bluuebunny/crossref_metadata_2025_split huggingface dataset:
AUTONOMOUS VEHICLES AND EUROPEAN DATA PROTECTION LAW
Authors: Fialová Eva 
Published: April 2021

Autonomous vehicles process a huge amount of data about the driver, or rather passengers of the vehicle, as well as about other persons (pedestrians and passengers of other vehicles). This is why the autonomous vehicles raise questions about the protection of personal data. In 2018 a new European data protection legislation came into force. The General Data Protection Regulation places new obligations on controllers of personal data and provides new rights to data subjects, which will relate to operations of autonomous vehicles and their infrastructure. The providers thereof will have to implement the principles of data protection legislation into their systems. In this context the personal data is not just data concerning the identity of the driver, a passenger or other persons, but any information relating to an identified or identifiable natural person who can be identified, directly or indirectly, in particular by reference to an identifier such as a name, an identification number, location data, or even due to a peculiar behaviour in the vehicle. The paper will focus on the new legal regulation in relation to the operation of autonomous vehicles.Autonomní vozidla zpracovávají velké množství údajů o řidiči vozidla, resp. cestujících ve vozidle, jakož i o dalších osobách (spolucestujících, chodcích a pasažérech v jiných vozidlech). To je důvod, proč provoz autonomních vozidel vyvolává řadu otázek týkajících se ochrany osobních údajů. V roce 2018 nabyla účinnosti nová evropská právní úprava regulující tuto oblast. Obecné nařízení o ochraně osobních údajů přináší nové povinnosti správcům osobních údajů, jakož i nová práva subjektům údajů, která se budou týkat provozu autonomních vozidel a infrastruktury. Výrobci a poskytovatelé služeb budou muset do svých systémů implementovat legislativu o ochraně osobních údajů. Osobními údaji nejsou pouze údaje týkající se totožnosti řidiče, cestujících nebo jiných osob, ale veškeré informace vztahujících se k identifikované nebo identifikovatelné fyzické osobě, kterou lze přímo nebo nepřímo identifikovat, zejména odkazem na identifikátor, jako je např. název, identifikační číslo, lokalizační údaje, nebo třeba i kvůli osobitému chování ve vozidle. Tento článek se zaměřuje na novou právní úpravu ve vztahu k provozu autonomních vozidel.
Magneto-optical properties of two – layer film systems based on Fe and Pt
Authors: Bezdidko O.V. , Shkurdoda Yu.O. , Vashchenko S.M. 
Published: April 2021

The paper shows the experimental results of the study of magneto - optical properties and phase composition of thin films and multilayers based on Fe and Pt. Samples were obtained in a high-vacuum chamber (10–8 Pa) by layer-by-layer deposition from pots at room temperature. It has been shown that FCC solid solution of FePt is formed already in the process of deposition on the substrate (sital plates). Depending on the concentration of the atoms of the components in the unannealed samples, three phases can be formed: (i) s.s. Fe(Pt); (ii) Fe3Pt; (iii) FePt. The first sign of the beginning of ordering in the FCC phase of FePt should be considered the appearance of superreflections in the form of lines (001) and (002) during heat treatment. Depending on the total thickness of the multilayer or individual layers, the annealing temperature at which extrareflexes appear can vary in the range of 300–570 K. All the samples obtained have a low coercivity (0.25 - 0.4 mT). Magneto-optical studies have shown that an increase in the content of the non-magnetic component decreases the main magnetic characteristics. However, In [Fe(3)/Pt(3)]n/S multilayers with the number of repeatable elements from 2 to 8 an increase in the main magnetic parameters is observed compared with bilayer films at the same effective thickness.
Effect of Serotonin Receptor Antagonist on Phosphate Excretion
Authors: GROSS JENNIFER M. , BERNDT THERESA J. , KNOX FRANKLYN G. 
Published: April 2021

