Search

Thrips are one of the most challenging pests in agricultural crops, including Chrysanthemum . In this study we tested via two plant assays whether solutions containing sticky rice germ oil (RGO) droplets could effectively trap thrips and lower thrips damage on Chrysanthemum . In the first assay, we additionally assessed the metabolomic effects of these RGO droplet sprays and thrips presence on plant chemistry via 1 H NMR and headspace GC-MS on multiple timepoints to investigate which plant metabolites were affected by spraying and their potential relation to plant resistance against thrips. In the second assay, we tested the individual RGO solution constituents against thrips. Our results suggested that the adhesive RGO droplets were not effective as a physical trap as only three out of 600 adult thrips were caught at the achieved coverage. However, average thrips damage was still reduced up to 50% and no negative effects on plant growth were observed up to 25 days. Results from the second plant assay indicated that the individual constituents of the solution containing RGO droplets may have direct effects against thrips. Metabolomics analysis of sprayed leaves via headspace GC-MS and 1 H NMR indicated that fatty acids and several volatile compounds such as 4(10)-thujene (sabinene), eucalyptol, cis -4-thujanol, and isocaryophyllene were highest on day 10, while sucrose, malic acid, o -Cymene, and 3-Methyl-2-butenoic acid were highest on day 25. Plants with thrips showed higher flavonoid, carbohydrate and glutamine acetic acid levels, and lower fatty acids and malic acid levels. RGO application increased the levels of fatty acids and alcohols present on top of and inside the Chrysanthemum leaves, while decreasing the concentrations of volatile compounds such as eucalyptol, chrysanthenone and eugenol in the Chrysanthemum leaves. Most interestingly, the thrips effect on the plant metabolome was no longer visible in RGO treated plants at the later harvesttime, suggesting that RGO application may overrule or prevent the metabolomic effects of thrips infestation. In conclusion, our study provides new information on how the application of a new plant-based plant protection product affects insect herbivores and alters crop phytochemistry for improved herbivore resistance., Competing Interests: A patent for the method to fabricate solutions with adhesive plant-derived oil droplets has been filed with the European Patent Office, application no. 22202752.6; EP4356732A1, by Wageningen University. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2025 Bierman, Fernandes, Choi, Seo, Vrieling, Macel, Knegt, Kodger, van Zwieten, Klinkhamer and Bezemer.)

With a continuous increase in world population and food production, chemical pesticide use is growing accordingly, yet unsustainably. As chemical pesticides are harmful to the environment and developmental resistance in pests is increasing, a sustainable and effective pesticide alternative is needed. Inspired by nature, we mimic one defense strategy of plants, glandular trichomes, to shift away from using chemical pesticides by moving toward a physical immobilization strategy via adhesive particles. Through controlled oxidation of a biobased starting material, triglyceride oils, an adhesive material is created while monitoring the reactive intermediates. After being milled into particles, nanoindentation shows these particles to be adhesive even at low contact forces. A suspension of particles is then sprayed and found to be effective at immobilizing a target pest, thrips, Frankliniella occidentalis . Small arthropod pests, like thrips, can cause crop damage through virus transfer, which is prevented by their immobilization. We show that through a scalable fabrication process, biosourced materials can be used to create an effective, sustainable physical pesticide., Competing Interests: Competing interests statement:A patent pertaining to this research has been filed with the European Patent Office Application No. EP22202752.

Senescence of erythrocytes is characterized by a series of changes that precede their removal from the circulation, including loss of red cell hydration, membrane shedding, loss of deformability, phosphatidyl serine exposure, reduced membrane sialic acid content, and adhesion molecule activation. Little is known about the mechanisms that initiate these changes nor is it known whether they are interrelated. In this study, we show that Ca2+-dependent K+ efflux (the Gardos effect) drives erythrocyte senescence. We found that increased intracellular Ca2+ activates the Gardos channel, leading to shedding of glycophorin-C (GPC)-containing vesicles. This results in a loss of erythrocyte deformability but also in a marked loss of membrane sialic acid content. We found that GPC-derived sialic acid residues suppress activity of both Lutheran/basal cell adhesion molecule (Lu/BCAM) and CD44 by the formation of a complex on the erythrocyte membrane, and Gardos channel-mediated shedding of GPC results in Lu/BCAM and CD44 activation. This phenomenon was observed as erythrocytes aged and on erythrocytes that were otherwise prone to clearance from the circulation, such as sickle erythrocytes, erythrocytes stored for transfusion, or artificially dehydrated erythrocytes. These novel findings provide a unifying concept on erythrocyte senescence in health and disease through initiation of the Gardos effect., (© 2020 by The American Society of Hematology.)

