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Current Status of Whole Slide Image (WSI) Standardization in Japan. 日本全幻灯片图像(WSI)标准化现状。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-06-29 Epub Date: 2022-06-25 DOI: 10.1267/ahc.22-00009
Ichiro Mori

A whole slide image (WSI) is a digitized microscopic image that is particularly useful in histochemistry and cytochemistry. Several WSI scanners have been introduced in Japan and all use their own native format. Thus, there is basically no interchangeability. However, the Digital Imaging and Communications in Medicine (DICOM) standard format for WSI has been available since 2010. In this review, the configuration and differences among the native WSI and DICOM formats are examined, and the advantages and issues of DICOM standardization are discussed.

全幻灯片图像(WSI)是一种数字化的显微图像,在组织化学和细胞化学中特别有用。日本已经引进了几种WSI扫描仪,它们都使用自己的本机格式。因此,基本上没有互换性。然而,自2010年以来,WSI的数字成像和医学通信(DICOM)标准格式已经可用。本文分析了本地WSI和DICOM格式的配置和差异,并讨论了DICOM标准化的优点和问题。
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引用次数: 1
A Histochemical Analysis of Neurofibrillary Tangles in Olfactory Epithelium, a Study Based on an Autopsy Case of Juvenile Alzheimer's Disease. 嗅觉上皮中神经原纤维缠结的组织化学分析,基于一例青少年阿尔茨海默病的尸检研究。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-06-29 Epub Date: 2022-06-25 DOI: 10.1267/ahc.22-00048
Shino Shimizu, Ichiro Tojima, Keigo Nakamura, Hideaki Kouzaki, Takeshi Kanesaka, Norihiro Ogawa, Yoshio Hashizume, Hiroyasu Akatsu, Akira Hori, Ikuo Tooyama, Takeshi Shimizu

The pathological changes of Alzheimer's disease (AD) begin 10-20 years before clinical onset, and it is therefore desirable to identify effective methods for early diagnosis. The nasal mucosa is a target tissue for measuring AD-related biomarkers because the olfactory nerve is the only cranial nerve that is exposed to the external environment. We describe an autopsy case of rapidly advanced juvenile AD (JAD), focusing on the olfactory system. The formation of senile plaques, neurofibrillary tangles (NFTs), and neuropil threads was examined in the temporal cortex, hippocampus, olfactory bulb, and olfactory and respiratory epithelia in the bilateral olfactory clefts. Neurodegenerative changes in the olfactory and respiratory epithelia and the pathological deposition of amyloid β42 (Aβ42) and phosphorylated tau were also examined. As a result, senile plaques, NFTs, and neuropil threads were found in the temporal cortex, hippocampus, and olfactory bulb. NFTs were also found in the olfactory epithelium. Degenerated olfactory cells and their axons stained positive for phosphorylated tau. Supporting cells in the degenerated olfactory epithelium stained positive for Aβ42. In conclusion, pathological biomarkers of AD were expressed in the degenerated olfactory epithelium of this JAD patient. This observation suggests that nasal samples may be useful for the diagnosis of AD.

