bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insulin-Like Growth Factor I Plays a Role in Regulating Erythropoiesis in Patients with End-Stage Renal Disease and Erythrocytosis
Authors: SHIH LEE-YUNG , HUANG JENG-YI , LEE CHING-TAI 
Published: May 2021

Abstract.
Erythroid progenitor growth, the serum hormones that regulate erythropoiesis, and the effect of patient's serum on the growth of normal erythroid progenitors were assessed in eight patients with end-stage renal disease (ESRD) and erythrocytosis. All patients were male and had been on maintenance dialysis, they had a hematocrit >50% and/or a red blood cell count >6 × 1012/L and an arterial oxygen saturation >95%. Four had acquired cystic disease of the kidney (ACDK), and four other non-ACDK patients did not have known causes of secondary erythrocytosis after appropriate investigations and long-term follow-up. The methylcellulose culture technique was used to assay the erythroid progenitor (BFU-E/CFU-E) growth. Serum erythropoietin (EPO) and insulin-like growth factor I (IGF-I) levels were measured by RIA. Paired experiments were performed to determine the effects of 10% sera from ESRD patients and control subjects on normal marrow CFU-E growth. The numbers of EPO-dependent BFU-E in marrow and/or blood of patients with ESRD and erythrocytosis were higher than those of normal controls. No EPO-independent erythroid colonies were found. Serum EPO levels were constantly normal in one patient and elevated in three patients with ACDK; for non-ACDK patients, EPO levels were normal or low in two patients and persistently increased in one, but fluctuated in the remaining one on serial assays. There was no correlation between serum EPO levels and hematocrit values. The serum IGF-I levels in patients with ESRD and erythrocytosis were significantly increased compared with normal subjects or ESRD patients with anemia. We found an inverse correlation between serum EPO and IGF-I levels. Sera from patients with ESRD and erythrocytosis exhibited a stimulating effect on normal marrow CFU-E growth. The stimulating effect of sera from patients who had a normal serum EPO level and an elevated IGF-I level could be partially blocked by anti-IGF-I. The present study suggests that IGF-I plays an important role in the regulation of erythropoiesis in patients with ESRD and erythrocytosis who did not have an increased EPO production.
Non-Insulin-Dependent Diabetes Mellitus and Hypertriglyceridemia Impair Lipoprotein Metabolism in Chronic Hemodialysis Patients
Authors: QUASCHNING THOMAS , SCHÖMIG MICHAEL , KELLER MARKUS , THIERY JOACHIM , NAUCK MATTHIAS , SCHOLLMEYER PETER , WANNER CHRISTOPH , KRÄMER-GUTH ANNETTE 
Published: May 2021

Abstract.
Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk.
Tissue Sources and Blood Flow Limitations of Osmotic Water Transport Across the Peritoneum
Authors: DEMISSACHEW HAILU , LOFTHOUSE JOANNE , FLESSNER MICHAEL F. 
Published: May 2021

Abstract.
Despite the daily use of hypertonic solutions to remove fluid from patients throughout the world who are undergoing peritoneal dialysis, the tissue sources of this water flow are unknown. To study this phenomenon in specific tissues, small plastic chambers were affixed to parietal and visceral surfaces of the peritoneum and were filled with either an isotonic or hypertonic solution. The volume changes over 60 to 90 min were determined and divided by the chamber area to yield the volume flux. The hypertonic solution produced a positive flux into the chamber of 0.6 to 1.1 μl/min per cm2 in all tissues tested. In contrast, the isotonic solution resulted in a net loss or an insignificant change in the chamber volume. Additional experiments tested the influence of blood flow on the hypertonic water flux during periods of control, reduced (50 to 80%), or postmortem (no) blood flow, as determined by laser Doppler flowmetry. With the exception of the liver, small but insignificant changes in the flux into the chamber were observed during the period of reduced flow; all water fluxes were markedly depressed during the postmortem period. It is concluded that both parietal and visceral tissues are sources of osmotically induced water flow into the cavity. Except for the liver, marked blood flow reductions have small but insignificant effects on osmotic water transport.
Effect of High Glucose on Mesangial Cell Protein Kinase C-δ and -ε is Polyol Pathway-Dependent
Authors: KAPOR-DREZGIC JOVANA , ZHOU XIAOPENG , BABAZONO TETSUYA , DLUGOSZ JOHN A. , HOHMAN THOMAS , WHITESIDE CATHARINE 
Published: May 2021

