Cell & developmental biology最新文献_第6页

Apoptosis in Bcl2l13 epididymal cells Bcl2l13附睾细胞的凋亡

Cell & developmental biology

Pub Date : 2017-07-07 DOI: 10.4172/2168-9296.1000187

Donato Dalonzo, Hong Zhang

Apoptosis, i.e., controlled cell death, occurs in response to many different environmental stimuli and it plays an indispensable role in the development and maintenance of homeostasis within all multicellular organisms. The apoptotic cascade that occurs within the cell in response to these cues, leads to morphological and biochemical changes that trigger the death of the cell. Bcl2 (B-cell lymphoma 2), encoded in humans by the BCL2 gene, is the founding member of the Bcl-2 family of regulator proteins that regulate cell death (apoptosis), by either inducing (proapoptotic) or inhibiting (anti-apoptotic) apoptosis and thus represents a crucial part in the cascade of cell death. We analyzed the effect of BCL2l13 in murine knockout (k.o.) following apoptosis. These mice show a phenotype in the epididymis; A gland that is prerequisite to guarantee fertility. By inducing apoptosis and thereafter observing the cell death, the results did not indicate a significant difference between k.o. and wild type suggesting BCL2l13 having less of importance in the BCL2 protein family.

细胞凋亡，即受控的细胞死亡，是对许多不同环境刺激的反应，它在所有多细胞生物的体内平衡的发展和维持中起着不可或缺的作用。细胞内发生的凋亡级联反应是对这些信号的反应，导致形态和生化变化，从而引发细胞死亡。Bcl2 (b细胞淋巴瘤2)由Bcl2基因在人体内编码，是Bcl-2调节蛋白家族的创始成员，通过诱导(促凋亡)或抑制(抗凋亡)凋亡来调节细胞死亡(凋亡)，因此在细胞死亡的级联反应中起关键作用。我们分析了bcl213在小鼠细胞凋亡后基因敲除(k.o)中的作用。这些小鼠显示附睾表型;腺体是保证生育能力的先决条件通过诱导细胞凋亡和随后观察细胞死亡，结果显示k.o.与野生型之间没有显著差异，表明bcl213在BCL2蛋白家族中的重要性较低。

引用次数: 0

Microbial Growth in Planktonic Conditions 浮游条件下微生物的生长

Cell & developmental biology

Pub Date : 2017-06-12 DOI: 10.4172/2168-9296.1000185

A. Schiraldi

A two-parameter model describes the microbial growth trend of planktonic cultures. Based on the assumption that cell duplication underlies the growth, the model defines an average generation time that depends on time and complies with the phenomenological evidence that the growth rate is naught at the start and at the end of the process. This is tantamount as to replace the real growth process with a virtual one, where all the generation lines stemming from the inoculum are synchronous and imply a duplication tree with no truncated branches. A simple function that complies with these constraints is τ=(a/t+bt), where a and b are parameters defined through a best fit treatment of the experimental plate count data. Surprisingly simple relationships come out for specific items of the growth trend, like maximum specific growth rate, eventual cell number, Nmax, duration of lag phase, etc., as well as some intriguing correlations between them. Published plate count data allowed testing the reliability of the model. The agreement is satisfactory being in line with the accuracy of the data (R2 ≥ 0.98).

一个双参数模型描述了浮游生物培养的微生物生长趋势。基于细胞复制是生长的基础这一假设，该模型定义了一个平均世代时间，该时间取决于时间，并符合现象证据，即生长速率在过程开始和结束时为零。这就等于用虚拟的生长过程来代替真实的生长过程，在虚拟的生长过程中，从接种物产生的所有代线都是同步的，意味着一个没有截断分支的复制树。符合这些约束的一个简单函数是τ=(A /t+bt)，其中A和b是通过对实验板计数数据进行最佳拟合处理而定义的参数。在生长趋势的特定项上，如最大特定生长率、最终细胞数、Nmax、滞后期持续时间等，得出了令人惊讶的简单关系，以及它们之间一些有趣的相关性。公布的车牌计数数据允许测试模型的可靠性。一致性令人满意，符合数据的准确性(R2≥0.98)。

引用次数: 8

Relationship of Metabolic Alterations and PD-L1 Expression in Cisplatin Resistant Lung Cancer. 顺铂耐药肺癌中代谢改变与 PD-L1 表达的关系

