[go: up one dir, main page]

 
 
Sign in to use this feature.

Years

Between: -

Subjects

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Journals

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Article Types

Countries / Regions

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Search Results (3,608)

Search Parameters:
Keywords = infusions

Order results
Result details
Results per page
Select all
Export citation of selected articles as:
30 pages, 9406 KiB  
Article
Potential Use and Chemical Analysis of Some Natural Plant Extracts for Controlling Listeria spp. Growth In Vitro and in Food
by Abdul-Raouf Al-Mohammadi, Seham Abdel-Shafi, Ahmed H. Moustafa, Nehal Fouad, Gamal Enan and Rehab A. Ibrahim
Foods 2024, 13(18), 2915; https://doi.org/10.3390/foods13182915 (registering DOI) - 14 Sep 2024
Viewed by 343
Abstract
Listeria are Gram-negative intracellular foodborne pathogens that can cause invasive infections with high mortality rates. In this work, the antibacterial activity of ten essential oils, infusion extracts, and decoction extracts of some medicinal plants was tested against Listeria monocytogenes and listeria ivanovii strains. [...] Read more.
Listeria are Gram-negative intracellular foodborne pathogens that can cause invasive infections with high mortality rates. In this work, the antibacterial activity of ten essential oils, infusion extracts, and decoction extracts of some medicinal plants was tested against Listeria monocytogenes and listeria ivanovii strains. The effects of different physical conditions including temperature, pH, sodium chloride, and some organic acids were studied. The results showed that the water extracts gave the maximum bacterial inhibition, while ethanolic extract was inactive against the tested Listeria spp. The antibiotic sensitivity of L. monocytogenes LMG10470 and L. ivanovii LMZ11352 was tested against five antibiotics including imipenem, levofloxacin, amikacin, ampicillin, and amoxicillin. Imipenem was the most effective antibiotic, resulting in inhibition zones of 40 mm and 31 mm for L. monocytogenes and L. ivanovii, respectively. When imipenem mixed with Syzygium aromaticum oil, Salvia officinalis oil, Pimpinella anisum infusion, and Mentha piperita infusion each, the water extract of Moringa oleifera leaves and seeds against LMG10470 and LMZ11352 resulted in broader antibacterial activity. The antimicrobial activity of both Pimpinella anisum and Mentha piperita plant extracts is related to a variety of bioactive compounds indicated by gas chromatography–mass spectrometry analysis of these two plant extracts. These two plant extracts seemed to contain many chemical compounds elucidated by gas chromatography–mass spectrometry (GC-MS) and infrared radiation spectra. These compounds could be classified into different chemical groups such as ethers, heterocyclic compounds, aromatic aldehydes, condensed heterocyclic compounds, ketones, alicyclic compounds, aromatics, esters, herbicides, saturated fatty acids, and unsaturated fatty acids. The use of these natural compounds seems to be a useful technological adjuvant for the control of Listeria spp. in foods. Full article
(This article belongs to the Special Issue Detection and Control of Food-Borne Pathogens)
Show Figures

Figure 1

Figure 1
<p>Thermal death point of <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 after 15 min of exposure to different temperatures different temperature exposure.</p>
Full article ">Figure 2
<p>Effect of different pH values on <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 growth.</p>
Full article ">Figure 3
<p>Effect of different NaCl concentrations on <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 growth.</p>
Full article ">Figure 4
<p>Effect of citric acid concentration on <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 growth.</p>
Full article ">Figure 5
<p>Effect of oxalic acid concentrations on <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 growth.</p>
Full article ">Figure 6
<p>Effect of salicylic acid concentrations on <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 growth.</p>
Full article ">Figure 7
<p>Antibacterial activity of different concentrations of infusion extracts of <span class="html-italic">Mentha piperita</span> and <span class="html-italic">Pimpinella anisum</span> against <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 by the disc assay method. The numbers 1, 2, 3, 4, and 5 show inhibition zone diameters of 10%, 25%, 50%, 75%, and 100%.</p>
Full article ">Figure 8
<p>Growth curves of (<b>A</b>) Pimpinella anisum, (<b>B</b>) Mentha piperita, (<b>C</b>) Zingiber officinalis, (<b>D</b>) Rosemarinus officinalis, (<b>E</b>) Salvia officinalis, and (<b>F</b>) Martricaria chamomilla against L. monocytogenes LMG10470 in nutrient broth incubated at 37 °C for 24 h.</p>
Full article ">Figure 8 Cont.
<p>Growth curves of (<b>A</b>) Pimpinella anisum, (<b>B</b>) Mentha piperita, (<b>C</b>) Zingiber officinalis, (<b>D</b>) Rosemarinus officinalis, (<b>E</b>) Salvia officinalis, and (<b>F</b>) Martricaria chamomilla against L. monocytogenes LMG10470 in nutrient broth incubated at 37 °C for 24 h.</p>
Full article ">Figure 9
<p>Growth curves of (<b>A</b>) <span class="html-italic">Pimpinella anisum</span>, (<b>B</b>) <span class="html-italic">Mentha piperita</span>, (<b>C</b>) <span class="html-italic">Zingiber officinalis</span>, (<b>D</b>) <span class="html-italic">Rosemarinus officinalis</span>, (<b>E</b>) <span class="html-italic">Salvia officinalis</span>, and (<b>F</b>) <span class="html-italic">Martricaria chamomilla</span> against <span class="html-italic">L. ivanovii</span> LMZ11352 in nutrient broth incubated at 37 °C for 24 h.</p>
Full article ">Figure 9 Cont.
<p>Growth curves of (<b>A</b>) <span class="html-italic">Pimpinella anisum</span>, (<b>B</b>) <span class="html-italic">Mentha piperita</span>, (<b>C</b>) <span class="html-italic">Zingiber officinalis</span>, (<b>D</b>) <span class="html-italic">Rosemarinus officinalis</span>, (<b>E</b>) <span class="html-italic">Salvia officinalis</span>, and (<b>F</b>) <span class="html-italic">Martricaria chamomilla</span> against <span class="html-italic">L. ivanovii</span> LMZ11352 in nutrient broth incubated at 37 °C for 24 h.</p>
Full article ">Figure 10
<p>Quantitative inhibition of decoction extract of the test medicinal plants against <span class="html-italic">L. monocytogenes</span> LMG10470. (<b>A</b>) <span class="html-italic">Pimpinella anisum</span>, (<b>B</b>) <span class="html-italic">Rosemarinus officinalis</span>, (<b>C</b>) <span class="html-italic">Cinnamum zeylanieum</span>, and (<b>D</b>) <span class="html-italic">Syzygium aromaticum</span>.</p>
Full article ">Figure 10 Cont.
<p>Quantitative inhibition of decoction extract of the test medicinal plants against <span class="html-italic">L. monocytogenes</span> LMG10470. (<b>A</b>) <span class="html-italic">Pimpinella anisum</span>, (<b>B</b>) <span class="html-italic">Rosemarinus officinalis</span>, (<b>C</b>) <span class="html-italic">Cinnamum zeylanieum</span>, and (<b>D</b>) <span class="html-italic">Syzygium aromaticum</span>.</p>
Full article ">Figure 11
<p>Quantitative inhibition of decoction extract of test medicinal plants against <span class="html-italic">L. ivanovii</span> LMZ11352. (<b>A</b>) <span class="html-italic">Pimpinella anisum</span>, (<b>B</b>) <span class="html-italic">Rosemarinus officinalis</span>, (<b>C</b>) <span class="html-italic">Cinnamum zeylanieum</span>, and (<b>D</b>) <span class="html-italic">Syzygium aromaticum</span>.</p>
Full article ">Figure 12
<p>Antibacterial activity of <span class="html-italic">Moringa oleifera</span> extracts (leaves) against <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 using disc assay and agar well diffusion methods. WE: water extract of leaves. ME: methanol extract of leaves.</p>
Full article ">Figure 13
<p>Antibacterial activity of <span class="html-italic">Moringa oleifera</span> extracts (Seeds) against <span class="html-italic">L. monocytogenes</span> LMG10470 and <span class="html-italic">L. ivanovii</span> LMZ11352 using disc assay and agar well diffusion methods. WE: water extract of seeds. ME: methanol extract of seeds.</p>
Full article ">Figure 14
<p>Antibacterial activity of mixed combinations of natural extracts and an antibiotic (imipenem) against <span class="html-italic">L. monocytogenes</span> by the disc assay method. (<b>A</b>) imipenem against <span class="html-italic">L. monocytogenes</span>. (<b>B</b>) (imipenem–natural extract) mixture combination against <span class="html-italic">L. monocytogenes</span>. (<b>C</b>) natural extract against <span class="html-italic">L. monocytogenes</span>.</p>
Full article ">Figure 14 Cont.
<p>Antibacterial activity of mixed combinations of natural extracts and an antibiotic (imipenem) against <span class="html-italic">L. monocytogenes</span> by the disc assay method. (<b>A</b>) imipenem against <span class="html-italic">L. monocytogenes</span>. (<b>B</b>) (imipenem–natural extract) mixture combination against <span class="html-italic">L. monocytogenes</span>. (<b>C</b>) natural extract against <span class="html-italic">L. monocytogenes</span>.</p>
Full article ">Figure 15
<p>Antibacterial activity of mixed combinations of natural extracts and an antibiotic (imipenem) against <span class="html-italic">L. ivanovii</span> by the disc assay method. (<b>A</b>): imipenem against <span class="html-italic">L. ivanovii</span>. (<b>B</b>): (imipenem—natural extract) mixture combination against <span class="html-italic">L. ivanovii.</span> (<b>C</b>): natural extract against <span class="html-italic">L. ivanovii</span>.</p>
Full article ">Figure 15 Cont.
<p>Antibacterial activity of mixed combinations of natural extracts and an antibiotic (imipenem) against <span class="html-italic">L. ivanovii</span> by the disc assay method. (<b>A</b>): imipenem against <span class="html-italic">L. ivanovii</span>. (<b>B</b>): (imipenem—natural extract) mixture combination against <span class="html-italic">L. ivanovii.</span> (<b>C</b>): natural extract against <span class="html-italic">L. ivanovii</span>.</p>
Full article ">Figure 16
<p>IR spectrum of <span class="html-italic">Pimpinella anisum.</span> Growth of <span class="html-italic">L. monocytogenes</span> LMG10470 (CFU/mL) in the presence of <span class="html-italic">L. delbreukii</span> subsp. <span class="html-italic">bulgaricus</span> Z55, <span class="html-italic">E. faecium</span> NM2, and <span class="html-italic">L. plantarum</span> LPS10 in vitro.</p>
Full article ">Figure 17
<p>IR spectrum of <span class="html-italic">Mentha pipertia</span>.</p>
Full article ">
20 pages, 2961 KiB  
Article
Leveraging Large Language Models with Chain-of-Thought and Prompt Engineering for Traffic Crash Severity Analysis and Inference
by Hao Zhen, Yucheng Shi, Yongcan Huang, Jidong J. Yang and Ninghao Liu
Computers 2024, 13(9), 232; https://doi.org/10.3390/computers13090232 (registering DOI) - 14 Sep 2024
Viewed by 218
Abstract
Harnessing the power of Large Language Models (LLMs), this study explores the use of three state-of-the-art LLMs, specifically GPT-3.5-turbo, LLaMA3-8B, and LLaMA3-70B, for crash severity analysis and inference, framing it as a classification task. We generate textual narratives from original traffic crash tabular [...] Read more.
Harnessing the power of Large Language Models (LLMs), this study explores the use of three state-of-the-art LLMs, specifically GPT-3.5-turbo, LLaMA3-8B, and LLaMA3-70B, for crash severity analysis and inference, framing it as a classification task. We generate textual narratives from original traffic crash tabular data using a pre-built template infused with domain knowledge. Additionally, we incorporated Chain-of-Thought (CoT) reasoning to guide the LLMs in analyzing the crash causes and then inferring the severity. This study also examine the impact of prompt engineering specifically designed for crash severity inference. The LLMs were tasked with crash severity inference to: (1) evaluate the models’ capabilities in crash severity analysis, (2) assess the effectiveness of CoT and domain-informed prompt engineering, and (3) examine the reasoning abilities with the CoT framework. Our results showed that LLaMA3-70B consistently outperformed the other models, particularly in zero-shot settings. The CoT and Prompt Engineering techniques significantly enhanced performance, improving logical reasoning and addressing alignment issues. Notably, the CoT offers valuable insights into LLMs’ reasoning process, unleashing their capacity to consider diverse factors such as environmental conditions, driver behavior, and vehicle characteristics in severity analysis and inference. Full article
(This article belongs to the Special Issue Natural Language Processing (NLP) and Large Language Modelling)
Show Figures

