The sorption of naphthalene (NAP) and 1-naphthoic acid (1-NAPA) onto giant Miscanthus–derived biochar was investigated in methanol volume fractions (fc) of 0–0.6 as a function of ionic composition ...(5mM CaCl2 and 10mM KCl) and liquid pH (2 and 7). The sorption onto biochar was nonlinear with 0.42≤N≤0.95; thus, a concentration-specific sorption constant (Km) was compared. The Km log linearly decreased with increasing fc, except for 1-NAPA from a CaCl2 mixture at pH7. Isotherm data was fitted with a cosolvency sorption model through which the slope (ασ) of the inverse log linear Km-fc plot and empirical constant (α) were obtained. NAP sorption was well described by the cosolvency model with the α value being 0.41–0.53, indicating a methanol–biochar interaction favoring more sorption than the cosolvency based prediction. In particular, the slope (ασ) of 1-NAPA was lower than that of NAP, indicating less reduction of 1-NAPA sorption (i.e., lower α value) by methanol. In comparison with other sorbents, the α value was approximately intermediate between a humic substance and kaolinite clay. An analysis of FT-IR spectra suggested the transformation of O-containing functional groups by methanol, which will subsequently boost the π–π interaction between an organic solute and biochar. Moreover, Ca2+-induced sorption between anionic 1-NAPA and a negatively charged biochar surface was also fortified in the methanol mixture. The results revealed unexplored cosolvent effects on organic solute sorption onto biochar and identified the hydrophobic and hydrophilic sorption moieties of biochar as affected by the cosolvent.
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•Naphthalene sorption to biochar in methanol was well explained by the cosolvency model.•1-Naphthoic acid sorption decreased less with empirical constant (α) between −0.07 and 0. 31.•Ca2+-induced sorption was in part responsible for a low α value for anionic 1-NAPA.•FT-IR spectra revealed the enhanced π electron-acceptor ability of biochar by methanol.•The results will help in assessing the fate of organic solutes in biochar-applied sites.
Despite of the routine use of erythropoietin in hemodialysis patients to correct anemia, its administration route's effects on hemoglobin variability and cardiovascular events remain elusive. Herein, ...we determined different erythropoietin administration routes' effects on hemoglobin variability in hemodialysis patients and the associated factors of hemoglobin variability and cardiovascular events.
This is a post hoc analysis of a prospective, controlled, randomized, unblinded study with 78 Korean hemodialysis patients receiving intravenous (n = 40) or subcutaneous (n = 38) erythropoietin therapy. We evaluated hemoglobin variability by calculating the frequency of hemoglobin measurements outside the target range during all visits. The high-frequency group was defined by those with hemoglobin variability over the median value (25%) while the low-frequency group was defined by those with hemoglobin variability of <25%.
In this analysis, 37 patients (51.1%) were male, and the mean age was 50.6 ± 12.5 years. The frequency of the value being outside the target hemoglobin range was higher in the subcutaneous group compared to the intravenous group (p = 0.03). The low-frequency group required significantly lower erythropoietin doses compared to the high-frequency group. In the adjusted Cox analysis, the parameter high group was a significant independent risk factor for cardiovascular events (p = 0.03).
The risk out of the target hemoglobin range increased with subcutaneous administration compared with intravenous erythropoietin administration in hemodialysis patients. An increased frequency of the value being outside the target hemoglobin range was also associated with an increased risk of cardiovascular events.
Patients with end-stage kidney disease face increased risk of cardiovascular events, and left ventricular diastolic dysfunction (LVDD) contributes to the high occurrence of cardiovascular mortality ...(CM). Although a high serum aldosterone (sALD) level is involved in the development of cardiovascular complications in the general population, this association is unclear in patients undergoing hemodialysis. We aimed to determine the impact of sALD on LVDD and CM among hemodialysis patients (HDPs).
We performed a prospective cohort study of maintenance HDPs without cardiovascular disease. The patients were divided into two groups according to the median level of sALD. All patients underwent baseline echocardiography to evaluate diastolic dysfunction (E/e' ratio > 15). The LVDD and CM rates were compared between the high and low aldosterone groups.
We enrolled a total of 60 adult patients (mean age, 57.9 ± 12.1 years; males, 30.0%). The low aldosterone group had an increased left ventricular diastolic dimension compared with the high aldosterone group (52.2 ± 8.4 mm vs. 50.3 ± 5.2 mm, respectively; p = 0.03). Low log-aldosterone (odds ratio OR, 0.40; 95% confidence interval CI, 0.19-0.86) and large left atrial dimension (OR, 1.31; 95% CI, 1.11-1.54) were independent risk factors for LVDD at baseline. In addition, Cox regression analysis demonstrated that low sALD was an independent predictor of CM in HDPs (hazard ratio, 0.46; 95% CI, 0.25-0.85; p = 0.01) during follow-up.
Low sALD was not only associated with LVDD but was also an independent predictor of CM among HDPs regardless of their interdialytic weight gain.
