (NSCLC) and asymptomatic brain metastases, a patient subgroup in which these regimens have remained untested.Materials and methods: This multicenter phase 1b study (RELAY-Brain) consisted of two cohorts with three patients each. The two cohorts were assessed independently of one another and were not compared. Patients whose asymptomatic brain metastases had or had not undergone prior local therapy received ramucirumab (10 mg/kg) every 2 weeks plus either erlotinib (150 mg/day) or osimertinib (80 mg/day) until disease progression or intolerable toxicity. The primary objective of the study was to assess dose-limiting toxicity (DLT), defined as central nervous system (CNS) hemorrhage of grade ³2. Secondary end points included safety profile, objective response (systemic and intracranial), and disease control rate.Results: Six patients were enrolled in the study. Neither DLT nor serious or unexpected adverse events were observed. At the time of this analysis, discontinuation of the study drugs had also not occurred. One treatment-related adverse event of grade ³3 (hypertension of grade 3) was apparent. Common adverse events were generally manageable. The median number of ramucirumab administrations was 18.5 (range, 13 to 31), and there were no detected episodes of CNS hemorrhage. Four patients experienced at least one dose delay for ramucirumab, but there were no dose reductions or omissions for this drug. Five of the six patients showed an objective systemic response. Although only one patient had a measurable CNS lesion at baseline, a confirmed intracranial partial response was observed. Conclusion: Ramucirumab in combination with erlotinib or osimertinib showed promising safety and efficacy for EGFR-mutated NSCLC with brain metastases.Clinical trial registration: Japan Registry of Clinical Trials (jRCTs2051190027)

Multiple primary lung cancers (MPLCs) harbour various genetic profiles among the tumours, even from individuals with same non-intrinsic risk factors. Paired mutational analyses were performed to obtain a census of mutational events in MPLC and assess their relationship with non-intrinsic risk factors. Thirty-eight surgical specimens from 17 patients diagnosed as MPLC were used. Extracted DNAs were sequenced for somatic mutations in 409 cancer-associated genes from a comprehensive cancer panel. We statistically analysed the correlation between each driver mutation frequency and non-intrinsic risk factors using Fisher's exact test, and whether genetic mutations occurred concomitantly or randomly in MPLC using an exact test. Comprehensive genetic analyses suggested different mutation profiles in tumours within the same individuals, with some exceptions. EGFR, KRAS, TP53, or PARP1 mutations were concomitantly detected in some MPLC cases. EGFR mutations were significantly more frequent in never or light smokers and females. Concomitant EGFR or KRAS mutations in MPLCs were significantly more frequent than expected by chance (P = .0023 and .0049, respectively) suggesting a more prominent role of non-intrinsic risk factors in EGFR and KRAS mutations than other mutations, which occurred more randomly. Concomitant EGFR or KRAS mutations were particularly prominent in never or light smokers and males.

本学には，教員研修の高度化，体系化，組織化の実現に一層寄与することを目的としてNITS 四国アライアンス鳴門教育大学センターが設置された。本稿は，そこでの県教育委員会と連携して実 施している管理職養成講座についてまとめたものである。, The NITS Shikoku Alliance Naruto University of Education Center was established at this university with the aim to further contribute to the sophistication, systematization, and organization of teacher training. This paper is a summary of the Manager Training Course conducted in collaboration with the Prefectural Board of Education.

A 68-year-old Japanese man was diagnosed with lung adenocarcinoma stage IVB. We introduced a first-line chemotherapy of four cycles of carboplatin and pemetrexed and pembrolizumab, followed by pemetrexed and pembrolizumab maintenance therapy. Approximately four months after anticancer therapy, a small nodule appeared in the right peripheral S3 lesion. After five months, the nodule was confirmed as a Mycobacterium tuberculosis (TB) nodule. We initiated anti-TB therapy without stopping pembrolizumab, and the right S3 nodule shrank immediately. This report supports the concurrent use of anti-TB treatment with an immune checkpoint inhibitor when the TB infection area is limited.

