Biomedical Research-tokyo最新文献_第6页

Visualization of the localization of phospholipids in developing rat teeth by matrix-assisted laser desorption/ionization imaging mass spectrometry. 基质辅助激光解吸/电离成像质谱法观察发育中的大鼠牙齿中磷脂的定位。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2023-01-01 DOI: 10.2220/biomedres.44.173

Yasuyuki Sasano, Alu Konno, Megumi Nakamura, Akiko Henmi, Miyuki Mayanagi, Mu-Chen Yang, Ikuko Yao

{"title":"Visualization of the localization of phospholipids in developing rat teeth by matrix-assisted laser desorption/ionization imaging mass spectrometry.","authors":"Yasuyuki Sasano, Alu Konno, Megumi Nakamura, Akiko Henmi, Miyuki Mayanagi, Mu-Chen Yang, Ikuko Yao","doi":"10.2220/biomedres.44.173","DOIUrl":"https://doi.org/10.2220/biomedres.44.173","url":null,"abstract":"Matrix-assisted laser desorption/ionization imaging mass spectrometry (IMS) is used to comprehensively visualize the spatial distribution of numerous biomolecules. The present study was designed to investigate the distribution of phospholipids in developing rat teeth by IMS to identify the characteristic phospholipid molecules for tooth development, and to evaluate the suitability of tissue preparation methods. Rats at postnatal day 3 were euthanized, and the resected head specimens were either fixed or not fixed with 4% paraformaldehyde (PFA), and decalcified or not decalcified in 10% ethylenediaminetetraacetic acid (EDTA) before being frozen. Subsequently, sections were prepared and mounted on glass slides coated with indium tin oxide, and analyzed by IMS. The mass spectra showed the highest peaks around m/z 706, 732, and 734 in the region of interest. Characteristic localization of signals in the tooth buds was seen around m/z 706 and 732, and a database search indicated that the corresponding molecules were phosphatidylcholines. The signals were localized to the dental papillae and enamel epithelia in the tooth buds. The PFA-fixed specimens with or without EDTA decalcification showed preserved IMS signals, while the non-fixed specimens showed fewer signals. Thus, PFA fixation with EDTA decalcification appears to be suitable for IMS analysis of calcified tissues.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"44 4","pages":"173-179"},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9943309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Allergic inflammation disrupts epithelial electrogenic electrolyte transport through cholinergic regulation in the mouse colon. 变应性炎症通过小鼠结肠胆碱能调节破坏上皮电致电解质运输。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2023-01-01 DOI: 10.2220/biomedres.44.31

Takeshi Yamamoto, Yosuke Katsuki, Yuya Kanauchi, Shusaku Hayashi, Makoto Kadowaki

{"title":"Allergic inflammation disrupts epithelial electrogenic electrolyte transport through cholinergic regulation in the mouse colon.","authors":"Takeshi Yamamoto, Yosuke Katsuki, Yuya Kanauchi, Shusaku Hayashi, Makoto Kadowaki","doi":"10.2220/biomedres.44.31","DOIUrl":"https://doi.org/10.2220/biomedres.44.31","url":null,"abstract":"Intestinal transport of electrolytes is regulated by the enteric nervous system. Acetylcholine (ACh) is considered the most important neurotransmitter for electrolyte transport in the colon. However, electrolyte transport regulated by ACh is not fully understood in the colon. We investigated the regulation of electrogenic electrolyte transport by cholinergic agonists in the mouse colon by measuring the short-circuit current (Isc) using an Ussing chamber system. Muscarinic stimulation induced transient electrogenic Cl- secretion, and nicotinic stimulation induced electrogenic K+ secretion to the apical side in the normal mouse colon, and these effects were reduced in the colon of mice with food allergy (FA). Administration of prednisolone to mice with FA suppressed mild inflammation in the colon and allergic symptoms and thereby ameliorated the disruption of electrogenic electrolyte transport induced not only by cholinergic pathway activation but also by electrical field stimulation and intracellular cAMP signaling pathway activation in the colon. These results suggest that the electrogenic electrolyte transport function in the colon is impaired by FA-induced colonic inflammation and that the suppression of inflammation ameliorates the dysfunction of electrogenic electrolyte transport in the colon of mice with FA.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"44 1","pages":"31-40"},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9145537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Validation of mitotic harvesting method with human cervical carcinoma HeLa cells expressing fluorescent ubiquitination-based cell cycle indicators for radiation research. 用表达基于荧光泛素化的细胞周期指标的人宫颈癌HeLa细胞进行有丝分裂收获方法的验证，用于辐射研究。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2023-01-01 DOI: 10.2220/biomedres.44.181