Activation of hypoxia‐inducible factor 1α (HIF1α) contributes to blood‐retinal barrier (BRB) breakdown and pathological neovascularization responsible for vision loss in ischemic retinal diseases. ...During disease progression, mitochondrial biology is altered to adapt to the ischemic environment created by initial vascular dysfunction, but the mitochondrial adaptive mechanisms, which ultimately contribute to the pathogenesis of ischemic retinopathy, remain incompletely understood. In the present study, it is identified that expression of mitochondrial chaperone tumor necrosis factor receptor‐associated protein 1 (TRAP1) is essential for BRB breakdown and pathologic retinal neovascularization in mouse models mimicking ischemic retinopathies. Genetic Trap1 ablation or treatment with small molecule TRAP1 inhibitors, such as mitoquinone (MitoQ) and SB‐U015, alleviate retinal pathologies via proteolytic HIF1α degradation, which is mediated by opening of the mitochondrial permeability transition pore and activation of calcium‐dependent protease calpain‐1. These findings suggest that TRAP1 can be a promising target for the development of new treatments against ischemic retinopathy, such as retinopathy of prematurity and proliferative diabetic retinopathy.
This study reveals that the mitochondrial chaperone TRAP1 is vital for stabilizing HIF1α, a key transcription factor in pathologic microvascular changes in ischemic retinopathies. Therefore, inhibiting TRAP1 genetically or pharmacologically alleviates retinal vascular pathologies by inducing HIF1α proteolytic degradation, indicating that TRAP1 can be a promising target for the development of therapies for ischemic retinopathy.
The antigen-independent, strong proliferative responses of naive CD8
T cells have been well demonstrated in a particular strain of mice lacking IL-2 receptors. This type of proliferation is mainly ...driven by common gamma-chain (γ
) cytokines, such as IL-2, IL-7, and IL-15, present at abnormally high levels in these mice. Similarly, in the present study, we showed that mice lacking Janus kinase 3 (Jak3), a tyrosine kinase crucial for γ
cytokine signaling, could induce strong proliferation of adoptively transferred naive CD8
T cells. This proliferation was also independent of antigenic stimulation, but heavily dependent on IL-2, as evidenced by the failure of proliferation of adoptively transferred IL-2 receptor alpha- and beta-chain-deficient naive CD8
T cells. Consistent with this,
mice showed elevated serum levels of IL-2 compared to wild-type mice, and interestingly, IL-2 production was due to high levels of accumulation of activated CD4
T cells in
mice along with defective CD4
T regulatory cells. Collectively, these findings reveal previously unidentified unique immune contexts of
mice that cause robust IL-2-driven T cell expansion and have a clinical implication for designing a treatment strategy for human patients with loss-of-function genetic mutations of
.
A relatively high affinity/avidity of T cell receptor (TCR) recognition for self-peptide bound to major histocompatibility complex II (self-pMHC) ligands is a distinctive feature of CD4 T regulatory ...(Treg) cells, including their development in the thymus and maintenance of their suppressive functions in the periphery. Despite such high self-reactivity, however, all thymic-derived peripheral Treg populations are neither homogenous in their phenotype nor uniformly immune-suppressive in their function under steady state condition. We show here that based on the previously defined heterogeneity in the phenotype of peripheral Treg populations, Ly6C expression on Treg marks a lower degree of activation, proliferation, and differentiation status as well as functional incompetence. We also demonstrate that Ly6C expression on Treg in a steady state is either up- or downregulated depending on relative amounts of tonic TCR signals derived from its contacts with self-ligands. Interestingly, peripheral appearance and maintenance of these Ly6C-expressing Treg cells largely differed in an age-dependent manner, with their proportion being continuously increased from perinatal to young adult period but then being gradually declined with age. The reduction of Ly6C
Treg in the aged mice was not due to their augmented cell death but rather resulted from downregulation of Ly6C expression. The Ly6C downregulation was accompanied by proliferation of Ly6C
Treg cells and subsequent change into Ly6C
effector Treg with concomitant restoration of immune-suppressive activity. Importantly, we found that this phenotypic and functional change of Ly6C
Treg is largely driven by conventional effector T cell population. Collectively, these findings suggest a potential cross-talk between peripheral Treg subsets and effector T cells and provides better understanding for Treg homeostasis and function on maintaining self-tolerance.
Foxp3 ＋ regulatory CD4 ＋ T (Treg) cells play an essential role in preventing overt immune responses against self and innocuous foreign antigens. Selective expansion of endogenous Treg cells in ...response to the administration of interleukin (IL)-2/antibody complex, such as the IL-2/JES6-1 complex (IL-2C) in mice, is considered an attractive therapeutic approach to various immune disorders. Here, we investigated the therapeutic potential of IL-2C in allergic airway inflammation models. IL-2C treatment ameliorated Th17-mediated airway inflammation; however, unexpectedly, IL-2C treatment exacerbated Th2-mediated allergic airway inflammation by inducing the selective expansion of Th2 cells and type-2 innate lymphoid cells. We also found that IL-2 signaling is required for the expansion of Th2 cells in lymphoproliferative disease caused by Treg cell depletion. Our data suggest that IL-2C is selectively applicable to the treatment of allergic airway diseases depending on the characteristics of airway inflammation. BMB Reports 2019; 52(4): 283-288
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