Abstract.
In diabetes mellitus, enhanced activity of mesangial cell protein kinase C (PKC) may contribute to nephropathy. The purpose of this study was to determine whether high glucose alters mesangial cell diacylglycerol-sensitive PKC-α, -β2, -δ, and -ε content, cellular distribution, and activity through polyol pathway activation. Primary cultured rat mesangial cells (passage 10) were growth-arrested in 0.5% fetal bovine serum and cultured in 5.6 mM glucose (NG) or 30 mM glucose (HG) for 48 h, with or without the aldose reductase inhibitor tolrestat or ARI-509. PKC isoform content in total cell lysates, or cytosol, membrane (Triton X-soluble), and particulate (sodium dodecyl sulfate-soluble) fractions was analyzed by immunoblotting, and band density in HG was expressed as a percentage of corresponding NG values. In HG at 48 h, increased total PKC-α (222 ± 17% of NG, P < 0.001), -β2 (209 ± 12%, P < 0.001), and -ε (195 ± 19%, P < 0.001) were observed. L-Glucose had no effect on total PKC isoform content. HG caused increased membrane- and particulate-associated PKC-α (257 ± 87 and 327 ± 66%, respectively, P < 0.05), membrane-associated PKC-δ (143 ± 10%, P < 0.05), and membrane-associated PKC-ε (186 ± 11%, P < 0.001), with no change in cytosol contents. The HG effects were not mimicked by L-glucose. In NG or HG, PKC-β2 was not detected in the cytosol fraction, and membrane and particulate association were unchanged with phorbol ester stimulation. Confocal immunofluorescence imaging revealed that in HG, PKC-α, -δ, and -ε translocate to the nucleus and plasma membrane. Total PKC activity measured by in situ
32P-phosphorylation of the epidermal growth factor receptor substrate increased from 18 ± 1 pmol/min per mg cell protein in NG to 33 ± 3 pmol/min per mg cell protein in HG (P < 0.002 versus NG). In NG, tolrestat and ARI-509 exposure caused increased PKC activity, enhanced accumulation of total PKC-α and -β2, with no change in total or fractional recovery of PKC-δ or -ε. In HG, tolrestat and ARI-509 prevented the increase in total PKC-ε and membrane-associated PKC-δ and -ε. It is concluded that within 48 h of HG, enhanced mesangial cell PKC activity is associated with accumulation and cellular redistribution of diacylglycerol-sensitive PKC isoforms, and that increased PKC-ε content and membrane-associated PKC-δ and -ε are dependent on polyol pathway activation.
Induction of Monocyte Chemoattractant Protein-1 by Albumin Is Mediated by Nuclear Factor κB in Proximal Tubule Cells
Authors: WANG YIPING , RANGAN GOPALA K. , TAY YUET-CHING , WANG YAO , HARRIS DAVID C. H. 
Published: May 2021

Abstract.
The transcription and translation of monocyte chemoattractant protein-1 (MCP-1), a CC chemokine, are increased in proximal tubule epithelial cells (PTC) stimulated with pathophysiologically relevant concentrations of albumin. The purpose of this study was to investigate whether nuclear factor κB (NFκB)/Rel proteins play a role in albumin-induced MCP-1 transcription. Confluent monolayers of rat PTC in primary culture were stimulated with delipidated bovine serum albumin. NFκB, the NFκB inhibitory protein (IκB), and MCP-1 transcription were assessed using electrophoretic mobility shift assays, Western immunoblotting, semiquantitative reverse transcription-PCR, and ribonuclease protection assays. Activation of NFκB by delipidated bovine serum albumin (15 mg/ml) was detectable within 2 h, maximal after 8 h, and maintained for at least 16 h of continuous exposure. Supershift analysis showed that the activated proteins were composed of p50/p50, p50/p65, and p50/c-Rel dimers. dimers. Cytoplasmic IκBα levels were decreased 30 min after stimulation and returned to unstimulated levels by 4 to 8 h. IκBβ levels were decreased at 2 h and there was no recovery until 8 h. Inhibition of NFκB with pharmacologic agents (N-tosyl-phenylalanine chloromethyl ketone and dexamethasone) and an antisense oligonucleotide to the rat p65 subunit of NFκB significantly reduced MCP-1 transcription. The 3.6-kb 5′ flanking region of the rat MCP-1 gene was cloned and sequenced, and two putative κB binding sites were identified within the enhancer region. Therefore, albumin increased NFκB and reduced IκB levels in PTC, and MCP-1 expression was dependent on NFκB activation. It is concluded that the activation of NFκB/Rel proteins modulates chemokine production in PTC in response to albumin and is likely to have an important role in the mediation of tubulointerstitial injury in proteinuric renal disease.
Hematocrit Levels and Hospitalization Risks in Hemodialysis Patients
Authors: XIA HONG , EBBEN JIM , MA JENNIE Z. , COLLINS ALLAN J. 
Published: May 2021

