Biological fingerprint using scout computed tomographic images for positive patient identification

Purpose: Management of patient identification is an important issue that should be addressed to ensure patient safety while using modern healthcare systems. Patient identification errors can be mainly attributed to human errors or system problems. An error-tolerant system, such as a biometric system, should be able to prevent or mitigate potential misidentification occurrences. Herein, we propose the use of scout computed tomography (CT) images for biometric patient identity verification and present the quantitative accuracy outcomes of using this technique in a clinical setting. Methods: Scout CT images acquired from routine examinations of the chest, abdomen, and pelvis were used as biological fingerprints. We evaluated the resemblance of the follow-up with the baseline image by comparing the estimates of the image characteristics using local feature extraction and matching algorithms. The verification performance was evaluated according to the receiver operating characteristic (ROC) curves, area under the ROC curves (AUC), and equal error rates (EER). The closed-set identification performance was evaluated according to the cumulative match characteristic curves and rank-one identification rates (R1). Results: A total of 619 (383 males, 236 females, age range 21–92 years) patients who underwent baseline and follow-up chest–abdomen–pelvis CT scans on the same CT system were analyzed for verification and closed-set identification. The highest performances of AUC, EER, and R1 were 0.998, 1.22%, and 99.7%, respectively, in the considered evaluation range. Furthermore, to determine whether the performance decreased in the presence of metal artifacts, the patients were classified into two groups, namely scout images with (255 patients) and without (364 patients) metal artifacts, and the significance test was performed for two ROC curves using the unpaired Delong's test. No significant differences were found between the ROC performances in the presence and absence of metal artifacts when using a sufficient number of local features. Our proposed technique demonstrated that the performance was comparable to that of conventional biometrics methods when using chest, abdomen, and pelvis scout CT images. Thus, this method has the potential to discover inadequate patient information using the available chest, abdomen, and pelvis scout CT image; moreover, it can be applied widely to routine adult CT scans where no significant body structure effects due to illness or aging are present. Conclusions: Our proposed method can obtain accurate patient information available at the point-of-care and help healthcare providers verify whether a patient’s identity is matched accurately. We believe the method to be a key solution for patient misidentification problems.This is the peer reviewed version of the following article: Ueda, Y., Morishita, J. and Hongyo, T. (2019), Biological fingerprint using scout computed tomographic images for positive patient identification. Med. Phys., 46: 4600-4609, which has been published in final form at https://doi.org/10.1002/mp.13779. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited

Increased fibrosis and impaired intratumoral accumulation of macromolecules in a murine model of pancreatic cancer co-administered with FGF-2

Pancreatic cancer is notorious for its poor prognosis. The histopathologic characteristic of pancreatic ductal adenocarcinoma (PDAC), which is the most common type of pancreatic cancer, is fibrosis within tumor tissue. Although fibrosis within tumor tissue is thought to impede drug therapy by interfering with the intratumoral accumulation of anti-tumor drugs, this hypothesis has yet to be proven directly in preclinical models. Here, we evaluated the effect of enhanced fibrosis on intratumoral accumulation of macromolecular drugs by increasing fibrosis in a murine tumor model of subcutaneously xenografted BxPC-3, a human PDAC cell line. When fibroblast growth factor-2 (FGF-2) was co-administered upon BxPC-3 inoculation, stromal fibrotic area was increased and was characterized by augmented murine collagen accumulation compared to inoculation of BxPC-3 alone, which correlated with increased monocyte/macrophage contents in the tumor tissues. We further discovered that the intratumoral accumulation of intravenously administrated fluorescein isothiocyanate-dextran of 2,000,000 Da (2 MDa) was significantly reduced in the FGF-2 co-administered tumors despite unaltered hyaluronan accumulation and pericyte coverage of the tumor neovasculature and increased lymphangiogenesis. Finally, we found that FGF-2 co-administered tumors are more refractory to macromolecular drug therapy using nab-paclitaxel (Abraxane). The model established and analyzed in this study, characterized by increased fibrotic component, provides a preclinical animal model suited to predict the intratumoral accumulation of macromolecular drugs and to evaluate the efficacy of drugs targeting the tumor stroma