Cell & developmental biology

Pub Date : 2017-06-01 Epub Date: 2017-04-28 DOI: 10.4172/2168-9296.1000183

M Wangpaichitr, H Kandemir, Y Y Li, C Wu, Djm Nguyen, L G Feun, M T Kuo, N Savaraj

Despite numerous reports on immune checkpoint inhibitor for the treatment of non-small cell lung cancer (NSCLC), the response rate remains low but durable. Thus cisplatin still plays a major role in the treatment of NSCLC. While there are many mechanisms involved in cisplatin resistance, alteration in metabolic phenotypes with elevated levels of reactive oxygen species (ROS) are found in several cisplatin resistant tumors. These resistant cells become more reliant on mitochondria oxidative metabolism instead of glucose. Consequently, high ROS and metabolic alteration contributed to epithelial-mesenchymal transition (EMT). Importantly, recent findings indicated that EMT has a crucial role in upregulating PD-L1 expression in cancer cells. Thus, it is very likely that cisplatin resistance will lead to high expression of PD-L1/PD-1 which makes them vulnerable to anti PD-1 or anti PD-L1 antibody treatment. An understanding of the interactions between cancer cells metabolic reprogramming and immune checkpoints is critical for combining metabolism targeted therapies with immunotherapies.

尽管有大量关于免疫检查点抑制剂治疗非小细胞肺癌（NSCLC）的报道，但反应率仍然很低，但却很持久。因此，顺铂仍在治疗非小细胞肺癌中发挥着重要作用。虽然顺铂耐药涉及多种机制，但在一些顺铂耐药的肿瘤中发现了代谢表型的改变和活性氧（ROS）水平的升高。这些耐药细胞变得更加依赖线粒体氧化代谢，而不是葡萄糖。因此，高 ROS 和新陈代谢的改变促成了上皮-间质转化（EMT）。重要的是，最近的研究结果表明，EMT 在上调癌细胞中 PD-L1 的表达方面起着至关重要的作用。因此，顺铂耐药很可能会导致 PD-L1/PD-1 的高表达，从而使其易受抗 PD-1 或抗 PD-L1 抗体治疗的影响。了解癌细胞代谢重编程与免疫检查点之间的相互作用对于将代谢靶向疗法与免疫疗法相结合至关重要。

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引用次数: 0

Mitochondrial Dysfunction and Mitophagy in Neurodegenerative Diseases 神经退行性疾病中的线粒体功能障碍和线粒体自噬

Cell & developmental biology

Pub Date : 2017-05-18 DOI: 10.4172/2168-9296.1000184

Li‐Pin Kao, E. Wolvetang

Mitochondria are critical in providing energy for neuronal development. They provide the majority of intracellular energy and perform important metabolic functions such as the Krebs cycle. Mitochondria contain their own mitochondrial DNA in a circular form, similar to bacterial genomes. Mitochondrial genomes encode several essential genes of the eukaryotic respiratory machinery, but most respiratory machinery components and factors controlling mitochondrial biogenesis are encoded in the nucleus. Mitochondria and the nucleus cooperate and communicate via retrograde signals, such as energy supply and redox signaling. This poorly understood communication is essential for balancing intracellular energy production and demand. Mitochondrial mutations could lead to dysfunctions in ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Thus, mitochondrial dysfunction has been reported and discussed as part of neurodegenerative etiologies. There is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics, and mitophagic degradation occur in neurodegenerative diseases. Mitochondrial turnover maintains cellular homeostasis by eliminating defective mitochondria through a specific form of autophagy, an evolutionarily conserved eukaryotic response to stress conditions by which lysosome contents are used to breakdown cytoplasmic proteins and organelles. Both number of ‘healthy’ and ‘mutated’ mitochondria could be increased or decreased by fusion and fission. Selective uptake of mitochondria by autophagosomes is called mitophagy. Mitophagic events are highly selective processes controlled by oxidative stress and are accompanied by loss of membrane potential and ensuing mitochondrial degradation. This review discusses the role of mitochondria in neurodegenerative diseases. This review also explores the connection between neurodegeneration and mitophagy, a highly selective autophagic process of oxidative stress-induced mitochondrial degradation. It will further discuss the role of fusion and fission processes in maintaining homeostasis.