Figure 1

Figure 1
<p>Illustration of textual narrative generation.</p>
Full article ">Figure 2
<p>Zero-shot (ZS).</p>
Full article ">Figure 3
<p>Zero-shot with CoT (ZS_CoT).</p>
Full article ">Figure 4
<p>Zero-shot with prompt engineering (ZS_PE).</p>
Full article ">Figure 5
<p>Zero-shot with prompt engineering &amp; CoT (ZS_PE_CoT).</p>
Full article ">Figure 6
<p>Few shot (FS).</p>
Full article ">Figure 7
<p>Exemplar responses of LLMs in different settings.</p>
Full article ">Figure 8
<p>Effect of PE or CoT separately.</p>
Full article ">Figure 9
<p>Performance comparison of models in ZS, ZS_PE, and ZS_PE_CoT.</p>
Full article ">Figure 10
<p>Word cloud for correctly inferred “Minor or non-injury accident” in the ZS_CoT setting.</p>
Full article ">Figure 11
<p>Word cloud for correctly inferred “Serious injury accident” in the ZS_CoT setting.</p>
Full article ">Figure 12
<p>Word cloud for correctly inferred “Fatal accident” in the ZS_CoT setting.</p>
Full article ">Figure 13
<p>Output examples for fatal accidents from LLaMA3-70B in ZS_CoT setting.</p>
Full article ">
14 pages, 647 KiB  
Article
Bayesian Knowledge Infusion for Studying Historical Sunspot Numbers
by Wenxin Jiang and Haisheng Ji
Universe 2024, 10(9), 370; https://doi.org/10.3390/universe10090370 (registering DOI) - 14 Sep 2024
Viewed by 135
Abstract
A scientific method that proposes a value Y to estimate a target value ρ is often subject to some level of uncertainty. In the Bayesian framework, the level of uncertainty can be measured by the width of the 68% interval, which is [...] Read more.
A scientific method that proposes a value Y to estimate a target value ρ is often subject to some level of uncertainty. In the Bayesian framework, the level of uncertainty can be measured by the width of the 68% interval, which is the range of the middle 68% of the ranked ρ values sampled from the posterior distribution p(ρ|Y). This paper considers Bayesian knowledge infusion (BKI) to reduce the uncertainty of the posterior distribution p(ρ|Y) based on additional knowledge that an event A happens. BKI is achieved by using a conditional prior distribution p(ρ|A) in the Bayes theorem, assuming that given the true ρ, its error-contaminated value Y is independent of event A. We use two examples to illustrate how to study whether or not it is possible to reduce uncertainty from 14C reconstruction (Y) of the annual sunspot number (SSN) (ρ) by infusing additional information (A) using BKI. Information (A) that SSN is from a year that has a Far Eastern record of naked eye sunspots is found to be not so effective in reducing the uncertainty. In contrast, information that SSN is from a year at a cycle minimum is found to be very effective, producing much narrower 68% intervals. The resulting Bayesian point estimates of SSN (the posterior medians of ρ) are cross-validated and tested on a subset of telescopically observed SSNs that were unused in the process of Bayes computation. Full article
(This article belongs to the Section Astroinformatics and Astrostatistics)
Show Figures

Figure 1

Figure 1
<p>Bayesian point estimates and 68% intervals (symbolized by red dots with vertical error bars) for the SSNs, computed using post-1818 SSNs at years with NES observations, plotted over the years before 1818, and compared to the <sup>14</sup>C reconstruction (solid curve with shade for 68% uncertainty) and to the telescopically observed SSNs (dashed curve).</p>
Full article ">Figure 2
<p>Information of cycle minimums does further reduce uncertainty of SSN estimated from <sup>14</sup>C construction. Each boxplot is from 28 widths of the 68% intervals for the 28 years of plausible cycle minima found from the <sup>14</sup>C reconstruction (listed in <a href="#universe-10-00370-t001" class="html-table">Table 1</a>). For the boxplot above ‘<sup>14</sup>C’, the interval width for year <span class="html-italic">j</span> is <math display="inline"><semantics> <mrow> <mn>2</mn> <msub> <mi>σ</mi> <mi>j</mi> </msub> </mrow> </semantics></math>; for the boxplot above ‘0-truncated <sup>14</sup>C’, the interval width for year <span class="html-italic">j</span> is <math display="inline"><semantics> <mrow> <mo movablelimits="true" form="prefix">max</mo> <mrow> <mo>{</mo> <msub> <mi>Y</mi> <mi>j</mi> </msub> <mo>+</mo> <msub> <mi>σ</mi> <mi>j</mi> </msub> <mo>,</mo> <mn>0</mn> <mo>}</mo> </mrow> <mo>−</mo> <mo movablelimits="true" form="prefix">max</mo> <mrow> <mo>{</mo> <msub> <mi>Y</mi> <mi>j</mi> </msub> <mo>−</mo> <msub> <mi>σ</mi> <mi>j</mi> </msub> <mo>,</mo> <mn>0</mn> <mo>}</mo> </mrow> </mrow> </semantics></math>, where <math display="inline"><semantics> <msub> <mi>Y</mi> <mi>j</mi> </msub> </semantics></math> is the <sup>14</sup>C reconstruction and <math display="inline"><semantics> <msub> <mi>σ</mi> <mi>j</mi> </msub> </semantics></math> is the 1-sigma uncertainty. For both the boxplots above ‘Bayes’ and above ‘Bayes with cycle min’, each interval width is computed as the difference of the 84% quantile and the 16% quantile of the posterior distribution. For ‘Bayes with cycle min’, the prior distribution uses the telescopic observations of annual SSNs, only at years of cycle minima, between years 1818 and 2023. For ‘Bayes’, the prior distribution uses all the telescopic observations of annual SSNs, whether or not at cycle minima, between years 1818 and 2023.</p>
Full article ">Figure 3
<p>Bayesian point estimates and 68% intervals (symbolized by red dots with vertical errorbars) of the SSNs, incorporating telescopic data after 1818, at plausible cycle minimums before 1818, plotted over the years, compared to the <sup>14</sup>C reconstruction (solid curve with shade for 68% uncertainty) and to the telescopic SSNs in the later years (dashed curve).</p>
Full article ">Figure 4
<p>Bayesian reconstruction for SSNs at 11 cycle minimums before 1899, using post-1899 telescopic data at the cycle minimums, plotted over the years, compared to the <sup>14</sup>C reconstruction (solid curve with shade for 68% uncertainty) and to the unused information on telescopic SSNs (dashed curve). The red dots and the vertical error bars display the Bayesian point estimate (posterior median) and the nominal 68% intervals. The horizontal error bars extend to the year of the nearest plausible cycle minimum according to the <sup>14</sup>C reconstruction, as defined in note 3, with ties averaged. Therefore, the lengths of the horizontal error bars reflect the errors of placements of the cycle minimums by the <sup>14</sup>C reconstruction.</p>
Full article ">
9 pages, 1565 KiB  
Article
Orbital Adipose Tissue: The Optimal Control for Back-Table Fluorescence Imaging of Orbital Tumors
by Lan Yao, Wenhua Zhang, Xuedong Wang, Lishuang Guo, Wenlu Liu, Yueyue Li, Rui Ma, Yan Hei, Xinji Yang, Zeyu Zhang and Wei Wu
Bioengineering 2024, 11(9), 922; https://doi.org/10.3390/bioengineering11090922 (registering DOI) - 14 Sep 2024
Viewed by 163
Abstract
Control tissue is essential for ensuring the precision of semiquantitative analysis in back-table fluorescence imaging. However, there remains a lack of agreement on the appropriate selection of control tissues. To evaluate the back-table fluorescence imaging performance of different normal tissues and identify the [...] Read more.
Control tissue is essential for ensuring the precision of semiquantitative analysis in back-table fluorescence imaging. However, there remains a lack of agreement on the appropriate selection of control tissues. To evaluate the back-table fluorescence imaging performance of different normal tissues and identify the optimal normal tissue, a cohort of 39 patients with orbital tumors were enrolled in the study. Prior to surgery, these patients received indocyanine green (ICG) and following resection, 43 normal control tissues (34 adipose tissues, 3 skin tissues, 3 periosteal tissues, and 3 muscle tissues) were examined using back-table fluorescence imaging. The skin tissue demonstrated significantly elevated fluorescence intensity in comparison to the diseased tissue, whereas the muscle tissue exhibited a broad range and standard deviation of fluorescence signal intensity. Conversely, the adipose and periosteum displayed weak fluorescence signals with a relatively consistent distribution. Additionally, no significant correlations were found between the signal-to-background ratio (SBR) of adipose tissue and patients’ ages, genders, weights, disease duration, tumor origins, dosing of administration of ICG infusion, and the time interval between ICG infusion and surgery. However, a positive correlation was observed between the SBR of adipose tissue and its size, with larger adipose tissues (>1 cm) showing an average SBR 27% higher than smaller adipose tissues (≤1 cm). In conclusion, the findings of this study demonstrated that adipose tissue consistently exhibited homogeneous hypofluorescence during back-table fluorescence imaging, regardless of patient clinical variables or imaging parameters. The size of the adipose tissue was identified as the primary factor influencing its fluorescence imaging characteristics, supporting its utility as an ideal control tissue for back-table fluorescence imaging. Full article
(This article belongs to the Special Issue Recent Advances and Trends in Ophthalmic Diseases Treatment)
Show Figures

Figure 1

Figure 1
<p>Fluorescence signal distribution in different control tissues. (<b>A</b>) White light and fluorescence imaging results in a representative skin tissue. The red dotted line outlines the diseased tissue and the arrow indicates the normal tissue. (<b>B</b>–<b>D</b>) White light and fluorescence imaging results in tumor tissues and patient-matched normal tissues (adipose, muscle, and periosteum tissues). (<b>E</b>,<b>F</b>) The range and standard deviation of gray values in the fluorescence imaging results of adipose, periosteum, and muscle tissues.</p>
Full article ">Figure 2
<p>Correlation between the SBR of adipose tissue and the dose of ICG (<b>A</b>,<b>B</b>) or the time of ICG injection (<b>C</b>).</p>
Full article ">Figure 3
<p>The fluorescence imaging results of adipose tissues might be affected by their sizes. (<b>A</b>) In four typical adipose tissues, the large ones (&gt;1 cm) showed stronger fluorescence than the small ones (≤1 cm). (<b>B</b>) The calculated SBR of adipose tissues was also in proportion to the tissue size. The SBR of large tissues (&gt;1 cm) is significantly higher than that of small tissues (≤1 cm). ** <span class="html-italic">p</span> &lt; 0.01.</p>
Full article ">
20 pages, 4248 KiB  
Article
Reducing Flow Resistance via Introduction and Enlargement of Microcracks in Convection Enhanced Delivery (CED) in Porous Tumors
by Md Jawed Naseem, Ronghui Ma and Liang Zhu
Fluids 2024, 9(9), 215; https://doi.org/10.3390/fluids9090215 - 13 Sep 2024
Viewed by 179
Abstract
A theoretical simulation is performed to evaluate how microcracks affect the flow resistance in tumors during the convection-enhanced delivery (CED) of nanofluids. Both Darcy’s law and the theory of poroelasticity are used to understand fluid transport with or without microcrack introduction and/or enlargement. [...] Read more.
A theoretical simulation is performed to evaluate how microcracks affect the flow resistance in tumors during the convection-enhanced delivery (CED) of nanofluids. Both Darcy’s law and the theory of poroelasticity are used to understand fluid transport with or without microcrack introduction and/or enlargement. The results demonstrate significantly altered pressure and velocity fields in a spherical tumor with a radius of 10 mm due to the presence of a microcrack with a radius of 0.05 mm and length of 3 mm. The non-uniform fluid pressure field enlarges the original cylindrical microcrack to a frustum, with the crack volume more than doubled. Due to the larger permeability and porosity in the microcrack, flow in the tumor is much easier. One finds that the flow resistance with the enlarged microcrack is reduced by 14% from the control without a microcrack. Parametric studies are conducted to show that larger crack radii, longer crack lengths and higher infusing pressures result in further resistance reductions. The largest resistance reduction occurs when the infusing pressure is 4 × 105 Pa and the microcrack is 9 mm long, up to 18% from the control. We conclude that introducing a microcrack is an effective way to facilitate nanofluid delivery in porous tumors using CED. Full article
Show Figures

