Fluoride removal from coal mining water using novel polymeric aluminum modified activated carbon prepared through mechanochemical process.

Defluoridation of coal mining water is of great significance for sustainable development of coal industry in western China. A novel one-step mechanochemical method was developed to prepare polymeric aluminum modified powder activated carbon (PAC) for effective fluoride removal from coal mining water. Aluminum was stably loaded on the PAC through facile solid-phase reaction between polymeric aluminum (polyaluminum chloride (PACl) or polyaluminum ferric chloride (PAFC)) and PAC (1:15 W/W). Fluoride adsorption on PACl and PAFC modified PAC (C-PACl and C-PAFC) all reached equilibrium within 5 min, at rate of 2.56 g mg-1 sec-1 and 1.31 g mg-1 sec-1 respectively. Larger increase of binding energy of Al on C-PACl (AlF bond: 76.64 eV and AlFOH bond: 77.70 eV) relative to that of Al on C-PAFC (AlF bond: 76.52 eV) explained higher fluoride uptake capacity of C-PACl. Less chloride was released from C-PACl than that from C-PAFC due to its higher proportion of covalent chlorine and lower proportion of ionic chlorine. The elements mapping and atomic composition proved the stability of Al loaded on the PAC as well as the enrichment of fluoride on both C-PACl and C-PAFC. The Bader charge, formation energy and bond length obtained from DFT computational results explained the fluoride adsorption mechanism further. The carbon emission was 7.73 kg CO2-eq/kg adsorbent prepared through mechanochemical process, which was as low as 1:82.3 to 1:8.07 × 104 compared with the ones prepared by conventional hydrothermal methods.

Renal tubular epithelial cell necroptosis promotes tubulointerstitial fibrosis in patients with chronic kidney disease.

Renal fibrosis, a common pathological manifestation of virtually all types of chronic kidney disease (CKD), ultimately predisposes patients to end-stage renal disease. However, there is no effective therapy for renal fibrosis. Our earlier studies proved that RIP3-mediated necroptosis might be an important mode of renal tubular cell death in rats with chronic renal injury. Under transmission electron microscopy (TEM), we found morphological changes in the necrosis of human renal tissue, and the percentage of necrotic cells increased significantly in patients with stages 2 and 3a CKD. Immunofluorescence analyses showed that the percentages of TUNEL+ /RIP3+ double-positive and TUNEL+ /MLKL+ double-positive tubular epithelial cells in renal tubules of patients with stages 2 and 3a CKD were significantly increased compared to those in control patients without renal disease. Immunohistochemistry analyses of renal biopsy specimens from patients with CKD revealed RIP3, MLKL, and p-MLKL upregulation in patients with stages 2 and 3a CKD, suggesting that necroptosis of renal tubular epithelial cells in CKD patients occurs, and the peak of necroptosis was in stages 2 and 3a CKD. We showed that profibrotic factor proteins (TGF-ß1, Smad2 and Smad3) and fibroblast activation markers (α-SMA and Vimentin) were specifically upregulated in stage 2 and 3a CKD patients. In addition, Pearson correlation analysis showed that the percentage of necroptotic renal tubular epithelial cells was positively correlated with TGF-ß1 and collagen-I. We also showed that RIP1/3 or MLKL inhibitors decreased the expression of RIP3, MLKL, TGF-ß1, and Smad3 in HK-2 cells treated with TNF-α. FGF-2, α-SMA, Vimentin and FN were overexpressed in the hRIFs cultured with the supernatant of necroptotic HK-2 cells, whereas necroptosis blockers (Nec-1s, GSK'872 and NSA) and TGF-ß1/Smad3 pathway antagonists (LY364947 and SIS3) reduced FGF-2, α-SMA, Vimentin and FN levels. Collectively, necroptosis of renal tubular epithelial cells in CKD patients occurs, and the peak of necroptosis was in stages 2 and 3a CKD. Renal tubular epithelial cell necroptosis mediates renal tubulointerstitial fibrosis in patients with chronic kidney disease, which is related to the TGF-ß1/Smad3 signaling pathway.

Hippocampal subfield morphology in regular hemodialysis patients.