线粒体在为神经元发育提供能量方面是至关重要的。它们提供大部分细胞内能量，并执行重要的代谢功能，如克雷布斯循环。线粒体含有自己的线粒体DNA，呈圆形，类似于细菌基因组。线粒体基因组编码真核生物呼吸机制的几个必要基因，但大多数呼吸机制成分和控制线粒体生物发生的因素都在细胞核中编码。线粒体和细胞核通过逆行信号进行合作和交流，如能量供应和氧化还原信号。这种难以理解的交流对于平衡细胞内能量生产和需求至关重要。线粒体突变可导致ATP产生、钙稳态、活性氧产生和凋亡信号的功能障碍。因此，线粒体功能障碍作为神经退行性病因的一部分被报道和讨论。毫无疑问，线粒体功能障碍、线粒体动力学异常和线粒体自噬降解发生在神经退行性疾病中。线粒体转换通过一种特殊形式的自噬来消除有缺陷的线粒体，从而维持细胞稳态。自噬是一种进化上保守的真核生物对应激条件的反应，溶酶体的内容物被用来分解细胞质蛋白质和细胞器。“健康”和“突变”线粒体的数量都可以通过融合和裂变来增加或减少。自噬体选择性摄取线粒体称为线粒体自噬。线粒体自噬事件是由氧化应激控制的高度选择性过程，伴随着膜电位的丧失和随后的线粒体降解。本文就线粒体在神经退行性疾病中的作用作一综述。这篇综述还探讨了神经变性和线粒体自噬之间的联系，线粒体自噬是氧化应激诱导的线粒体降解的高度选择性自噬过程。它将进一步讨论聚变和裂变过程在维持体内平衡中的作用。

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引用次数: 1

The Hormone Exocytosis in Prolactinoma and Normal Adenohypophysis Cell Cultures by the Effects of Hypocalcaemia 低钙对泌乳素瘤和正常腺垂体细胞激素分泌的影响

Cell & developmental biology

Pub Date : 2017-03-28 DOI: 10.4172/2168-9296.1000182

K. Sepp, A. László, M. Radács, A. Serester, Z. Valkusz, M. Gálfi, Z. Molnár

The biological systems are opened, complex objects, which can regularly exchange feedbacks with their environment. The calcium ion is a universal messenger, which can regulate several cellular functions e.g. exocytosis machinery. The primary aim of this study was to investigate the response mechanisms of normal adenohypophysis and adenohypophyseal prolactinoma cell populations at different extracellular Ca2+ levels with an otherwise isoionic milieu of all other essential ions. We focused on prolactin (PRL) and adrenocorticotrophic hormone (ACTH) release. In our experimental study, female Wistar rats (n=10) were treated with estrone-acetate (150 μg/kg b.w/week) for 6 months to induce prolactinomas in the adenohypophysis. Primary, monolayer cell cultures were prepared by enzymatic and mechanical digestion. PRL and ACTH hormone presence was measured by radioimmunoassay or immuno- chemiluminescence assay. Repeated measurements of ACTH and PRL hormone release in different treatment groups on cell cultures during 80 minutes were compared using marginal models. Differences between the effects of hypocalcaemia on normal adenohypophysis cultures and prolactinoma cell populations were investigated. Significant alteration (p<0.001, n=12) in hormone exocytosis was detected in Ca2+ treated adenohypophyseal and prolactinoma cell cultures, compared to untreated groups. Diminution of Ca2+ may inhibit the SNARE mediated fusion of hormone containing vesicles to plasma membrane. In conclusion, the main finding of this study is that a strict correlation exists among certain biophysical properties, especially extracellular Ca2+ milieu and hormone vesicle exocytosis.

生物系统是开放的、复杂的物体，它们可以定期与环境交换反馈。钙离子是一种通用信使，可以调节多种细胞功能，如胞吐机制。本研究的主要目的是研究正常腺垂体和腺垂体泌乳素瘤细胞群在不同的细胞外Ca2+水平和其他所有必需离子的等离子环境下的反应机制。我们关注催乳素(PRL)和促肾上腺皮质激素(ACTH)的释放。在我们的实验研究中，雌性Wistar大鼠(n=10)给予150 μg/kg b.w/周的雌酮醋酸酯治疗6个月，诱导垂体泌乳素瘤。用酶和机械消化法制备原代单层细胞培养物。用放射免疫法或免疫化学发光法测定PRL和ACTH激素的存在。使用边缘模型比较不同处理组细胞培养80分钟内ACTH和PRL激素释放的重复测量。研究了低钙对正常腺垂体培养和泌乳素瘤细胞群影响的差异。与未处理组相比，Ca2+处理的腺垂体和泌乳素瘤细胞培养中激素分泌显著改变(p<0.001, n=12)。Ca2+的减少可能会抑制SNARE介导的含激素囊泡与质膜的融合。总之，本研究的主要发现是某些生物物理特性，特别是细胞外Ca2+环境与激素囊泡胞吐之间存在着严格的相关性。