阿尔茨海默病(AD)的病理变化在临床发病前10-20年就开始了,因此需要找到有效的早期诊断方法。鼻黏膜是测量ad相关生物标志物的靶组织,因为嗅觉神经是唯一暴露于外部环境的颅神经。我们描述了一个快速晚期青少年AD (JAD)的尸检病例,重点是嗅觉系统。在双侧嗅裂的颞叶皮层、海马、嗅球、嗅上皮和呼吸上皮中检测老年斑、神经原纤维缠结(nft)和神经丝的形成。嗅觉和呼吸上皮的神经退行性改变以及淀粉样蛋白β42 (Aβ42)和磷酸化tau的病理沉积也被检查。结果,在颞叶皮层、海马体和嗅球中发现了老年斑、nft和神经丝。在嗅上皮中也发现了nft。退化的嗅觉细胞及其轴突磷酸化tau蛋白呈阳性。变性嗅上皮内的支持细胞a - β42染色阳性。综上所述,AD的病理生物标志物在该JAD患者退化的嗅上皮中表达。这一观察结果表明,鼻腔样本可能对阿尔茨海默病的诊断有用。
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引用次数: 1
Pulmonary Neuroendocrine Cells and Small Cell Lung Carcinoma: Immunohistochemical Study Focusing on Mechanisms of Neuroendocrine Differentiation. 肺神经内分泌细胞与小细胞肺癌:神经内分泌分化机制的免疫组化研究。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-06-29 Epub Date: 2022-05-24 DOI: 10.1267/ahc.22-00031
Takaaki Ito, Shinji Kudoh, Kosuke Fujino, Mune Sanada, Yuki Tenjin, Haruki Saito, Yuko Nakaishi-Fukuchi, Hiroki Kameyama, Takaya Ichimura, Naoko Udaka, Noritaka Kudo, Akira Matsuo, Younosuke Sato

Neuroendocrine (NE) differentiation has been histochemically detected in normal and cancer tissues and cells. Immunohistochemical analyses have provided a more detailed understanding of NE biology and pathology. Pulmonary NE cells are a rare lung epithelial type, and small cell carcinoma of the lung (SCLC) is a high-grade NE tumor. Pulmonary NE and SCLC cells share common mechanisms for NE differentiation. Neural or NE cell lineage-specific transcription factors, such as achaete-scute homologue 1 (Ascl1) and insulinoma-associated protein 1 (INSM1), are crucial for the development of pulmonary NE cells, and NE differentiation is influenced by the balance between Ascl1 and the suppressive neural transcription factor, hairy-enhancer of split 1, a representative target molecule of the Notch signaling pathway. In this review, we discuss the importance of Ascl1 and INSM1 in identifying pulmonary NE and SCLC cells and introduce Ascl1-related molecules detected by comparative RNA-sequence analyses. The molecular classification of SCLC based on the expression of lineage-specific transcription or co-transcription factors, including ASCL1, NEUROD1, POU2F3, and YAP1, was recently proposed. We attempted to characterize these 4 SCLC subtypes using integrated immunohistochemical studies, which will provide insights into the molecular characteristics of these subtypes and clarify the inter- and intratumor heterogeneities of SCLC.

神经内分泌(NE)分化已在正常和癌组织和细胞中被组织化学检测到。免疫组织化学分析为NE的生物学和病理学提供了更详细的了解。肺NE细胞是一种罕见的肺上皮类型,肺小细胞癌(SCLC)是一种高级别的NE肿瘤。肺NE和SCLC细胞具有相同的NE分化机制。神经或NE细胞谱系特异性转录因子,如无毛鳞片同源物1 (Ascl1)和胰岛素瘤相关蛋白1 (INSM1),对肺NE细胞的发育至关重要,而NE的分化受Ascl1与抑制神经转录因子、分裂1的毛发增强因子(Notch信号通路的代表性靶分子)之间的平衡影响。在这篇综述中,我们讨论了Ascl1和INSM1在鉴别肺NE和SCLC细胞中的重要性,并介绍了通过比较rna序列分析检测到的Ascl1相关分子。最近提出了基于谱系特异性转录或共转录因子(包括ASCL1、NEUROD1、POU2F3和YAP1)表达的SCLC分子分类。我们试图利用综合免疫组织化学研究来表征这4种SCLC亚型,这将为这些亚型的分子特征提供见解,并阐明SCLC肿瘤间和肿瘤内的异质性。
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引用次数: 2
Colonic Lymphoid Follicle Hyperplasia after Gastrectomy in Rats 大鼠胃切除术后结肠淋巴滤泡增生
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-04-23 DOI: 10.1267/ahc.22-00015
Tomoko Kagiya, K. Shiogama, K. Inada, H. Utsunomiya, Masayuki Kitano
Nodular lymphoid hyperplasia (NLH) of the human colon has been associated with multiple diseases and symptoms. Causes include food allergies, infections, inflammatory bowel disease, and immunodeficiency, and gastrectomy is not usually considered to be the etiology. Nine rats two weeks after total gastrectomy and 12 control rats were sacrificed and submitted for histological examination. In the gastrectomy group, we found lymphoid hyperplasia throughout the entire colon mucosa. The cross-sectional area of lymphoid follicles was increased to be five-fold larger than that in the rats in the control group (sham surgery). Lymphoid follicles were classified into primary and secondary follicles according to the presence/absence of germinal centers; the gastrectomy group had a significantly larger number of secondary follicles. When T cell and B cell classification of lymphocytes was performed, there was no difference between gastrectomy and control groups at T:B = 40:60. When the lymphoid follicles were classified, the proportion of T lymphocytes increased in the secondary follicle (T:B = 40:60) compared with in the primary follicle (T:B = 20:80). Gastrectomy significantly activated lymphocytic intestinal immunity by altering the intestinal environment, causing colonic NLH. Gastrectomy in rats is a good animal model for the study of NLH in colorectal diseases.
