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The Japanese government established Japan Agriculture Standards (JAS) in 1999 for the production of chicken meat using native Japanese chicken breeds, abbreviated as ‘Jidori JAS’, for the effective use of native chickens. “Jidori” means “native chickens” in Japanese. The Jidori JAS has designated the Japanese chicken breeds that were established in Japan and/or imported before the end of the Meiji period (until 1912). According to the Jidori JAS, the percentage of native blood in chickens to be marketed as certified Jidori JAS must be 50% or more. This indicates that the Japanese government has permitted the commercial production of hybrid chickens under the Jidori JAS certification. Jidori JAS was introduced to increase the number of chicks available for fattening and improve the growth performance of Jidori JAS certified production. While farmers have to buy chicks from hatcheries each time they produce poultry, this ensures stable production, and the meat quality of the chicken remains consistent. It should be noted that Jidori JAS certification does not guarantee a specific flavor for Jidori meat products. Currently, marker-assisted selection for growth improvement has been successfully implemented in Japan for several Jidori JAS-certified chickens, enhancing their growth performance.

A new term, the occupancy rate (OR) of the ancestors of a breed, defined as the proportion of autosomal genomic information inherited from a common ancestor, has been proposed. The associations between the ORs of three paternal ancestors (Tajiri, Kedaka, and Fujiyoshi) of Japanese Black cattle (JBK) and carcass traits of the progeny of sire candidates were analyzed using data from the field progeny test conducted by the Livestock Improvement Association of Japan. The results suggest that further Kedaka OR accumulation will positively affect beef marbling score (BMS) and carcass weight (CW) and further Fujiyoshi OR accumulation will positively affect BMS. Thus, the optimal range that intersects the Fujiyoshi and Kedaka proportions produce the best CW and BMS. Moreover, further Tajiri OR accumulation negatively affects CW. Additionally, further Tajiri OR accumulation will positively affect BMS, but the effect is less than those of Kedaka and Fujiyoshi ORs. I conclude that the OR is a useful index for evaluating economic traits in animal genetic resources. Sustainable livestock industry development plays a crucial role in achieving Sustainable Development Goals. Maintaining genetic diversity is crucial for conserving animal genetic resources. The genetic diversity of cattle breeds, particularly in developed countries, has rapidly decreased owing to the introduction of artificial insemination using frozen semen in the 1960s. This is due to the limited number of sires with high productivity used for offspring production, even after they pass away. In beef and dairy cattle, sire candidate performance has been evaluated primarily using the economic traits of their progeny meat and production as indexes. Therefore, sire breeding is time-consuming and laborious. My goal is to establish an innovative sire breeding program that utilizes innovative selection indexes to minimize the time and effort required.

This study analyzed outcomes of systemic chemotherapy for advanced neuroendocrine carcinoma (NEC) of the digestive system. Clinical data from 258 patients with unresectable or recurrent NEC of the gastrointestinal tract (GI) or hepato‐biliary‐pancreatic system (HBP), who received chemotherapy, were collected from 23 Japanese institutions and analyzed retrospectively. Patients had primary sites in the esophagus (n = 85), stomach (n = 70), small bowel (n = 6), colorectum (n = 31), hepato‐biliary system (n = 31) and pancreas (n = 31). Median overall survival (OS) was 13.4 months the esophagus, 13.3 months for the stomach, 29.7 months for the small bowel, 7.6 months for the colorectum, 7.9 months for the hepato‐biliary system and 8.5 months for the pancreas. Irinotecan plus cisplatin (IP) and etoposide plus cisplatin (EP) were most commonly selected for GI‐NEC and HBP‐NEC. For patients treated with IP/EP (n = 160/46), the response rate was 50/28% and median OS was 13.0/7.3 months. Multivariate analysis among patients treated with IP or EP showed that the primary site (GI vs HBP; hazard ratio [HR] 0.58, 95% confidence interval [CI] 0.35–0.97) and baseline serum lactate dehydrogenase levels (not elevated vs elevated; HR 0.65, 95% CI 0.46–0.94) were independent prognostic factors for OS, while the efficacy of IP was slightly better than for EP (HR 0.80, 95% CI 0.48–1.33; P = 0.389). IP and EP are the most common treatment regimens for NEC of the digestive system. HBP primary sites and elevated lactate dehydrogenase levels are unfavorable prognostic factors for survival. A randomized controlled trial is required to establish the appropriate chemotherapy regimen for advanced NEC of the digestive system. This study was registered at UMIN as trial number 000005176. Clinical data from patients with unresectable or recurrent NEC of the gastrointestinal tract (GI) or hepato‐biliary‐pancreatic system (HBP), who received chemotherapy, were collected from 23 Japanese institutions and analyzed retrospectively. This study included 258 patients. Multivariate analysis among the patients treated with IP or EP showed that the primary site (GI vs. HBP; HR 0.58, 95% CI 0.35–0.97) and baseline serum lactate dehydrogenase (LDH) levels (not elevated vs elevated; HR 0.65, 95% CI 0.46–0.94) were independent prognostic factors for OS, while the efficacy of IP was slightly better than EP (HR 0.80, 95% CI 0.48–1.33; P = 0.389).

