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- Beal, Jacob, et al.
(author)
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Robust estimation of bacterial cell count from optical density
- 2020
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In: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1
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Journal article (peer-reviewed)abstract
- Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data.
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| 2. |
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| 3. |
- Tang, Ting-Ting, et al.
(author)
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Impaired thymic export and apoptosis contribute to regulatory T-cell defects in patients with chronic heart failure.
- 2011
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In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203 .- 1932-6203. ; 6:9, s. e24272-
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Journal article (peer-reviewed)abstract
- Animal studies suggest that regulatory T (T(reg)) cells play a beneficial role in ventricular remodeling and our previous data have demonstrated defects of T(reg) cells in patients with chronic heart failure (CHF). However, the mechanisms behind T(reg-)cell defects remained unknown. We here sought to elucidate the mechanism of T(reg-)cell defects in CHF patients.
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| 4. |
- Yang, Shao-Nian
(author)
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Reciprocal interactions of neuropeptide y and angiotensin II receptors with a2-adrenoceptors in the nucleus tractus solitarii of the rat
- 1996
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Doctoral thesis (other academic/artistic)abstract
- Neuropeptide Y (NPY), angiotensin II (Ang II) and adrenergic transmission lines in the nucleus tractus solitarii (NTS), the major relay nucleus involved in the cardiovascular reflex, play an important role in central cardiovascular control. The present work explored reciprocal interactions of NPY and Ang II receptor subtypes with a2-adrenoceptors in the NTS of the normotensive Sprague-Dawley rat (SD), the normotensive Wistar Kyoto rat (WKY) and the spontaneously hypertensive rat (SHR) by using a cardiovascular analysis, quantitative receptor autoradiography, immunocytochemistry and in situ hybridization techniques. a2A-Adrenoceptors have been shown to be present in almost allcatecholaminergic neurons in the brainstem including the NTS. NPY Yl or AngII ATl receptor-like immunoreactivity (-LI) was found to be colocalized with tyrosine hydroxylase-LI in the NTS suggesting colocalization of these receptors with a2-adrenoceptors in catecholaminergic neurons of the NTS. In the NTS of the SD, the NPY Yl and Y2 receptor agonists decreased the affinity and transduction of a2-adrenoceptors. In contrast, a2-adrenoceptor agonists increased NPY Y2 receptor affinity but reduced the NPY Y2 receptor functions, i.e., the NPY Y2 receptor-mediated cardiovascular actions and the NPY-induced c-Fos expression in the NTS. NPY Y2 receptor agonists reduced transduction over NPY Yl receptors in the NTS. In the SHR, a2A-adrenoceptor mRNA levels and a2-adrenoceptor binding sites in the NTS were lower than those in the WKY. NPY in the NTS of the SHR had an increased potency to antagonize a2-adrenoceptor function. This suggests that abnormal NPY/a2-adrenergic receptor interaction may contribute to the development of hypertension. In the NTS of the SD, activation of Ang II ATI receptors reduced the affinity and transduction of a2-adrenoceptors, whereas a2-adrenoceptor activation had the opposite effect on Ang II receptors. Ang II differentially regulates a2-adrenoceptors in the NTS of the WKY and the SHR. In the WKY, Ang II reduced the affinity and function of a2-adrenoceptors. In the SHR, however, Ang II increased them. This opposite effectin the SHR may be one compensatory mechanism to counteract the development of high blood pressure in the SHR. In conclusion, the present work provides evidence for reciprocal interactions of NPY and Ang II receptors with a2-adrenoceptors in the NTS participating in cardiovascular regulation which are altered in relation to spontaneous hypertension.
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