人类结肠结节性淋巴样增生(NLH)与多种疾病和症状有关。病因包括食物过敏、感染、炎症性肠病和免疫缺陷,而胃切除术通常不被认为是病因。全胃切除2周后处死大鼠9只,对照组12只,行组织学检查。在胃切除术组,我们发现淋巴样增生遍及整个结肠粘膜。淋巴滤泡横截面积比对照组(假手术)大5倍。根据生发中心的有无,将淋巴滤泡分为原发性和继发性;胃切除术组的继发卵泡数量明显增多。当进行淋巴细胞T细胞和B细胞分类时,在T:B = 40:60时,胃切除术组与对照组之间无差异。对淋巴滤泡进行分类时,继发滤泡(T:B = 40:60)中T淋巴细胞的比例高于原发性滤泡(T:B = 20:80)。胃切除术通过改变肠道环境显著激活肠道淋巴细胞免疫,引起结肠NLH。大鼠胃切除术是研究NLH在结直肠疾病中的良好动物模型。
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引用次数: 0
Histomorphological Changes in a Rat Model of Polycystic Ovary Syndrome and the Contribution of Stevia Leaf Extract in Modulating the Ovarian Fibrosis, VEGF, and TGF-β Immunoexpressions: Comparison with Metformin. 多囊卵巢综合征大鼠模型的组织形态学改变及甜菊叶提取物对卵巢纤维化、VEGF和TGF-β免疫表达的调节作用:与二甲双胍的比较
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-02-26 Epub Date: 2022-01-27 DOI: 10.1267/ahc.21-00081
Ahmed A Morsi, Ezat A Mersal, Abdel Razik H Farrag, Ahmed M Abdelmoneim, Alshaymaa M Abdelmenem, Mohamed S Salim

Polycystic ovary syndrome (PCOS) is a common endocrine disorder of fertile females. It has been reported that stevia leaf extract (SLE) has antidiabetic and antihyperlipidemic properties. Therefore, the current study hypothesized and investigated the role and mechanistic aspects of a natural sweetener; SLE in treating a rat model of letrozole-induced PCOS and to compare it with metformin. Thirty-five female Wistar albino rats were divided into 5 groups: control, PCOS-induced group (letrozole, 1 mg/kg/d, for 21 days), SLE, metformin, and combination-treated groups (300 mg/kg/d, for the next 28 days in SLE and metformin-treated groups). Vaginal smears were done. The levels of glucose, lipid, and hormonal profiles were measured in the serum meanwhile, malonyl dialdehyde (MDA), superoxide dismutase (SOD), and tumour necrosis factor (TNF-α) were measured in the ovary. Ovarian sections were subjected to hematoxylin and eosin, Masson, and immunohistochemical identification of VEGF and TGF-β followed by morphometric analysis. PCOS rats showed altered hormonal and lipid profiles, in addition to hyperglycemia. Also, the ovarian tissue levels of MDA and TNF-α were elevated, and SOD was decreased. Numerous cystic follicles, decrease/absence of corpora lutea, interstitial fibrosis with positive VEGF and TGF-β immunoreactivity were evident. SLE improved all altered parameters. SLE showed potential therapeutic merits in letrozole-induced PCOS via anti-inflammatory, antioxidant, anti-fibrotic, and angiogenesis regulating mechanisms. Its effects were almost comparable to metformin, and the combination of both has no further synergistic effect.