Ryosuke Seino, Hiroto Uno, Hisanori Fukunaga

引用次数: 0

Fractalkine's dual role in inflammation and hard tissue formation in cultured human dental pulp cells. Fractalkine在培养的人牙髓细胞炎症和硬组织形成中的双重作用。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2023-01-01 DOI: 10.2220/biomedres.44.257

Natsuko Gomyo-Furuya, Naoto Kamio, Takahiro Watanabe, Tomomi Hayama, Joji Fukai, Kosei Kuramochi, Kento Nakanishi, Arata Watanabe, Tatsu Okabe, Kiyoshi Matsushima

{"title":"Fractalkine's dual role in inflammation and hard tissue formation in cultured human dental pulp cells.","authors":"Natsuko Gomyo-Furuya, Naoto Kamio, Takahiro Watanabe, Tomomi Hayama, Joji Fukai, Kosei Kuramochi, Kento Nakanishi, Arata Watanabe, Tatsu Okabe, Kiyoshi Matsushima","doi":"10.2220/biomedres.44.257","DOIUrl":"10.2220/biomedres.44.257","url":null,"abstract":"This study aimed to explore the potential roles of fractalkine/CX3CR1, primarily expressed in vascular endothelial cells and has recently been identified in dental pulp cells at sites of pulp tissue inflammation, not only in inflammation but also in pulp hard tissue formation. To this end, cultured human dental pulp cells were grown in 10% FBS-supplemented α-MEM. Fractalkine was introduced to the culture, and COX-2 and dentin sialophosphoprotein (DSPP) expression levels were evaluated via western blotting. Real-time PCR was used to examine BMP-2 and Osterix mRNA expression. Calcified nodule formation was evaluated with Alizarin red staining. Results revealed that fractalkine increased COX-2 protein expression, calcified nodule formation, and BMP-2 and Osterix mRNA expression in a concentration- and time-dependent manner. DSPP protein expression also increased upon fractalkine addition. This effect of fractalkine on expression of DSPP protein was inhibited in the presence of the CX3CR1 inhibiter ADZ8797. In conclusion, our findings suggest a dual role for fractalkine in promoting pulp inflammation via COX-2 production and contributing to pulp hard tissue formation by stimulating the expression of hard tissue formation markers.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"44 6","pages":"257-264"},"PeriodicalIF":1.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138440247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Editorial. Indications for arachnoid cyst surgery. 社论。蛛网膜囊肿手术的适应症。

IF 2.1 4区医学

Biomedical Research-tokyo Pub Date : 2022-05-20 Print Date: 2022-08-01 DOI: 10.3171/2022.1.PEDS21540

Cormac O Maher

引用次数: 0

Silibinin promotes melanogenesis through the PKA and p38 MAPK signaling pathways in melanoma cells. 水飞蓟宾素通过黑色素瘤细胞中的PKA和p38 MAPK信号通路促进黑色素生成。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2022-04-15 DOI: 10.2220/biomedres.43.31

