| 1. |
- Beal, Jacob, et al.
(författare)
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Robust estimation of bacterial cell count from optical density
- 2020
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Ingår i: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1
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Tidskriftsartikel (refereegranskat)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. |
- Ablikim, M., et al.
(författare)
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Measurement of the absolute branching fraction for Lambda(+)(c) -> Lambda mu(+)nu(mu)
- 2017
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Ingår i: Physics Letters B. - : ELSEVIER SCIENCE BV. - 0370-2693 .- 1873-2445. ; 767, s. 42-47
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Tidskriftsartikel (refereegranskat)abstract
- We report the first measurement of the absolute branching fraction for Lambda(+)(c) -> Lambda mu(+)nu(mu).This measurement is based on a sample of e+e(-) annihilation data produced at a center-of-mass energy root s = 4.6 GeV, collected with the BESIII detector at the BEPCII storage rings. The sample corresponds to an integrated luminosity of 567 pb(-1). The branching fraction is determined to be B( Lambda(+)(c) -> Lambda mu(+)nu(mu)) = (3.49 +/- 0.46( stat) +/- 0.27( syst))%. In addition, we calculate the ratio B( Lambda(+)(c) -> Lambda mu(+)nu(mu))/B(Lambda(+)(c) -> Lambda e(+)nu(e) to be 0.96 +/- 0.16( stat) +/- 0.04( syst).
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| 3. |
- Ablikim, M., et al.
(författare)
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Measurement of branching fractions for psi(3686) -> gamma eta ', gamma eta, and gamma pi(0)
- 2017
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Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 96:5
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Tidskriftsartikel (refereegranskat)abstract
- Using a data sample of 448 x 10(6) psi(3686) events collected with the BESIII detector operating at the BEPCII storage ring, the decays psi(3686) -> gamma eta and psi(3686) -> gamma pi(0) are observed with a statistical significance of 7.3 sigma and 6.7 sigma, respectively. The branching fractions are measured to be B(psi(3686) -> gamma eta) = (0.85 +/- 0.18 +/- 0.05) x 10(-6) and B(psi(3686) ->gamma pi(0)) = (0.95 +/- 0.16 +/- 0.05) x 10(-6). In addition, we measure the branching fraction of psi(3686) -> gamma eta' to be B(psi(3686) -> gamma eta') = (125.1 +/- 2.2 +/- 6.2)x10(-6), which represents an improvement of precision over previous results.
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| 4. |
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- 2019
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Tidskriftsartikel (refereegranskat)
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| 5. |
- Guan, Pei-Pei, et al.
(författare)
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By activating matrix metalloproteinase-7, shear stress promotes chondrosarcoma cell motility, invasion and lung colonization.
- 2015
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Ingår i: Oncotarget. - : Impact Journals, LLC. - 1949-2553. ; 6:11, s. 9140-9159
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Tidskriftsartikel (refereegranskat)abstract
- Interstitial fluid flow and associated shear stress are relevant mechanical signals in cartilage and bone (patho)physiology. However, their effects on chondrosarcoma cell motility, invasion and metastasis have yet to be delineated. Using human SW1353, HS.819.T and CH2879 chondrosarcoma cell lines as model systems, we found that fluid shear stress induces the accumulation of cyclic AMP (cAMP) and interleukin-1β (IL-1β), which in turn markedly enhance chondrosarcoma cell motility and invasion via the induction of matrix metalloproteinase-7 (MMP-7). Specifically, shear-induced cAMP and IL-1β activate PI3-K, ERK1/2 and p38 signaling pathways, which lead to the synthesis of MMP-7 via transactivating NF-κB and c-Jun in human chondrosarcoma cells. Importantly, MMP-7 upregulation in response to shear stress exposure has the ability to promote lung colonization of chondrosarcomas in vivo. These findings offer a better understanding of the mechanisms underlying MMP-7 activation in shear-stimulated chondrosarcoma cells, and provide insights on designing new therapeutic strategies to interfere with chondrosarcoma invasion and metastasis.
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| 6. |
- Chi, Zhi-Hong, et al.
(författare)
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Zinc transporter 7 is located in the cis-Golgi apparatus of mouse choroid epithelial cells.
- 2006
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Ingår i: Neuroreport. - : Ovid Technologies (Wolters Kluwer Health). - 0959-4965. ; 17:17, s. 1807-11
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Tidskriftsartikel (refereegranskat)abstract
- The cellular localization of zinc transporter 7 protein in the mouse choroid plexus was examined in this study. Zinc transporter 7 immunoreactive cells were detected in the third, lateral, and fourth ventricles of CD-1 mouse brain. Distinct zinc transporter 7 immunoreactivity was concentrated in the perinuclear regions of the positive cells. The results from zinc autometallography showed that zinc-positive grains were also predominantly located in the perinuclear areas. Ultrastructural localization showed that zinc transporter 7 immunostaining was predominantly present in the membrane and cisternae of the cis-Golgi networks and some vesicle compartments. The results support the notion that zinc transporter 7 may participate in the transport of the cytoplasmic zinc into the Golgi apparatus, and may be involved in local packaging of zinc-binding proteins in the mouse choroid plexus.
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| 7. |
- Gao, Hui-Ling, et al.
(författare)
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Expression of zinc transporter ZnT7 in mouse superior cervical ganglion.