多囊卵巢综合征(PCOS)是一种常见于生殖期女性的内分泌疾病。据报道,甜菊叶提取物(SLE)具有抗糖尿病和抗高血脂的特性。因此,目前的研究假设并调查了天然甜味剂的作用和机制方面;SLE治疗来曲唑诱导的多囊卵巢综合征大鼠模型并与二甲双胍比较。将35只雌性Wistar白化大鼠分为5组:对照组、pcos诱导组(来曲唑,1 mg/kg/d,持续21 d)、SLE、二甲双胍和联合治疗组(SLE和二甲双胍治疗组,300 mg/kg/d,持续28 d)。进行阴道涂片检查。测定血清中葡萄糖、血脂和激素水平,同时测定卵巢中丙二醛(MDA)、超氧化物歧化酶(SOD)和肿瘤坏死因子(TNF-α)。卵巢切片进行苏木精、伊红、马松染色,免疫组化检测VEGF和TGF-β,并进行形态计量学分析。多囊卵巢综合征大鼠除了高血糖外,还表现出激素和脂质谱的改变。卵巢组织MDA、TNF-α水平升高,SOD水平降低。可见大量囊泡,黄体减少或缺失,间质纤维化伴VEGF和TGF-β免疫反应阳性。SLE改善了所有改变的参数。SLE通过抗炎、抗氧化、抗纤维化和血管生成调节机制在来曲唑诱导的多囊卵巢综合征中显示出潜在的治疗优势。其作用几乎与二甲双胍相当,两者联合使用没有进一步的协同作用。
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引用次数: 0
Identification of Brain Regions Activated by Sevoflurane and Propofol and Regional Changes in Gene Expression 七氟醚和异丙酚激活脑区的鉴定及基因表达的区域变化
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-02-22 DOI: 10.1267/ahc.21-00091
N. Kamei, Shimpei Higo, Tomoki Mizuno, Keisuke Mori, A. Sakamoto, H. Ozawa
General anesthetics have different efficacies and side effect incidences based on their mechanism of action. However, detailed comparative studies of anesthetics are incomplete. In this study, target brain regions and gene expression changes in these brain regions were determined for sevoflurane and propofol to understand the mechanisms that cause differences among anesthetics. Rats were anesthetized with sevoflurane or propofol for 1 hr, and brain regions with anesthesia-induced changes in neuronal activity were examined by immunohistochemistry and in situ hybridization for c-Fos. Among the identified target brain regions, gene expression analysis was performed in the habenula, the solitary nucleus and the medial vestibular nucleus from laser microdissected samples. Genes altered by sevoflurane and propofol were different and included genes involved in the incidence of postoperative nausea and vomiting and emergence agitation, such as Egr1 and Gad2. GO enrichment analysis showed that the altered genes tended to be evenly distributed in all functional category. The detailed profiles of target brain regions and induced gene expression changes of sevoflurane and propofol in this study will provide a basis for analyzing the effects of each anesthetic agent and the risk of adverse events.
全身麻醉剂根据其作用机制有不同的疗效和副作用发生率。然而,麻醉剂的详细比较研究尚不完整。在这项研究中,确定了七氟醚和丙泊酚的靶脑区域和这些脑区域的基因表达变化,以了解导致麻醉剂之间差异的机制。用七氟醚或丙泊酚麻醉大鼠1小时,并通过免疫组织化学和c-Fos原位杂交检测麻醉诱导的神经元活动变化的大脑区域。在确定的靶脑区域中,对激光显微切割样本的缰核、孤立核和前庭内侧核进行了基因表达分析。七氟醚和丙泊酚改变的基因是不同的,包括与术后恶心呕吐和苏醒激动发生率有关的基因,如Egr1和Gad2。GO富集分析表明,改变的基因倾向于均匀分布在所有功能类别中。本研究中七氟醚和丙泊酚靶脑区域的详细图谱和诱导的基因表达变化将为分析每种麻醉剂的效果和不良事件的风险提供基础。
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引用次数: 2
Specific Expression of KCC2 in the α Cells of Normal and Type 1 Diabetes Model Mouse Pancreatic Islets KCC2在正常和1型糖尿病模型小鼠胰岛α细胞中的特异性表达
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-02-22 DOI: 10.1267/ahc.21-00078
C. Shimizu-Okabe, Shigeki Okada, S. Okamoto, H. Masuzaki, C. Takayama
Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the mature brain; however, it acts excitatory during development. This difference in action depends on the intracellular chloride ion concentration, primarily regulated by potassium chloride co-transporter2 (KCC2). Sufficient KCC2 expression results in its inhibitory action. GABA is also abundant in pancreatic islets, where it acts differentially on the islet cells, and is involved in carbohydrate metabolism. However, the mechanisms underlying the differential action remain unknown. We performed immunohistochemistry for glutamic