Figure 1

Figure 1
<p>Three models generated in this study for simulation. (<b>Left</b>): the first model without a crack; (<b>middle</b>): the second model with a cylindrical microcrack; and (<b>right</b>): the third model with an enlarged microcrack.</p>
Full article ">Figure 2
<p>Simulated pressure field (<b>left</b>) and velocity field (<b>right</b>) in the tumor without a microcrack. The inset images are the enlarged pressure and velocity fields near the infusion surface.</p>
Full article ">Figure 3
<p>Simulated pressure field (<b>left</b>) and velocity field (<b>right</b>) in the tumor with a cylindrical microcrack. The inset images are the enlarged pressure and velocity fields near the infusion surface and along the microcrack.</p>
Full article ">Figure 4
<p>Components of the displacement vector in the lateral (<b>Left</b>) and axial (<b>Right</b>) directions of the microcrack in the tumor with a cylindrical microcrack.</p>
Full article ">Figure 5
<p>The original (green dots) interface and post-deformation (red dots) interface of the microcrack and tissue plotted in Excel. A frustum-shaped microcrack is generated using curve fitting.</p>
Full article ">Figure 6
<p>Simulated pressure field (<b>left</b>) and velocity field (<b>right</b>) in the tumor with an enlarged frustum microcrack. The inset images are the enlarged pressure and velocity fields near the infusion surface and along the microcrack after deformation.</p>
Full article ">Figure 7
<p>The original (blue dots) and post-deformation (orange dots) interfaces between the microcrack and tumor region, as affected by the length of the microcrack.</p>
Full article ">Figure 8
<p>The original (blue dots) and post-deformation (orange dots) interfaces between the microcrack and tumor region, as affected by the radius of the original cylindrical microcrack.</p>
Full article ">Figure 9
<p>Details of the pressure field near the infusion surface and along the microcrack as influenced by the permeability of the microcrack: (<b>a</b>) <span class="html-italic">Κ</span><sub>2</sub> = 1 × 10<sup>−13</sup> m<sup>2</sup>, (<b>b</b>) <span class="html-italic">Κ</span><sub>2</sub> = 2.0173 × 10<sup>−13</sup> m<sup>2</sup>, and (<b>c</b>) <span class="html-italic">Κ</span><sub>2</sub> = 3 × 10<sup>−13</sup> m<sup>2</sup>.</p>
Full article ">Figure 10
<p>The original (blue dots) and post-deformation (orange dots) interfaces between the microcrack and tumor region, as affected by the permeability of the microcrack: (<b>a</b>) <span class="html-italic">Κ</span><sub>2</sub> = 1 × 10<sup>−13</sup> m<sup>2</sup>, (<b>b</b>) <span class="html-italic">Κ</span><sub>2</sub> = 2.0173 × 10<sup>−13</sup> m<sup>2</sup>, and (<b>c</b>) <span class="html-italic">Κ</span><sub>2</sub> = 3 × 10<sup>−13</sup> m<sup>2</sup>.</p>
Full article ">Figure 11
<p>Obtained enlargements of the microcrack from the original locations (blue dots) to later locations (orange dots) at different infusion pressures.</p>
Full article ">
16 pages, 2063 KiB  
Article
Postoperative Intravenous Iron Infusion in Anemic Colorectal Cancer Patients: An Observational Study
by Leonidas Chardalias, Androniki-Maria Skreka, Nikolaos Memos, Alexandra-Stavroula Nieri, Dimitrios Politis, Marianna Politou, Theodosios Theodosopoulos and Ioannis Papaconstantinou
Biomedicines 2024, 12(9), 2094; https://doi.org/10.3390/biomedicines12092094 - 13 Sep 2024
Viewed by 207
Abstract
Anemia is the most common extraintestinal symptom of colorectal cancer, with a prevalence of 30–75%. While the preoperative anemia in this patient population has been well studied and its correction 4–6 weeks prior to surgery is recommended when feasible, there is a paucity [...] Read more.
Anemia is the most common extraintestinal symptom of colorectal cancer, with a prevalence of 30–75%. While the preoperative anemia in this patient population has been well studied and its correction 4–6 weeks prior to surgery is recommended when feasible, there is a paucity of data regarding the management of postoperative anemia, which has a prevalence of up to 87% in these patients. To address this issue, we conducted an observational cohort study of surgically treated postoperative anemic patients with colorectal cancer. The objective of this study was to evaluate the effect of intravenous ferric carboxymaltose on the correction of postoperative anemia by postoperative day 30 (POD30). The primary outcome was the change in hemoglobin on POD30, while the secondary outcomes were the change in iron and other laboratory parameters, postoperative complications and transfusions. The results demonstrated that patients treated with intravenous iron exhibited a significant increase in hemoglobin levels by POD30, along with a concomitant increase in hematocrit, ferritin, and transferrin saturation levels, compared to the control group. The findings imply that patients undergoing colorectal cancer surgery with anemia that was not corrected in the preoperative setting may benefit from early postoperative intravenous iron infusion. Full article
(This article belongs to the Special Issue Advances in Iron Deficiency and Iron-Related Disorders)
Show Figures

Figure 1

Figure 1
<p>Hemoglobin levels from preoperative to POD30 in males.</p>
Full article ">Figure 2
<p>Hemoglobin levels from preoperative to postoperative day 30, female.</p>
Full article ">Figure 3
<p>Red blood cell levels from preoperative to postoperative day 30.</p>
Full article ">Figure 4
<p>(<b>a</b>) Ferritin levels from preoperative to postoperative day 30 in the male cohort. (<b>b</b>) Ferritin levels from preoperative to postoperative day 30 in the female cohort. The full black circle is an indication that an extreme outlier is present in the data. The circle is an indication that an outlier is present in the data.</p>
Full article ">Figure 4 Cont.
<p>(<b>a</b>) Ferritin levels from preoperative to postoperative day 30 in the male cohort. (<b>b</b>) Ferritin levels from preoperative to postoperative day 30 in the female cohort. The full black circle is an indication that an extreme outlier is present in the data. The circle is an indication that an outlier is present in the data.</p>
Full article ">Figure 5
<p>TSAT levels from preoperative to postoperative day 30. The asterisk (*) is an indication that an extreme outlier is present in the data. The circle is an indication that an outlier is present in the data.</p>
Full article ">
22 pages, 4974 KiB  
Article
E3 Ubiquitin Ligase CHIP Inhibits Haemocyte Proliferation and Differentiation via the Ubiquitination of Runx in the Pacific Oyster
by Miren Dong, Ying Song, Weilin Wang, Xiaorui Song, Wei Wu, Lingling Wang and Linsheng Song
Cells 2024, 13(18), 1535; https://doi.org/10.3390/cells13181535 - 13 Sep 2024
Viewed by 210
Abstract
Mollusca first evolve primitive immune cells (namely, haemocytes), which assemble a notable complex innate immune system, which are continuously produced through proliferation and differentiation and infused in the haemolymph. As a typical E3 ligase, CHIP is critical for immune cell turnover and homeostasis [...] Read more.
Mollusca first evolve primitive immune cells (namely, haemocytes), which assemble a notable complex innate immune system, which are continuously produced through proliferation and differentiation and infused in the haemolymph. As a typical E3 ligase, CHIP is critical for immune cell turnover and homeostasis in vertebrates. In this study, a CHIP homolog (CgCHIP) with a high expression in haemocytes was identified in oysters to investigate its role in the proliferation and differentiation of ancient innate immune cells. CgCHIP exhibited a widespread distribution across all haemocyte subpopulations, and the knockdown of CgCHIP altered the composition of haemocytes as examined by flow cytometry. Mechanistically screened with bioinformatics and immunoprecipitation, a key haematopoietic transcription factor CgRunx was identified as a substrate of CgCHIP. Moreover, amino acids in the interacted intervals of CgCHIP and CgRunx were determined by molecular docking. Experimental evidence from an in vitro culture model of an agranulocyte subpopulation and an in vivo oyster model revealed that the knockdown of CgCHIP and CgRunx had opposing effects on agranulocyte (precursor cells) differentiation and granulocyte (effector cells) proliferation. In summary, CgCHIP negatively regulated agranulocyte differentiation and granulocyte proliferation by mediating the ubiquitination and degradation of CgRunx in oysters. These results offer insight into the involvement of ubiquitylation in controlling haemocyte turnover in primitive invertebrates. Full article
Show Figures

