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Transfer of natural radionuclides from soil to water spinach (Ipomoea aquatica Forssk) in Hanoi, Vietnam have been investigated using a low background gamma spectrometer with an HPGe detector (Model-GC5019). Twenty pairs of soil and water spinach samples in two environmental conditions, i.e., flooded and unflooded, were collected for measuring the activity concentrations and determining the soil-to-plant transfer factors (TFs) of natural radionuclides. For water spinach, stems and leaves were collected as the main parts for human consumption and livestock food. The TF of 40 K is within the range of 0.32-2.49, which is greater than that of 228 Ra (0.01-0.17) and 226 Ra (0.01-0.13). The geometric means (geometric standard deviations) of the TFs are 1.17(1.89), 0.05(2.41) and 0.04(1.88) for flooded sites, and 0.89(1.73), 0.03(2.12) and 0.03(1.82) for unflooded sites, respectively. Comparing between the flooded and unflooded sites, the TFs are all greater at the flooded sites., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Extensive scientific evidence consistently demonstrates the clinical validity and utility of HLA-B*15:02 pre-screening in averting severe cutaneous adverse reactions (SCARs), namely Stevens-Johnson syndrome and toxic epidermal necrolysis, associated with carbamazepine or oxcarbazepine usage. Current practice guidelines and drug labeling actively advocate for pharmacogenetic pre-screening before initiating these antiepileptic drugs (AED), with particular emphasis on patients of Asian descent. However, there is a potential need to strengthen compliance with these recommendations. This retrospective study aimed to describe the pharmacogenetic pre-screening, documentation, and SCARs incidence for patients of Asian ancestry initiated on carbamazepine or oxcarbazepine at a large Northeastern USA healthcare system. Between 1 July 2016 and August 1, 2021, 27 patients with documented Asian heritage in the electronic health record (EHR) were included. The overall rate of HLA-B*15:02 pre-screening before carbamazepine or oxcarbazepine initiation was 4%. None who underwent pharmacogenetic pre-screening carried the associated HLA-B risk allele, and no SCARs were reported. Notably, pharmacogenetic results were not discretely entered into the EHR, and the results were only found as attached documents in the miscellaneous section of the EHR. There remains a significant opportunity for improving HLA-B*15:02 pre-screening for patients starting carbamazepine and oxcarbazepine to prevent SCARs in the USA., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

226 Ra, 238 U, 4  K, and 232 Th ( 228 Ra) activity concentrations of 61 soil samples distributed surrounding the rare earth element mine (NORM), MH, Lao Cai, Vietnam have been measured by HPGe detector. The activity concentrations of 226 Ra, 238 U, 4  K, and 232 Th ( 228 Ra) range from 1179 to 6291 Bq/kg, from 1024 to 8351 Bq/kg, from 260 to 3519 Bq/kg, and from 1476 to 35546 Bq/kg in the ore body and from 21.3 to 964 Bq/kg, from 23.4 to 1635 Bq/kg, from 124 to 3788 Bq/kg, and from 40.9 to 6107 Bq/kg outside the ore body in respective. The study area is considered as the high local natural background radiation with the concentration of 226 Ra, 238 U, 4  K, and 232 Th ( 228 Ra) of 156, 254, 647, and 908 Bq/kg in respective. Regarding the spatial distribution, the measured radionuclide concentrations are independent of the distance from measured points to the ore body. With regard to the hazard indices, the average calculated radiological hazard indices, including absorbed gamma dose rate, effective dose equivalent, and excess lifetime cancer risk significantly exceed the global average values. There is a disequilibrium between 238 U/ 226 Ra concentrations in studied soil samples. The results also found that the 232 Th ( 228 Ra) concentration and total absorbed gamma dose rate show a strong positive correlation (coefficient of determination, R 2  = 1)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Introduction : Cardiovascular disease is a leading comorbidity in rheumatoid arthritis. Timely introduction of biologic therapies in a treat-to-target approach has optimized disease-related outcomes and attenuated accrual of comorbidities, including cardiovascular risk. Areas covered : A literature search in MEDLINE (via PubMed) was performed between January 2009 and November 2020. This manuscript explores recent developments in atherosclerotic cardiovascular risk in RA compared with non-RA individuals; it synopsizes differences in vascular function and inflammation, prevalence, burden, vulnerability, and progression of atherosclerotic plaque and their underlying cellular and molecular mechanisms. Finally, it reviews the recent literature on cardioprotective benefits of biologics and draws mechanistic links with inhibition of new plaque formation, stabilization of high-risk lesions and improvement in endothelial function, arterial stiffness, lipid metabolism, and traditional cardiac risk factors. Expert opinion : Increasing evidence points to a solid cardioprotective influence of earlier, longer, and ongoing use of biologic treatments in RA. Nevertheless, the precise mechanistic effects of plaque progression and remodeling, vascular stiffness, endothelial dysfunction, lipid metabolism, and traditional cardiac risk factors are less rigorously characterized.