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引用次数: 1

Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth. 沉默miR-16表达可促进血管紧张素II刺激血管平滑肌细胞生长。

Cell & developmental biology

Pub Date : 2017-03-01 Epub Date: 2017-03-24 DOI: 10.4172/2168-9296.1000181

Qingqing Gu, Guannan Zhao, Yinan Wang, Biao Xu, Junming Yue

miRNAs are a class of non-coding endogenous small RNAs that control gene expression at the posttranscriptional level and involved in cell proliferation, migration and differentiation. Dysregulation of miRNA expression is involved in a variety of human diseases including cardiovascular diseases. miRNAs have been shown to regulate vascular smooth muscle cell (VSMC) function and play vital roles in hypertension, restenosis and atherosclerosis. Here we reported that miR-16 as one of miRNAs in the miR-15 family was highly expressed in vascular smooth muscle cells (VSMCs) and involved in angiotensin II (Ang II) mediated VSMC signaling pathways. Ang II downregulated miR-16 expression in VSMCs. Lentiviral vector mediated miR-16 knockdown promoted Ang II-induced cell proliferation and migration. Moreover, silencing miR-16 enhanced Ang II induced cell cycle associated gene expression and promoted Ang II-activated cell proliferative pathways ERK1/2 and p38. Our finding demonstrated for the first time that miR-16 was a potential therapeutic target by participating in the Ang II-associated multiple signaling pathways in cardiovascular diseases.

mirna是一类非编码的内源性小rna，在转录后水平控制基因表达，参与细胞增殖、迁移和分化。miRNA表达失调与包括心血管疾病在内的多种人类疾病有关。mirna已被证明可以调节血管平滑肌细胞(VSMC)的功能，并在高血压、再狭窄和动脉粥样硬化中发挥重要作用。在这里，我们报道了miR-16作为miR-15家族中的mirna之一，在血管平滑肌细胞(VSMC)中高表达，并参与血管紧张素II (Ang II)介导的VSMC信号通路。Ang II下调VSMCs中miR-16的表达。慢病毒载体介导的miR-16敲低促进了Ang ii诱导的细胞增殖和迁移。此外，沉默miR-16可增强Ang II诱导的细胞周期相关基因表达，促进Ang II激活的细胞增殖途径ERK1/2和p38。我们的发现首次证明了miR-16是一个潜在的治疗靶点，通过参与心血管疾病中Ang ii相关的多种信号通路。

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引用次数: 6

Treatments for Sickle Cell Disease: A Global Problem in Cell and Developmental Biology 镰状细胞病的治疗:细胞和发育生物学中的一个全球性问题

Cell & developmental biology

Pub Date : 2017-02-28 DOI: 10.4172/2168-9296.1000E141

R. Broyles

Copyright: © 2017 Broyles RH. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Sickle cell disease (SCD) is the world’s most common genetic disorder, being most prevalent among populations in the regions where malaria has been endemic [1]. SCD is caused by a point mutation (A → T) in the sixth codon of the β-globin gene on chromosome 11, resulting in the substitution of the amino acid valine for glutamic acid in the expressed protein. The result is that the mutated hemoglobin S (HbS) polymerizes and precipitates within the red blood cells (RBCs) during deoxygenation or dehydration, altering the RBC’s form from a flexible biconcave disc to a rigid elongated cell that is often in the shape of a crescent or sickle. Sickling results in a vascular train wreck, producing abnormally increased adhesion to other blood cells and to the vascular walls, hyper-coagulation, hemolysis, hypoxia, widespread inflammation, organ damage, and premature death. There are approximately 340,000 deaths per year attributed to the effects of SCD, most of the deaths being children under five years of age. Although the molecular basis of sickle cell has been understood for over sixty years [2,3], there is still no treatment that is highly effective and available to the millions of affected individuals worldwide.

