bluuebunny/crossref_metadata_2025_split huggingface dataset:
A comparative study on the performance of photo/sono/peroxone processes for the removal and mineralization of reactive dye red 198 from aquatic environments
Authors: Safari Hasan , Zaeimdar Mojgan , Kashefi ALasl Morteza , Dadban Shahamat Yousef , Marandi Reza 
Published: April 2021

Abstract
Colored wastewater is the most important problem of textile manufacturing factories, because it contains pollutants with complex structure and toxic, carcinogenic, and mutagenic properties which are non-biodegradable and sustainable in the environment. Reactive Red 198 (RR198) is one of the types of azo dyes which are widely used in the textile industries. Therefore, in this study, the rate of degradation and mineralization of RR198 by UV/US/H2O2/O3 hybrid process was investigated. Influencing factors including: initial dye concentration (100, 200, 300, 400, 500 mg/L), contact time (12.5, 30, 47.5, 65, 82.5 min), pH (3, 5, 7, 9, 11), UV (125-W), H2O2 (10, 20, 30, 40, 50 mg/L), US (160 KHz) and O3 (33 mg/(L·min)) on the removal and mineralization efficiency of RR198 were investigated. Optimization and modeling of the process was done by CCD method. Based on the results of ANOVA analysis, most effective parameters on the RR198 removal efficiency were ozone, US, UV, time, initial dye concentration, pH, and H2O2, respectively, with an impact percentage of 96.86 and less than 1% for ozone and the rest parameters, respectively. Highest removal efficiency of RR198 was obtained by UV/US/H2O2/O3 hybrid process. Optimal conditions for dye removal including: initial dye concentration of 200 mg/L, reaction time of 34 min, H2O2 concentration of 27 mg/L and pH of seven were determined in the presence of ozone gas, UV, and US waves. In these conditions, the removal efficiency of RR198 and TOC were estimated to be 100 and 40.5, respectively. UV/US/H2O2/O3 hybrid process as an advanced oxidation process (AOP) with advantages such as high performance and speed, no sludge production and toxic residues in the treated effluent containing hard biodegradable compounds such as RR198 from aqueous solutions, so can be recommended and used.
Layoutoptimierung für kleinskalige modulare Förderanlagen
Authors: Aurich Paul , Stonis Malte , Overmeyer Ludger 
Published: April 2021

Abstract
Kleinskalige modulare Fördertechnik ermöglicht es, mehrere Förderaufgaben gleichzeitig und auf kleinstem Raum durchzuführen, und bietet so ein großes Potenzial zur Flexibilisierung und Effizienzsteigerung von Förderanlagen. Aktuell existiert keine einfach anwendbare Methode, die Unternehmen dabei unterstützt, diese neuartige Fördertechnik auf Prozessebene unter Berücksichtigung logistischer und wirtschaftlicher Zielstellungen in konventionelle Fördersysteme zu integrieren. Daher wird in einem Forschungsprojekt derzeit eine Optimierungsmethode für Förderanlagenlayouts entwickelt, mit der Unternehmen die Potenziale der neuartigen Fördertechnik bewerten können.
Predicting the Need for Phototherapy After Discharge
Authors: Kuzniewicz Michael W. , Park Jina , Niki Hamid , Walsh Eileen M. , McCulloch Charles E. , Newman Thomas B. 
Published: April 2021

BACKGROUND AND OBJECTIVES:
Bilirubin screening before discharge is performed to identify neonates at risk for future hyperbilirubinemia. The American Academy of Pediatrics recommends using a graph of bilirubin levels by age (the Bhutani Nomogram) to guide follow-up and a different graph to determine phototherapy recommendations. Our objective was to evaluate predictive models that incorporate the difference between the last total serum bilirubin (TSB) before discharge and the American Academy of Pediatrics phototherapy threshold (Δ-TSB) to predict a postdischarge TSB above the phototherapy threshold by using a single graph.