A replication study confirmed the EDAR gene to be a major contributor to population differentiation regarding head hair thickness in Asia

Hair morphology is a highly divergent phenotype among human populations. We recently reported that a nonsynonymous SNP in the ectodysplasin A receptor (EDAR 1540T/C) is associated with head hair fiber thickness in an ethnic group in Thailand (Thai-Mai) and an Indonesian population. However, these Southeast Asian populations are genetically and geographically close, and thus the genetic contribution of EDAR to hair morphological variation in the other Asian populations has remained unclear. In this study, we examined the association of 1540T/C with hair morphology in a Japanese population (Northeast Asian). As observed in our previous study, 1540T/C showed a significant association with hair cross-sectional area (P = 2.7 × 10−6) in Japanese. When all populations (Thai-Mai, Indonesian, and Japanese) were combined, the association of 1540T/C was stronger (P = 3.8 × 10−10) than those of age, sex, and population. These results indicate that EDAR is the genetic determinant of hair thickness as well as a strong contributor to hair fiber thickness variation among Asian populations

Ras signaling directs endothelial specification of VEGFR2+ vascular progenitor cells

Vascular endothelial growth factor receptor 2 (VEGFR2) transmits signals of crucial importance to vasculogenesis, including proliferation, migration, and differentiation of vascular progenitor cells. Embryonic stem cell–derived VEGFR2+ mesodermal cells differentiate into mural lineage in the presence of platelet derived growth factor (PDGF)–BB or serum but into endothelial lineage in response to VEGF-A. We found that inhibition of H-Ras function by a farnesyltransferase inhibitor or a knockdown technique results in selective suppression of VEGF-A–induced endothelial specification. Experiments with ex vivo whole-embryo culture as well as analysis of H-ras−/− mice also supported this conclusion. Furthermore, expression of a constitutively active H-Ras[G12V] in VEGFR2+ progenitor cells resulted in endothelial differentiation through the extracellular signal-related kinase (Erk) pathway. Both VEGF-A and PDGF-BB activated Ras in VEGFR2+ progenitor cells 5 min after treatment. However, VEGF-A, but not PDGF-BB, activated Ras 6–9 h after treatment, preceding the induction of endothelial markers. VEGF-A thus activates temporally distinct Ras–Erk signaling to direct endothelial specification of VEGFR2+ vascular progenitor cells

Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction

In autoimmune arthritis, traditionally classified as a T helper (Th) type 1 disease, the activation of T cells results in bone destruction mediated by osteoclasts, but how T cells enhance osteoclastogenesis despite the anti-osteoclastogenic effect of interferon (IFN)-γ remains to be elucidated. Here, we examine the effect of various Th cell subsets on osteoclastogenesis and identify Th17, a specialized inflammatory subset, as an osteoclastogenic Th cell subset that links T cell activation and bone resorption. The interleukin (IL)-23–IL-17 axis, rather than the IL-12–IFN-γ axis, is critical not only for the onset phase, but also for the bone destruction phase of autoimmune arthritis. Thus, Th17 is a powerful therapeutic target for the bone destruction associated with T cell activation

Muscle-specific deletion of BDK amplifies loss of myofibrillar protein during protein undernutrition

Ishikawa, T., Kitaura, Y., Kadota, Y. et al. Muscle-specific deletion of BDK amplifies loss of myofibrillar protein during protein undernutrition. Sci Rep 7, 39825 (2017). https://doi.org/10.1038/srep3982