The solid tumour microenvironment includes nerve fibres that arise from the peripheral nervous system 1 , 2 . Recent work indicates that newly formed adrenergic nerve fibres promote tumour growth, but the origin of these nerves and the mechanism of their inception are unknown 1 , 3 . Here, by comparing the transcriptomes of cancer-associated trigeminal sensory neurons with those of endogenous neurons in mouse models of oral cancer, we identified an adrenergic differentiation signature. We show that loss of TP53 leads to adrenergic transdifferentiation of tumour-associated sensory nerves through loss of the microRNA miR-34a. Tumour growth was inhibited by sensory denervation or pharmacological blockade of adrenergic receptors, but not by chemical sympathectomy of pre-existing adrenergic nerves. A retrospective analysis of samples from oral cancer revealed that p53 status was associated with nerve density, which was in turn associated with poor clinical outcomes. This crosstalk between cancer cells and neurons represents mechanism by which tumour-associated neurons are reprogrammed towards an adrenergic phenotype that can stimulate tumour progression, and is a potential target for anticancer therapy. MicroRNAs from head and neck cancer cells, shuttled to sensory neurons by extracellular vesicles, cause a shift to an adrenergic neuronal phenotype that promotes tumour progression.

It is well known that corrosion protection of pure Al is enormously improved by the formation of porous anodic oxide films and by pore sealing treatment. However, the effects of anodizing and pore sealing on corrosion protection for Al alloys are unclear, because the alloying elements included in Al alloys affect the structure of anodic oxide films. In the present study, porous anodic oxide films are formed on pure Al, 1050-, 3003- and 5052-Al alloys, and pore sealing was carried out in boiling water. Changes in the structure and corrosion protection ability of porous anodic oxide films on pure Al and the Al alloys by pore sealing, were examined by scanning electron microscopy (SEM) and electrochemical impedance spectroscopy (EIS). SEM observation showed that anodic oxide films formed on pure Al have a smooth surface after pore sealing, and that cracks are formed in anodic oxide films on 1050-, 3003- and 5052-aluminum alloys, after pore sealing. Corrosion protection after pore sealing increased with anodizing time on pure Al, but only slightly increased with anodizing time on the Al alloys.