Objectives: To evaluate whether anti-Beta-2-Glycoprotein-I (anti-β2GPI) IgA antibodies associate with progression of coronary atherosclerosis and cardiovascular disease (CVD) events in rheumatoid arthritis (RA)., Methods: One hundred-fifty patients underwent plaque evaluation (total, non-calcified, mixed and calcified) with coronary computed tomography angiography; 101 were re-imaged within 6.9±0.3 years to assess progression. The Framingham-D'Agostino score assessed cardiovascular risk. Coronary artery calcium (CAC) and segment involvement score quantified plaque burden., Results: Anti-β2GPI IgA were seen in 45 (30%) patients. Despite no link to baseline plaque burden, anti-β2GPI IgA associated with segment involvement score increase (adjusted-RR=1.64 [95%CI 1.02-2.63]), CAC change (adjusted-β=0.33 [95%CI 0.002-0.656]) and developing new extensive or obstructive plaque at follow-up (adjusted-OR=4.24 [95%CI 1.30-13.87]). Adding anti-β2GPI IgA to logistic regression models with conventional risk factors predicting plaque progression outcomes increased Area under the receiver-operator curve and improved Net Reclassification and Integrated Discrimination Improvement indices (all P<0.05). In per-segment analyses, anti-β2GPI IgA predicted mixed plaque formation (adjusted-OR=3.20 [95%CI 1.01-10.09]) and lower likelihood of transition of mixed to calcified plaque (adjusted-OR=0.19 [95%CI 0.04-0.96]). Anti-β2GPI IgA moderated the effect of C-reactive protein on CAC change such that C-reactive protein associated with CAC change (β=0.26 [95%CI 0.14-0.38]) and CVD risk (adjusted-HR=1.89 [95%CI 1.02-3.51]) only in anti-β2GPI IgA positive patients., Conclusion: Anti-β2GPI IgA addition to clinical risk models improved prediction accuracy of CAC, plaque progression and transition to extensive/obstructive disease. They associated with new high-risk mixed plaques and delayed healing to calcified lesions. Anti-β2GPI IgA further modified the effect of inflammation on plaque progression and CVD events., Competing Interests: Declaration of Competing Interest This study was supported by grants from American Heart Association and Pfizer to GAK. The authors have no conflict of interest to declare., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Macrophages reprogram their lipid metabolism in response to activation signals. However, a systems-level understanding of how different pro-inflammatory stimuli reshape the macrophage lipidome is lacking. Here, we use complementary "shotgun" and isotope tracer mass spectrometry approaches to define the changes in lipid biosynthesis, import, and composition of macrophages induced by various Toll-like receptors (TLRs) and inflammatory cytokines. "Shotgun" lipidomics data revealed that different TLRs and cytokines induce macrophages to acquire distinct lipidomes, indicating their specificity in reshaping lipid composition. Mechanistic studies showed that differential reprogramming of lipid composition is mediated by the opposing effects of MyD88- and TRIF-interferon-signaling pathways. Finally, we applied these insights to show that perturbing reprogramming of lipid composition can enhance inflammation and promote host defense to bacterial challenge. These studies provide a framework for understanding how inflammatory stimuli reprogram lipid composition of macrophages while providing a knowledge platform to exploit differential lipidomics to influence immunity., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Plasma membranes of animal cells are enriched for cholesterol. Cholesterol-dependent cytolysins (CDCs) are pore-forming toxins secreted by bacteria that target membrane cholesterol for their effector function. Phagocytes are essential for clearance of CDC-producing bacteria; however, the mechanisms by which these cells evade the deleterious effects of CDCs are largely unknown. Here, we report that interferon (IFN) signals convey resistance to CDC-induced pores on macrophages and neutrophils. We traced IFN-mediated resistance to CDCs to the rapid modulation of a specific pool of cholesterol in the plasma membrane of macrophages without changes to total cholesterol levels. Resistance to CDC-induced pore formation requires the production of the oxysterol 25-hydroxycholesterol (25HC), inhibition of cholesterol synthesis and redistribution of cholesterol to an esterified cholesterol pool. Accordingly, blocking the ability of IFN to reprogram cholesterol metabolism abrogates cellular protection and renders mice more susceptible to CDC-induced tissue damage. These studies illuminate targeted regulation of membrane cholesterol content as a host defense strategy.