BACKGROUND: Differences in carcinogenesis and therapeutic efficacy according to ethnicity have been reported for lung cancer, and understanding differences in genetic mutation profiles among ethnicities is important for interpreting the results of clinical trials, preventing carcinogenesis, and individualizing treatment. However, no studies have focused on differences in mutation profiles among different ethnicities using large-scale genomic analysis data with detailed information on smoking history, the main cause of lung cancer. METHODS: To clarify the differences in genetic mutation profiles between Caucasian and Japanese subjects, we compared data from The Cancer Genome Atlas, which mainly included Caucasians, with results from the Japan Molecular Epidemiology for lung cancer study, which is an epidemiological study only involving Japanese subjects. We divided the participants into four groups according to smoking status and performed comparative analysis by tissue type (lung adenocarcinoma and squamous cell lung cancer). RESULTS: In patients with lung adenocarcinoma, the frequency of EGFR mutations was lower in Caucasian subjects than in Japanese subjects (14.6% vs. 51.1%), whereas the frequencies of mutations in other genes, namely KRAS (32.9% vs. 9.3%), TP53 (45.2% vs. 20.7%), BRAF (9.6% vs. 1.3%), PIK3CA (5.9% vs. 2.6%), KEAP1 (17.8% vs. 0.5%), NF1 (10.9% vs. 0.5%), STK11 (17.8% vs. 0.7%), RBM10 (8.7% vs. 0.1%), and MET (7.8% vs. 0.1%), were higher in Caucasian subjects. Among patients with squamous cell carcinoma, TP53 (81.2% vs. 49.1%), PIK3CA (14.5% vs. 6.8%), KEAP1 (12.7% vs. 0.9%), and NFE2L2 mutations (15.8% vs. 13.6%) were more common in Caucasian subjects. CONCLUSIONS: Ethnicity is an important and complex characteristic that must be recognized and considered, even in the era of precision medicine. We should collaborate to share data for different ethnicities and incorporate them into clinical practice and the design of global clinical studies. Carefully designed molecular epidemiological studies focusing on ethnic differences are warranted.

Highlights • Tumor microenvironment (TME) was compared among multiple primary lung cancers (MPLCs). • Sex and smoking status concomitantly impacted PD-L1 expression in paired tumors. • EGFR mutations were independently associated with PD-L1 expression. • KRAS mutations altered the TMEs according to the types of co-mutations. • The number of FOXP3-positive t cells reflected histological subtypes., Introduction Multiple primary lung cancers (MPLCs) occur in common carcinogenetic risks such as lifestyle, biological aging, immune responses, hormones, and metabolism. Although MPLCs harbor various genetic profiles within the same individuals, differences in the tumor microenvironment (TME) are unclear. We investigated the impact of genetic aberrations, non-intrinsic factors, and pathological subtypes on tumor immunity. Materials and Methods In total, 73 surgically resected specimens from 32 patients with MPLC were analyzed. PD-L1 expression in tumor cells (TCs) and immune cells (ICs), CD3-positive tumor-infiltrating lymphocytes (TILs), CD8/CD3 ratios, and FOXP3-positive TILs that compose TMEs were evaluated by immunohistochemistry and classified on a score of 0–2. 38 tumors were sequenced for somatic mutations in 409 cancer-associated genes. Results Females and never or light smokers had a higher incidence of PD-L1-negative tumors and a higher concordance rate. PD-L1 positivity in TCs and ICs was significantly less frequent in EGFR-mutated than in wild-type tumors. Differences in the score of TMEs were observed between the KRAS-mutated-only tumor and the KRAS and TP53-co-mutated tumors, and between the KRAS-mutated-only tumor and the KRAS and STK11-co-mutated tumors. Significantly more FOXP3-high TILs were observed in invasive pathological subtypes than in non-invasive ones. Conclusion Comparing TMEs among MPLCs revealed that non-smokers or light smokers and females were unlikely to express PD-L1 regardless of tumor site and confirmed that the EGFR mutations and co-occurring KRAS and STK11 or TP53 mutations were associated with TME. Pathological subtypes may impact the efficacy of immune therapy due to their potential correlations with regulatory T cells.