The expression of the human β-like globin genes follows a well-orchestrated developmental pattern, undergoing two essential switches, the first one during the first weeks of gestation (ε to γ), and the second one during the perinatal period (γ to β). The γ- to β-globin gene switching mechanism includes suppression of fetal (γ-globin, HbF) and activation of adult (β-globin, HbA) globin gene transcription. In hereditary persistence of fetal hemoglobin (HPFH), the γ-globin suppression mechanism is impaired leaving these individuals with unusual elevated levels of fetal hemoglobin (HbF) in adulthood. Recently, the transcription factors KLF1 and BCL11A have been established as master regulators of the γ- to β-globin switch. Previously, a genomic variant in the KLF1 gene, identified by linkage analysis performed on twenty-seven members of a Maltese family, was found to be associated with HPFH. However, variation in the levels of HbF among family members, and those from other reported families carrying genetic variants in KLF1, suggests additional contributors to globin switching. ASF1B was downregulated in the family members with HPFH. Here, we investigate the role of ASF1B in γ- to β-globin switching and erythropoiesis in vivo. Mouse-human interspecies ASF1B protein identity is 91.6%. By means of knockdown functional assays in human primary erythroid cultures and analysis of the erythroid lineage in Asf1b knockout mice, we provide evidence that ASF1B is a novel contributor to steady-state erythroid differentiation, and while its loss affects the balance of globin expression, it has no major role in hemoglobin switching.

A 4-year-old boy, a β-thalassemia (β-thal) carrier, with an unexplained severe chronic microcytic anemia was referred to us. Sequencing of the α-globin genes revealed a Hb Charlieu [α106(G13)Leu→Pro, HBA1 : c.320T>C, p.Leu107Pro] mutation present on both HBA1 genes. Quantitative polymerase chain reaction (qPCR) confirmed α Charlieu mRNA in the proband and his parents, showing that the mutation does not affect mRNA stability. However, we were unable to detect the Hb Charlieu protein by capillary electrophoresis (CE), reverse phase electrophoresis, cation exchange electrophoresis or isoelectric focusing. Mass spectrometry (MS) allowed us to confirm the presence of the Hb Charlieu peptide in erythrocyte progenitors. These findings suggest that the mutation affects the stability of α Charlieu . As hemoglobin (Hb) heat stability tests showed no abnormalities in erythrocytes, we speculated that α Charlieu is already degraded during red blood cell (RBC) development. The clinical severity in the proband and the presence of new methylene blue-stained aggregates in his reticulocytes indicates that incorporation of α Charlieu destabilizes Hb. This, combined with an excess of unstable free α-globins as the result of β-thal minor, results in severely impaired erythropoiesis and, as a consequence, severe and chronic microcytic anemia in the proband.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency worldwide. Detection of heterozygously deficient females can be difficult as residual activity in G6PD-sufficient red blood cells (RBCs) can mask deficiency. In this study, we compared accuracy of 4 methods for detection of G6PD deficiency in females. Blood samples from females more than 3 months of age were used for spectrophotometric measurement of G6PD activity and for determination of the percentage G6PD-negative RBCs by cytofluorometry. An additional sample from females suspected to have G6PD deficiency based on the spectrophotometric G6PD activity was used for measuring chromate inhibition and sequencing of the G6PD gene. Of 165 included females, 114 were suspected to have heterozygous deficiency. From 75 females, an extra sample was obtained. In this group, mutation analysis detected 27 heterozygously deficient females. The sensitivity of spectrophotometry, cytofluorometry, and chromate inhibition was calculated to be 0.52 (confidence interval [CI]: 0.32-0.71), 0.85 (CI: 0.66-0.96), and 0.96 (CI: 0.71-1.00, respectively, and the specificity was 1.00 (CI: 0.93-1.00), 0.88 (CI: 0.75-0.95), and 0.98 (CI: 0.89-1.00), respectively. Heterozygously G6PD-deficient females with a larger percentage of G6PD-sufficient RBCs are missed by routine methods measuring total G6PD activity. However, the majority of these females can be detected with both chromate inhibition and cytofluorometry.

