L-Calc Software for Limiting Dilution Analysis

总览

有限稀释分析（LDA）被应用于造血干细胞（HSC）的体外定量，如长期培养起始细胞（LTC-IC）测定（Conneally et al.）和鹅卵石区域形成细胞（CAFC）测定（Wang et al.）。有限稀释方法也被用于定量人和小鼠造血干细胞在竞争性再生单位（CRU）检测（Ploemacher et al.; Szilvassy et al.）和SCID再生细胞（SRC）检测（Dick et al.）中在体内产生所有造血谱系的成熟细胞的能力。

L-Calc™将帮助您分析LDA的结果。对于每个实验，输入值包括：剂量（dose，即每孔细胞数）；每个剂量获得的阳性反应总数；以及测试的复孔总数（即每个细胞剂量使用的孔总数）。根据这些数据，可以确定给定细胞群中能够产生特定反应的细胞的频率。L-Calc™也可用于指导评估LDA配对组间差异。建议咨询统计学家以进行适当的比较。

软件免费下载：lcsetup.exe

适用于Microsoft®Windows。

请注意，我们不再为L-Calc软件提供支持或更新。

L-Calc™将帮助您分析LDA的结果。对于每个实验，输入值包括：剂量（dose，即每孔细胞数）；每个剂量获得的阳性反应总数；以及测试的复孔总数（即每个细胞剂量使用的孔总数）。根据这些数据，可以确定给定细胞群中能够产生特定反应的细胞的频率。L-Calc™也可用于指导评估LDA配对组间差异。建议咨询统计学家以进行适当的比较。

软件免费下载：lcsetup.exe

适用于Microsoft®Windows。

请注意，我们不再为L-Calc软件提供支持或更新。

L-Calc™将帮助您分析LDA的结果。对于每个实验，输入值包括：剂量（dose，即每孔细胞数）；每个剂量获得的阳性反应总数；以及测试的复孔总数（即每个细胞剂量使用的孔总数）。根据这些数据，可以确定给定细胞群中能够产生特定反应的细胞的频率。L-Calc™也可用于指导评估LDA配对组间差异。建议咨询统计学家以进行适当的比较。

软件免费下载：lcsetup.exe

适用于Microsoft®Windows。

请注意，我们不再为L-Calc软件提供支持或更新。

L-Calc™将帮助您分析LDA的结果。对于每个实验，输入值包括：剂量（dose，即每孔细胞数）；每个剂量获得的阳性反应总数；以及测试的复孔总数（即每个细胞剂量使用的孔总数）。根据这些数据，可以确定给定细胞群中能够产生特定反应的细胞的频率。L-Calc™也可用于指导评估LDA配对组间差异。建议咨询统计学家以进行适当的比较。

软件免费下载：lcsetup.exe

适用于Microsoft®Windows。

请注意，我们不再为L-Calc软件提供支持或更新。

应用
功能学筛选

研究领域
干细胞生物学

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应用领域

本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。

Research Area

Workflow Stages

Workflow Stages for Hematopoietic Stem and Progenitor Cell Research

Cell Sourcing and Isolation

Expansion and Differentiation

Analysis

相关材料与文献

p53-TP53-Induced Glycolysis Regulator Mediated Glycolytic Suppression Attenuates DNA Damage and Genomic Instability in Fanconi Anemia Hematopoietic Stem Cells. X. Li et al. Stem cells (Dayton, Ohio) 2019 jul