SMARCA4-deficient thoracic sarcoma (SMARCA4-DTS) is a recently described entity of thoracic sarcomas with an undifferentiated rhabdoid morphology and SMARCA4 inactivation. Regardless of some reports about the histopathological findings so far, there have been only a few reports about the cytological features. In this article, we present the pathological features of 2 SMARCA4-DTS cases, including the cytological findings. Histopathologically, the tumor cells showed atypical loosely cohesive large epithelioid cells focally with geographic necrosis. Some cells were characterized by rhabdoid cells. Both patients showed intrathoracic masses with a history of smoking, and loss of SMARCA4 expression was confirmed with histopathological specimens. Immunohistochemically, tumor cells of both cases were at least focally positive for cytokeratin, CD34, CD99, synaptophysin, SOX2, and SALL4. In addition, tumor cells demonstrated significantly reduced expression of BRG1/SMARCA4 and SMARCA2. In conclusion, SMARCA4-DTS should be taken into consideration in the differential diagnosis of tumors with undifferentiated rhabdoid morphology involving the thoracic region.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common and progressive disease characterised by chronic cough, airflow limitation and recurrent exacerbations. Since COPD exacerbations are linked to rising mortality and reduced quality of life, the condition poses a substantial burden on individuals, society and the healthcare system. Effective management of COPD exacerbations that includes treatment of related conditions in people with COPD is thus recognised as a relevant clinical question and an important research topic. Gastroesophageal reflux disease (GERD) is a known comorbidity of COPD, and pulmonary microaspiration of gastric acid is thought to be a possible cause of COPD exacerbations. Therefore, reducing gastric acid secretion may lead to a reduction in COPD exacerbations. Proton pump inhibitors (PPIs) are one of the most commonly prescribed medications and are recommended as first‐line therapy for people with GERD because of their inhibitory effects on gastric acid secretion. Treatment with PPIs may present a viable treatment option for people with COPD. OBJECTIVES: To evaluate the efficacy and safety of PPI administration for people with COPD, focusing on COPD‐specific outcomes. SEARCH METHODS: We searched the Cochrane Airways Register of Trials and conventional clinical trial registers from inception to 22 May 2020. We also screened bibliographies of relevant studies. SELECTION CRITERIA: Parallel‐group and cluster‐randomised controlled trials (RCTs) that compared oral PPIs versus placebo, usual care or low‐dose PPIs in adults with COPD were eligible for inclusion. We excluded cross‐over RCTs, as well as studies with a duration of less than two months. DATA COLLECTION AND ANALYSIS: Two independent review authors screened search results, selected studies for inclusion, extracted study characteristics and outcome data, and assessed risk of bias according to standard Cochrane methodology. We resolved discrepancies by involving a third review author. Primary outcomes of interest were COPD exacerbations, pneumonia and other serious adverse events. Secondary outcomes were quality of life, lung function test indices, acute respiratory infections and disease‐specific adverse events. We extracted data on these outcome measures and entered into them into Review Manager software for analysis. MAIN RESULTS: The search identified 99 records, and we included one multicentre RCT that randomised 103 adults with COPD. The 12‐month RCT compared an oral PPI (lansoprazole) and usual care versus usual care alone. It was conducted at one tertiary care hospital and three secondary care hospitals in Japan. This study recruited participants with a mean age of 75 years, and excluded people with symptoms or history of GERD. No placebo was used in the usual care arm. Among the primary and secondary outcomes of this review, the study only reported data on COPD exacerbations and acute respiratory infections (the common cold). As we only included one study, we could not conduct a meta‐analysis. The included study reported that 12 of the 50 people on lansoprazole had at least one exacerbation over a year, compared to 26 out of 50 on usual care (risk ratio 0.46, 95% CI 0.26 to 0.81). The frequency of COPD exacerbations per person in a year was also lower in the PPI plus usual care group than in the usual care alone group（0.34 ± 0.72 vs 1.18 ± 1.40; P < 0.001). The number of people with at least one cold over the year was similar in both groups: 26 people on lansoprazole and 27 people in the usual care group. We judged the evidence to be of low to very low certainty, according to GRADE criteria. The study reported no data on pneumonia and other serious adverse events, quality of life, lung function test indices or disease‐specific adverse events. The risk of bias was largely low or unclear for the majority of domains, though the performance bias was a high risk, as the study was not blinded. AUTHORS' CONCLUSIONS: Evidence identified by this review is insufficient to determine whether treatment with PPIs is a potential option for COPD. The sample size of the included trial is small, and the evidence is low to very low‐certainty. The efficacy and safety profile of PPIs for people with COPD remains uncertain. Future large‐scale, high‐quality studies are warranted, which investigate major clinical outcomes such as COPD exacerbation rate, serious adverse events and quality of life.

