| 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. |
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| 3. |
- Carney Almroth, Bethanie, 1974, et al.
(författare)
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Assessing the effects of textile leachates in fish using multiple testing methods: From gene expression to behavior
- 2021
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Ingår i: Ecotoxicology and Environmental Safety. - : Elsevier BV. - 0147-6513 .- 1090-2414. ; 207
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Tidskriftsartikel (refereegranskat)abstract
- The textile industry, while of major importance in the world economy, is a toxic industry utilizing and emitting thousands of chemical substances into the aquatic environment. The aim of this project was to study the potentially harmful effects associated with the leaching of chemical residues from three different types of textiles: sportswear, children’s bath towels, and denim using different fish models (cell lines, fish larvae and juvenile fish). A combination of in vitro and in vivo test systems was used. Numerous biomarkers, ranging from gene expression, cytotoxicity and biochemical analysis to behavior, were measured to detect effects of leached chemicals. Principle findings indicate that leachates from all three types of textiles induced cytotoxicity on fish cell lines (RTgill-W1). Leachates from sportswear and towels induced mortality in zebrafish embryos, and chemical residues from sportswear reduced locomotion responses in developing larval fish. Sportswear leachate increased Cyp1a mRNA expression and EROD activity in liver of exposed brown trout. Leachates from towels induced EROD activity and VTG in rainbow trout, and these effects were mitigated by the temperature of the extraction process. All indicators of toxicity tested showed that exposure to textile leachate can cause adverse reactions in fish. These findings suggested that chemical leaching from textiles from domestic households could pose an ecotoxicological threat to the health of the aquatic environment.
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| 4. |
- Chen, Yue, et al.
(författare)
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A novel nanoparticle system targeting damaged mitochondria for the treatment of Parkinson's disease
- 2022
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Ingår i: Biomaterials Advances. - : Elsevier BV. - 2772-9516 .- 2772-9508. ; 138
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Tidskriftsartikel (refereegranskat)abstract
- Mitochondrial damage is one of the primary causes of neuronal cell death in Parkinson's disease (PD). In PD patients, the mitochondrial damage can be repaired or irreversible. Therefore, mitochondrial damage repair becomes a promising strategy for PD treatment. In this research, hyaluronic acid nanoparticles (HA-NPs) of different molecular weights are used to protect the mitochondria and salvage the mild and limited damage in mitochondria. The HA-NPs with 2190 k Dalton (kDa) HA can improve the mitochondrial function of SH-SY5Y cells and PTEN induced putative kinase 1 (PINK1) knockout mouse embryo fibroblast (MEF) cells. In cases of irreversible damage, NPs with ubiquitin specific peptidase 30 (USP30) siRNA are used to promote mitophagy. Meanwhile, by adding PINK1 antibodies, the NPs can selectively target the irreversibly damaged mitochondria, preventing the excessive clearance of healthy mitochondria.
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| 5. |
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| 6. |
- Lu, Qiongxuan, et al.
(författare)
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IL-17 undermines longevity and stress tolerance by inhibiting a protective transcriptional network
- 2024
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Aberrant cytokine secretion contributes to the pathogenesis of autoimmune diseases and age-related disorders, but the molecular mechanism underlying this is not entirely clear. Here, we elucidate how interleukin-17 (IL-17) overactivation shortens lifespan and damages defense mechanisms against stress inC. elegans. Our analysis reveals that NHR-49, theC. elegansortholog of human PPARα and HNF4, is the central component in the transcriptional network undermined by increased IL-17 signaling. Both NHR-49 and its coactivator MDT-15 physically interact with the downstream components of IL-17 pathway, and their expression is significantly decreased when IL-17 signaling is enhanced. IL-17 overactivation also induces the expression and nucleus entry of theC. elegansortholog of NF-κB inhibitor NFKI-1/IκBζ to repress the activity of transcriptional coactivator MDT-15 and CBP-1. IL-17 signaling acts on neurons to modulate the activity of NFKI-1/IκBζ and NHR-49. In addition, persistent IL-17 activation decreases the expression of HLH-30/TFEB, leading to the reduced transcription of lysosomal lipase genes in the distal tissues. All these jointly contribute to the increased sensitivity to oxidative stress of animals with enhanced IL-17 signaling. Collectively, our work illustrates a transcription system undermined by IL-17 overactivation in the animals without NF-κB, and provides mechanistic insight into the pathogenesis of abnormal IL-17 secretion.
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| 7. |
- Naghibi, Seyed Amir, et al.
(författare)
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Spatiotemporal variability of dust storm source susceptibility during wet and dry periods: The Tigris-Euphrates River Basin
- 2024
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Ingår i: Atmospheric Pollution Research. - 1309-1042. ; 15:1
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Tidskriftsartikel (refereegranskat)abstract
- This study develops a framework for spatiotemporal modeling of dust storm source susceptibility in a critical case study, the Tigris-Euphrates River Basin, as a significant source of dust storms in the Middle East. The study period was divided into four periods, 2000–2004 (hydrological dry year), 2005–2007 (hydrological wet year), 2008–2012 (hydrological dry year), and 2013–2021 (hydrological wet year) representing hydrological conditions in the study area. Initially, visual interpretations of true color composites of the MODIS satellite images were conducted to spot dust storm sources in the studied periods. Topographical, hydrological, soil texture, and vegetation health datasets were prepared to model dust storm source susceptibility in each period. The random forest algorithm was implemented on the four study periods’ datasets. For each period, 70% of dust and non-dust storm sources and conditioning factors were used for training the models. The models were then validated using the validation datasets (remaining 30%), and the importance of the variables was determined for each study period. In the 2008–2012 period, experiencing an extensive drought in the region, a higher number of dust storm sources were detected, and 383 locations (pixels) in the area were considered highly susceptible to dust storm sources. In all study periods, as well as in the ensemble model (integrating the results of four study periods into one overall model), high susceptibility to dust storms was detected in areas where lakes and marshlands had dried up due to climate factors, inappropriate water management strategies, and land use policies. The results also depicted that elevation, wind speed, precipitation, vegetation coverage, slope degree, distance from rivers, and soil texture had high impacts on the susceptibility of land to be a dust storm source.