Recurrent, metastatic disease represents the most frequent cause of death for patients with thyroid cancer, and radioactive iodine (RAI) remains a mainstay of therapy for these patients. Unfortunately, many thyroid cancer patients have tumors that no longer trap iodine, and hence are refractory to RAI, heralding a poor prognosis. RAI-refractory (RAI-R) cancer cells result from the loss of thyroid differentiation features, such as iodide uptake and organification. This loss of differentiation features correlates with the degree of mitogen-activated protein kinase (MAPK) activation, which is higher in tumors with BRAF (B-Raf proto-oncogene) mutations than in those with RTK (receptor tyrosine kinase) or RAS (rat sarcoma) mutations. Hence, inhibition of the mitogen-activated protein kinase kinase-1 and -2 (MEK-1 and -2) downstream of RAF (rapidly accelerated fibrosarcoma) could sensitize RAI refractivity in thyroid cancer. However, a significant hurdle is the development of secondary tumor resistance (escape mechanisms) to these drugs through upregulation of tyrosine kinase receptors or another alternative signaling pathway. The sodium iodide symporter (NIS) is a plasma membrane glycoprotein, a member of solute carrier family 5A (SLC5A5), located on the basolateral surfaces of the thyroid follicular epithelial cells, which mediates active iodide transport into thyroid follicular cells. The mechanisms responsible for NIS loss of function in RAI-R thyroid cancer remains unclear. In a study of patients with recurrent thyroid cancer, expression levels of specific ribosomal machinery—namely PIGU (phosphatidylinositol glycan anchor biosynthesis class U), a subunit of the GPI (glycosylphosphatidylinositol transamidase complex—correlated with RAI avidity in radioiodine scanning, NIS levels, and biochemical response to RAI treatment. Here, we review the proposed mechanisms for RAI refractivity and the management of RAI-refractive metastatic, recurrent thyroid cancer. We also describe novel targeted systemic agents that are in use or under investigation for RAI-refractory disease, their mechanisms of action, and their adverse events.

Advances in narrowband imaging (NBI) have revealed that squamous epithelial lesions form alongside changes in squamous epithelial cells and intrapapillary capillary loops (IPCLs) in the head and neck. However, the molecular interactions between squamous epithelial cells and endothelial cells (ECs) that promote IPCL proliferation are unclear. This study aimed to identify the mechanisms of cooperation between parenchymal squamous cells and stromal IPCLs during the formation of head and neck squamous cell carcinoma (SCC). We investigated ligand‐receptor interactions between squamous epithelial and endothelial cells of IPCLs using Visium analysis on frozen, formalin‐fixed and paraffin‐embedded (FFPE) tissues from hypopharyngeal squamous epithelial lesions. We examined the protein expression in hypopharyngeal superficial squamous epithelial lesions using immunohistochemistry and immunofluorescence. mRNA expression levels of these genes in SCC and non‐tumor tissues were analyzed using RT‐qPCR. Phenotypic changes were analyzed by inducing candidate genes into SCC cell lines via a lentivirus system. Visium analysis revealed that Fibronectin 1 (FN1) acted as a ligand in endothelial cells, Cellular communication network factor 1 (CCN1) as a ligand in SCC cells, and Integrin subunit alpha V (ITGAV) as a receptor for both FN1 and CCN1. The expression of these three candidates increased in low‐grade dysplasia, an early stage of neoplastic lesions, and was significantly higher in invasive SCCs, except for CCN1. When ITGAV was introduced into SCC cell lines (FaDu and Detroit 562) and HaCaT cells treated with FN1, the cells showed increased proliferation ability. SCC develops via ligand‐receptor molecular interactions between squamous epithelial and vascular endothelial cells in IPCLs. SCC develops via ligand‐receptor molecular interactions between squamous epithelial and vascular endothelial cells in IPCLs.