TUFT1 interacts with RABGAP1 and regulates mTORC1 signaling

The mammalian target of rapamycin (mTOR) pathway is commonly activated in human cancers. The activity of mTOR complex 1 (mTORC1) signaling is supported by the intracellular positioning of cellular compartments and vesicle trafficking, regulated by Rab GTPases. Here we showed that tuftelin 1 (TUFT1) was involved in the activation of mTORC1 through modulating the Rab GTPase-regulated process. TUFT1 promoted tumor growth and metastasis. Consistently, the expression of TUFT1 correlated with poor prognosis in lung, breast and gastric cancers. Mechanistically, TUFT1 physically interacted with RABGAP1, thereby modulating intracellular lysosomal positioning and vesicular trafficking, and promoted mTORC1 signaling. In addition, expression of TUFT1 predicted sensitivity to perifosine, an alkylphospholipid that alters the composition of lipid rafts. Perifosine treatment altered the positioning and trafficking of cellular compartments to inhibit mTORC1. Our observations indicate that TUFT1 is a key regulator of the mTORC1 pathway and suggest that it is a promising therapeutic target or a biomarker for tumor progression.UTokyo FOCUS Articles掲載「がんの増殖・転移を促進する新規因子の同定 小胞輸送を標的とする新しいがん治療戦略への可能性」 https://www.u-tokyo.ac.jp/focus/ja/articles/z0508_00119.htmlUTokyo FOCUS Articles "Possible target for future cancer treatment : Deregulation of system to move molecules in the cell may promote tumor growth, metastasis" https://www.u-tokyo.ac.jp/focus/en/articles/z0508_00120.htm

古代アンデス文明と日本人─放送大学特別講義と展示会

　1898年に秋田で生まれた天野芳太郎は、30歳のときに中南米にわたって実業家として成功し、後にペルーのリマ市に考古学博物館を創設した人物である。　天野は少年時代から考古学に関心をもっていたが、その関心を決定づけたのは、1935年のマチュピチュ訪問であった。天野はマチュピチュで、そこに住んでいた野内与吉という日本人に出会い、彼の案内で一週間ほどマチュピチュを踏査した。　しかし、第二次世界大戦が始まると、天野は総てを失い、北米の収容所に入れられたあと、日本に送還された。戦後の1951年に再び南米に向かい、ペルーで事業を再開し成功するが、後半生は古代アンデス文明の研究と土器、織物などの考古遺物のコレクションに身を投じ、1964年リマに博物館を設立したのである。　それに先立つ1956年、当時東京大学助教授であった泉靖一がリマで天野芳太郎と出会った。泉はすぐにアンデス研究を始め、調査団を組織し発掘を始めた。最初のコトシュ遺跡の発掘で、アメリカ大陸最古の神殿を発掘した。東京大学はそれ以来アンデスの研究で大きな実績を重ねてきた。　岡山出身の実業家森下精一は、1969年リマで天野芳太郎の博物館を訪問し、古代アンデスの土器や織物のすばらしさに衝撃を受け、中南米の考古遺物を蒐集し、1975年自らも岡山県に博物館を開設した。　筆者らは、放送大学のTV特別講義「古代アンデス文明と日本人」を制作し、2015年秋田でそのテーマの展示会を企画し実現した。本稿では、それらの内容を中心に、日本人による古代アンデス文明研究、その背景としての先人たちの「運命的」な出会い、そして秋田で開催した展示会について論じる

Ultrasonographic characteristics of small hepatocellular carcinoma.

The ultrasonographic characteristics of hepatocellular carcinomas (HCC) were investigated. Four typical features of HCCs, "mosaic internal echo pattern", "halo", "lateral shadow" and "posterior echo enhancement", were not recognized in minute HCCs smaller than 2 cm in diameter. These characteristics developed as the tumors grew. Only hypoechoic space-occupying lesions can be considered as small HCCs. In differentiating small HCCs from hypoechoic non-malignant space-occupying lesions in the cirrhotic liver, the ratios of short to long dimensions of the lesions seemed to be important since the ratios of HCCs were significantly larger than those of non-malignant lesions. The fact that 3 hyperechoic small HCCs could not be diagnosed even by celiac arteriography has suggested to us that ultrasonically guided biopsies should be performed in order to differentiate from small hemangiomas. Serum alpha-fetoprotein (AFP) levels of 1/3 of the patients with HCCs were below 100 ng/ml, indicating that it is impossible to detect small HCCs only by measuring serum AFP.</p