T. Uto, Tomoe Ohta, Koki Katayama, Y. Shoyama

{"title":"Silibinin promotes melanogenesis through the PKA and p38 MAPK signaling pathways in melanoma cells.","authors":"T. Uto, Tomoe Ohta, Koki Katayama, Y. Shoyama","doi":"10.2220/biomedres.43.31","DOIUrl":"https://doi.org/10.2220/biomedres.43.31","url":null,"abstract":"Silibinin is a flavonolignan isolated from milk thistle (Silybum marianum). Silibinin has been reported to possess multiple biological activities; however, its effect on melanogenesis remains unclear. This study investigated the effect of silibinin on melanogenesis in melanoma cells and the associated molecular mechanism. Our findings demonstrated that silibinin markedly increased melanin content in murine B16-F1 and human HMV-II melanoma cells. Silibinin activated intracellular tyrosinase activity and expression of tyrosinase, tyrosinase-related protein (TRP)-1, TRP-2, and microphthalmia-associated transcription factor (MITF). Furthermore, silibinin enhanced the phosphorylation of cyclic AMP-responsive element-binding protein (CREB), protein kinase A (PKA), and p38 mitogen-activated protein kinase (MAPK) but not of Akt and extracellular signal-regulated kinase (ERK). The specific PKA (H-89) and p38 (SB203580) inhibitors significantly attenuated silibinin-mediated melanin synthesis. These results suggest that silibinin is an effective stimulator of melanogenesis through upregulation of the protein expression of melanogenic enzymes activated by the PKA and p38 pathways, leading to CREB phosphorylation and MITF expression. Therefore, silibinin may have potential for use in the treatment of hypopigmentation disorders.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"43 2 1","pages":"31-39"},"PeriodicalIF":1.2,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45388504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Oncostatin M reduces the synthesis of macrophage-colony stimulating factor stimulated by TGF-β via suppression of p44/p42 MAP kinase and JNK in osteoblasts. 肿瘤抑制素M通过抑制成骨细胞中p44/p42 MAP激酶和JNK来减少TGF-β刺激的巨噬细胞集落刺激因子的合成。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2022-04-15 DOI: 10.2220/biomedres.43.41

T. Doi, Tomoyuki Hioki, Junko Tachi, K. Ueda, R. Matsushima‐Nishiwaki, H. Iida, S. Ogura, O. Kozawa, H. Tokuda

{"title":"Oncostatin M reduces the synthesis of macrophage-colony stimulating factor stimulated by TGF-β via suppression of p44/p42 MAP kinase and JNK in osteoblasts.","authors":"T. Doi, Tomoyuki Hioki, Junko Tachi, K. Ueda, R. Matsushima‐Nishiwaki, H. Iida, S. Ogura, O. Kozawa, H. Tokuda","doi":"10.2220/biomedres.43.41","DOIUrl":"https://doi.org/10.2220/biomedres.43.41","url":null,"abstract":"Bone fracture is an important trauma frequently encountered into emergency medicine as well as orthopedics reflecting an aging society. Oncostatin M, an inflammatory cytokine produced by osteal macrophages, has been considered to play a crucial role in fracture healing. Macrophage colony-stimulating factor (M-CSF) secreted from osteoblasts is essential in osteoclastgenesis, and the secretion is stimulated by transforming growth factor-β (TGF-β). The aim of this study is to elucidate the effects of oncostatin M on the TGF-β-induced M-CSF synthesis in osteoblast-like MC3T3-E1 cells and the underlying mechanisms. Oncostatin M attenuated the TGF-β-stimulated M-CSF release and the mRNA expressions. SMAD3 inhibitor SIS3, p38 MAP kinase inhibitor SB203580, MEK1/2 inhibitor PD98059, and SAPK/JNK inhibitor SP600125 significantly suppressed the M-CSF release. Oncostatin M suppressed the TGF-β-induced phosphorylation of p44/p42 MAP kinase and SAPK/JNK, but failed to affect the phosphorylation of SMAD3 and p38 MAP kinase. Oncostatin M attenuated the TGF-β-stimulated vascular endothelial growth factor (VEGF) release and the TGF-β-induced mRNA expressions of VEGF. These results strongly suggest that oncostatin M downregulates TGF-β signaling upstream of p44/p42 MAP kinase and SAPK/JNK, but not SMAD 2/3 and p38 MAP kinase, in osteoblasts, leading to the attenuation of M-CSF synthesis. Our findings might provide a new therapeutic strategy for the acceleration of fracture healing process.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"43 2 1","pages":"41-51"},"PeriodicalIF":1.2,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46053933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Suncus murinus as a novel model animal that is suitable for elucidating the mechanism of daily torpor. 墨丘子是一种新型的模型动物，适合于阐明日常嗜睡的机制。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2022-04-15 DOI: 10.2220/biomedres.43.53

Yuuki Horii, Kanako Okadera, Shingo Miyawaki, T. Shiina, Y. Shimizu

引用次数: 0

Consensus molecular subtyping improves the clinical usefulness of canonical tumor markers for colorectal cancer. 共识分子分型提高了结直肠癌典型肿瘤标志物的临床应用价值。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2022-01-01 DOI: 10.2220/biomedres.43.201