版权所有:©2017 Broyles RH。这是一篇根据知识共享署名许可协议发布的开放获取文章，该协议允许在任何媒体上不受限制地使用、分发和复制，前提是要注明原作者和来源。镰状细胞病(SCD)是世界上最常见的遗传性疾病，在疟疾流行地区的人群中最为流行。SCD是由11号染色体上β-珠蛋白基因第6个密码子点突变(a→T)引起的，导致表达蛋白中的氨基酸缬氨酸取代了谷氨酸。结果是，在脱氧或脱水过程中，突变的血红蛋白S (HbS)在红细胞(RBC)内聚合和沉淀，将红细胞的形状从灵活的双凹圆盘改变为刚性的细长细胞，通常呈新月形或镰刀形。镰状坏死导致血管列车失事，产生与其他血细胞和血管壁的粘附异常增加、高凝、溶血、缺氧、广泛的炎症、器官损伤和过早死亡。每年约有34万人死于慢性阻塞性肺病，其中大多数是五岁以下的儿童。尽管镰状细胞的分子基础已经被了解了60多年[2,3]，但仍然没有一种非常有效的治疗方法可供全世界数百万患者使用。

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引用次数: 0

Cflarb Complemented the Function of Cflara to Allow Cflara Knock out Zebrafish To Normal Development Cflara补充了Cflara的功能，使Cflara敲昏斑马鱼恢复正常发育

Cell & developmental biology

Pub Date : 2017-02-28 DOI: 10.4172/2168-9296.1000180

S. Huh, Kyu-Seok Hwang, S. Koppula, C. Kim, Cheol‐Hee Kim, Chan Gil Kim

Cellular FLICE-inhibitory protein (cFLIP, cflara) is a regulator of death receptor (DR)-induced apoptosis and NF-κB activation. cFLIP is known to prevent activation of the caspase cascade by binding to FADD/caspase-8. Up-regulated cFLIP has been identified in many tumor types, and therefore restoring apoptosis by silencing cFLIP may be one of the more potent strategies in cancer therapeutics. The zebrafish cFLIP gene, cflara, has 2 death effector domains (DEDs) and a single caspase-like domain. Expression of cflara was detected in the zebrafish embryo by RT-PCR and whole-mount in situ hybridization. To study the in vivo function of cflara, we generated a cflara knockout mutant zebrafish using transcription activator-like effector nucleases (TALENs). Frame shift mutation is caused by a 10-bp deletion in the first DED domain. By inbreeding the F1 generation, a homozygous mutant fish was produced and confirmed by PCR. Knockout of cflara leads to abnormal heart development and embryonic lethality in mice. However, mutant zebrafish did not show any differences from wild type in heartbeat rate, survival rate or development. Zebrafish have analogues of both cflara and cflarb. Quantitative PCR showed that cflarb mRNA levels of mutant zebrafish were higher than those in the wild type. In a chemical exposure experiment, mutant zebrafish larvae showed a longer survival rate compared with wild type after CoCl2 treatment. However, no significant difference was observed from cisplatin treatment. This data suggests that cflarb may contribute to normal development and causes a difference in chemical resistance.

细胞fflip抑制蛋白(cFLIP, cflara)是死亡受体(DR)诱导的细胞凋亡和NF-κB活化的调节因子。已知cFLIP通过结合FADD/caspase-8来阻止caspase级联的激活。上调的cFLIP已经在许多肿瘤类型中被发现，因此通过沉默cFLIP来恢复细胞凋亡可能是癌症治疗中更有效的策略之一。斑马鱼的cFLIP基因，cflara，有2个死亡效应域(ded)和一个caspase样域。采用RT-PCR和全载原位杂交技术检测了cflara在斑马鱼胚胎中的表达。为了研究cflara在体内的功能，我们利用转录激活因子样效应核酸酶(TALENs)产生了一个cflara敲除突变体斑马鱼。帧移位突变是由第一个DED结构域的10bp缺失引起的。通过对F1代进行近交，获得了一个纯合突变体，并经PCR证实。敲除clara可导致小鼠心脏发育异常和胚胎死亡。然而，突变斑马鱼在心率、存活率和发育方面与野生斑马鱼没有任何差异。斑马鱼有两种类似的细胞。定量PCR结果显示，突变斑马鱼的cflarb mRNA水平高于野生型斑马鱼。在化学暴露实验中，突变斑马鱼幼虫在CoCl2处理后的存活率比野生型更长。然而，与顺铂治疗相比，无显著差异。这一数据表明，氯虫可能有助于正常发育，并导致化学抗性的差异。