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| 8. |
- Nduwayezu, Gilbert, et al.
(författare)
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Understanding the spatial non-stationarity in the relationships between malaria incidence and environmental risk factors using Geographically Weighted Random Forest : A case study in Rwanda
- 2023
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Ingår i: Geospatial health. - 1970-7096. ; 18:1
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Tidskriftsartikel (refereegranskat)abstract
- As found in the health studies literature, the levels of climate association between epidemiological diseases have been found to vary across regions. Therefore, it seems reasonable to allow for the possibility that relationships might vary spatially within regions. We implemented the geographically weighted random forest (GWRF) machine learning method to analyze ecological disease patterns caused by spatially non-stationary processes using a malaria incidence dataset for Rwanda. We first compared the geographically weighted regression (WGR), the global random forest (GRF), and the geographically weighted random forest (GWRF) to examine the spatial non-stationarity in the non-linear relationships between malaria incidence and their risk factors. We used the Gaussian areal kriging model to disaggregate the malaria incidence at the local administrative cell level to understand the relationships at a fine scale since the model goodness of fit was not satisfactory to explain malaria incidence due to the limited number of sample values. Our results show that in terms of the coefficients of determination and prediction accuracy, the geographical random forest model performs better than the GWR and the global random forest model. The coefficients of determination of the geographically weighted regression (R2), the global RF (R2), and the GWRF (R2) were 4.74, 0.76, and 0.79, respectively. The GWRF algorithm achieves the best result and reveals that risk factors (rainfall, land surface temperature, elevation, and air temperature) have a strong non-linear relationship with the spatial distribution of malaria incidence rates, which could have implications for supporting local initiatives for malaria elimination in Rwanda.
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| 9. |
- Peng, Ningxin, et al.
(författare)
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Platelet mitochondrial DNA methylation : A novel biomarker for myocardial infarction – A preliminary study
- 2023
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Ingår i: International Journal of Cardiology. - 0167-5273.
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Tidskriftsartikel (refereegranskat)abstract
- Background: Platelet activation and thrombus formation play critical roles in the pathogenesis of myocardial infarction (MI). In addition to their role in energy production, platelet mitochondria also regulate cellular functions related to apoptosis, oxidative stress, and inflammation. Epigenetic modifications of platelet mitochondrial DNA (mtDNA) may influence platelet function and are believed to be an important factor in MI. Therefore, the aim of this study was to investigate the differences in platelet mtDNA methylation levels between MI patients and controls. Methods: The present study utilized propensity score matching to generate 45 multivariate matched apparently healthy controls for 45 patients with newly-onset acute MI. Platelet mtDNA methylation levels were assessed through bisulfite-PCR pyrosequencing and compared between the two groups, with further adjustments made in the sensitivity analysis. Results: Among the measured mitochondrial genes (MT-COX1, MT-COX2, MT-COX3, MT-ND5, MT-ATP6 and tRNA_Leu), patients with MI exhibited statistically significant differences in mtDNA methylation levels as compared to matched controls. Specifically, higher levels of mtDNA methylation were observed in MT-COX1, MT-COX3, and tRNA_Leu, while a lower level was observed in MT-ATP6 (all p < 0.0001). These results remained robust in the sensitivity analysis. Conclusion: Our study demonstrated significant variations in platelet mtDNA methylation levels between patients with MI and controls. Platelet mtDNA methylation may serve as a novel biomarker for MI. This observation also provided some insights into the etiology of MI.
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| 10. |
- Pu, Longjun, et al.
(författare)
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Dissecting the genetic landscape of GPCR signaling through phenotypic profiling in C. elegans
- 2023
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Ingår i: Nature Communications. - : Springer Nature. - 2041-1723. ; 14
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Tidskriftsartikel (refereegranskat)abstract
- G protein-coupled receptors (GPCRs) mediate responses to various extracellular and intracellular cues. However, the large number of GPCR genes and their substantial functional redundancy make it challenging to systematically dissect GPCR functions in vivo. Here, we employ a CRISPR/Cas9-based approach, disrupting 1654 GPCR-encoding genes in 284 strains and mutating 152 neuropeptide-encoding genes in 38 strains in C. elegans. These two mutant libraries enable effective deorphanization of chemoreceptors, and characterization of receptors for neuropeptides in various cellular processes. Mutating a set of closely related GPCRs in a single strain permits the assignment of functions to GPCRs with functional redundancy. Our analyses identify a neuropeptide that interacts with three receptors in hypoxia-evoked locomotory responses, unveil a collection of regulators in pathogen-induced immune responses, and define receptors for the volatile food-related odorants. These results establish our GPCR and neuropeptide mutant libraries as valuable resources for the C. elegans community to expedite studies of GPCR signaling in multiple contexts.
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