BACKGROUND: Hippocampal alterations have been implicated in the pathophysiology of cognitive impairment in hemodialysis patients. The hippocampus consists of several distinct subfields, and the molecular mechanisms underlying cognition might be associated with specific hippocampal subfield volume changes. However, this has not yet been investigated in hemodialysis patients. This study aimed to explore volumetric abnormalities in hippocampal subfields in regular hemodialysis patients. METHODS: High-resolution T1-weighted structural images were collected in 61 subjects including 36 hemodialysis patients and 25 healthy controls. A state-of-the-art hippocampal segmentation approach was adopted to segment the hippocampal subfields. Group differences in hippocampal subfield volumes were assessed in Python with a statsmodels module using an ordinary least squares regression with age and sex as nuisance effects. RESULTS: Hemodialysis patients had significantly smaller volumes in the bilateral hippocampus (P < .05/2, Bonferroni corrected), cornu ammonis 1 (CA1), CA4, granule cell and molecular layer of the dentate gyrus, hippocampus-amygdala transition area and molecular layer of the hippocampus than healthy controls (P < .05/24, Bonferroni corrected). Hemodialysis patients also had lower volumes in the left hippocampal tail and right fimbria than healthy controls (P < .05/24, Bonferroni corrected). Hippocampal subfield volumes were associated with neuropsychological test scores, the duration of disease and hemoglobin levels. CONCLUSIONS: We found smaller hippocampal subfield volumes in hemodialysis patients, which were associated with impaired cognition, supporting their role in memory disturbance in the hemodialysis population. However, multiple clinical factors may have confounded the results, and therefore, the interpretation of these results needs to be cautious.

Abnormal white matter along fibers by automated fiber quantification in patients undergoing hemodialysis.

BACKGROUND: Abnormal white matter has been reported in patients with end-stage renal disease (ESRD). However, few studies have investigated the relationship between specific damage segments and cognition in ESRD. This study aimed to delineate white matter alterations in ESRD and its relationship with cognition. METHODS: A total of 36 patients undergoing hemodialysis and 25 healthy controls underwent diffusion tensor imaging (DTI) and a series of neuropsychiatric tests. Automated fiber quantification was used to extract distinct DTI indices, and the relationship between the specific segment of the white matter and clinical properties was investigated. Furthermore, a support vector machine was applied to differentiate patients with ESRD from healthy controls. RESULTS: Fractional anisotropy values decreased in multiple fiber bundles, including bilateral thalamic radiata, cingulum cingulate, inferior fronto-occipital fasciculus (IFOF), uncinate, Callosum_Forceps_Major/Callosum_Forceps_Minor (CFMaj/CFMin), and left uncinate from the tract level in patients with ESRD. Specific damaged segments were detected in 8 fiber bundles, including bilateral thalamic radiation, cingulum cingulate, IFOF, CFMin, and left corticospinal tract. Few alterations in these fiber bundles were correlated with cognition impairment and hemoglobin levels. The tract profiles of the left thalamic radiata and left cingulum cingulate could be used to differentiate hemodialysis patients from healthy controls, with an accuracy of 76.9% and 67.6%, respectively. CONCLUSIONS: This study revealed white matter damage in hemodialysis patients. This damage occurred in specific segments of the tract, especially in the left thalamic radiata and left cingulum cingulate, which might become a new biomarker for patients with ESRD and cognition impairment.

Overexpression of miR-204-5p Alleviates Osteogenic Differentiation and Calcification of Human Aortic Vascular Smooth Muscle Cells by Targeting Calcium/Calmodulin-dependent Protein Kinase 1.

ABSTRACT: Vascular calcification (VC), a major complication in chronic kidney disease (CKD), is predominantly driven by osteoblastic differentiation. Recent studies have highlighted the crucial role of microRNAs in CKD's pathogenesis. Here, our research focused on the effects of miR-204-5p and its molecular mechanisms within VC. We initially found a notable decrease in miR-204-5p levels in human aortic vascular smooth muscle cells stimulated with inorganic phosphate, using this as a VC model in vitro. Following the overexpression of miR-204-5p, a decrease in VC was observed, as indicated by alizarin red S staining and measurements of calcium content. This decrease was accompanied by lower levels of the osteogenic marker, runt-related transcription factor 2, and higher levels of α-smooth muscle actin, a marker of contractility. Further investigation showed that calcium/calmodulin-dependent protein kinase 1 (CAMK1), which is a predicted target of miR-204-5p, promotes VC. Conversely, overexpressing miR-204-5p reduced VC by suppressing CAMK1 activity. Overexpressing miR-204-5p also effectively mitigated aortic calcification in an in vivo rat model. In summary, our research indicated that targeting the miR-204-5p/CAMK1 pathway could be a viable strategy for mitigating VC in CKD patients.

Clinical significance of serum CDC42 in the prediction of uremic vascular calcification incidence and progression.

Vascular calcification (VC) is prevalent in uremia patients, lacking effective molecular biomarkers. This study was conducted to explore the role of serum cell division cycle 42 (CDC42) in the diagnosis of uremic VC incidence and progression. We enrolled 104 uremia patients and selected arcus aortae calcification (AAC) as the outcome phenotype. Levels of CDC42, 1,25-dihydroxy vitamin D (1,25(OH) 2-D), fibroblast growth factor-23 (FGF-23), and other laboratory parameters in the blood were measured. The receiver operator characteristic curve, the Pearson test, and the multivariate Logistic regression were used for the analysis of CDC42 diagnostic values, correlation analysis, and screening of VC risk factors, respectively. CDC42 was higher in the serum of uremia patients with VC and elevated with the increase in AAC level. Serum CDC42 level>1.025 was predictive of VC incidence with 83.58% sensitivity and 56.76% specificity, and CDC42 level>1.280 was predictive of VC progression with 73.33% sensitivity and 68.18% specificity. Serum CDC42 was positively correlated with 1,25(OH) 2-D and FGF-23. Uremia patients with higher serum CDC42 had a higher probability of VC incidence and progression. Generally, serum CDC42 helped the diagnosis of uremic VC incidence and progression and was an independent risk factor for uremic VC progression.