Figure 1

Figure 1
<p>Evolutionary properties of ubiquitin E3 ligase CHIP from oyster <span class="html-italic">C</span>. <span class="html-italic">gigas</span>. (<b>A</b>) Domain and tertiary structure prediction of CHIP from oyster <span class="html-italic">C</span><b>.</b> <span class="html-italic">gigas</span> by SMART and SWISS-MODEL program. (<b>B</b>) Domain and tertiary structure prediction of CHIP from <span class="html-italic">Homo sapiens</span> by SMART and SWISS-MODEL program. The pink box indicates a low complexity domain. (<b>C</b>) Multisequence alignment analysis of <span class="html-italic">Cg</span>CHIP with its homologues from other vertebrate and invertebrate species. Amino acids with 100% identity are in black, and similar amino acids are in gray. (<b>D</b>) A phylogenetic tree for CHIP was constructed with the amino acid sequences from the indicated species including <span class="html-italic">H. sapiens</span>, <span class="html-italic">M. musculus</span>, <span class="html-italic">D. rerio</span>, <span class="html-italic">L. anatine</span>, <span class="html-italic">D. melanogaster</span>, <span class="html-italic">A. californica</span>, <span class="html-italic">B. glabrata</span>, <span class="html-italic">M. yessoensis</span>, <span class="html-italic">C</span>. <span class="html-italic">gigas</span>, <span class="html-italic">C. virginica</span>, and <span class="html-italic">C. elegans</span>. The trees were constructed using the neighbor-joining (NJ) algorithm in the Mega 6.0 program based on multiple sequence alignment by ClustalW. Bootstrap values of 1000 replicates (%) are indicated for the branches. CHIP from <span class="html-italic">C</span>. <span class="html-italic">gigas</span> was marked with a grey arrow.</p>
Full article ">Figure 2
<p><span class="html-italic">Cg</span>CHIP is highly expressed in oyster haemocytes and alters the proportion of their three subpopulations. (<b>A</b>) The mRNA transcripts of <span class="html-italic">Cg</span>CHIP in the indicated tissues and haemocytes examined by qRT-PCR, normalized to <span class="html-italic">Cg</span>EF1-α. Hep: hepatopancreas; Man: mantle; Gon: gonad; Amu: adductor muscle; Lap: labial palp; Gil: gill; Hae: haemocytes. <span class="html-italic">p</span>-values, <sup>a</sup> <span class="html-italic">p</span> &gt; 0.05, <sup>b</sup> <span class="html-italic">p</span> &lt; 0.05, and <sup>c</sup> <span class="html-italic">p</span> &lt; 0.01, were calculated using a one-way ANOVA with Dunnett’s correction for multiple comparisons. (<b>B</b>) Relative temporal levels of <span class="html-italic">Cg</span>CHIP mRNA in haemocytes with or without <span class="html-italic">V. splendidus</span> infection examined by qRT-PCR, normalized to <span class="html-italic">Cg</span>EF1-α. Error bars show mean ± standard deviation. <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, were calculated using a two-tailed, unpaired <span class="html-italic">t</span>-test. Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). (<b>C</b>) SDS-PAGE analysis showed the recombinant-<span class="html-italic">Cg</span>CHIP (r<span class="html-italic">Cg</span>CHIP) proteins. Lane M: protein molecular marker; Lane 1: negative control (without IPTG induction); Lane 2: induced recombinant protein with IPTG; Lane 3: purified r<span class="html-italic">Cg</span>CHIP protein. (<b>D</b>) The specificity of the <span class="html-italic">Cg</span>CHIP polyclonal antibody determined by Western blotting. Lane M: protein molecular marker; Lane 1: in vitro recombinant proteins; Lane 2: haemocyte lysate. (<b>E</b>) Transcriptome data analysis shows the mRNA transcripts of <span class="html-italic">Cg</span>CHIP in the three haemocyte subpopulations (<span class="html-italic">n</span> = 7). <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, were calculated using a one-way ANOVA with Dunnett’s correction for multiple comparisons. ns indicates no significant difference. (<b>F</b>) Haemocytes collected from oyster haematocoel, and morphology observed under confocal. (<b>G</b>) Haemocytes observed following Giemsa staining. (<b>H</b>) Three subpopulations of haemocytes morphologically identified and separated as agranulocytes (A), semi-granulocytes (SG), and granulocytes (G), by flow cytometry. (<b>I</b>) Representative immunofluorescence image shows the localization of <span class="html-italic">Cg</span>CHIP (green) in haemocytes and the nuclei stained with DAPI (blue). The localization region marked with yellow circles. (<b>J</b>) Bar graph shows the mean fluorescence intensity of <span class="html-italic">Cg</span>CHIP in the three haemocyte subpopulations. The per cell compartment was outlined, and the fluorescence intensity of positive signals within per cell was measured using ImageJ software. For each haemocyte subpopulation, the mean fluorescence value of ten cells from five fields were calculated as one replicate, and there were three replicates (<span class="html-italic">n</span> = 3). Abbreviations: Ara: agranulocytes; Semi-gra: semi-granulocytes; and Gra: granulocytes. (<b>K</b>) The percentages of three subpopulations in total haemocytes measured by flow cytometry (<span class="html-italic">n</span> = 3). (<b>L</b>) The bar graph shows the percentage of three haemocyte subpopulations (<span class="html-italic">n</span> = 3). <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, were calculated using a two-tailed, unpaired <span class="html-italic">t</span>-test.</p>
Full article ">Figure 3
<p><span class="html-italic">Cg</span>CHIP targets the <span class="html-italic">Cg</span>Runx protein. (<b>A</b>) CHIP was known to interact with Runx1 as predicted by UbiBrowser 2.0 program. (<b>B</b>) The typical and conserved ubiquitination sites within the Runx protein. The Runt domain is marked with a red box. A Met-1 ubiquitination site is marked with a blue asterisk. Four conserved Lys ubiquitination sites are labeled with a red triangle. (<b>C</b>) Co-IP-based interaction detection of <span class="html-italic">Cg</span>CHIP and <span class="html-italic">Cg</span>Runx in oyster haemocytes. (<b>D</b>) Docking model analysis of <span class="html-italic">Cg</span>CHIP and <span class="html-italic">Cg</span>Runx. (<b>E</b>) The binding coefficients of <span class="html-italic">Cg</span>CHIP and <span class="html-italic">Cg</span>Runx protein interaction sites. (<b>F</b>) Ubiquitination activity of <span class="html-italic">Cg</span>CHIP detected with Western blotting in vitro. (<b>G</b>) <span class="html-italic">Cg</span>Runx ubiquitination assessed by Western blotting. (<b>H</b>) The levels of <span class="html-italic">Cg</span>Runx in oyster haemocytes treated with MG132 (20 μM), quantified by Western blotting.</p>
Full article ">Figure 4
<p><span class="html-italic">Cg</span>CHIP enhances the ubiquitination and degradation of <span class="html-italic">Cg</span>Runx. (<b>A</b>) Representative immunofluorescence image shows the localization of <span class="html-italic">Cg</span>Runx (green) in haemocytes and the nuclei stained with DAPI (blue). (<b>B</b>) Transcriptome data analysis shows the mRNA transcripts of <span class="html-italic">Cg</span>Runx in the three haemocyte subpopulations (<span class="html-italic">n</span> = 7). <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, were calculated using a one-way ANOVA with Dunnett’s correction for multiple comparisons. ns indicates no significant difference. (<b>C</b>) Bar graph shows the mean fluorescence intensity of <span class="html-italic">Cg</span>Runx in the three haemocyte subpopulations. (<b>D</b>) An injection cartoon of dsRNA in the interference assay. (<b>E</b>) The RNAi efficiency of <span class="html-italic">Cg</span>CHIP in haemocytes quantified via qRT-PCR, normalized to <span class="html-italic">Cg</span>EF1-α. Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). <span class="html-italic">p</span>-values, ** <span class="html-italic">p</span> &lt; 0.01, were calculated using a two-tailed, unpaired <span class="html-italic">t</span>-test. (<b>F</b>) Protein abundance of <span class="html-italic">Cg</span>CHIP (RNAi efficiency) and <span class="html-italic">Cg</span>Runx examined with Western blotting. (<b>G</b>) Gray analysis of protein band, normalized to β-Tubulin and Histone H3, respectively. <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, were calculated using a two-tailed, unpaired <span class="html-italic">t</span>-test.</p>
Full article ">Figure 5
<p><span class="html-italic">Cg</span>CHIP inhibits agranulocyte differentiation. (<b>A</b>) Schematic of the induced differentiation in cultured agranulocytes. (<b>B</b>) Representative flow cytometry dot-plots show the gated semi-granulocyte and granulocyte populations differentiated from agranulocytes using the agranulocyte differentiation protocol. (<span class="html-italic">n</span> = 3). (<b>C</b>) The bar graph shows the percentage of differentiated agranulocytes (<span class="html-italic">n</span> = 3). * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, determined by a two-tailed Student’s <span class="html-italic">t</span>-test. (<b>D</b>,<b>E</b>) Protein expression levels of the proliferative marker <span class="html-italic">Cg</span>PCNA, immature agranulocyte marker <span class="html-italic">Cg</span>Integrin α4, and mature granulocyte marker <span class="html-italic">Cg</span>AATase, in agranulocytes. β-Tubulin was used as an internal control. Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, determined by a two-tailed Student’s <span class="html-italic">t</span>-test.</p>
Full article ">Figure 6
<p><span class="html-italic">Cg</span>CHIP inhibits granulocyte proliferation. (<b>A</b>) Representative flow cytometry peak diagrams show the proliferation rate of gated EdU labeling agranulocytes in total agranulocytes. (<b>B</b>) The bar graph shows the proliferation rate of agranulocytes (<span class="html-italic">n</span> = 3). (<b>C</b>) Representative flow cytometry peak diagrams showing the proliferation rate of gated EdU labeling granulocytes in total granulocytes. (<b>D</b>) The bar graph shows the proliferation rate of granulocytes (<span class="html-italic">n</span> = 3). * <span class="html-italic">p</span> &lt; 0.05, determined by a two-tailed Student’s <span class="html-italic">t</span> test. (<b>E</b>) Schematic of granulocyte isolation for cell cycle and Western blotting analyses. (<b>F</b>) The percentage changes of granulocytes in different cell cycle phases. (<b>G</b>) The bar graph shows the percentage of agranulocytes in different cell cycle phases (<span class="html-italic">n</span> = 3). Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). <span class="html-italic">p</span>-values, * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, were calculated using a one-way ANOVA with Dunnett’s correction for multiple comparisons. (<b>H</b>,<b>I</b>) Protein expression levels of proliferative genes <span class="html-italic">Cg</span>Cyclin B1 and <span class="html-italic">Cg</span>CDK2 in granulocytes. β-Tubulin was used as an internal control. Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). The data shown are representative of three independent experiments. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, determined by a two-tailed Student’s <span class="html-italic">t</span> test.</p>
Full article ">Figure 7
<p><span class="html-italic">Cg</span>CHIP attenuates phagocytosis in a <span class="html-italic">Cg</span>Runx-dependent manner. (<b>A</b>,<b>B</b>) Representative flow cytometry peak diagrams show the gated phagocytic haemocytes that are defined according to the red positive signal of latex beads. Phagocytic rate in haemocytes was defined by the percentage of phagocytic haemocytes taking in latex beads in total haemocytes. Error bars show mean ± standard deviation (<span class="html-italic">n</span> = 3). <span class="html-italic">p</span>-values were calculated using a one-way ANOVA with Dunnett’s correction for multiple comparisons. The asterisk * and ** indicated a significant difference at <span class="html-italic">p</span> &lt; 0.05 and extremely significant difference at <span class="html-italic">p</span> &lt; 0.01.</p>
Full article ">Figure 8
<p>A graphical abstract. A conceptual framework for the ubiquitination and degradation of <span class="html-italic">Cg</span>Runx mediated by <span class="html-italic">Cg</span>CHIP, which inhibits the differentiation of agranulocytes and the proliferation of granulocytes in the Pacific oyster <span class="html-italic">C</span>. <span class="html-italic">gigas</span>.</p>
Full article ">
18 pages, 8248 KiB  
Article
Gastrodin Alleviates Angiotensin II-Induced Hypertension and Myocardial Apoptosis via Inhibition of the PRDX2/p53 Pathway In Vivo and In Vitro
by Nanhui Xu, Qiurong Xie, Youqin Chen, Jiapeng Li, Xiuli Zhang, Huifang Zheng, Ying Cheng, Meizhu Wu, Aling Shen, Lihui Wei, Mengying Yao, Yanyan Yang, Thomas J. Sferra, Anjum Jafri, Yi Fang and Jun Peng
Pharmaceuticals 2024, 17(9), 1200; https://doi.org/10.3390/ph17091200 - 12 Sep 2024
Viewed by 397
Abstract
Gastrodin, a highly potent compound found in the traditional Chinese medicine Gastrodia elata Blume, exhibits significant antihypertensive properties. However, its role and the mechanism behind its protective effects on hypertensive cardiac conditions are not well understood. This study aims to investigate the cardiac [...] Read more.
Gastrodin, a highly potent compound found in the traditional Chinese medicine Gastrodia elata Blume, exhibits significant antihypertensive properties. However, its role and the mechanism behind its protective effects on hypertensive cardiac conditions are not well understood. This study aims to investigate the cardiac protective effects and underlying mechanisms of gastrodin in angiotensin II (Ang II)-induced hypertensive models, both in vivo and in vitro. Treatment with gastrodin significantly decreased blood pressure and the heart weight/tibial length (HW/TL) ratio and attenuated cardiac dysfunction and pathological damage in Ang II-infused C57BL/6 mice. RNA sequencing analysis (RNA-seq) revealed 697 up-regulated and 714 down-regulated transcripts, along with 1105 signaling pathways, in Ang II-infused C57BL/6 mice following gastrodin treatment, compared to Ang II-induced hypertensive mice. Furthermore, the analyses of the top 30 Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway indicated significant enrichment in apoptosis and the peroxiredoxin 2 (PRDX2)/p53 pathway. Consistently, gastrodin treatment significantly reduced myocardial apoptosis in both the cardiac tissues of Ang II-induced hypertensive mice and Ang II-stimulated H9c2 cells. Additionally, gastrodin treatment significantly decreased the protein levels of PRDX2, p53, cleaved caspase-3, cleaved caspase-9, and Bax/Bcl-2 ratio in the cardiac tissues of Ang II-infused mice and H9c2 cells stimulated with Ang II. In conclusion, gastrodin treatment can mitigate hypertension-induced myocardial apoptosis in hypertensive mice by inhibiting the PRDX2/p53 pathway. Full article
(This article belongs to the Section Pharmacology)
Show Figures