The observation of the 239 keV gamma line from 232 U decay in high-enriched uranium (HEU) samples prompted us to utilize 232 U (with main gamma energies of its daughters at 239, 583, 763, and 860 keV) as a mediator isotope for performing relative (intrinsic) efficiency calibration among 232 U, 234 U, 235 U, 238 U, and 214 Bi isotopes. By this way, the isotopic composition and age of HEU samples can be derived from activity ratios constituted between pairs of these isotopes on the basis of a common relative efficiency calibration curve. The method proved to be a useful tool for γ-spectrometric characterization of HEU items, especially of weapon grade, shielded uranium material., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Whether the recently identified innate lymphocyte population coexpressing natural killer cell receptors (NKRs) and the nuclear receptor RORγt is part of the NK or lymphoid tissue inducer (LTi) cell lineage remains unclear. By using adoptive transfer of genetically tagged LTi-like cells, we demonstrate that NKR⁻RORγt(+) innate lymphocytes but not NK cells were direct progenitors to NKR(+)RORγt(+) cells in vivo. Genetic lineage tracing revealed that the differentiation of LTi-like cells was characterized by the stable upregulation of NKRs and a progressive loss of RORγt expression. Whereas interleukin-7 (IL-7) and intestinal microbiota stabilized RORγt expression within such NKR-LTi cells, IL-12 and IL-15 accelerated RORγt loss. RORγt(+) NKR-LTi cells produced IL-22, whereas RORγt⁻ NKR-LTi cells released IFN-γ and were potent inducers of colitis. Thus, the RORγt gradient in NKR-LTi cells serves as a tunable rheostat for their functional program. Our data also define a previously unappreciated role of RORγt⁻ NKR-LTi cells for the onset or maintenance of inflammatory bowel diseases., (Copyright © 2010 Elsevier Inc. All rights reserved.)

The mucosal immune system of the intestine is separated from a vast array of microbes by a single layer of epithelial cells. Cues from the commensal microflora are needed to maintain epithelial homeostasis, but the molecular and cellular identities of these cues are unclear. Here we provide evidence that signals from the commensal microflora contribute to the differentiation of a lymphocyte population coexpressing stimulatory natural killer cell receptors and the transcription factor RORgammat that produced interleukin 22 (IL-22). The emergence of these IL-22-producing RORgammathiNKp46+NK1.1(int) cells depended on RORgammat expression, which indicated that these cells may have been derived from lymphoid tissue-inducer cells. IL-22 released by these cells promoted the production of antimicrobial molecules important in the maintenance of mucosal homeostasis.

In this work, the C3-type form of Sorghum phosphoenolpyruvate carboxylase (PyrPC) was produced in PyrPC-deficient strains of Escherichia coli transformed by a plasmid bearing the corresponding full-length cDNA (CPR1). The full-sized protein was purified to homogeneity by immunoaffinity chromatography. Some functional and regulatory properties were described; notably, the immunopurified PyrPC could be phosphorylated in reconstituted assay by 1) both a mammalian PKA and the PyrPC protein serine kinase purified from Sorghum leaves and 2) a novel protein kinase affinity-purified from Sorghum roots. In all cases phosphorylation was accompanied by a marked reduction in its malate sensitivity.