Objective: Here, we present a 7-year-old patient suffering from severe haemolytic anaemia. The most common cause of chronic hereditary non-spherocytic haemolytic anaemia is red blood cell pyruvate kinase (PK-R) deficiency. Because red blood cells rely solely on glycolysis to generate ATP, PK-R deficiency can severely impact energy supply and cause reduction in red blood cell lifespan. We determined the underlying cause of the anaemia and investigated how erythroid precursors in the patient survive., Methods: PK activity assays, Western blot and Sanger sequencing were employed to determine the underlying cause of the anaemia. Patient erythroblasts were cultured and reticulocytes were isolated to determine PK-R and PKM2 contribution to glycolytic activity during erythrocyte development., Results: We found a novel homozygous mutation (c.583G>A) in the PK-R coding gene (PKLR). Although this mutation did not influence PKLR mRNA production, no PK-R protein could be detected in the red blood cells nor in its precursors. In spite of the absence of PK-R, the reticulocytes of the patient exhibited 20% PK activity compared with control. Western blotting revealed that patient erythroid precursors, like controls, express residual PKM2., Conclusions: We conclude that PKM2 rescues glycolysis in PK-R-deficient erythroid precursors., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Cavitation Intensifying Bags (CIBs), a novel reactor type for use with ultrasound, have been recently proposed as a scaled-up microreactor with increased energy efficiencies. We now report on the use of the CIBs for the preparation of emulsions out of hexadecane and an SDS aqueous solution. The CIBs have been designed in such a way that cavitation effects created by the ultrasound are increased. It was found that the CIBs were 60 times more effective in breaking up droplets than conventional bags, therewith showing a proof of principle for the CIBs for the preparation of emulsions. Droplets of 0.2μm could easily be obtained. To our knowledge, no other technology results in the same droplet size more easily in terms of energy usage. Without depending on the wettability changes of the membrane, the CIBs score similarly as membrane emulsification, which is the most energy friendly emulsification method known in literature. Out of the frequencies used, 37kHz was found to require the lowest treatment time. The treatment time decreased at higher temperatures. While the energy usage in the current non-optimised experiments was on the order of 10 7 -10 9 J/m 3 , which is comparable to that of a high-pressure homogenizer, we expect that the use of CIBs for the preparation of fine emulsions can still be improved considerably. The process presented can be applied for other uses such as water treatment, synthesis of nanomaterials and food processing., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Congenital dyserythropoietic anaemia type II (CDAII) is a rare autosomal recessive disease characterized by ineffective erythropoiesis, haemolysis, erythroblast morphological abnormalities, hypoglycosylation of some red blood cell membrane proteins, particularly band 3, and mutations in the SEC23B gene. We report the analysis of 101 patients from 91 families with a median follow-up of 23 years (range 0-65); 68 patients are newly reported. Clinical and haematological parameters were separately analysed in early infancy and thereafter, when feasible. Molecular analysis of the SEC23B gene confirmed the high heterogeneity of the defect, leading to the identification of 54 different mutations, 24 of which are newly described. To evaluate the genotype-phenotype correlation, patients were grouped according to their genotype (two missense mutations vs. one missense/one drastic mutation) and assigned to two different severity gradings based on laboratory data and on therapeutic needs; by this approach only a weak genotype-phenotype correlation was observed in the analysed groups., (© 2016 John Wiley & Sons Ltd.)

Familial hemophagocytic lymphohistiocytosis type 5 (FHL-5) is a rare genetic disorder caused by mutations in STXBP2/Munc18-2. Munc18-2 plays a role in the degranulation machinery of natural killer cells and cytotoxic T lymphocytes. Mutations in STXBP2/Munc18-2 lead to impaired killing of target cells by natural killer cells and cytotoxic T lymphocytes, which in turn results in elevated levels of the inflammatory cytokine interferon γ, macrophage activation, and hemophagocytosis. Even though patients with FHL-5 present with anemia and hemolysis, no link between the disease and the erythroid lineage has been established. Here we report that red blood cells express Munc18-2 and that erythroid cells from patients with FHL-5 exhibit intrinsic defects caused by STXBP2/Munc18-2 mutations. Red blood cells from patients with FHL-5 expose less phosphatidylserine on their surface upon Ca(2+) ionophore ionomycin treatment. Furthermore, cultured erythroblasts from patients with FHL-5 display defective erythropoiesis characterized by decreased CD235a expression and aberrant cell morphology., (Copyright © 2015 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.)

In a family with mild dominant spherocytosis, affected members showed partial band 3 deficiency. The index patient showed more severe clinical symptoms than his relatives, and his red blood cells displayed concomitant low pyruvate kinase activity. We investigated the contribution of partial PK deficiency to the phenotypic expression of mutant band 3 in this family. Pyruvate kinase deficiency and band 3 deficiency were characterized by DNA analysis. Results of red cell osmotic fragility testing, the results of cell deformability obtained by the Automated Rheoscope and Cell Analyzer and the results obtained by Osmotic Gradient Ektacytometry, which is a combination of these tests, were related to the red cell ATP content. Spherocytosis in this family was due to a novel heterozygous mutation in SLC4A1, the gene for band 3. Reduced PK activity of the index patient was attributed to a novel mutation in PKLR inherited from his mother, who was without clinical symptoms. Partial PK deficiency was associated with decreased red cell ATP content and markedly increased osmotic fragility. This suggests an aggravating effect of low ATP levels on the phenotypic expression of band 3 deficiency., (© 2014 Wiley Periodicals, Inc.)