METHODS:
We studied 148 162 infants born at ≥35 weeks’ gestation at 11 Kaiser Permanente Northern California facilities from 2012 to 2017 whose TSB did not exceed phototherapy levels and who did not receive phototherapy during the birth hospitalization. We compared 3 logistic models (Δ-TSB; Δ-TSB-Plus, which included additional variables; and the Bhutani Nomogram) by using the area under the receiver operating characteristic curve (AUC) in a 20% validation subset.

RESULTS:
A total of 2623 infants (1.8%) exceeded the phototherapy threshold postdischarge. The predicted probability of exceeding the phototherapy threshold after discharge ranged from 56% for a predischarge Δ-TSB 0 to 1 mg/dL below the threshold to 0.008% for Δ-TSB &gt;7 mg/dL below the threshold. Discrimination was better for the Δ-TSB model (AUC 0.93) and the Δ-TSB-Plus model (AUC 0.95) than for the Bhutani Nomogram (AUC 0.88).

CONCLUSIONS:
The use of Δ-TSB models had excellent ability to predict postdischarge TSB above phototherapy thresholds and may be simpler to use than the Bhutani Nomogram.
The Decorin High Glucose Response Element and Mechanism of Its Activation in Human Mesangial Cells
Authors: WAHAB NADIA ABDEL , PARKER SUSAN , SRAER JEAN-DANIEL , MASON ROGER M. 
Published: April 2021

Abstract.
The decorin gene encodes a proteoglycan with putative structural and regulatory functions whose expression is markedly increased in human mesangial cells (HMC) exposed to high concentrations of glucose (15 to 30 mM). The gene has two promoters (P1 and P2) upstream of two alternative first exons. Transcripts driven by both promoters are present in HMC maintained in 4 mM D-glucose medium. After exposure to 30 mM D-glucose for 7 to 21 d, transcripts driven by P1 are markedly increased, whereas those driven by P2 decrease. Culture in 4 mM D-glucose medium containing transforming growth factor-β1 (TGF-β1) (1.25 ng/ml) has the same effect. However, addition of an excess of TGF-β neutralizing antibody to the 30 mM D-glucose cultures only partly suppressed increased decorin transcription from P1. In transformed HMC transfected with a reporter (p-SAEP) driven by P1 or P2, P1 activity increased twofold on treatment with either 30 mM D-glucose or TGF-β1 in 4 mM medium. P2 had little activity under any conditions. 5′ deletion of P1 showed that basal transcriptional activity lies within the proximal 378 bp, while the major high glucose and TGF-β response element is located in the -683 to -583-bp region. A putative cAMP response-like sequence (TGACGTTT) lies within this region. Electrophoretic mobility shift assays revealed the same pattern of multiple complexes between oligonucleotides containing this sequence and nuclear proteins extracted from HMC maintained in either 4 or 30 mM D-glucose conditions, but the latter were more prominent. cAMP response element binding protein (CREB) was identified as one transcription factor forming these complexes but other factors remain unidentified. Increased levels of phospho-(Ser 133) CREB were found in HMC exposed to 30 mM D-glucose. High glucose also activated and led to nuclear translocation of p42/44 mitogen-activated protein kinase and p38 mitogen-activated protein kinase, both of which can activate CREB by phosphorylation of serine 133.
Molecular Genetics of Nephronophthisis and Medullary Cystic Kidney Disease
Authors: HILDEBRANDT FRIEDHELM , OTTO EDGAR 
Published: April 2021