Figure 1

Figure 1
<p>The effects of gastrodin on blood pressure in Ang II-infused mice. Blood pressure was measured in mice from each group using the tail-cuff plethysmograph method once a week for a total of 4 weeks. (<b>a</b>) Systolic blood pressure (SBP), (<b>b</b>) diastolic blood pressure (DBP), (<b>c</b>) mean arterial pressure (MAP). (<b>d</b>) Body weight of mice from each group. All values are presented as mean ± SD, <span class="html-italic">n</span> = 6. * <span class="html-italic">p</span> &lt; 0.05 vs. the Control group; # <span class="html-italic">p</span> &lt; 0.05 vs. the Ang II group.</p>
Full article ">Figure 2
<p>Gastrodin alleviates Ang II-induced cardiac dysfunction. (<b>a</b>) Representative images of M-mode echocardiography from each group of mice. (<b>b</b>) LVFS, (<b>c</b>) LVEF, (<b>d</b>) LV vol.s, (<b>e</b>) LV vol.d, (<b>f</b>) LV Mass. (<b>g</b>) The ratio of HW/T in each group. (<b>h</b>) Cardiac tissues of mice from each group were stained with HE, and representative images were taken at a magnification of ×400. The Arrow indicates infiltrating inflammatory cells in cardiac tissue. All values are presented as mean ± SD, <span class="html-italic">n</span> = 6. * <span class="html-italic">p</span> &lt; 0.05 vs. the Control group; # <span class="html-italic">p</span> &lt; 0.05 vs. the Ang II group.</p>
Full article ">Figure 3
<p>RNA-seq analysis of differentially expressed genes and signaling pathways in the cardiac tissues of Ang II-infused mice after gastrodin treatment. (<b>a</b>) Hierarchical clustering plots and (<b>b</b>) volcano plots were used to compare gene expression profiles (|fold change| ≥ 2, <span class="html-italic">p</span> &lt; 0.05). (<b>c</b>) The overlapping KEGG pathways in the comparisons of Ang II + gastrodin vs. Ang II. The top 30 enriched items of the (<b>d</b>) biological processes, (<b>e</b>) cellular composition, and (<b>f</b>) molecular function. GO analysis was performed based on the DETs from comparisons of Ang II + gastrodin vs. Ang II. All values are represented as mean ± SD, <span class="html-italic">n</span> = 6.</p>
Full article ">Figure 4
<p>Gastrodin reduces Ang II-induced cardiac apoptosis in the cardiac tissues of Ang II-infused mice. (<b>a</b>) Cardiac tissues of mice from each group were stained with TUNEL (<span class="html-italic">n</span> = 6), and representative images were taken at a magnification of ×400. (<b>b</b>) The percentage of TUNEL-positive cells in each group was analyzed. (<b>c</b>) Western blot analysis was performed to determine the protein expression of Bax and Bcl-2. (<b>d</b>) The ratio of Bax/Bcl-2 was analyzed by Image J (version 2022). (<b>e</b>) Western blot analysis was performed to determine the protein expression of cleaved caspase-3 and cleaved caspase-9. (<b>f</b>,<b>g</b>) The ratio of cleaved caspase-3 and cleaved caspase-9 were analyzed by Image J (version 2022) and β-actin was used as the internal Control. All values are represented as mean ± SD. * <span class="html-italic">p</span> &lt; 0.05 vs. the Control group; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. the Ang II group.</p>
Full article ">Figure 5
<p>Gastrodin reduces Ang II-induced cardiac apoptosis in Ang II-stimulated H9c2 cells. (<b>a</b>) H9c2 cells from each group were stained with Hoechst. Representative images were taken at a magnification of ×200. (<b>b</b>) Representative dot plot of Annexin V and PI-stained cells. The result involved setting up quadrant gates based on negative cell groups, as well as using single staining with Annexin V and PI. Specifically, Annexin V (−)/PI (−) represents normal living cells, Annexin V (+)/PI (−) represents apoptotic cells at early stage, Annexin V (−)/PI (+) represents apoptotic cells at late stage, and Annexin V (+)/PI (+) represents cells undergoing necrosis or with severe mechanical damage. (<b>c</b>) The percentage of total apoptosis in H9c2 cells. (<b>d</b>) Western blot analysis was performed to determine the protein expression of Bax and Bcl-2. (<b>e</b>) The ratio of Bax/Bcl-2 was analyzed by Image J (version 2022). (<b>f</b>) Western blot analysis was performed to determine the protein expression of cle-caspase-3 and cle-caspase-9. (<b>g</b>,<b>h</b>) The ratio of cle-caspase-3 and cle-caspase-9 were analyzed by Image J (version 2022), and β-actin was used as the internal Control. All values are represented as mean ± SD, <span class="html-italic">n</span> = 3. * <span class="html-italic">p</span> &lt; 0.05 vs. the Control group; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. the Ang II group.</p>
Full article ">Figure 6
<p>Gastrodin inhibits Ang II-induced PRDX2/p53 pathway activation in vivo and in vitro. Representative images of PRDX2 (<b>a</b>) and p53 (<b>c</b>) protein stained by IHC analysis (<span class="html-italic">n</span> = 6). Representative images were taken at a magnification of ×400. Arrow indicates PRDX2 protein expressed in cardiac tissue. PRDX2 (<b>b</b>) and p53 (<b>d</b>) protein expression in the cardiac tissues of mice from each group was analyzed. (<b>e</b>–<b>g</b>) Western blot analysis was performed to determine the protein expression of PRDX2 and p53 in H9c2 cells from each group. All values are represented as mean ± SD. * <span class="html-italic">p</span> &lt; 0.05 vs. the Control group; <sup>#</sup> <span class="html-italic">p</span> &lt; 0.05 vs. the Ang II group.</p>
Full article ">
24 pages, 13331 KiB  
Article
Decimeter-Level Accuracy for Smartphone Real-Time Kinematic Positioning Implementing a Robust Kalman Filter Approach and Inertial Navigation System Infusion in Complex Urban Environments
by Amir Hossein Pourmina, Mohamad Mahdi Alizadeh and Harald Schuh
Sensors 2024, 24(18), 5907; https://doi.org/10.3390/s24185907 - 11 Sep 2024
Viewed by 450
Abstract
New smartphones provide real-time access to GNSS pseudorange, Doppler, or carrier-phase measurement data at 1 Hz. Simultaneously, they can receive corrections broadcast by GNSS reference stations to perform real-time kinematic (RTK) positioning. This study aims at the real-time positioning capabilities of smartphones using [...] Read more.
New smartphones provide real-time access to GNSS pseudorange, Doppler, or carrier-phase measurement data at 1 Hz. Simultaneously, they can receive corrections broadcast by GNSS reference stations to perform real-time kinematic (RTK) positioning. This study aims at the real-time positioning capabilities of smartphones using raw GNSS measurements as a conventional method and proposes an improvement to the positioning through the integration of Inertial Navigation System (INS) measurements. A U-Blox GNSS receiver, model ZED-F9R, was used as a benchmark for comparison. We propose an enhanced ambiguity resolution algorithm that integrates the traditional LAMBDA method with an adaptive thresholding mechanism based on real-time quality metrics. The RTK/INS fusion method integrates RTK and INS measurements using an extended Kalman filter (EKF), where the state vector x includes the position, velocity, orientation, and their respective biases. The innovation here is the inclusion of a real-time weighting scheme that adjusts the contribution of the RTK and INS measurements based on their current estimated accuracy. Also, we use the tightly coupled (TC) RTK/INS fusion framework. By leveraging INS data, the system can maintain accurate positioning even when the GNSS data are unreliable, allowing for the detection and exclusion of abnormal GNSS measurements. However, in complex urban areas such as Qazvin City in Iran, the fusion method achieved positioning accuracies of approximately 0.380 m and 0.415 m for the Xiaomi Mi 8 and Samsung Galaxy S21 Ultra smartphones, respectively. The subsequent detailed analysis across different urban streets emphasized the significance of choosing the right positioning method based on the environmental conditions. In most cases, RTK positioning outperformed Single-Point Positioning (SPP), offering decimeter-level precision, while the fusion method bridged the gap between the two, showcasing improved stability accuracy. The comparative performance between the Samsung Galaxy S21 Ultra and Xiaomi Mi 8 revealed minor differences, likely attributed to variations in the hardware design and software algorithms. The fusion method emerged as a valuable alternative when the RTK signals were unavailable or impractical. This demonstrates the potential of integrating RTK and INS measurements for enhanced real-time smartphone positioning, particularly in challenging urban environments. Full article
(This article belongs to the Section Navigation and Positioning)
Show Figures

Figure 1

Figure 1
<p>Flowchart depicting the TC RTK/INS integration architecture.</p>
Full article ">Figure 2
<p>The U-Blox antenna installed on the car roof (<b>a</b>), the Xiaomi Mi8 (left) and Samsung Galaxy S21 Ultra (right) mounted in the car (<b>b</b>), the Stonex S3II SE geodetic receiver (<b>c</b>), and the ZED-F9R receiver chipset used for the U-Blox antenna (<b>d</b>).</p>
Full article ">Figure 3
<p>The vehicle’s path while logging measurements using smartphones and the U-Blox receiver (<b>a</b>). (<b>b</b>–<b>e</b>) Field photos of the 4 selected parts of paths 1, 2, 3, and 4 in (<b>a</b>), respectively.</p>
Full article ">Figure 4
<p>GNSS raw observations processed by three methods, SPP, RTK, and fusion, respectively, on four streets, Daneshgah, Naderi, Peighambarieh, and Khorramshahr. The figures on the right (i.e., <b>b</b>,<b>d</b>,<b>f</b>,<b>h</b>) show the results of the Mi 8, and the figures on the left (i.e., <b>a</b>,<b>c</b>,<b>e</b>,<b>g</b>) show the results of the S21 Ultra.</p>
Full article ">Figure 4 Cont.
<p>GNSS raw observations processed by three methods, SPP, RTK, and fusion, respectively, on four streets, Daneshgah, Naderi, Peighambarieh, and Khorramshahr. The figures on the right (i.e., <b>b</b>,<b>d</b>,<b>f</b>,<b>h</b>) show the results of the Mi 8, and the figures on the left (i.e., <b>a</b>,<b>c</b>,<b>e</b>,<b>g</b>) show the results of the S21 Ultra.</p>
Full article ">Figure 5
<p>Easting and Northing errors regarding the reference trajectory for the Samsung Ultra S21 (<b>a</b>,<b>c</b>), and Xiaomi Mi8 (<b>b</b>,<b>d</b>), on Daneshgah Street, respectively. The dotted line is the zero-error axis.</p>
Full article ">Figure 6
<p>Easting and Northing errors regarding the reference trajectory for the Samsung Ultra S21 (<b>a</b>,<b>c</b>), and Xiaomi Mi8 (<b>b</b>,<b>d</b>), on Naderi Street, respectively. The dotted line is the zero-error axis.</p>
Full article ">Figure 7
<p>Easting and Northing errors regarding the reference trajectory for the Samsung Ultra S21 (<b>a</b>,<b>c</b>), and Xiaomi Mi8 (<b>b</b>,<b>d</b>), on Peyghambariyeh street, respectively. The dotted line is the zero-error axis.</p>
Full article ">Figure 8
<p>Easting and Northing errors regarding the reference trajectory for the Samsung Ultra S21 (<b>a</b>,<b>c</b>), and Xiaomi Mi8 (<b>b</b>,<b>d</b>), on Khorramshahr Street, respectively. The dotted line is the zero-error axis.</p>
Full article ">Figure 9
<p>(<b>a</b>) Satellite sky plot from the Samsung S21 Ultra, and (<b>b</b>) satellite sky plot from the Xiaomi Mi8, including observations from the multi-GNSS in the first part of the operation.</p>
Full article ">
35 pages, 4530 KiB  
Review
Current Approaches for the Prevention and Treatment of Acute and Chronic GVHD
by Attilio Olivieri and Giorgia Mancini
Cells 2024, 13(18), 1524; https://doi.org/10.3390/cells13181524 - 11 Sep 2024
Viewed by 267
Abstract
Whereas aGVHD has strong inflammatory components, cGVHD displays autoimmune and fibrotic features; incidence and risk factors are similar but not identical; indeed, the aGVHD is the main risk factor for cGVHD. Calcineurin Inhibitors (CNI) with either Methotrexate (MTX) or Mycophenolate (MMF) still represent [...] Read more.
Whereas aGVHD has strong inflammatory components, cGVHD displays autoimmune and fibrotic features; incidence and risk factors are similar but not identical; indeed, the aGVHD is the main risk factor for cGVHD. Calcineurin Inhibitors (CNI) with either Methotrexate (MTX) or Mycophenolate (MMF) still represent the standard prophylaxis in HLA-matched allogeneic stem cell transplantation (HSCT); other strategies focused on ATG, Post-Transplant Cyclophosphamide (PTCy), Abatacept and graft manipulation. Despite the high rate, first-line treatment for aGVHD is represented by corticosteroids, and Ruxolitinib is the standard second-line therapy; investigational approaches include Microbiota transplant and the infusion of Mesenchymal stem cells. GVHD is a pleiotropic disease involving any anatomical district; also, Ruxolitinib represents the standard for steroid-refractory cGVHD in this setting. It is a pleiotropic disease involving any anatomical district; also, Ruxolitinib represents the standard for steroid-refractory cGVHD in this setting. Extracorporeal Photopheresis (ECP) is still an option used for steroid refractoriness or to achieve a steroid-sparing. For Ruxolitinib-refractory cGVHD, Belumosudil and Axatilimab represent the most promising agents. Bronchiolitis obliterans syndrome (BOS) still represents a challenge; among the compounds targeting non-immune effectors, Alvelestat, a Neutrophil elastase inhibitor, seems promising in BOS. Finally, in both aGVHD and cGVHD, the association of biological markers with specific disease manifestations could help refine risk stratification and the availability of reliable biomarkers for specific treatments. Full article
Show Figures