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引用次数: 0

Characterization of Cell Cycle Phase-Based Micrornas in Pluripotency and Differentiation 细胞周期期微rna在多能性和分化中的特性研究

Cell & developmental biology

Pub Date : 2017-01-25 DOI: 10.4172/2168-9296.1000178

X. Ming, T. Wan, Lin Chen, M. Garcia-Barceló, C. Lo, X. Q. Wang

In addition to signaling pathways, transcription factors and epigenetic regulators, microRNAs (miRNAs) are emerging as important regulators of human pluripotent stem cells (hPSCs). Pluripotent miRNAs that regulate G1-S transition and pluripotency factors to maintain self-renewal have been identified. However, only 4-5 clusters of miRNAs have been identified in human embryonic stem cells (hESCs). We performed cell cycle phase-based (G1, S, and G2/M phases) miRNA array in pluripotent and differentiated hESCs. We demonstrated that embryonic stem cell-cell cycle (ESCC) regulating miRNAs were all highly expressed in three cell cycle phases of undifferentiated hESCs suggesting a non-cell phase regulated mechanism. From cell phase-dependent miRNAs, G2/M-miRNAs was extracted by principle component analysis (PCA) as a significant component in pluripotent hESCs, whereas G1-miRNAs was a significant component in differentiated hESCs. The results indicate that G2/M-miRNAs might function to maintain pluripotency and G1-miRNAs might function to enhance differentiation. By miRNA target site prediction, G2/M-phase miRNA displayed potential target sites on differentiation factors GATA6 and GATA4, G1-phase miRNAs displayed potential target sites on pluripotency gene OCT4, NANOG, and SOX2, which warrant further confirmation and functional study. By statistical and computation analysis of the miRNA array data, we demonstrated that the G2/M-miRNAs could potentially repress differentiation factors to maintain pluripotency, and G1-miRNAs could potentially target pluripotency genes to enhance differentiation.

除了信号通路、转录因子和表观遗传调控因子外，microRNAs (miRNAs)也成为人类多能干细胞(hPSCs)的重要调控因子。调控G1-S转化和多能性因子以维持自我更新的多能性mirna已经被确定。然而，在人胚胎干细胞(hESCs)中仅鉴定出4-5个mirna簇。我们在多能和分化hESCs中进行了基于细胞周期期(G1、S和G2/M期)的miRNA阵列。我们证明了胚胎干细胞-细胞周期(ESCC)调节mirna在未分化hESCs的三个细胞周期阶段都高度表达，这表明非细胞期调节机制。从细胞相依赖性mirna中，通过主成分分析(PCA)提取出G2/ m - mirna作为多能hESCs的重要组成部分，而g1 - mirna是分化hESCs的重要组成部分。结果表明，G2/M-miRNAs可能具有维持多能性的功能，而G1-miRNAs可能具有增强分化的功能。通过miRNA靶位点预测，G2/ m期miRNA显示分化因子GATA6和GATA4的潜在靶位点，g1期miRNA显示多能基因OCT4、NANOG和SOX2的潜在靶位点，有待进一步证实和功能研究。通过对miRNA阵列数据的统计和计算分析，我们证明了G2/M-miRNAs可能潜在地抑制分化因子以维持多能性，G1-miRNAs可能潜在地靶向多能性基因以增强分化。

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引用次数: 0

The Acquisition of Mathematical Language in Biomedical Articles 生物医学文章中数学语言的习得

Cell & developmental biology

Pub Date : 2017-01-01 DOI: 10.13140/RG.2.2.18390.75841

D. Lu

Mathematical equations are a universal language suitable for all areas of scientific disciplines. Yet, currently, only limited biomedical scientists like to use mathematical equations to introduce new ideas in their articles. To change this situation, a great deal of effort must be made in the biomedical field. This article tries to urge more biomedical scientists to do that by providing new ideologies and initiatives.

数学方程是一种适用于所有科学学科领域的通用语言。然而，目前只有有限的生物医学科学家喜欢在他们的文章中使用数学方程来引入新的思想。要改变这一现状，必须在生物医学领域做出巨大努力。本文试图通过提供新的思想和倡议来敦促更多的生物医学科学家这样做。

引用次数: 8