Abstract.
Nephronophthisis (NPH) and medullary cystic kidney disease (MCKD) constitute a group of renal cystic diseases that share the macroscopic feature of cyst development at the corticomedullary border of the kidneys. The disease variants also have in common a characteristic renal histologic triad of tubular basement membrane disintegration, tubular atrophy with cyst development, and interstitial cell infiltration with fibrosis. NPH and, in most instances, MCKD lead to chronic renal failure with an onset in the first two decades of life for recessive NPH and onset in adult life for autosomal dominant MCKD. There is extensive genetic heterogeneity with at least three different loci for NPH (NPHP1, NPHP2, and NPHP3) and two different loci for MCKD (MCKD1 and MCKD2). Juvenile nephronophthisis, in addition, can be associated with extrarenal organ involvement. As a first step toward understanding the pathogenesis of this disease group, the gene (NPH1) for juvenile nephronophthisis (NPH1) has been identified by positional cloning. Its gene product, nephrocystin, is a novel protein of unknown function that contains a src-homology 3 domain. It is hypothesized that the pathogenesis of NPH might be related to signaling processes at focal adhesions (the contact points between cells and extracellular matrix) and/or adherens junctions (the contact points between cells). This hypothesis is based on the fact that most src-homology 3-containing proteins are part of focal adhesion signaling complexes, on animal models that exhibit an NPH-like phenotype, and on the recent finding that nephrocystin binds to the protein p130cas, a major mediator of focal adhesion signaling.
Renal Function and Intensive Lowering of Blood Pressure in Hypertensive Participants of the Hypertension Optimal Treatment (HOT) Study
Authors: RUILOPE LUIS M. , SALVETTI ANTONIO , JAMERSON KENNETH , HANSSON LENNART , WARNOLD INGRID , WEDEL HANS , ZANCHETTI ALBERTO 
Published: April 2021

Abstract.
This article reports further analyses of the Hypertension Optimal Treatment (HOT) Study data with the aim to describe (1) the value of baseline serum creatinine and its clearance (estimated by Cockroft and Gault formula) as predictors of cardiovascular events, (2) the effects of intensive lowering of BP on cardiovascular events and renal function in patients with reduced renal function, and (3) the effects on cardiovascular events of adding acetylsalicylic acid to antihypertensive therapy in patients with reduced renal function. The results show that (1) baseline elevation in serum creatinine and a reduction in estimated creatinine clearance are powerful predictors of cardiovascular events and death. (2) Reduced renal function at baseline did not preclude the desired control of BP. In contrast to patients with normal renal function, the incidence of major cardiovascular events did not differ in the three groups of patients with mild renal insufficiency randomized to different diastolic BP targets. No significant changes in serum creatinine were seen at the end of the 3.8-yr treatment period in the great majority of patients. However, there was a small group of patients (0.58% of the total study population) whose renal function deteriorated (increase ≥30% over baseline and final serum creatinine concentration ≥2 mg/dl) despite satisfactory reduction of diastolic BP. (3) The results of this reanalysis of the HOT Study suggest though do not prove that the association of acetylsalicylic acid with intensive antihypertensive therapy offers additional benefit in hypertensive patients with reduced renal function.
Hyperphosphorylation of Na-Pump Contributes to Defective Renal Dopamine Response in Old Rats
Authors: ASGHAR MOHAMMAD , KANSRA VIKRAM , HUSSAIN TAHIR , LOKHANDWALA MUSTAFA F. 
Published: April 2021

Abstract.
Dopamine D1-like receptor activation causes phosphorylation and inhibition of Na,K-ATPase (Na-pump) activity in the proximal tubules, which is associated with an increase in sodium excretion. It has been shown that dopamine and SKF 38393, a D1-like receptor agonist, caused inhibition of Na,K-ATPase activity in the proximal tubules of adult (6 mo) but not of old (24 mo) Fischer 344 rats. The present study demonstrated that SKF 38393 and PDBu, a phorbol ester and protein kinase C (PKC) activator, increased phosphorylation of the α1-subunit of Na,K-ATPase in adult but not in old rats. In adult rats, SKF 38393-mediated phosphorylation was antagonized by SCH 23390, a D1-like receptor antagonist. Similarly, Na,K-ATPase activity was inhibited by SKF 38393 and PDBu in adult but not in old rats. The basal activity of Na,K-ATPase was decreased and the basal phosphorylation state of the enzyme was increased in old compared with adult rats. Basal activity of PKC was higher in old compared with adult rats, and SKF 38393 and PDBu stimulated PKC activity in adult but not in old rats. The conclusion is that the failure of D1-like receptor agonist and phorbol ester to stimulate PKC and inhibit Na,K-ATPase activity in old rats is due, at least in part, to the higher basal PKC activity and Na,K-ATPase phosphorylation in old compared with adult rats.
Identification of Receptor Ligands by Screening Phage-Display Peptide Libraries Ex Vivo on Microdissected Kidney Tubules
Authors: ODERMATT ALEX , AUDIGÉ ANNETTE , FRICK CHRISTOPH , VOGT BRUNO , FREY BRIGITTE M. , FREY FELIX J. , MAZZUCCHELLI LUCA 
Published: April 2021