Figure 1

Figure 1
<p>Pathogenesis of aGVHD and main targetable pathways for prophylaxis and treatment. Simplified outline of the aGVHD pathogenesis and the possible specific interventions according to some targetable steps. 1—The conditioning damages host tissues and causes the release of inflammatory mediators with the activation of host APCs; this process is amplified in the GIT lumen, where the altered microbiota and the destruction of the intestinal barrier facilitate the stimulation of innate immunity. 2—Host APCs activate donor T cells in the secondary satellite lymphoid organs 3—After expansion in the lymph nodes, activated T cells are primed, differentiating to type 1 T helper (Th1)/type 1 CD8+ T (Tc1) or Th17/Tc17 cells, and become able to target specific organs; 4—The lymphocyte traffic to the target organs is mediated by adhesion molecules such as L-selectin, CCR7, integrin a4b7; 5—activated T-cells can induce the tissue damage, both directly and by recruiting non-immune effector cells, (such as monocytes, PMN and NK) cells, and cytokines, such as TNF. The progressive loss of Treg contributes to the uncontrolled expansion of alloreactive T cells. Targetable pathways for Prophylaxis: 1—alloreactive T-cell depletion (in vivo/ex vivo): ATG; Campath; 2—early PTCy blocks alloreactive donor T cell expansion; 3—CD34 + selection/a-b depletion; 4—inactivating TCR (CNI: CSA, Tac); Sirolimus is a mTOR inhibitor which inhibits effector T-lymphocytes; 5—Abatacept (CTLA4-Ig) blocks T cell-APC co-stimulation; 6—Anti-homing compounds interfere with the alloreactive T-cell migration in the target organs (Vedolizumab; Maraviroc). Targetable pathways for Therapy: 1—anti-inflammasome treatment (Prednisone; Ruxolitinib/Itacitinib; Tocilizumab; Etanercept/Infliximab; 2—blocking T-cell priming: anti-IL2 (Basiliximab); 3—Primed T cells are susceptible to the Jak1/2 inhibitor Ruxolitinib or anti-IL-6R-antibodies (Tocilizumab) anti-TNF-antibodies; 4—Begelomab (anti-CD26) blocks alloreactive T cell migration to target organs; 5—treatments aimed to protect or regenerate target organs: IL22, FMT, anti-1 anti-trypsin; 6—Agents with pleiotropic activity: MSC; PDSC; multitarget treatments (ECP induces tolerogenic dendritic cells; reduces inflammasome; augments Treg). Abbreviations: aGVHD, acute GVHD; GIT, gastrointestinal tract; GIsc, gastrointestinal stem cells; PAMPs, pathogen-associated molecular patterns; DAMPs, damage-associated molecular patterns; HP APC, hematopoietic antigen-presenting cell; non-HP APC, non-hematopoietic antigen-presenting cell; TCR, T cell receptor; IFN, interferon; IL, interleukin; Th, helper T lymphocyte; Tc, cytotoxic T lymphocyte; T reg; regulatory T cells; PMN, polymorphonucleated cells; NK, natural killer cells; PTCY, post-transplant cyclophosphamide; CNI, Calcineurin Inhibitor; CSA, cyclosporine A; Tac, Tacrolimus; MTX, Methotrexate; MMF, Mycophenolate; ECP, Extracorporeal Photopheresis; FMT, fecal microbial transplant; MSC, mensenchimal stem cell; PDSC, placenta-derived stem cells.</p>
Full article ">Figure 2
<p>Pathogenesis of cGVHD and main targetable pathways for prophylaxis and treatment. The three-step development of c-GVHD with the treatment targeting the specific pathways. Phase I: Inflammasome is the starting point of cGVHD and could be clinically undetectable; conditioning and aGVHD cause thymus injury with loss of central tolerance. Phase II: T and B cell dysregulation; thymic dysfunction impairs donor Treg generation and the negative selection of autoreactive donor T cell clones that escape into the periphery. Tfh cells expand in lymphoid organs and promote the development of allo/autoreactive B cells in germinal centers; BAFF facilitates survival and expansion of the aberrant B cell clones; the aberrant B cells produce auto or allo-antibodies which induce macrophage polarization in presence of IL17/GM-CSF Phase III: Fibrosis and tissue remodeling; activated macrophages produce high levels of profibrotic cytokines (TGF-b, PDGF) with continuous stimulation of fibroblast which in turn produce exaggerated collagen matrix with tissue fibrotic remodeling. Targetable pathways: 1—The inflammasome and the subsequent phase of deregulation can be targeted by drugs/treatments with anti-inflammatory properties (PDN/ECP/Ruxolitinib); 2—Immune dysregulation and aberrant B-cell activity. The imbalanced Treg/T effector cell reconstitution (and the altered ROCK-2 signal) can be restored by Belumosudil, low-dose IL-2 treatment or by Treg infusions; ECP preserves Treg function. Belumosudil blocks Th17 differentiation and GC reactions by inhibiting Tfh cell generation (like Ruxolitinib); constitutive B cell receptor signaling (BTK) and intracellular downstream Syk can be inhibited by BTK Ibrutinib or Fostamatinib, while Rituximab blocks auto-antibodies production and Bortezomib inhibits long-lived autoreactive plasma cells. 3—Macrophage polarization and fibroblast activation with exaggerated collagen production: fibrosis and tissue remodeling. Axatilimab inhibits CSF1-R+ macrophages secreting profibrotic cytokines; -TGF-β production is inhibited by Belumosudil, Nintedanib, Pirfenidone or by Imatinib; these compounds also inhibit the fibrotic process via PDGF-R. Abbreviations: cGVHD, chronic GVHD; aGVHD, acute GVHD; T reg, regulatory T cell; Tfh, helper T follicular lymphocyte; GC, germinal center; BAFF, B cell activating factor; PDN, prednisone; ECP, Extracorporeal Photopheresis; BTK, Bruton tyrosine kinase; TKI, tyrosine kinase inhibitor.</p>
Full article ">Figure 3
<p>How we manage GIT-GVHD. Proposal of a clinical algorithm for managing patients with grade II–IVlower GIT aGVHD: first of all, do not wait for histologic confirmation in case of suspected GIT GVHD; check the chance to enroll the patient in a clinical trial: if not, start immediately standard first-line therapy with PDN 2 mg/kg and monitor response every day. If worsening after 72 h or without improvement after 5–7 days, a treatment change is strongly suggested (check again for a clinical trial availability). In the case of CR, a quick steroid tapering (or a slow tapering in the case of PR) should be considered; in our personal view, we consider the early ECP association in order to allow an easier steroid tapering, preventing possible flares and reducing the risk of infections. The standard second-line treatment is represented by Ruxolitinib (Etanercept or ECP represents possible alternative treatments), but enrollment in clinical trials (if available) is a valuable option both in steroid-refractory and in Ruxolitinib-refractory aGVHD. Fecal Microbiota Transplant or Mesenchymal Stem cell infusions are currently under evaluation: 1—NCT04769895: MaaT013 as Salvage Therapy in Ruxolitinib Refractory GI-aGVHD Patients; 2—NCT06075706 Treatment Of Steroid-Refractory Acute Graft-versus-host-Disease With Mesenchymal Stromal Cells Versus Best Available. GIT, gastro-intestinal tract; Neg, negative; PDN, Prednisone; CR, complete response; PR, partial response; ECP, Extracorporeal Photopheresis.</p>
Full article ">Figure 4
<p>Approach to the patient with suspected pulmonary GVHD involvement: the onset of dyspnea on (with or without other symptoms) and/or the deterioration of the LFTs require a careful work-up based on both imaging and Bronchoalveolar lavage, in order to exclude infectious complications; DLCO testing, although not mandatory, is useful since its reduction is frequent in restrictive syndromes. An isolated reduction in FEV1 (or FEV1/VC ratio) of at least 10% over 3 months, if associated with distinctive imaging findings (bronchiectasis, air trapping; bronchial wall thickening) points towards typical lung GVHD (BOS). Alteration of the LFTs, but with a preserved FEV1/VC ratio (often with reduced DLCO) instead points towards a restrictive syndrome or a mixed form (which may be referred to an atypical form of cGVHD). In this case (in the absence of microbiological/virological isolations) radiological imaging can be indicative of either rare forms (PPFE; NSIP) or may show consolidations indicative of COP. Steroid treatment can be rapidly curative in COP while it rarely is in BOS; in the case of SR-cGVHD or steroid-dependence, the association of ECP for 10-12 months is an option; Ruxolitinib is indicated in any case in SR-cGVHD forms, while in Ruxolitinib-refractory forms, consider the use of Belumosudil (if available); other options include the use of Imatinib and Ibrutinib. Ancillary treatment with FAM is generally recommended in BOS forms, while in young patients with severe impairment of lung function the option of a lung transplant should be considered. Abbreviations: LFT: lung functional test; BAL: Broncho-Alveolar Lavage; DLCO: Diffusion Lung Carbon Monoxide; FEV1: Forced Expiratory Volume in the first second; VC: vital capacity; BOS: Bronchiolitis obliterans syndrome; RLD: Restrictive Lung Disease; PDN: Prednisone; FAM: Fluticasone-Azithromycin-Montelukast; ECP: Extracorporeal Photopheresis; CT: Computed Thomography; PPFE: Pleuropaenchimal fibroelastosis; NSIP: Non-specific interstitial Pneumonia; BOOP: Bronchiolitis obliterans organizing pneumonia; COP: Cryptogenic organizing pneumonia; SR-cGVHD: Steroid-refractory chronic GVHD.</p>
Full article ">
18 pages, 1722 KiB  
Article
Zeaxanthin and Lutein Ameliorate Alzheimer’s Disease-like Pathology: Modulation of Insulin Resistance, Neuroinflammation, and Acetylcholinesterase Activity in an Amyloid-β Rat Model
by Da-Sol Kim, Suna Kang, Na-Rang Moon, Bae-Keun Shin and Sunmin Park
Int. J. Mol. Sci. 2024, 25(18), 9828; https://doi.org/10.3390/ijms25189828 - 11 Sep 2024
Viewed by 247
Abstract
Alzheimer’s disease (AD) is characterized by impaired insulin/insulin-like growth factor-1 signaling in the hippocampus. Zeaxanthin and lutein, known for their antioxidant and anti-inflammatory properties, have been reported to protect against brain damage and cognitive decline. However, their mechanisms related to insulin signaling in [...] Read more.
Alzheimer’s disease (AD) is characterized by impaired insulin/insulin-like growth factor-1 signaling in the hippocampus. Zeaxanthin and lutein, known for their antioxidant and anti-inflammatory properties, have been reported to protect against brain damage and cognitive decline. However, their mechanisms related to insulin signaling in AD remain unclear. This study investigated the efficacy and mechanisms of zeaxanthin, lutein, and resveratrol in modulating an AD-like pathology in an amyloid-β rat model. Rats were administered hippocampal infusions of 3.6 nmol/day amyloid-β (Aβ)(25-35) for 14 days to induce AD-like memory deficits (AD-CON). Normal control rats received Aβ(35-25) (Normal-CON). All rats had a high-fat diet. Daily, AD rats consumed 200 mg/kg body weight of zeaxanthin (AD-ZXT), lutein (AD-LTN), and resveratrol (AD-RVT; positive-control) or resistant dextrin as a placebo (AD-CON) for eight weeks. The AD-CON rats exhibited a higher Aβ deposition, attenuated hippocampal insulin signaling (reduced phosphorylation of protein kinase B [pAkt] and glycogen synthase kinase-3β [pGSK-3β]), increased neuroinflammation, elevated acetylcholinesterase activity, and memory deficits compared to the Normal-CON group. They also showed systemic insulin resistance and high hepatic glucose output. Zeaxanthin and lutein prevented memory impairment more effectively than the positive-control resveratrol by suppressing acetylcholinesterase activity, lipid peroxidation, and pro-inflammatory cytokines (TNF-α, IL-1β). They also potentiated hippocampal insulin signaling and increased brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CTNF) mRNA expression to levels comparable to the Normal-CON rats. Additionally, zeaxanthin and lutein improved glucose disposal, reduced hepatic glucose output, and normalized insulin secretion patterns. In conclusion, zeaxanthin and lutein supplementation at doses equivalent to 1.5–2.0 g daily in humans may have practical implications for preventing or slowing human AD progression by reducing neuroinflammation and maintaining systemic and central glucose homeostasis, showing promise even when compared to the established neuroprotective compound resveratrol. However, further clinical trials are needed to evaluate their efficacy and safety in human populations. Full article
Show Figures