acid decarboxylase (GAD), a synthetic enzyme for GABA, and KCC2 in normal adult islets. GAD was co-localized with insulin in β cells, whereas KCC2 was expressed in glucagon-positive α cells. These results are in line with previous observations that GABA decreases glucagon release but increases insulin release, and suggest that GABA and insulin may work together in reducing blood glucose levels under hyperglycemia. Next, we examined the streptozotocin-induced type1 diabetes mellitus mouse model. GAD and insulin expression levels were markedly decreased. KCC2 was expressed in glucagon-positive cells, whereas insulin- and somatostatin-positive cells were KCC2-negative. These findings suggest that in diabetes model, reduced GABA release may cause disinhibition of glucagon release, resulting in increased blood sugar levels and the maintenance of hyperglycemic state.
γ-氨基丁酸(GABA)是成熟大脑中的一种抑制性神经递质;然而,它在发育过程中起兴奋作用。这种作用差异取决于细胞内氯离子浓度,主要由氯化钾共转运蛋白2(KCC2)调节。充分的KCC2表达导致其抑制作用。GABA在胰岛中也很丰富,它对胰岛细胞有不同的作用,并参与碳水化合物代谢。然而,差异作用的机制仍然未知。我们对正常成年胰岛中的谷氨酸脱羧酶(GAD)、GABA的合成酶和KCC2进行了免疫组织化学检测。GAD与胰岛素在β细胞中共定位,而KCC2在胰高血糖素阳性的α细胞中表达。这些结果与先前的观察结果一致,即GABA降低胰高血糖素的释放,但增加胰岛素的释放,并表明GABA和胰岛素可能在高血糖下共同降低血糖水平。接下来,我们检测链脲佐菌素诱导的1型糖尿病小鼠模型。GAD和胰岛素表达水平显著降低。KCC2在胰高血糖素阳性细胞中表达,而胰岛素和生长抑素阳性细胞为KCC2阴性。这些发现表明,在糖尿病模型中,GABA释放减少可能会导致胰高血糖素释放的抑制作用减弱,导致血糖水平升高并维持高血糖状态。
{"title":"Specific Expression of KCC2 in the α Cells of Normal and Type 1 Diabetes Model Mouse Pancreatic Islets","authors":"C. Shimizu-Okabe, Shigeki Okada, S. Okamoto, H. Masuzaki, C. Takayama","doi":"10.1267/ahc.21-00078","DOIUrl":"https://doi.org/10.1267/ahc.21-00078","url":null,"abstract":"Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the mature brain; however, it acts excitatory during development. This difference in action depends on the intracellular chloride ion concentration, primarily regulated by potassium chloride co-transporter2 (KCC2). Sufficient KCC2 expression results in its inhibitory action. GABA is also abundant in pancreatic islets, where it acts differentially on the islet cells, and is involved in carbohydrate metabolism. However, the mechanisms underlying the differential action remain unknown. We performed immunohistochemistry for glutamic acid decarboxylase (GAD), a synthetic enzyme for GABA, and KCC2 in normal adult islets. GAD was co-localized with insulin in β cells, whereas KCC2 was expressed in glucagon-positive α cells. These results are in line with previous observations that GABA decreases glucagon release but increases insulin release, and suggest that GABA and insulin may work together in reducing blood glucose levels under hyperglycemia. Next, we examined the streptozotocin-induced type1 diabetes mellitus mouse model. GAD and insulin expression levels were markedly decreased. KCC2 was expressed in glucagon-positive cells, whereas insulin- and somatostatin-positive cells were KCC2-negative. These findings suggest that in diabetes model, reduced GABA release may cause disinhibition of glucagon release, resulting in increased blood sugar levels and the maintenance of hyperglycemic state.","PeriodicalId":6888,"journal":{"name":"Acta Histochemica Et Cytochemica","volume":"55 1","pages":"47 - 56"},"PeriodicalIF":2.4,"publicationDate":"2022-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44680212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Immunolocalization of CD80 and CD86 in Non-Small Cell Lung Carcinoma: CD80 as a Potent Prognostic Factor CD80和CD86在非小细胞肺癌中的免疫定位:CD80是一个有效的预后因素