Abstract.
A novel method to identify receptor ligands for defined renal tubular segments has been developed. Ex vivo screening of phage-display peptide libraries on isolated intact rat proximal convoluted tubules (PCT) and cortical collecting ducts (CCD) allowed the direct access of phage to the basolateral surface of tubular epithelial cells. Two distinct peptide motifs were selected for CCD and PCT, indicating differential expression of some membrane receptors on the basolateral surface of defined kidney tubule segments. Using the linear peptide motif ELRGD(R/M)AX(W/L), recovered from freshly isolated rat CCD, mediated 16-fold selectivity of phage binding to CCD compared with PCT. Binding to CCD was 39-fold higher than that of a random control phage. Binding and subsequent internalization of phage, most likely by an integrin-mediated endocytosis pathway, was abolished by the addition of the corresponding synthetic peptide. Furthermore, the results demonstrate that presentation and flanking amino acids determine the specific binding properties of RGD ligands to their putative integrin receptors. The results emphasize the need of a native cell system for the identification of renal epithelial cell surface ligands. Such ligands are of potential relevance for the analysis of interactions between extracellular matrix and kidney tubules or for the development of improved vectors for kidney-specific drug delivery or gene transfer.
Downregulation of Hepatic Cytochrome P450 in Chronic Renal Failure
Authors: LEBLOND FRANCOIS , GUÉVIN CARL , DEMERS CHRISTIAN , PELLERIN ISABELLE , GASCON-BARRÉ MARIELLE , PICHETTE VINCENT 
Published: April 2021

Abstract.
Chronic renal failure (CRF) is associated with a decrease in drug metabolism. The mechanism remains poorly understood. The present study investigated the repercussions of CRF on liver cytochrome P450 (CYP450). Three groups of rats were defined: control, control paired-fed, and CRF. Total CYP450 activity, protein expression of several CYP450 isoforms as well as their mRNA, and the in vitro N-demethylation of erythromycin were assessed in liver microsomes. The regulation of liver CYP450 by dexamethasone and phenobarbital was assessed in CRF rats. Compared with control and control paired-fed rats, creatinine clearance was reduced by 60% (P < 0.01) in CRF rats. Weight was reduced by 30% (P < 0.01) in control paired-fed and CRF rats, compared with control animals. There was no difference in the CYP450 parameters between control and control paired-fed. Compared with control paired-fed rats, total CYP450 was reduced by 47% (P < 0.001) in CRF rats. Protein expression of CYP2C11, CYP3A1, and CYP3A2 were considerably reduced (>40%, P < 0.001) in rats with CRF. The levels of CYP1A2, CYP2C6, CYP2D, and CYP2E1 were the same in the three groups. Northern blot analysis revealed a marked downregulation in gene expression of CYP2C11, 3A1, and 3A2 in CRF rats. Although liver CYP450 was reduced in CRF, its induction by dexamethasone and phenobarbital was present. N-demethylation of erythromycin was decreased by 50% in CRF rats compared with control (P < 0.001). In conclusion, CRF in rats is associated with a decrease in liver cytochrome P450 activity (mainly in CYP2C11, CYP3A1, and 3A2), secondary to reduced gene expression.
Rise in Albuminuria and Blood Pressure in Patients Who Progressed to Diabetic Nephropathy in the Diabetes Control and Complications Trial
Authors: THOMAS WILLIAM , SHEN YINGJIA , MOLITCH MARK E. , STEFFES MICHAEL W. 
Published: April 2021