Abstract.
To determine whether endogenous intrarenal 5-hydroxytryptamine affects phosphate excretion, the serotonin receptor antagonist methiothepin (20 μg/kg, +6 μg/kg per h) was infused into the renal interstitium of rats fed a normal phosphate diet (0.7% phosphate [Pi]) in the presence of endogenous parathyroid hormone (PTH). Renal interstitial infusion of methiothepin significantly increased fractional phosphate excretion (FEPi) from 23 ± 4 to 30 ± 4% (n = 8, P < 0.05). To determine whether serotonin modulates the phosphaturic response to PTH during conditions of dietary phosphate excess or deprivation, rats were fed either a high (1.8% Pi, HPD) or low (0.07% Pi, LPD) phosphate diet, and methiothepin (100 μg/kg, +30 μg/kg per h) or saline vehicle was infused intravenously before and during PTH infusion (33 U/kg, +1 U/kg per min). Methiothepin infusion significantly increased FEPi in thyroparathyroidectomized rats fed a HPD from 25 ± 4 to 32 ± 4% (n = 9, P < 0.05), and the subsequent administration of PTH further increased the FEPi to 64 ± 3% (P < 0.05). The increase in FEPi during PTH infusion was similar in the absence (Δ27 ± 5%, n = 7) and presence (Δ33 ± 6%) of methiothepin, P > 0.05. In thyroparathyroidectomized rats fed a LPD, methiothepin infusion did not increase phosphate excretion (0.8 ± 0.4 to 1.3 ± 0.9%, n = 7, P > 0.05). However, the increase in FEPi during PTH infusion was significantly greater in the presence of methiothepin (1.3 ± 0.9 to 20.0 ± 4.0%, Δ18.7 ± 3.5%) than in the vehicle-infused rats (0.5 ± 0.2 to 8.8 ± 1.1%, Δ8.3 ± 1.2%; n = 8, P < 0.05). In conclusion, these observations suggest that endogenous intrarenal serotonin enhances phosphate reabsorption in phosphate-replete rats, and attenuates the phosphaturic response to PTH in phosphate-deprived rats.
Luminal and Basolateral Membrane Transport of Glutathione in Isolated Perfused S1, S2, and S3 Segments of the Rabbit Proximal Tubule
Authors: PARKS LISA D. , ZALUPS RUDOLFS K. , BARFUSS DELON W. 
Published: April 2021

Abstract.
Lumen-to-bath and bath-to-lumen transport rates of glutathione (GSH) were measured in isolated perfused S1, S2, and S3 segments of the rabbit proximal tubule. In lumen-to-bath experiments, the perfusion solution contained 4.6 μM 3H-GSH with or without 1.0 mM acivicin. In all three segments perfused without acivicin, luminal disappearance rate (J
DL) and bath appearance rate (J
AB) of 3H-GSH were 14.5 ± 0.5 and 2.2 ± 0.8 fmol/min per mm tubule length, respectively. With acivicin present, J
DL and J
AB were reduced to 1.3 ± 0.4 and 0.5 ± 0.3, respectively, with no differences among segments. Cellular concentrations of 3H-GSH in S1, S2, and S3 segments when acivicin was absent were 23.1 ± 2.0, 31.7 ± 11.4, and 143.5 ± 17.9 μM, respectively. With acivicin in perfusate, cellular concentrations were reduced but there was no change in the heterogeneity profile. In bath-to-lumen transport experiments (S2 segments only), the bathing solution contained 2.3 μM 3H-GSH. 3H-GSH appearance in the lumen (J
AL, fmol/min per mm) and cellular accumulation from the bath were studied with and without acivicin in the perfusate. J
AL values were 3.0 ± 0.2 and 0.2 ± 0.03 while cellular concentrations were 9.5 ± 1.0 and 6.1 ± 0.5 μM, respectively. It is concluded that: (1) GSH is primarily removed from the luminal fluid after degradation to glycine, cysteine, and glutamate, which are absorbed; (2) GSH can be absorbed intact at the luminal membrane; (3) the S3 segment has the greatest GSH cellular concentration because its basolateral membrane has less capacity for cell-to-bath transport of GSH; and (4) GSH can be secreted intact from the peritubular compartment into the tubular lumen.
Regenerative and Proinflammatory Effects of Thrombin on Human Proximal Tubular Cells
Authors: GRANDALIANO GIUSEPPE , MONNO RAFFAELLA , RANIERI ELENA , GESUALDO LORETO , SCHENA FRANCESCO P. , MARTINO CARMELA , URSI MICHELE 
Published: April 2021