Impact of impaired renal function on outcomes of chronic total occlusion undergoing revascularization: a systemic review and meta-analysis.

PURPOSE: Patients with chronic kidney disease (CKD) have an associated burden of coronary artery disease, including chronic total occlusions (CTO). It is unclear how the presence of CKD affects the outcomes of CTO revascularization. Previous reviews have not taken into account all relevant published studies that examined the association of CKD with outcomes of CTO revascularization. METHODS: A systematic search was conducted using PubMed, Scopus, and Google Scholar databases for studies investigating patients with or without CKD who also had coronary chronic total occlusion undergoing revascularization procedures Statistical analysis was performed using STATA software. Effect sizes were reported as pooled relative risk (RR). RESULTS: A total of 13 studies were included. CKD patients showed elevated risk of in-hospital mortality (RR 4.25, 95% CI 2.64, 6.82) and mortality at latest follow-up (RR 3.24, 95% CI 2.56, 4.11), elevated risk of major cardio or cerebrovascular events (RR 1.65, 95% CI 1.38, 1.98), major bleeding (RR 2.85, 95% CI 1.96, 4.13), and contrast-induced acute kidney injury (RR 3.06, 95% CI 1.70, 5.52). CKD patients also showed lower chances of technical success (RR 0.95, 95% CI 0.91, 1.00). CONCLUSIONS: The presence of CKD increases the risk of mortality, complications and adversely affects the success of CTO revascularization. Patients with CKD undergoing revascularization should have their kidney function comprehensively evaluated and these patients should be carefully monitored.

[Simulating site index of Juglans mandshurica using a random effect model in three provinces of Northeast China]. / 利用随机效应模型模拟东北三省胡桃楸地位指数.

To evaluate site quality and provide scientific evidence, the mixed effect model of polymorphic site index of Juglans mandshurica was accurately simulated in the three provinces of Northeast China. A total of 197 plots in the 23 typical regions of Liaoning, Jilin and Heilongjiang provinces were set by the sample circle method, from which we got 1537 height-age data of J. mandshurica. The site factors were divided, assigned and calculated using variance analysis and model fitting. The results showed that slope position was the dominant factor affecting the growth of dominant wood of J. mandshurica, followed by soil depth, slope and aspect. After fitting and analyzing eight common basic models, we found that the logistic model H=a/[1+exp(b+cA)] was the optimal one (R2=0.70), with a mean absolute error (MAE) of 2.52. When the four main influen-cing factors were randomly combined, the optimal site index model of the stochastic combination (M8.15) was obtained with R2 of 0.90, which improved the fitting accuracy of the base model. The K-means clustering method was used to further divide the initial groups of site types into six groups. We established the nonlinear mixed effect model Mfinal, H=(20.1837+ui)/[1+exp (1.7352-0.0961A)]+εij, with R2 and Akaike's information criterion (AIC) being 0.92 and 912.65, respectively, which could significantly improve the fitting and accuracy of the model. The equation could be used for the accurate evaluation of site quality of J. mandshurica under the complex site types in the three provinces of Northeast China.

Enantioseparation of racemic bupivacaine via ultrasonic-assisted diastereomeric crystallization using 12,14-dinitrodehydroabietic acid.

12,14-Dinitrodehydroabietic acid (12,14-dinitroDHAA), a chiral acid obtained by the nitration of optical dehydroabietic acid (DHAA), was successfully employed as resolving agent. The resolution of racemic bupivacaine by ultrasonic-assisted diastereomeric crystallization in ethanol was investigated. The results indicated that ultrasonic-assist can well facilitate resolution of (R,S)-bupivacaine and a higher enantiomeric excess (ee) and yield was obtained for (S)-bupivacaine, and while without ultrasound, the ee value decreases by increasing the crystallization time. A Box-Behnken experimental design with four factors (amount of 12,14-dinitroDHAA, ethanol amount, ultrasonic power and crystallization temperature) combined with response surface methodology (RSM) was applied to explore resolution effects. A second-order polynomial equation was adequate to model the relationship between the ee (or yield) and the dependent variables. When maintaining a lower limit of 90% for the yield of (S)-bupivacaine, the optimal resolution conditions by RSM were 12,14-dinitroDHAA/bupivacaine molar ratio of 1.6, solvent/propranolol ratio of 16.5 mL/g, 63.2 W ultrasonic power and crystallization temperature of 0 °C, respectively. Under the optimal conditions, the experimental ee and yield of (S)-bupivacaine were 69.8% and 87.5%.