Abstract.
The Diabetes Control and Complications Trial (DCCT) enrolled 1441 participants to address the role of intensive therapy for type 1 diabetes mellitus on the onset and progression of microvascular complications. To examine the timing of elevated systolic BP (SBP) and diastolic BP (DBP) and increased albumin excretion rate (AER) in the progression to clinical diabetic nephropathy (AER > 300 mg/24 h on two consecutive visits from a baseline of <100 mg/24 h) and, importantly, to control for initial values of hemoglobin A1c, a retrospective case-control study was assembled from the records of the publicly released DCCT data. Participants who progressed to clinical diabetic nephropathy—progressors—were matched with participants of the same gender and treatment group who had similar baseline values for DBP, SBP, AER AER and hemoglobin A1c, but who did not progress to clinical diabetic nephropathy—matched controls. In the conventional treatment group, the 21 progressors exhibited a significant rise in mean AER (above their own baseline levels and above values in the matched controls) at year 2 of the DCCT. In contrast, the progressors' mean DBP and SBP were not significantly higher than baseline until year 3 (DBP) or year 4 (SBP) and not significantly higher than the matched controls until year 4 (both DBP and SBP). On the individual level, 19 of 21 (90%) progressors reached clinical diabetic nephropathy before the diagnosis of hypertension (140/90 mmHg). In the intensive treatment group, however, the rise in DBP preceded the rise in AER by 1 to 2 yr among the six progressors. Both intensively treated progressors who experienced hypertension reached this before AER > 300 mg/24 h. These results underline the early and prognostic rise in AER in diabetic patients, but only in those who received conventional treatment. The evolution of diabetic renal disease may follow a different course in patients who receive intensive diabetic treatment.
Hereditary Hypophosphatemic Rickets with Hypercalciuria Is Not Caused by Mutations in the Na/Pi Cotransporter NPT2 Gene
Authors: JONES ANDREW O. , TZENOVA JORDANA , FRAPPIER DANIELLE , CRUMLEY M. JOYCE , ROSLIN NICOLE M. , KOS CLAUDINE H. , TIEDER MARTIN , LANGMAN CRAIG B. , PROESMANS WILLEM , CARPENTER THOMAS O. , RICE ALLAN , ANDERSON DONALD , MORGAN KENNETH , FUJIWARA T. MARY , TENENHOUSE HARRIET S. 
Published: April 2021

Abstract.
Hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a renal phosphate (Pi) wasting disease first described in an extended Bedouin kindred, is characterized by hypophosphatemia, elevated serum 1,25-dihydroxyvitamin D levels, hypercalciuria, rickets, and osteomalacia. Correction of all abnormalities, except for renal Pi wasting, can be achieved by oral Pi supplementation. These findings and the demonstration that mice that are homozygous for the disrupted Na/Pi cotransporter gene Npt2 exhibit many of the biochemical features of HHRH suggested that mutations in the human orthologue NPT2 might be responsible for HHRH. The NPT2 gene in affected individuals from the Bedouin kindred and four small families was screened for mutations to test this hypothesis. No putative disease-causing mutation was found. Two single nucleotide polymorphisms (SNP), a silent substitution in exon 7 and a nucleotide substitution in intron 4, were identified, and neither consistently segregated with HHRH in the Bedouin kindred. Linkage analysis indicated that the two NPT2 intragenic SNP as well as five microsatellite markers in the NPT2 gene region were not linked to HHRH in the Bedouin kindred. Therefore, this is evidence to exclude NPT2 as a candidate gene for HHRH in the families that were studied.
Chronic Humoral Rejection
Authors: MAUIYYEDI SHAMILA , PELLE PATRICIA DELLA , SAIDMAN SUSAN , COLLINS A. BERNARD , PASCUAL MANUEL , TOLKOFF-RUBIN NINA E. , WILLIAMS WINFRED W. , COSIMI A. BENEDICT , SCHNEEBERGER EVELINE E. , COLVIN ROBERT B. 
Published: April 2021