Abstract.
Interstitial fibrin deposition is a common histologic feature of tubulointerstitial diseases, which suggests that the coagulation system is activated. Thrombin, generated during the activation of the coagulation cascade, is a powerful activating factor for different cell types. Although proximal tubular cells are potential targets for this coagulation factor, no information is available on the effect of thrombin on these cells. Thus, the expression of protease-activated receptor-1 (PAR-1), the main thrombin receptor, was investigated in human proximal tubular cells (hPTC) in vivo and in vitro. A diffuse expression of PAR-1 was observed by immunohistochemistry along the basolateral membrane of PTC in normal human kidney. This observation was confirmed in vitro in cultured hPTC. Because tubular damage and monocyte infiltration are two hallmarks of tubulointerstitial injury, the effect of thrombin on DNA synthesis and monocyte chemotactic peptide-1 (MCP-1) gene and protein expression was evaluated in cultured hPTC. Thrombin induced a significant and dose-dependent increase in thymidine uptake and a striking upregulation of MCP-1 mRNA expression and protein release into the supernatant. Although PAR-1 is a G protein-coupled receptor, its activation in hPTC, as in other cell systems, resulted in a transient increase in cellular levels of tyrosine-phosphorylated proteins. An increased level of tyrosine-phosphorylated c-src suggested the activation of this cytoplasmic tyrosine kinase in response to thrombin and its potential role in thrombin-induced protein-tyrosine phosphorylation. Interestingly, thrombin-induced DNA synthesis and MCP-1 gene expression were completely blocked by genistein, a specific tyrosine kinase inhibitor, but not by its inactive analogue daidzein, demonstrating a central role for tyrosine kinase activation in the thrombin effects on hPTC. Moreover, the specific src inhibitor PP1 abolished the thrombin effect on DNA synthesis. In conclusion, thrombin might represent a powerful regenerative and proinflammatory stimulus for hPTC in acute and chronic tubulointerstitial diseases.
Functional Relevance of Activated β1 Integrins in Mercury-Induced Nephritis
Authors: ESCUDERO ESTHER , MARTÍN ANA , NIETO MARTA , NIETO ELENA , NAVARRO ELENA , LUQUE ALFONSO , CABAN[Combining Tilde]AS CARLOS , SÁNCHEZ-MADRID FRANCISCO , MAMPASO FRANCISCO 
Published: April 2021