Immune checkpoint inhibitors (ICIs) have improved the overall survival of many patients with advanced cancers. However, unlike cytotoxic and targeted drugs, ICIs may cause various immune-related adverse events (irAEs). Among these irAEs, autoimmune meningitis is very rare. Here, we report a case of early-onset, atezolizumab-induced meningitis after administration of one dose of atezolizumab. A 56-year-old man with lung adenocarcinoma had received seventh-line treatment with atezolizumab when he experienced dysarthria. Blood examinations, including the measurement of electrolytes, glucose, and organ functions, were unremarkable, but enhanced head magnetic resonance imaging T1-weighted images showed meningeal enhancement. Although cerebral spinal fluid (CSF) examinations revealed elevated lymphocyte and protein levels, no cancer cells were detected in the CSF. CSF cultures and serological tests, including polymerase chain reaction for herpes simplex virus, were negative. The patient was therefore diagnosed with atezolizumab-triggered autoimmune meningitis. With steroid treatment, the patient's clinical and neurological state improved immediately and he recovered to baseline conditions. Prompt diagnosis and therapeutic intervention are essential for the effective treatment of autoimmune meningitis.

Background: Multiple primary lung cancers (MPLC) are reported to occur in 0.2-20 % of all primary lung cancer cases. MPLC are considered to harbor various genetic profiling patterns among the tumors even within the same individuals, though they developed from the same occupational and environmental exposure. In this study, we performed paired mutational analyses to clarify genetic mutations in MPLC and its relationship with environmental factors. Materials and methods: We obtained 38 surgical specimens from 17 patients who were pathologically diagnosed as MPLC and underwent surgery at Osaka City University Hospital between October 2007 and March 2019. In addition to the clinicopathological features, the patients' age, sex, smoking history, body mass index, radiologic features and surgical procedures were reviewed. Four of the 17 MPLC patients had metachronous lesions, whereas 13 patients only had synchronous lesions. For genetic profiling of MPLC patients, the extracted DNAs were deep-sequenced on Ion S5 sequencer (Thermo Fisher) for somatic mutations in 409 cancer-associated genes (Ion AmpliSeq Comprehensive Cancer Panel). The study was approved by institutional review board of Osaka City University Hospital and written informed consent was obtained from all of the patients. For statistically analyses, we assumed genetic mutations occurred by chance and calculated the frequency of concomitant mutations in multiple tumors within the same individuals based on a previous study (JME study; Kawaguchi T et al, J Clin Oncol 2016). Comparing the assumed frequency of mutations with the actual data, statistically analyses whether mutations would occur concomitantly or randomly were performed using an exact test. Results: Deep sequencing was successfully performed in all of the specimens with the mean coverage of 823. Results from comprehensive genetic analyses suggested that the mutation profiles differed among the tumors within the same individuals, whereas EGFR, KRAS, TP53, and PARP1 mutations were concomitantly detected in multiple tumors within the same individuals. In this study, the frequency of EGFR mutations was significantly higher in never or light -smokers and females. The occurrence of concomitant EGFR or KRAS mutations in multiple tumors within the same individuals was significantly more frequent than expected by chance (EGFR, P = .0023; KRAS, P = .0049), suggesting environmental factors play more role in EGFR and KRAS mutations than the other mutations including TP53 which occurred more randomly in individual tumors. Concomitant EGFR or KRAS mutations were particularly prominent in never or light-smokers and males. Conclusions: Results from our MPLC study confirmed that the development of EGFR or KRAS-mutated tumors were strongly related to environmental factors such as sex and smoking history, and suggested that the other mutations may occur randomly. Citation Format: Motohiro Izumi, Jun Oyanagi, Kenji Sawa, Mitsuru Fukui, Koichi Ogawa, Yoshiya Matsumoto, Yoko Tani, Tomohiro Suzumura, Tetsuya Watanabe, Hiroyasu Kaneda, Shigeki Mitsuoka, Kazuhisa Asai, Tatsuo Kimura, Nobuyuki Yamamoto, Tomoya Kawaguchi, Yasuhiro Koh. Mutational landscape of multiple primary lung cancers and its correlation with environmental factors [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 2333.