Abstract.
The pathogenesis of chronic renal allograft rejection (CR) remains obscure. The hypothesis that a subset of CR is mediated by antidonor antibody was tested by determining whether C4d is deposited in peritubular capillaries (PTC) and whether it correlates with circulating antidonor antibodies. All cases (from January 1, 1990, to July 31, 1999) that met histologic criteria for CR and had frozen tissue (28 biopsies, 10 nephrectomies) were included. Controls were renal allograft biopsies with chronic cyclosporine toxicity (n = 21) or nonspecific interstitial fibrosis (n = 10), and native kidneys with end-stage renal disease (n = 10) or chronic interstitial fibrosis (n = 5). Frozen sections were stained by two-color immunofluorescence for C4d, type IV collagen and Ulex europaeus agglutinin I. Antidonor HLA antibody was sought by panel-reactive antibody analysis and/or donor cross matching in sera within 7 wk of biopsy. Overall, 23 of 38 CR cases (61%) had PTC staining for C4d, compared with 1 of 46 (2%) of controls (P < 0.001). C4d in PTC was localized at the interface of endothelium and basement membrane. Most of the C4d-positive CR tested had antidonor HLA antibody (15 of 17; 88%); none of the C4d-negative CR tested (0 of 8) had antidonor antibody (P < 0.0002). The histology of C4d-positive CR was similar to C4d-negative CR, and 1-yr graft survival rates were 62% and 25%, respectively (P = 0.05). Since August 1998, five of six C4d-positive CR cases have been treated with mycophenolate mofetil ± tacrolimus with a 100% 1-yr graft survival, versus 40% before August 1998 (P < 0.03). These data support the hypothesis that a substantial fraction of CR is mediated by antibody (immunologically active). C4d can be used to separate this group of CR from the nonspecific category of chronic allograft nephropathy and may have the potential to guide successful therapeutic intervention.
Transferrin Synthesis Is Increased in Nephrotic Patients Insufficiently to Replace Urinary Losses
Authors: PRINSEN BERTHIL H. C. M. T. , DE SAIN-VAN DER VELDEN MONIQUE G. M. , KAYSEN GEORGE A. , STRAVER HELMA W. H. C. , VAN RIJN HERMAN J. M. , STELLAARD FRANS , BERGER RUUD , RABELINK TON J. 
Published: April 2021

Abstract.
The urinary loss of transferrin is sufficient to reduce plasma transferrin concentrations in the nephrotic syndrome. Hypotransferrinemia may lead to iron loss and microcytic anemia. The mechanism responsible for the hypotransferrinemia in the nephrotic syndrome is, however, unknown. In the present study, synthesis rate of transferrin was measured in vivo in nephrotic patients (n = 7) compared with control subjects (n = 6) using L-[1-13C]-valine. Plasma transferrin and iron concentration in the patients were significantly lower than in control subjects (transferrin, 1.39 ± 0.08 versus 2.57 ± 0.11 g/L, P < 0.0001; iron, 10.2 ± 0.8 versus 21.1 ± 4.5 μmol/L, P = 0.02). Furthermore, albuminuria correlated with transferrinuria (r2 = 0.901, P = 0.001). The absolute synthesis rate of transferrin was increased in the patients (10.0 ± 1.1 versus 7.4 ± 0.7 mg/kg per d, P = 0.07), although this value failed to achieve significance. C-reactive protein, plasma iron, and proteinuria did not correlate with transferrin synthesis. In contrast, transferrin synthesis correlated with albumin synthesis (r2 = 0.648, P = 0.03; n = 7). The present study indicates that increased transferrin synthesis occurs in nephrotic patients but is insufficient to compensate for urinary losses. Because, overall, no significant relationship was found between transferrin synthesis and either C-reactive protein or iron, it is unlikely that inflammation suppresses or that iron deficiency stimulates increased transferrin synthesis in these patients. The correlation between transferrin synthesis and albumin synthesis suggests that transferrin synthesis is a component of a general response in hepatic protein synthesis in the nephrotic syndrome. This suggests that a therapeutic approach to maximize plasma transferrin concentrations in nephrotic patients should be aimed primarily at reducing urinary protein excretion.