Abstract.
Cell adhesion through different adhesion molecules is a crucial event in the inflammatory response. Integrins can only bind and mediate cellular adhesion after their activation by different specific stimuli. The state of β1 integrin activation can be assessed by a group of monoclonal antibodies (HUTS) that selectively recognize β1 integrins in their active form. A similar activated epitope in the rat was defined using the anti-human monoclonal antibody HUTS-21, which recognizes an activation-dependent epitope on the β1 chain. It was found that the divalent cations Mn2+ and Hg2+ were able to induce in vitro the activation of β1 integrins on rat lymphocytes. The Hg2+ cation induces an autoimmune disease in the Brown Norway rat characterized by synthesis and glomerular deposits of anti-glomerular basement membrane antibodies, proteinuria, and interstitial nephritis. Using the mercury model of nephritis, it was found that the expression of HUTS-21 epitope is induced in vivo in rat lymphocytes, and its appearance is correlated with the other parameters at the onset of the disease. In addition, the administration of HUTS-21 monoclonal antibody to HgCl2-treated rats offered evidence of its protective effects (1) against infiltration of renal interstitium by leukocytes, and (2) in the reduction of anti-glomerular basement membrane synthesis and glomerular deposition. Nevertheless, urinary protein values remained unaffected. These results demonstrate a key role of β1-activated integrins in both leukocyte cell-cell interactions and leukocyte infiltration pathway mechanism, and also indicate that leukocyte migration may have less importance in the development of this disease than previously thought.
Pharmacokinetics of Once Daily Intraperitoneal Cefazolin in Continuous Ambulatory Peritoneal Dialysis Patients
Authors: LOW CHAI LUAN , GOPALAKRISHNA KAMANI , LYE WAI CHOONG 
Published: April 2021

Abstract.
This study determined the pharmacokinetic characteristics of once daily intraperitoneal (IP) cefazolin in continuous ambulatory peritoneal dialysis (CAPD) patients. Each of the 10 volunteer CAPD patients without active peritonitis received a single IP dose of 1 g of cefazolin sodium for a 6-h dwell. All patients underwent a fixed CAPD regimen comprising a first 6-h dwell followed by two 3-h dwells and a final 12-h overnight dwell. Blood and dialysate samples were collected at 0, 0.5, 1, 2, 3, 6 (end of first dwell), and 24 h after the administration of IP cefazolin. Any urine produced was collected over the 24-h study period. A validated HPLC method was used to analyze cefazolin in plasma, dialysate, and urine. The bioavailability was found to be 77.9 ± 3.1%, volume of distribution 0.20 ± 0.05 L/kg, and plasma half-life 39.9 ± 25.4 h. Mean total, renal, and peritoneal clearances were 4.5 ± 2.3, 1.4 ± 1.1, and 3.5 ± 1.8 ml/min, respectively. Mean plasma and dialysate concentrations at 24 h were 42.8 ± 14.3 and 31.8 ± 11.7 mcg/ml, respectively, well above the minimum inhibitory concentrations (MIC) of susceptible organisms. A once daily IP cefazolin dose of 500 mg/L gave desirable pharmacokinetic attributes for use as a suitable alternative to vancomycin for empiric treatment of CAPD-associated peritonitis.
Encrusted Pyelitis of Native Kidneys
Authors: HERTIG ALEXANDRE , DUVIC CHRISTIAN , CHRETIEN YVES , JUNGERS PAUL , GRU[Combining Diaeresis]NFELD JEAN-PIERRE , RIEU PHILIPPE 
Published: April 2021

Abstract.
This study reports the first four cases of encrusted pyelitis involving native kidneys. The clinical features, management, and outcome of these patients were analyzed. Predisposing factors were underlying urologic disease and/or urologic manipulations, debilitating diseases, hospitalization, and prolonged antibiotic therapies. Presenting symptoms were renal failure in three patients with ureteroileal urinary diversion and manifestations of cystitis in one patient. Computed tomography scan of the urinary tract was critical for diagnosis. Presence of struvite was demonstrated by crystalluria and infrared spectrophotometry analysis of the encrusted material. Corynebacterium urealyticum urinary infection was identified in one case. Surgery (one patient) and palliative ureteral diversion (one patient), respectively, led to death and end-stage renal failure. Successful dissolution of encrusted pyelitis was obtained in two patients treated with intravenous vancomycin and local acidification of the renal collecting system. Clinical observation shows that encrusted pyelitis is a threatening disorder that destroys the native kidneys and may lead to end-stage renal failure. Successful treatment of the disease by chemolysis and antibiotics depends on correct and early diagnosis. Diagnosis required recognition of the predisposing factors, computed tomography imaging of the urinary tract, crystalluria, and identification of urea-splitting bacteria with prolonged culture on selective medium.
Effect of Elevated Glucose on Endothelin-Induced Store-Operated and Non-Store-Operated Calcium Influx in Renal Mesangial Cells
Authors: NUTT LETA K. , O'NEIL ROGER G. 
Published: April 2021