Figure 1

Figure 1
<p>Amyloid-β accumulation in the hippocampus. Image amyloid-β deposition in the hippocampus (X100 magnification). Green dots are shown as amyloid-β deposition represented by immunohistochemistry with anti-amyloid-β antibody. The percentage of amyloid-β immunoreactivity in the hippocampus (n = 8 for each group) is shown. AD-CON (control), AD-LTN, AD-ZXT, and AD-RVT (positive-control) represent the groups of assigned 200 mg/kg bw/day resistant dextrin, luteolin, zeaxanthin, or resveratrol in amyloid-β-infused rats. Normal-Con rats infused with β-amyloid (35-25) received and consumed 200 mg/kg bw/day resistant dextrin. Different letters (a, b, c, d) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 2
<p>Memory function. (<b>A</b>). Latency time to enter the darkroom in the passive avoidance test (n = 16). (<b>B</b>). Latency time and frequencies of locating zone 5 located the platform on day 5 during the water maze test (n = 16). Each dot or bar with an error bar represents mean ± SD (n = 16 for each group). The β-amyloid (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw/day resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with β-amyloid (35-25) were fed a high-fat diet containing 200 mg/kg bw/day resistant dextrin, serving as normal controls (Normal-CON, Non-AD). * Significantly different at the time point among the groups at &lt;0.05. Different letters (a, b, c) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 3
<p>Hippocampal insulin signaling. (<b>A</b>). Immunoreactivity blots. (<b>B</b>). Intensity of the bands. After preparing the hippocampus lysates, the phosphorylation and expression of proteins related to insulin signaling were measured using a Western blot analysis, and their density was determined. Each dot and bar with error bars represent mean ± SD (n = 4 for each group). The amyloid-β (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with amyloid-β (35-25) were fed a high-fat diet containing 200 mg resistant dextrin per kg bw and served as the normal control (Normal-CON, Non-AD). Different letters (a, b, c, d) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different. Akt, protein kinase A; GSK-3β, glycogen synthase kinase-3β; STAT-3, signal transducer and activator of transcription 3; AMPK, AMP kinase.</p>
Full article ">Figure 4
<p>Oral glucose tolerance test with oral glucose intake (2 g/kg body weight). (<b>A</b>). Changes in the serum glucose levels (n = 16). (<b>B</b>). Area under the curve (AUC) of glucose. Each dot and bar with error bars represent (n = 16). Mean ± SD (n = 16 for each group). The β-amyloid (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with β-amyloid (35-25) were fed a high-fat diet containing 200 mg resistant dextrin per kg bw and served as the normal control (Normal-CON, Non-AD). * Significantly different at the time point among the groups at &lt;0.05. Different letters (a, b) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 4 Cont.
<p>Oral glucose tolerance test with oral glucose intake (2 g/kg body weight). (<b>A</b>). Changes in the serum glucose levels (n = 16). (<b>B</b>). Area under the curve (AUC) of glucose. Each dot and bar with error bars represent (n = 16). Mean ± SD (n = 16 for each group). The β-amyloid (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with β-amyloid (35-25) were fed a high-fat diet containing 200 mg resistant dextrin per kg bw and served as the normal control (Normal-CON, Non-AD). * Significantly different at the time point among the groups at &lt;0.05. Different letters (a, b) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 5
<p>Metabolic parameters during the hyperinsulinemic–euglycemic clamp. (<b>A</b>). Whole-body glucose infusion rates (GIR) and glucose uptake. (<b>B</b>). Hepatic glucose output at the basal and clamped states (n = 8). Bars and error bars represent mean ± standard deviation. Each dot and bar with error bars represent mean ± SD (n = 8 for each group). The β-amyloid (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with β-amyloid (35-25) were fed a high-fat diet containing 200 mg resistant dextrin per kg bw and served as normal controls (Normal-CON, Non-AD). Different letters (a, b, c) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 6
<p>Insulin secretion capacity during the hyperglycemic clamp. (<b>A</b>). Changes in the serum insulin concentrations during the hyperglycemic clamps (n = 8 for each group). Serum insulin levels were measured when serum glucose levels were maintained at 5.5 mM above fasting levels. (<b>B</b>). Area under the curve (AUC) of serum insulin concentration. Each dot and bar with error bars represent mean ± SD (n = 8). The β-amyloid (25-35)-infused rats were fed high-fat diets with 200 mg/kg bw resistant dextrin (AD-CON; control), lutein (AD-LTN), zeaxanthin (AD-ZXT), or resveratrol (AD-RVT; positive-control). The rats infused with β-amyloid (35-25) were fed a high-fat diet containing 200 mg resistant dextrin per kg bw and served as normal controls (Normal-CON, Non-AD). Dots and error bars represent mean ± standard deviation. * Significantly different at the time point among the four groups at <span class="html-italic">p</span> &lt; 0.05 by one-way ANOVA. Different letters (a, b) on the bars are significantly different from each other (<span class="html-italic">p</span> &lt; 0.05) by Tukey’s post hoc test. Bars with the same letter (a, a) are not significantly different.</p>
Full article ">Figure 7
<p>Experimental design. HE clamp, hyperinsulinemic–euglycemic clamp; HG clamp, hyperglycemic clamp.</p>
Full article ">
10 pages, 265 KiB  
Case Report
Modified Prophylactic Donor Lymphocyte Infusion (DLI) in an Adult T Cell Lymphoma/Leukemia (ATLL) Patient—Modality of Relapse Prevention
by Alexandra Ionete, Alexandru Bardas, Zsofia Varady, Madalina Vasilica, Orsolya Szegedi and Daniel Coriu
Diseases 2024, 12(9), 210; https://doi.org/10.3390/diseases12090210 - 11 Sep 2024
Viewed by 221
Abstract
Adult T-cell Leukemia/Lymphoma (ATLL) is a rare but aggressive malignancy associated with the human T-cell lymphotropic virus type 1 (HTLV-1). ATLL is a challenging malignancy characterized by its aggressive nature and poor prognosis. Despite advancements in treatment, relapse rates remain high. Donor lymphocyte [...] Read more.
Adult T-cell Leukemia/Lymphoma (ATLL) is a rare but aggressive malignancy associated with the human T-cell lymphotropic virus type 1 (HTLV-1). ATLL is a challenging malignancy characterized by its aggressive nature and poor prognosis. Despite advancements in treatment, relapse rates remain high. Donor lymphocyte infusion (DLI) is a promising therapeutic option post-hematopoietic stem cell transplantation (HSCT) to prevent relapse. However, the prophylactic use of DLI in ATLL patients remains underexplored. We report the case of a 45-year-old female diagnosed with ATLL. Following induction chemotherapy and successful HSCT, a modified prophylactic DLI regimen was administered, consisting of gradually increasing doses of donor lymphocytes. The patient demonstrated a favorable response with no significant graft-versus-host disease (GVHD) and maintained remission over a 40-month follow-up period, suggesting a potential benefit of this approach. This case highlights the potential efficacy and safety of modified prophylactic DLI in ATLL patients, warranting further investigation. Our findings suggest that modified prophylactic DLI is a viable option for ATLL patients post-HSCT, offering a balance between efficacy and safety. Future research should focus on optimizing DLI protocols and exploring biomarkers for response prediction. Full article
(This article belongs to the Section Oncology)
15 pages, 8170 KiB  
Article
Assessment of Mannitol-Induced Chronic Blood–Brain Barrier Dysfunction In Vivo Using Magnetic Resonance
by Ana Sampedro-Viana, Sabela Fernández-Rodicio, José Castillo, Pablo Hervella, María Luz Alonso-Alonso and Ramón Iglesias-Rey
Int. J. Mol. Sci. 2024, 25(18), 9792; https://doi.org/10.3390/ijms25189792 - 10 Sep 2024
Viewed by 293
Abstract
The blood–brain barrier (BBB) is essential for protection and plays a crucial role in chronic neurological disorders like small-vessel disease and Alzheimer’s disease. Its complexity poses significant challenges for effective diagnostics and treatments, highlighting the need for novel animal models and comprehensive BBB [...] Read more.
The blood–brain barrier (BBB) is essential for protection and plays a crucial role in chronic neurological disorders like small-vessel disease and Alzheimer’s disease. Its complexity poses significant challenges for effective diagnostics and treatments, highlighting the need for novel animal models and comprehensive BBB dysfunction studies. This study investigates chronic BBB dysfunction induction using osmotic disruption via mannitol in healthy adult male Sprague Dawley rats over 12 weeks. Group 1 received 1 bolus/week (2.0 g/kg), Group 2 received 3 boluses/week (1.5 g/kg), and Group 3 received 3 boluses/week (2.5 g/kg). BBB dysfunction was assessed using gadolinium (Gd) infusion and MRI to evaluate location, severity, evolution, and persistence. MR spectroscopy (MRS) examined the brain metabolism changes due to intravenous mannitol, with T2-weighted MRI assessing brain lesions. Biomarkers of neuroinflammation were analyzed in the highest mannitol dose group. Our data show chronic BBB dysfunction primarily in the cortex, hippocampus, and striatum, but not in the corpus callosum of rats under periodic mannitol dosing in groups 1 and 2. MRS identified a distinctive metabolite signature, including changes in alanine, choline, and N-acetyl aspartate in the striatum of Group 1. No significant differences were found in the serum levels of all pro- and anti-inflammatory cytokines analyzed in the high-dose Group 3. This study underscores the feasibility and implications of using osmotic disruption to model chronic BBB dysfunction, offering insights for future neuroprotection and therapeutic strategies research. Full article
Show Figures