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-02-11 DOI: 10.1267/ahc.21-00075
Takashi Sato, K. Takagi, M. Higuchi, H. Abe, Michie Kojimahara, Miho Sagawa, Megumi Tanaki, Y. Miki, Takashi Suzuki, H. Hojo
It has been demonstrated that tumor cells express programed cell death protein 1 (PD-L1) to escape T lymphocytes that express programed cell protein 1 (PD-1), and PD-1/PD-L1 immune checkpoint inhibitors have been regarded in lung cancer patients. CD80 and CD86 are members of B7 superfamily which regulates T lymphocyte activation and tolerance. However, immunolocalization of CD80 and CD86 has not been examined in the lung carcinoma tissues and their clinical significance remains unknown. Therefore, to clarify clinical significance of CD80 and CD86, we immunolocalized these in 75 non-small cell lung carcinomas (NSCLC) in this study. Immunoreactivities of CD80 and CD86 were mainly detected in tumor-infiltrating macrophages. Immunohistochemical CD80 status was high in 56% of NSCLC, and it was positively associated with stage, pathological T factor, distant metastasis, histological type and PD-L1 status. Moreover, multivariate analysis turned out that the CD80 status was an independent worse prognostic factor. CD86 status was high in 53% of the cases, but it was not significantly associated with any clinicopathological parameters. These findings suggest that CD80 is a potent worse prognostic factor possibly in association with escape from immune attack in NSCLC.
已经证明,肿瘤细胞表达程序性细胞死亡蛋白1(PD-L1)以逃避表达程序化细胞蛋白1(PD-1)的T淋巴细胞,并且PD-1/PD-L1免疫检查点抑制剂已被认为存在于癌症患者中。CD80和CD86是调节T淋巴细胞活化和耐受的B7超家族成员。然而,CD80和CD86的免疫定位尚未在肺癌组织中进行检测,其临床意义尚不清楚。因此,为了阐明CD80和CD86的临床意义,我们在本研究中对75例非小细胞肺癌(NSCLC)进行了免疫定位。CD80和CD86的免疫反应性主要在肿瘤浸润的巨噬细胞中检测到。免疫组织化学CD80在56%的NSCLC中高表达,并且与分期、病理T因子、远处转移、组织学类型和PD-L1状态呈正相关。此外,多变量分析表明,CD80状态是一个独立的预后较差的因素。53%的病例中CD86状态较高,但与任何临床病理参数均无显著相关性。这些发现表明,CD80是一种潜在的更差预后因素,可能与NSCLC免疫攻击的逃避有关。
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引用次数: 3
Histochemistry, Cytochemistry and Epigenetics 组织化学、细胞化学和表观遗传学
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2022-02-11 DOI: 10.1267/ahc.21-00095
S. Kitazawa, Teruyuki Ohno, Ryuma Haraguchi, R. Kitazawa
Over the past few decades, many researchers have individually identified tumor-related genes, and have accumulated information on their basic research in a database. With the development of technology that can comprehensively test the expression status within a short time, oncogene panel testing has become attainable. On the other hand, changes in gene expression that do not depend on changes in base sequences, that is, epigenetics, or more comprehensively, epigenomes, are also highly involved in the development and progression of disease. Oncogene panel tests tend to focus on DNA base mutations such as point mutations, deletions, duplications, and chimera formation. Elucidation leads to correct interpretation of diseases and treatment choices, and we are in an era where integrated understanding of the genome and epigenome is indispensable. In this review, we make every effort to cover a wide range of knowledge, including data on histone protein modification, non-coding (nc)RNA and DNA methylation, and recent application trials for demonstrating epigenetic alterations in histologic and cytologic specimens. We hope this review will help marshal the knowledge accumulated by researchers involved in genomic and epigenomic studies.