Abstract.
Early diabetic nephropathy exhibits renal glomerular hyperfiltration and an increase in renal plasma flow. The hyperfiltration is a dysfunctional state that may arise from a hyperglycemic-induced hypocontractility of glomerular mesangial cells that may be associated with depressed Ca2+ signaling events. The present study was designed to determine the effects of acute (minutes) and chronic (days) elevated glucose levels on endothelin-induced calcium signaling with a particular emphasis on the potential influence on stores and store-operated Ca2+ influx (SOCI; also called capacitative calcium entry) in glomerular mesangial cells. Primary cultures of rat mesangial cells were grown in either high (30 mM) or normal (5 mM) glucose-containing media and tested in the presence of either high (30 mM) or normal (5 mM) glucose levels. Intracellular calcium levels were monitored with the calcium-sensitive fluorophore fura-2 before and after treatment with either endothelin-1 (10 nM), to induce typical Ca2+ signals, or the endoplasmic reticulum (ER) Ca-ATPase inhibitor thapsagargin (1 μM), to unload ER Ca2+ stores. Both acute and chronic exposure to high glucose levels depressed the endothelin-induced calcium signal. However, neither release of Ca2+ from stores nor SOCI were depressed by high glucose levels. In contrast, an endothelin-induced calcium entry pathway (likely receptor-operated calcium influx), separate from SOCI, was markedly depressed in the presence of both acute and chronic high glucose levels. The depressant effect of high glucose was rapidly (minutes) reversible upon returning to normal glucose levels. It is concluded that high glucose levels depress endothelin-induced calcium signaling in rat mesangial cells by inhibiting non-SOCI Ca2+ entry pathways, namely the receptor-operated Ca2+ influx pathway. The glucose-induced alterations in the receptor-operated calcium influx pathway may, in part, contribute to the depressed contractile state of glomerular cells during periods of hyperglycemia.
In Vivo Administration of a Nuclear Transcription Factor-κB Decoy Suppresses Experimental Crescentic Glomerulonephritis
Authors: TOMITA NARUYA , MORISHITA RYUICHI , LAN HUI Y. , YAMAMOTO KEI , HASHIZUME MASAHIDE , NOTAKE MITSUE , TOYOSAWA KAORU , FUJITANI BUICHI , MU WEI , NIKOLIC-PATERSON DAVID J. , ATKINS ROBERT C. , KANEDA YASUFUMI , HIGAKI JITSUO , OGIHARA TOSHIO 
Published: April 2021

Abstract.
Glomerular expression of cytokines, interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α), together with leukocytic infiltration, are prominent features in crescentic glomerulonephritis. Because these cytokines are targets for nuclear transcription factor-κB (NF-κB), the use of NF-κB decoy oligodeoxynucleotide (ODN) treatment was evaluated in an experimental disease model. Crescentic glomerulonephritis was induced in primed Wistar rats by injection of sheep antiglomerular basement membrane serum. Thirty minutes after injection, rats were anesthetized and the left kidney was perfused with NF-κB decoy ODN or scrambled ODN control mixed with a virus-liposome complex, and then killed 7 d later. Animals given the scrambled control ODN developed severe glomerulonephritis by day 7 with heavy proteinuria, glomerular crescents and interstitial lesions, marked leukocytic infiltration, and upregulated renal expression of cytokines (IL-1 and TNF-α) and adhesion molecules (intercellular adhesion molecule-1). In contrast, NF-κB decoy ODN treatment substantially inhibited the disease with a 50% reduction in proteinuria, a threefold reduction in histologic damage, a 50% reduction in leukocytic infiltration, and a 50 to 80% reduction in the renal expression of cytokines and leukocyte adhesion molecules. In conclusion, this study has demonstrated that NF-κB plays a key role in cytokine-mediated renal injury and that NF-κB decoy ODN treatment has clear therapeutic potential in rapidly progressive glomerulonephritis.
Quantitative Trait Loci Modulate Renal Cystic Disease Severity in the Mouse bpk Model
Authors: GUAY-WOODFORD LISA M. , WRIGHT CHRISTOPHER J. , WALZ GERD , CHURCHILL GARY A. 
Published: April 2021