Figure 1

Figure 1
<p>(<b>a</b>) Temporal changes in the animals’ weight. (<b>b</b>) Corpus callosum and striatum volumes between groups 1 and 3 at 12 weeks. (<b>c</b>) Changes in Evans blue extravasation in the entire brain and both hemispheres of rats at the end of the study (<span class="html-italic">n</span> = 3 per group). Extravasation of Evans blue was expressed as ng/mg brain tissue. The data are shown as mean ± SEM. The red line indicates normal levels. (<b>d</b>) Relative levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-2) anti-inflammatory cytokines (IL-10) in the mannitol-induced BBB dysfunction. Basal levels represent the measurements taken at week 0, where each analyte value was normalized by dividing it by its corresponding baseline. Values from the subsequent weeks were also normalized to each animal’s baseline. The data are described as the mean ± SEM. * <span class="html-italic">p</span> &lt; 0.05.</p>
Full article ">Figure 2
<p>(<b>a</b>) Schematic representing the experimental protocol used for measuring the effects of repetitive mannitol i.v. injection on BBB dysfunction. In order to assess BBB permeability, magnetic resonance imaging with Gd contrast enhancement was performed at 0 (basal), 1, 3, and 12 weeks following the beginning of the study. Blood samples were collected at least 24 h after the last bolus at the same time to study inflammatory cytokines. MR spectroscopy was performed at identical time points in both groups 1 and 2, concluding with Evans blue staining. (<b>b</b>) Representative axial images of Gd-leakage in the brain at baseline (0 weeks), as well as at 6 and 12 weeks following the beginning of the study. Gd-leakage was calculated as the relative signal enhancement induced by Gd accumulation: the pre-contrast T1-weighted signal intensity was subtracted from the post-contrast signal intensity and divided by the pre-contrast signal intensity, as previously described [<a href="#B23-ijms-25-09792" class="html-bibr">23</a>,<a href="#B24-ijms-25-09792" class="html-bibr">24</a>]. The greater the number indicated by the color bar in the lower right corner, the closer the color on the image approaches white, indicating greater leakage. No significant Gd enhancement was detected in the brain before mannitol injections, except for the ventricles/circumventricular organs, which have an incomplete BBB. At 6 and 12 weeks, Gd-leakage was still detectable mainly in the hippocampus, striatum, and cortex. Arrows indicate higher extravasation values.</p>
Full article ">Figure 3
<p>Quantification of Gd-leakage at different follow-up points. T1-weighted MRI was performed to calculate the amount of Gd-leakage per region of interest (ROI) in the brain of the three groups studied. * <span class="html-italic">p</span> &lt; 0.05 , ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001 vs. groups, Kruskal–Wallis test followed by Mann–Whitney test.</p>
Full article ">Figure 4
<p>Metabolite differences between Group 1 (1 bolus/week (2.0 g/kg i.v., 25% solution)) and Group 2 (3 bolus/week (1.5 g/kg i.v., 25% solution)), * <span class="html-italic">p</span> &lt; 0.05. Metabolites: alanine (Ala), creatine (Cr), g-aminobutyric acid (GABA), glutamate (Glu), glutamine (Gln), glycine (Gly), N-acetylaspartate (NAA), phosphocholine (PCh or Ch), and taurine (Tau). Mannitol dosing periods correspond to the average metabolite levels observed in the subsequent weeks.</p>
Full article ">Figure 4 Cont.
<p>Metabolite differences between Group 1 (1 bolus/week (2.0 g/kg i.v., 25% solution)) and Group 2 (3 bolus/week (1.5 g/kg i.v., 25% solution)), * <span class="html-italic">p</span> &lt; 0.05. Metabolites: alanine (Ala), creatine (Cr), g-aminobutyric acid (GABA), glutamate (Glu), glutamine (Gln), glycine (Gly), N-acetylaspartate (NAA), phosphocholine (PCh or Ch), and taurine (Tau). Mannitol dosing periods correspond to the average metabolite levels observed in the subsequent weeks.</p>
Full article ">Figure 5
<p>Metabolite differences in Group 1 (1 bolus/week (2.0 g/kg i.v., 25% solution)), * <span class="html-italic">p</span> &lt; 0.05. Metabolites: alanine (Ala), creatine (Cr), g-aminobutyric acid (GABA), glutamate (Glu), glutamine (Gln), glycine (Gly), N-acetylaspartate (NAA), phosphocholine (PCh or Ch), and taurine (Tau). Basal levels represent the measurements taken at week 0, while the post-mannitol periods correspond to the average metabolite levels observed in the subsequent weeks.</p>
Full article ">Figure 5 Cont.
<p>Metabolite differences in Group 1 (1 bolus/week (2.0 g/kg i.v., 25% solution)), * <span class="html-italic">p</span> &lt; 0.05. Metabolites: alanine (Ala), creatine (Cr), g-aminobutyric acid (GABA), glutamate (Glu), glutamine (Gln), glycine (Gly), N-acetylaspartate (NAA), phosphocholine (PCh or Ch), and taurine (Tau). Basal levels represent the measurements taken at week 0, while the post-mannitol periods correspond to the average metabolite levels observed in the subsequent weeks.</p>
Full article ">
13 pages, 1177 KiB  
Article
An In Vitro Study on the Antioxidant Properties of Cistus incanus Extracts
by Małgorzata Olszowy-Tomczyk and Dorota Wianowska
Agriculture 2024, 14(9), 1559; https://doi.org/10.3390/agriculture14091559 - 9 Sep 2024
Viewed by 381
Abstract
This paper concerns the evaluation of the antioxidant activity (AA) of extracts obtained from cistus herbs grown in Albania and Turkey. The extracts were prepared in a Soxhlet apparatus, as well as by the maceration and infusion methods, similar to the home method [...] Read more.
This paper concerns the evaluation of the antioxidant activity (AA) of extracts obtained from cistus herbs grown in Albania and Turkey. The extracts were prepared in a Soxhlet apparatus, as well as by the maceration and infusion methods, similar to the home method of preparing herbal teas. AA was determined using the DPPH (2,2′-diphenyl-1-picrylhydrazyl), ABTS (2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid), FRAP (ferric reducing antioxidant power) and β-carotene methods. It was proven that the AA of extracts depends not only on the extraction technique and AA assessment method but also on the place of plant cultivation. The smallest activity was determined using the β-carotene bleaching method, while the highest values were obtained using the FRAP method. On the other hand, the ABTS method showed a greater activity of the Albanian herb prepared using the Soxhlet technique. In addition, the antioxidant properties of extracts were compared with those of rutin standard solutions, showing that this characteristic component of cistus is not the only one that determines AA of extracts. As a result, the rutin content is not an indicator of the antioxidant properties of extracts. The other polyphenolic compounds, although occurring at lower concentration levels compared to rutin, modify the resultant AA of extracts. These studies confirmed the biological activity of cistus as a valuable source of polyphenolic compounds in the human diet. Full article
(This article belongs to the Special Issue Natural Products: Phytochemical Extraction, Analysis and Application)
Show Figures

Figure 1

Figure 1
<p>Exemplary chromatograms of the extract obtained in the Soxhlet apparatus with the marked rutin peak (labelled as *).</p>
Full article ">Figure 2
<p>A summary of the antioxidant properties of cistus extracts obtained by extraction in the Soxhlet apparatus (blue bars), maceration (red bars) and infusion (green bars) using different plant materials (I or II or III) and methods for assessing antioxidant properties (ABTS, DPPH, β-carotene and FRAP). For comparison, orange bars represent the antioxidant properties of rutin solution with the same concentration as in the extract. The same letters indicate data that are not statistically different (Fcal &lt; Ftab and <span class="html-italic">p</span> &gt; 0.05).</p>
Full article ">
12 pages, 1599 KiB  
Communication
Antibacterial and Antioxidant Activities of Hydroalcoholic and Phenolic Extracts from Ternstroemia dentisepala and T. lineata Leaves
by Alexis Uriel Soto Díaz, María Luisa Villarreal, Marcelo Victorio-De los Santos and Alexandre Toshirrico Cardoso-Taketa
Plants 2024, 13(17), 2515; https://doi.org/10.3390/plants13172515 - 7 Sep 2024
Viewed by 322
Abstract
Traditional Mexican medicine commonly uses infusions of Ternstroemia spp. to treat insomnia, injuries, and infections. The antibacterial activities of Ternstroemia dentisepala and Ternstroemia lineata were evaluated for the first time against a panel of Gram-positive and Gram-negative bacteria that have implications for human health, [...] Read more.
Traditional Mexican medicine commonly uses infusions of Ternstroemia spp. to treat insomnia, injuries, and infections. The antibacterial activities of Ternstroemia dentisepala and Ternstroemia lineata were evaluated for the first time against a panel of Gram-positive and Gram-negative bacteria that have implications for human health, including Enterococcus faecalis, Streptococcus agalactiae, Streptococcus pyogenes, Salmonella typhi, Pseudomonas aeruginosa, and Vibrio parahaemolyticus. Furthermore, the scavenging potential of the hydroalcoholic (HAEs) and total phenolic extracts (TPEs) from the leaves of both plants by a 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) assay (ABTS•+) was determined. Also, the total phenolic contents of the HAEs using the Folin–Ciocalteu reagent were assayed. T. dentisepala HAE and TPE were active against all bacterial strains tested, with a minimum inhibitory concentration between 1.0 and 6.0 mg/mL, with the last one being the most active. However, the T. lineata extracts only demonstrated effectiveness against S. typhi and P. aeruginosa. The TPEs from T. dentisepala and T. lineata improved the activity by approximately 30% in all bacteria tested in comparison with the HAEs. The T. dentisepala HAE had a higher total phenolic content than the T. lineata extract, which was consistent with its ABTS•+-scavenging activity. The two HAEs had different chemical profiles, mostly because of the types and amounts of phenolic compounds they contained. These profiles were obtained using thin-layer chromatography (TLC), high-performance liquid chromatography (HPLC), and proton nuclear magnetic resonance (1H NMR) experiments. Full article
(This article belongs to the Special Issue Biological Activities of Plant Extracts 2023)
Show Figures

Figure 1

Figure 1
<p>HPLC analysis of the hydroalcoholic extracts from the leaves of <span class="html-italic">T. lineata</span> and <span class="html-italic">T. dentisepala</span>. Chromatographic conditions: C-18 column and a mobile phase of acetonitrile and water (85:15) with a flow of 1 mL/min and detection at 254 nm.</p>
Full article ">Figure 2
<p>Thin-layer chromatographic profiles of the hydroalcoholic extracts of five individuals of <span class="html-italic">T. dentisepala</span> and <span class="html-italic">T. lineata</span>. The numbers 1, 2, 3, 4, and 5 represent extracts from different individuals of the same species. (<b>A</b>) UV light at 365 nm; (<b>B</b>) UV light at 254 nm; (<b>C</b>) plate developed with vanillin/H<sub>2</sub>SO<sub>4</sub> and 120 °C; (<b>D</b>) plate developed with vanillin/H<sub>2</sub>SO<sub>4</sub> and observed with UV light at 365 nm. The elution system was composed of a mobile phase with chloroform and methanol (4:1) in silica gel.</p>
Full article ">Figure 3
<p><sup>1</sup>H NMR of the hydroalcoholic extracts from the leaves of <span class="html-italic">T. dentisepala</span>, in green color, and <span class="html-italic">T. lineata</span>, in brown color, at 600 MHz in a CD<sub>3</sub>OD solvent.</p>
Full article ">
Back to TopTop