Abstract

Emerging evidence has shown that resting quiescent hematopoietic stem cells (HSCs) prefer to utilize anaerobic glycolysis rather than mitochondrial respiration for energy production. Compelling evidence has also revealed that altered metabolic energetics in HSCs underlies the onset of certain blood diseases; however, the mechanisms responsible for energetic reprogramming remain elusive. We recently found that Fanconi anemia (FA) HSCs in their resting state are more dependent on mitochondrial respiration for energy metabolism than on glycolysis. In the present study, we investigated the role of deficient glycolysis in FA HSC maintenance. We observed significantly reduced glucose consumption, lactate production, and ATP production in HSCs but not in the less primitive multipotent progenitors or restricted hematopoietic progenitors of Fanca-/- and Fancc-/- mice compared with that of wild-type mice, which was associated with an overactivated p53 and TP53-induced glycolysis regulator, the TIGAR-mediated metabolic axis. We utilized Fanca-/- HSCs deficient for p53 to show that the p53-TIGAR axis suppressed glycolysis in FA HSCs, leading to enhanced pentose phosphate pathway and cellular antioxidant function and, consequently, reduced DNA damage and attenuated HSC exhaustion. Furthermore, by using Fanca-/- HSCs carrying the separation-of-function mutant p53R172P transgene that selectively impairs the p53 function in apoptosis but not cell-cycle control, we demonstrated that the cell-cycle function of p53 was not required for glycolytic suppression in FA HSCs. Finally, ectopic expression of the glycolytic rate-limiting enzyme PFKFB3 specifically antagonized p53-TIGAR-mediated metabolic reprogramming in FA HSCs. Together, our results suggest that p53-TIGAR metabolic axis-mediated glycolytic suppression may play a compensatory role in attenuating DNA damage and proliferative exhaustion in FA HSCs. Stem Cells 2019;37:937-947.

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Metformin blunts muscle hypertrophy in response to progressive resistance exercise training in older adults: A randomized, double-blind, placebo-controlled, multicenter trial: The MASTERS trial. R. G. Walton et al. Aging cell 2019 dec

Abstract

Progressive resistance exercise training (PRT) is the most effective known intervention for combating aging skeletal muscle atrophy. However, the hypertrophic response to PRT is variable, and this may be due to muscle inflammation susceptibility. Metformin reduces inflammation, so we hypothesized that metformin would augment the muscle response to PRT in healthy women and men aged 65 and older. In a randomized, double-blind trial, participants received 1,700 mg/day metformin (N = 46) or placebo (N = 48) throughout the study, and all subjects performed 14 weeks of supervised PRT. Although responses to PRT varied, placebo gained more lean body mass (p = .003) and thigh muscle mass (p {\textless} .001) than metformin. CT scan showed that increases in thigh muscle area (p = .005) and density (p = .020) were greater in placebo versus metformin. There was a trend for blunted strength gains in metformin that did not reach statistical significance. Analyses of vastus lateralis muscle biopsies showed that metformin did not affect fiber hypertrophy, or increases in satellite cell or macrophage abundance with PRT. However, placebo had decreased type I fiber percentage while metformin did not (p = .007). Metformin led to an increase in AMPK signaling, and a trend for blunted increases in mTORC1 signaling in response to PRT. These results underscore the benefits of PRT in older adults, but metformin negatively impacts the hypertrophic response to resistance training in healthy older individuals. ClinicalTrials.gov Identifier: NCT02308228.

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Revision of the Human Hematopoietic Tree: Granulocyte Subtypes Derive from Distinct Hematopoietic Lineages A. Gorgens et al. Cell Reports 2013 5

Abstract

The classical model of hematopoiesis predicts a dichotomous lineage restriction of multipotent hematopoietic progenitors (MPPs) into common lymphoid progenitors (CLPs) and common myeloid progenitors (CMPs). However, this idea has been challenged by the identification of lymphoid progenitors retaining partial myeloid potential (e.g., LMPPs), implying that granulocytes can arise within both the classical lymphoid and the myeloid branches. Here, we resolve this issue by using cell-surface CD133 expression to discriminate functional progenitor populations. We show that eosinophilic and basophilic granulocytes as well as erythrocytes and megakaryocytes derive from a common erythro-myeloid progenitor (EMP), whereas neutrophilic granulocytes arise independently within a lympho-myeloid branch with long-term progenitor function. These findings challenge the concept of a CMP and restore dichotomy to the classical hematopoietic model.

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