Abstract.
Numerous mouse models of polycystic kidney disease (PKD) have been described in which the mutant phenotypes closely resemble human PKD with regard to morphology, cyst localization, and disease progression. As in human PKD, genetic background affects the disease phenotype in mouse PKD models. Using experimental crosses, these modifying effects can be dissected into discrete genetic factors referred to as quantitative trait loci. The locus for the mouse bpk model was recently mapped to chromosome (Chr) 10. In the course of these studies, marked variability was observed in the renal cystic disease expressed in F2 bpk/bpk homozygotes of a (BALB/c-+/bpk × CAST/Ei)F1 intercross. The current study was undertaken to further characterize the renal cystic disease as quantitative trait in this F2 cohort and to map the genetic modifiers that modulate this phenotype. Whole-genome scans revealed a CAST-derived locus on distal Chr 6, near D6Mit14, that affects renal cystic disease severity. Additional analyses identified loci on Chr 1, Chr 2, and Chr 4, as well as a possible interaction between the Chr 6 locus and a locus on distal Chr 1, near D1Mit17. Interestingly, the gene encoding RGS7, a regulator of G protein signaling that binds to polycystin-1, was mapped to the same Chr 1 interval. It is concluded that the severity of the bpk renal cystic disease phenotype is modulated by multiple loci and possibly by epistatic interaction among them. It is hypothesized that the gene encoding the polycystin-binding partner RGS7 is a candidate for the Chr 1 genetic modifier.
Contribution of Angiotensin II to Late Renal Injury after Acute Ischemia
Authors: PAGTALUNAN MARIA ENRICA , OLSON JEAN L. , MEYER TIMOTHY W. 
Published: April 2021

Abstract.
Rats recovering from acute renal ischemia exhibit tubule loss and interstitial fibrosis followed by development of proteinuria and glomerular sclerosis. The current study assessed the contribution of angiotensin II (AngII) to these processes. The contribution of AngII to early tubule loss and interstitial fibrosis was assessed in rats studied for 35 d after right nephrectomy and transient occlusion of the left renal artery. One group of rats received no treatment, while a second group received losartan beginning at 2 d following ischemia. Studies at 35 d showed that losartan did not improve GFR (2.04 ± 0.30 ml/min treated, 2.16 ± 0.21 ml/min untreated), reduce the fraction of glomeruli that were no longer connected to normal tubule segments (42 ± 9% treated, 42 ± 13% untreated), or limit expansion of the interstitial volume fraction (25 ± 3% treated, 25 ± 4% untreated). The contribution of AngII to progressive glomerular injury following initial recovery from ischemia was assessed in similarly prepared rats studied for 140 d. One group of rats received no treatment, while a second group received enalapril beginning at 35 d following ischemia. Enalapril markedly reduced proteinuria (78 ± 17 mg/d treated, 229 ± 52 mg/d untreated) and the prevalence of segmental glomerular sclerosis (14 ± 9% treated, 45 ± 10% untreated). Untreated rats developed sclerotic lesions in glomeruli not connected to normal tubules, as well as in glomeruli connected to normal tubules. Enalapril prevented injury in both classes of glomeruli. These results indicate that AngII does not contribute to interstitial fibrosis during recovery from ischemic injury. Reduction of AngII activity, can, however, prevent secondary glomerular injury in kidneys initially damaged by ischemia.