e21035 Background: The role of estrogen receptor status in the carcinogenesis of lung cancer remains elusive. A census of clonal and sub-clonal mutations has been defined through the analyses of evolutionary histories of cancers. We previously reported a prospective multicenter molecular epidemiology study (JME study; Kawaguchi T, J Clin Oncol 2016), which included the expression levels of estrogen receptors β (ER) using immunohistochemistry(IHC) and the mutational profile using next generation sequencing as well as solid smoking information and reproductive/ hormonal risk factors from the detailed questionnaire. Methods: Utilizing the data of the JME study, the impact of ER in lung cancer development was explored. All the patients underwent surgery. In 441 ever- and 435 never-smokers, ER were observed in 46.4% and 53.5%, respectively. The cancer-associated 72 gene mutations and 5 gene amplifications examined in this study included EGFR, SMAD4, APC, FBXW7, BRAF, STK11, PIK3CA, TP53, PTEN, KRAS, CTNNB1, NFE2L2, NF1, and MET. ALK fusion was detected by IHC. Patients were enrolled between July 2012 and December 2013, with follow up until November 30th, 2017.Cox proportional hazards models were used to assess the ER expression on relapse free survival (RFS) and overall survival (OS). A logistic regression model was applied to assess the impact of ER (positive vs. negative) on gene alterations, using sex, smoking history, age and stage as independent variables. Results: ER expression was significantly higher in never smokers (vs. ever smokers; p = 0.022) and earlier stage (stage I vs. II-IV; p = 0.002). Patients with ER positive tumors had a longer RFS than those with negative tumors (RFS rate at 4 years: 33.7 vs. 26.5%; p = 0.021), however, there was no significant difference in OS between the two groups (p = 0.108). In the impact of ER status on the gene alterations, mutations in EGFR (p = 0.003), TP53 (p = 0.007) and CTNNB1 (p = 0.027) were significantly associated with ER expression. Multivariate analysis showed that EGFR mutations (OR = 1.394, 95%CI: 1.029-1.890, p = 0.032) and CTNNB1 mutations (OR = 0.272, 95%CI: 0.087-0.853, p = 0.026) were significantly associated with ER expression, while there was a trend for significance with TP53 mutations (OR = 0.737, 95%CI: 0.537-1.011, p = 0.059). Conclusions: ER positive status triggered the clonal EGFR mutations and suppressed the sub-clonal mutations of TP53 and CTNNB1. It is suggested that ER plays a critical role in the alterations of EGFR/TP53/ CTNNB1 axis in lung cancer evolution.

We describe a teaching−practice experience of graduate students for industrial arts education classes given at a junior high school. Naruto University of Education（NUE）has provided a task−oriented study course in which students are responsible for identifying and pursuing educational topics in elementary or secondary schools. In 2013, eight graduate students took part in the program. They have diversified backgrounds other than pedagogy, and are studying for acquiring teacher’s certificates. Prior to teaching a real class, weekly meetings were held for three months to generate and develop a feasible instructional content with teaching materials. The content was determined to be a topic in energy conversion learning from baking bread using Joule’s heat. A teaching plan was drawn up to standardize the educational context for student teachers with different backgrounds. Also, a safety guidance was formulated, taking into account the use of high−electric current. Then, laboratory experiments were repeated to optimize the amount of time required for the hands−on practice in a class. The lectures were successfully given to four classes in the Junior High School of NUE, receiving generally favorable feedbacks from the school students.

今までブラッシングマシーンは主に歯磨剤の歯や歯冠修復材料の摩耗性に関する基礎的研究に用いられてきた。その運動の大部分は水平運動と振動であり, しかも実際のブラッシング法とは必ずしも一致していない。そこで今回我々は, 最近開発したブラツシングマシーンの再現性について, まずスクラッビング法のプラーク除去効果をもとに比較検討した。ブラッシングシミュレーターに入力するデータを得る目的で, 本学保存科医局員10名を被験者とし, 2種の試作歯ブラシ (AおよびB) を用い, 著者らの方法に準じ, 臨床実験を行った。 得られたデータをブラッシングシミュレーターに入力し, 顎模型® (D15 D-500H, (株) ニッシン, 京都) 上で上顎左側中切歯部に人工の染色剤を塗布し, ブラッシングシミュレーター上で, 臨床実験と同じ試作歯ブラシを用いブラッシングを行わせ, 同様にプラーク除去率を算出した。 プラーク除去率は, Aの歯ブラシでは臨床実験上77.9±19.4%, ブラッシングシミュレーター上92.1±4.2%であり, Bの歯ブラシでは同様に92.4±18.0%, 90.4±3.4%であった。 以上の結果より, 今回のブラッシングシミュレーターは, ブラッシング圧の規定, 入力範囲の設定などを考慮すれば, 再現性は期待でき, ブラッシングマシーンとしての有用性はあると考えられる。