Hiroyasu Kagawa, Keiichi Hatakeyama, Akio Shiomi, Hitoshi Hino, Shoichi Manabe, Yusuke Yamaoka, Takeshi Nagashima, Keiichi Ohshima, Kenichi Urakami, Ken Yamaguchi

{"title":"Consensus molecular subtyping improves the clinical usefulness of canonical tumor markers for colorectal cancer.","authors":"Hiroyasu Kagawa, Keiichi Hatakeyama, Akio Shiomi, Hitoshi Hino, Shoichi Manabe, Yusuke Yamaoka, Takeshi Nagashima, Keiichi Ohshima, Kenichi Urakami, Ken Yamaguchi","doi":"10.2220/biomedres.43.201","DOIUrl":"https://doi.org/10.2220/biomedres.43.201","url":null,"abstract":"Transcriptome-based classification, such as consensus molecular subtyping, is expected to be applied to colorectal cancer (CRC). However, the relationship between molecular profiles and classical tumor markers, which are already used in clinical practice, has not been analyzed in a large cohort and remains unclear. We classified more than 1,500 Japanese patients with CRC based on consensus molecular subtyping and investigated the clinically available blood carcinoembryonic antigen (CEA) concentrations of each subgroup. To precisely distinguish CRCs, we allocated them to five subgroups, including tumors that were difficult to classify using the consensus molecular subtypes (CMSs), and extracted a heterogeneous population with somatic mutations and expression profiles that differed from those of the CMSs 1-4. For patients allocated to the CMS4 subgroup of stage III CRCs, elevated blood CEA concentrations may identify a subgroup with highly aggressive disease and contribute to improving therapeutic decisions. Furthermore, gene expression and pathway analyses of tumor and non-tumor tissues revealed that tumor immunity was \"cold\" in this subgroup with high CEA concentrations. The combination of emerging molecular profiling and classical tumor markers may have greater clinical utility than either used alone.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"43 6","pages":"201-209"},"PeriodicalIF":1.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9591832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Neonatal isoflurane exposure disturbs granule cell migration in the rat dentate gyrus. 新生儿异氟醚暴露干扰大鼠齿状回颗粒细胞迁移。

IF 1.2 4区医学

Biomedical Research-tokyo Pub Date : 2022-01-01 DOI: 10.2220/biomedres.43.1

Yosuke Uchida, Toshikazu Hashimoto, Hitoshi Saito, Koichi Takita, Yuji Morimoto

{"title":"Neonatal isoflurane exposure disturbs granule cell migration in the rat dentate gyrus.","authors":"Yosuke Uchida, Toshikazu Hashimoto, Hitoshi Saito, Koichi Takita, Yuji Morimoto","doi":"10.2220/biomedres.43.1","DOIUrl":"https://doi.org/10.2220/biomedres.43.1","url":null,"abstract":"It has been reported that neonatal isoflurane exposure causes behavioral abnormalities following neurodegeneration in animals and gamma-aminobutyric acid type A (GABAA) receptor activation during the synaptogenesis is considered to be one possible trigger. Additionally, the inhibitory effect of excitatory GABAA receptor signaling on the granule cell (GC) migration in the neonatal rat dentate gyrus (DG) was reported in a febrile seizure model. Then, we hypothesized that neonatal isoflurane exposure, which activates GABAA receptor, causes GC migration disturbances in the neonatal rat. Rat pups were injected with 5-bromo-2'-deoxyuridine (BrdU) and divided into five treatment groups, and double immunofluorescent staining targeting BrdU and homeobox prospero-like protein 1 (Prox1) was performed to examine the localization of BrdU/Prox1 colabeled cells, and then the GC migration was assessed. As a result, we found that the ectopic migration of GC after 2% isoflurane exposure on postnatal day 7 significantly increased after P21. The number of hilar ectopic GCs was influenced by the concentration of isoflurane and the exposure day but not by carbon dioxide exposure. Our main finding is that neonatal isoflurane anesthesia disturbs the migration of GCs in the rat DG, which may be one possible mechanism underlying the neurotoxicity following neonatal isoflurane anesthesia.","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":"43 1","pages":"1-9"},"PeriodicalIF":1.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39930230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3