Red-emitting CaTiO 3 :Pr 3+ phosphor nanoparticles were synthesized by a sol–gel method with a final heat treatment at a low temperature of 650 °C. For comparison, the CaTiO 3 :Pr 3+ phosphor was also synthesized by a conventional solid-state reaction method conducted at 1250 °C. The two kinds of resultant CaTiO 3 :Pr 3+ samples were revealed to differ largely in their microstructure and optical properties. Diffuse reflectance and photoluminescence measurements suggested that the sample from the solid-state reaction possessed a larger number of defects, which would deteriorate the optical properties, due to heating at high temperature. On the other hand, the sol–gel-derived sample exhibited much better optical properties and thus it was used for evaluating optical-switching phenomena upon redox treatments. In photoluminescence, three excitation bands were observed at 265, 335, and 375 nm for the red emission of the CaTiO 3 :Pr 3+ sample, and one of them (375 nm) was more effective for inducing luminescence quenching by a reduction treatment at room temperature. A body color of the CaTiO 3 :Pr 3+ sample was also changed from white to light yellow by the reduction due to the enhanced visible-light absorption. Such the dual luminescence/absorption switching was shown to be reversible with a subsequent oxidation and repeatable with a consecutive redox treatment. Graphical abstract Highlights CaTiO 3 :Pr 3+ phosphor nanoparticles were synthesized at low temperature by a sol–gel method. The nanoparticles showed more stable photoluminescence than larger particles obtained by a solid-state reaction method. Photoluminescence intensity of the nanoparticles was responsive to redox treatments at room temperature. A body color of the nanoparticles was also responsive to redox treatments, resulting in dual luminescence/absorption switching.

Background It has become clear that the intestinal microbiota plays a role in food allergies. The objective of this study was to assess the food allergy-preventive effects of combined intake of a short fructan (1-kestose [Kes]) and a long fructan (inulin ([Inu]) in an ovalbumin (OVA)-induced food allergy mouse model. Results Oral administration of fructans lowered the allergenic symptom score and alleviated the decreases in rectal temperature and total IgA levels and increases in OVA-specific IgE and IgA levels induced by high-dose OVA challenge, and in particular, combined intake of Kes and Inu significantly suppressed the changes in all these parameters. The expression of the pro-inflammatory cytokine IL-4, which was increased in the allergy model group, was significantly suppressed by fructan administration, and the expression of the anti-inflammatory cytokine IL-10 was significantly increased upon Kes administration. 16 S rRNA amplicon sequencing of the gut microbiota and beta diversity analysis revealed that fructan administration may induce gut microbiota resistance to food allergy sensitization, rather than returning the gut microbiota to a non-sensitized state. The relative abundances of the genera Parabacteroides B 862,066 and Alloprevotella , which were significantly reduced by food allergy sensitization, were restored by fructan administration. In Parabacteroides , the relative abundances of Parabacteroides distasonis , Parabacteroides goldsteinii , and their fructan-degrading glycoside hydrolase family 32 gene copy numbers were increased upon Kes or Inu administration. The concentrations of short-chain fatty acids (acetate and propionate) and lactate were increased by fructan administration, especially significantly in the Kes + Inu, Kes, and Inu-fed (Inu, Kes + Inu) groups. Conclusion Combined intake of Kes and Inu suppressed allergy scores more effectively than single intake, suggesting that Kes and Inu have different allergy-preventive mechanisms. This indicates that the combined intake of these short and long fructans may have an allergy-preventive benefit.

Comprehensive genomic profiling (CGP) is being increasingly used for the routine clinical management of solid cancers. In July 2018, the use of tumor tissue‐based CGP assays became available for all solid cancers under the universal health insurance system in Japan. Several restrictions presently exist, such as patient eligibility and limitations on the opportunities to perform such assays. The clinical implementation of CGP based on plasma circulating tumor DNA (ctDNA) is also expected to raise issues regarding the selection and use of tissue DNA and ctDNA CGP. A Joint Task Force for the Promotion of Cancer Genome Medicine comprised of three Japanese cancer‐related societies has formulated a policy proposal for the appropriate use of plasma CGP (in Japanese), available at https://www.jca.gr.jp/researcher/topics/2021/files/20210120.pdf, http://www.jsco.or.jp/jpn/user_data/upload/File/20210120.pdf, and https://www.jsmo.or.jp/file/dl/newsj/2765.pdf. Based on these recommendations, the working group has summarized the respective advantages and cautions regarding the use of tissue DNA CGP and ctDNA CGP with reference to the advice of a multidisciplinary expert panel, the preferred use of plasma specimens over tissue, and multiple ctDNA testing. These recommendations have been prepared to maximize the benefits of performing CGP assays and might be applicable in other countries and regions.