在过去的几十年里,许多研究人员已经单独鉴定了肿瘤相关基因,并在数据库中积累了他们基础研究的信息。随着能够在短时间内全面检测表达状态的技术的发展,癌基因小组检测已经成为可能。另一方面,不依赖于碱基序列变化的基因表达变化,即表观遗传学,或更全面地说,表观基因组,也高度参与疾病的发展和进展。癌基因小组测试往往侧重于DNA碱基突变,如点突变、缺失、重复和嵌合体形成。阐明导致对疾病和治疗选择的正确解释,我们正处于一个对基因组和表观基因组的综合理解不可或缺的时代。在这篇综述中,我们尽一切努力涵盖广泛的知识,包括组蛋白修饰、非编码(nc)RNA和DNA甲基化的数据,以及最近在组织学和细胞学标本中证明表观遗传学改变的应用试验。我们希望这篇综述将有助于汇集参与基因组和表观基因组研究的研究人员积累的知识。
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引用次数: 8
Differences in Regression Patterns of Complete and Incomplete Intestinal Metaplasia at Ten Years after Helicobacter pylori Eradication. 根除幽门螺旋杆菌十年后完全性和不完全性肠化生的回归模式差异。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2021-12-24 Epub Date: 2021-11-18 DOI: 10.1267/ahc.21-00069
Yasuhiro Wada, Masaaki Kodama, Kazuhiro Mizukami, Tadayoshi Okimoto, Takafumi Fuchino, Koshiro Tsutsumi, Masahide Fukuda, Yuka Hirashita, Kensuke Fukuda, Kazuhisa Okamoto, Ryo Ogawa, Ryoji Kushima, Kazunari Murakami

This study was conducted to reveal the reversibility of subtype of intestinal metaplasia (IM) and Paneth cells after H. pylori eradication (HPE). Among 75 patients, we retrospectively examined the proportions of patients with complete type of IM (CIM), incomplete type of IM (IIM) and Paneth cells in their biopsy specimens obtained from the greater curvature of the antrum (A2) and the greater curvature of the middle corpus (B2) before and during a follow-up period of 10 years after HPE. Immunohistochemistry was used to determine IM type. Compared to before HPE, the proportion of patients with CIM did not decrease significantly during the 10-year follow-up after HPE both in A2 (32% vs. 21.3%, P = 0.13) and in B2 (6.7% vs. 2.7%, P = 0.60). IIM rates in A2 was significantly lower during this time (26.7% vs. 10.7%, P = 0.04), whereas no patients showed IIM in B2 before HPE. The proportion of patients with Paneth cells decreased significantly in A2 after 3, 8, and 9 years of HPE and in B2 after 4, 6 and 9 years of HPE (P < 0.05 for all). Thus, IIM and Paneth cells regressed during a period of 10 years after HPE.

本研究旨在揭示根除幽门螺杆菌(HPE)后肠化生(IM)亚型和Paneth细胞的可逆性。在 75 例患者中,我们回顾性研究了在 HPE 前和 HPE 后 10 年随访期间,从胃窦大弯(A2)和胃窦中部大弯(B2)获得的活检标本中出现完全型 IM(CIM)、不完全型 IM(IIM)和 Paneth 细胞的患者比例。免疫组化用于确定 IM 类型。与 HPE 前相比,在 HPE 后的 10 年随访期间,A2(32% vs. 21.3%,P = 0.13)和 B2(6.7% vs. 2.7%,P = 0.60)的 CIM 患者比例没有明显下降。在此期间,A2的IIM率明显降低(26.7% vs. 10.7%,P = 0.04),而在HPE之前,B2中没有患者出现IIM。在 HPE 3、8 和 9 年后,A2 中出现 Paneth 细胞的患者比例明显降低,而在 HPE 4、6 和 9 年后,B2 中出现 Paneth 细胞的患者比例明显降低(P < 0.05)。因此,在 HPE 后的 10 年中,IIM 和 Paneth 细胞均有所减少。
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引用次数: 0
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