Eleven normal human temporal bone-eustachian tube (ET) specimens obtained from 11 individuals whose ages were 3 months to 88 years were studied to investigate the path length along the ET lumen and its postnatal development by means of a computer-aided 3-dimensional reconstruction and measurement method. The path length of the ET lumen of the 3-month-old infant was 21.2 mm, and its growth was in correlation with age to attain its adult length (average, 37.00 +/- 4.16 mm). The ratio of the length of the cartilaginous portion together with the junctional portion to the length of the bony portion was 8:1 in an infant at the age of 3 months and 4:1 in adults. That the bony portion of the ET develops relatively more than the cartilaginous and junctional portions may cause this finding. In addition, there is a developmental shift in the orientation of the cartilaginous portion with respect to the bony portion of the ET. In children, the cartilaginous and bony portions are both aligned with the line that connects the pharyngeal orifice and the tympanic orifice. In adults, however, the cartilaginous portion is angled inferiorly and laterally from the bony portion. This change may reflect the relative growth of the face.

Background Multitarget kinase inhibitors (m‐TKI), including lenvatinib, are now available as treatment options for radioiodine‐refractory differentiated thyroid cancer (RR‐DTC). However, the optimal timing of treatment initiation with m‐TKI in these patients remains to be defined. Methods We retrospectively reviewed the clinical records of 30 consecutive patients with RR‐DTC. The relationship between clinical characteristics was evaluated, including tumor growth parameters at pretreatment/post‐treatment and efficacy of lenvatinib. Results A total of 26 patients with RR‐DTC treated with lenvatinib were evaluable for response and eligible for analysis. From the results of multivariate analysis, baseline tumor size and tumor‐related symptoms were independent negative prognostic factors for overall survival (OS) and progression‐free survival (PFS). Pretreatment tumor growth parameters were not prognostic for either PFS or OS. Conclusions Patients with RR‐DTC with a high tumor burden and tumor‐related symptoms had significantly worse prognosis. Greater tumor reduction after starting lenvatinib may lead to better prognosis, irrespective of pretreatment high tumor growth rate.

Nine normal human temporal bones from persons 16 to 88 years old were studied by computer aided three-dimensional reconstruction and measurement. The length of the eustachian tube (ET) lumen in three portions (from pharyngeal orifice to tympanic orifice: cartilaginous, junctional, and bony) averaged 23.6 +/- 4.3 mm, 3.0 +/- 1.9 mm, and 6.4 +/- 2.6 mm. The narrowest portion of the ET lumen was in the cartilaginous portion in all cases: 20.5 +/- 4.2 mm from the pharyngeal orifice and 3.1 +/- 1.6 mm from the pharyngeal margin of the junctional portion. The cross-sectional area of the narrowest portion was 0.65 +/- 0.2 mm2. The tendon of the tensor veli palatini muscle (TVPM) inserted into the lateral lamina in the narrowest portion of the ET lumen in five of nine cases. These results suggest that contraction of the TVPM opens the narrowest portion of the ET lumen to ventilate the middle ear and that this portion also plays a role in protecting the middle ear.

Although field-emission scanning electron microscopy (FE-SEM) has proven very useful in biomedical research, the high vacuum required (10−3 to 10−7 Pa) precludes direct observations of living cells and tissues at high resolution and often produces unwanted structural changes. We have previously described a method that allows the investigator to keep a variety of insect larvae alive in the high vacuum environment of the electron microscope by encasing the organisms in a thin, vacuum-proof suit, the ‘NanoSuit®'. However, it was impossible to protect wet tissues freshly excised from intact organisms or cultured cells. Here we describe an improved ‘NanoSuit' technique to overcome this limitation. We protected the specimens with a surface shield enhancer (SSE) solution that consists of glycerine and electrolytes and found that the fine structure of the SSE-treated specimens is superior to that of conventionally prepared specimens. The SSE-based NanoSuit affords a much stronger barrier to gas and/or liquid loss than the previous NanoSuit did and, since it allows more detailed images, it could significantly help to elucidate the ‘real' organization of cells and their functions.

Patient‐derived xenograft (PDX) models are a useful tool in cancer biology research. However, the number of lung cancer PDX is limited. In the present study, we successfully established 10 PDX, including three adenocarcinoma (AD), six squamous cell carcinoma (SQ) and one large cell carcinoma (LA), from 30 patients with non‐small cell lung cancer (NSCLC) (18 AD, 10 SQ, and 2 LA), mainly in SCID hairless outbred (SHO) mice (Crlj:SHO‐PrkdcscidHrhr). Histology of SQ, advanced clinical stage (III‐IV), status of lymph node metastasis (N2‐3), and maximum standardized uptake value ≥10 when evaluated using a delayed 18F‐fluoro‐2‐deoxy‐d‐glucose positron emission tomography (FDG‐PET) scan was associated with successful PDX establishment. Histological analyses showed that PDX had histology similar to that of patients’ surgically resected tumors (SRT), whereas components of the microenvironment were replaced with murine cells after several passages. Next‐generation sequencing analyses showed that after two to six passages, PDX preserved the majority of the somatic mutations and mRNA expressions of the corresponding SRT. Two out of three PDX with AD histology had epidermal growth factor receptor (EGFR) mutations (L858R or exon 19 deletion) and were sensitive to EGFR tyrosine kinase inhibitors (EGFR‐TKI), such as gefitinib and osimertinib. Furthermore, in one of the two PDX with an EGFR mutation, osimertinib resistance was induced that was associated with epithelial‐to‐mesenchymal transition. This study presented 10 serially transplantable PDX of NSCLC in SHO mice and showed the use of PDX with an EGFR mutation for analyses of EGFR‐TKI resistance.