- 2008
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Ingår i: Autonomic neuroscience : basic & clinical. - : Elsevier BV. - 1566-0702. ; 140:1-2, s. 59-65
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Tidskriftsartikel (refereegranskat)abstract
- The superior cervical ganglion (SCG) neurons contain a considerable amount of zinc ions, but little is known about the zinc homeostasis in the SCG. It is known that zinc transporter 7 (ZnT7, Slc30a7), a member of the Slc30 ZnT family, is involved in mobilizing zinc ions from the cytoplasm into the Golgi apparatus. In the present study, we examined the expression and localization of ZnT7 and labile zinc ions in the mouse SCG using immunohistochemistry, Western blot and in vivo zinc selenium autometallography (AMG). Our immunohistochemical analysis revealed that the ZnT7 immunoreactivity in the SCG neurons was predominately present in the perinuclear region of the neurons, suggesting an affiliation to the Golgi apparatus. The Western blot results verified that ZnT7 protein was expressed in the mouse SCGs. The AMG reaction product was shown to have a similar distribution as ZnT7 immunoreactivity. These observations support the notion that ZnT7 may participate in zinc transport, storage, and incorporation of zinc into zinc-binding proteins in the Golgi apparatus of mouse SCG neurons.
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| 8. |
- Sun, Tian-Shu, et al.
(författare)
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Reciprocal functions of Cryptococcus neoformans copper homeostasis machinery during pulmonary infection and meningoencephalitis.
- 2014
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Copper homeostasis is important for virulence of the fungus Cryptococcus neoformans, which can cause lethal meningoencephalitis in humans. Cryptococcus cells encounter high copper levels in the lung, where infection is initiated, and low copper levels in the brain. Here we demonstrate that two Cryptococcus copper transporters, Ctr1 and Ctr4, differentially influence fungal survival during pulmonary infection and the onset of meningoencephalitis. Protein Ctr1 is rapidly degraded under the high-copper conditions found in infected lungs, and its loss has no effect in fungal virulence in mice. By contrast, deleting CTR4 results in a hypervirulent phenotype. Overexpressing either Ctr1 or Ctr4 leads to profound reductions in fungal burden in the lung. However, during the onset of meningoencephalitis, expression of the copper transporters is induced and is critical for Cryptococcus virulence. Our work demonstrates that the fungal cells switch between copper detoxification and acquisition to address different copper stresses in the host.
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| 9. |
- Wang, Min, et al.
(författare)
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Apolipoprotein M induces inhibition of inflammatory responses via the S1PR1 and DHCR24 pathways
- 2019
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Ingår i: Molecular Medicine Reports. - 1791-2997. ; 19:2, s. 1272-1283
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Tidskriftsartikel (refereegranskat)abstract
- © 2019 Spandidos Publications. All rights reserved. Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that high-density lipoprotein (HDL) decreases inflammatory responses via the apoM-sphingosine-1-phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM-/-) were employed to investigate the effects of ApoM on the expression of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), S1P receptor-1 (S1PR1) and 3β-hydroxysterol Δ-24-reductase (DHCR24), as compared with in wild-type mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (rec-apoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factor-α (TNF-α), in order to investigate the effects of ApoM on IL-1β and MCP-1. The results demonstrated that the mRNA expression levels of IL-1β and MCP-1 were significantly higher in the liver following administration of lipopolysaccharide in apoM-/- mice compared with in apoM+/+ mice. In cell culture experiments, when cells were pre-cultured with rec-apoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL-1β and MCP-1 following TNF-α treatment compared with in normal apoM-expressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL-1β and MCP-1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport-1 (BLT-1), in apoMTg cells prior to TNF-α treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT-1 prior to TNF-α treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.
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| 10. |
- Xu, Shuang Feng, et al.
(författare)
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Lactoferrin ameliorates dopaminergic neurodegeneration and motor deficits in MPTP-treated mice
- 2019
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Ingår i: Redox Biology. - : Elsevier BV. - 2213-2317. ; 21
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Tidskriftsartikel (refereegranskat)abstract
- Brain iron accumulation is common in patients with Parkinson's disease (PD). Iron chelators have been investigated for their ability to prevent neurodegenerative diseases with features of iron overload. Given the non-trivial side effects of classical iron chelators, lactoferrin (Lf), a multifunctional iron-binding globular glycoprotein, was screened to identify novel neuroprotective pathways against dopaminergic neuronal impairment. We found that Lf substantially ameliorated PD-like motor dysfunction in the subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. We further showed that Lf could alleviate MPTP-triggered apoptosis of DA neurons, neuroinflammation, and histological alterations. As expected, we also found that Lf suppressed MPTP-induced excessive iron accumulation and the upregulation of divalent metal transporter (DMT1) and transferrin receptor (TFR), which is the main intracellular iron regulation protein, and subsequently improved the activity of several antioxidant enzymes. We probed further and determined that the neuroprotection provided by Lf was involved in the upregulated levels of brain-derived neurotrophic factor (BDNF), hypoxia-inducible factor 1α (HIF-1α) and its downstream protein, accompanied by the activation of extracellular regulated protein kinases (ERK) and cAMP response element binding protein (CREB), as well as decreased phosphorylation of c-Jun N-terminal kinase (JNK) and mitogen activated protein kinase (MAPK)/P38 kinase in vitro and in vivo. Our findings suggest that Lf may be an alternative safe drug in ameliorating MPTP-induced brain abnormalities and movement disorder.
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