Abstract.
The association between hematocrit level and future hospitalization risks in hemodialysis patients has not been fully investigated on a national level. A total of 71,717 prevalent Medicare hemodialysis patients who survived a 6-mo entry period from July 1 through December 31, 1993 were studied, and their risk of hospitalizations was evaluated the next year. Five hematocrit groups were defined from Medicare recombinant human erythropoietin-treated patients: <27%, 27 to <30%, 30 to <33%, 33 to <36%, and ≥36%. A Cox regression model was used to investigate the association between hematocrit level and the risk of first hospitalization, and the Andersen-Gill regression model evaluated multiple hospitalizations during the next year, adjusting for patient comorbidity and severity of disease. Compared with the baseline group of 30 to <33%, patients with hematocrit levels <30% had a 14 to 30% increased risk of hospitalization without disease severity adjustment (p = 0.0001) and a 7 to 18% increased risk with disease severity adjustment (p = 0.0001). Patients in the 33 to <36% group had the lowest risk at 0.93 and 0.88 (p = 0.0001), with and without adjustment for disease severity. It is concluded that patients with hematocrits of <30% have an increased risk of future hospitalization, with hematocrit levels between 33 and 36% having the lowest associated risks.
Vascular Expression of Polycystin-2
Authors: TORRES VICENTE E. , CAI YIQUIANG , CHEN XI , WU GUANQUING Q. , GENG LIN , CLEGHORN KATHLEEN A. , JOHNSON CHRISTOPHER M. , SOMLO STEFAN 
Published: May 2021

Abstract.
The expression of polycystin-1 in the vascular smooth muscle cells (VSMC) of elastic and large distributive arteries suggests that some vascular manifestations of autosomal-dominant polycystic kidney disease (ADPKD) result directly from the genetic defect. Intracranial aneurysms have been reported in PKD2, as well as in PKD1 families. To determine whether the vascular expression of polycystin-2 is similar to that of polycystin-1, the expression of PKD2 mRNA and protein in cultured pig aortic VSMC was studied and immunofluorescence and immunohistochemistry were used to study the localization of polycystin-2 in cultured pig aortic VSMC, pig ascending thoracic aorta, and normal elastic and intracranial arteries and intracranial aneurysms obtained at autopsy from patients without or with ADPKD. Tissues derived from Pkd2 wild-type and Pkd2 null mice were used to confirm the specificity of the immunostaining for polycystin-2. Northern blots of VSMC revealed the expected 5.3-kb band. Western blotting detected a 110-kb band in a 100,000 × g fraction of VSMC homogenates. Cultured VSMC as well as VSMC between the elastic lamellae of pig thoracic aorta were positive for polycystin-2 by immunofluorescence. The staining pattern was cytoplasmic. Treatment of the cells before fixation with Taxol, colchicine, or cytochalasin-D altered the pattern of staining in a way suggesting alignment with the cytoskeleton. The immunohistochemical staining for polycystin-2 was abolished by extraction with 0.5% Triton X-100, indicating that polycystin-2 is not associated with the cytoskeleton. Weak immunoreactivity for polycystin-2, which was markedly enhanced by protease digestion, was detected in formaldehydefixed normal human elastic and intracranial arteries. Immunostaining of variable intensity for polycystin-2, which was not consistently enhanced by protease digestion, was seen in the spindle-shaped cells of the wall of the intracranial aneurysms. The similar expression of polycystin-1 and polycystin-2 in the vascular smooth muscle is consistent with the proposed interaction of these proteins in a single pathway. These observations suggest a direct pathogenic role for PKD1 and PKD2 mutations in the vascular complications of ADPKD.
Regulation of Potassium Channel Kir 1.1 (ROMK) Abundance in the Thick Ascending Limb of Henle's Loop
Authors: ECELBARGER CAROLYN A. , KIM GHEUN-HO , KNEPPER MARK A. , LIU JIE , TATE MARGARET , WELLING PAUL A. , WADE JAMES B. 
Published: May 2021

Abstract.
The renal outer medullary potassium channel (ROMK) of the thick ascending limb (TAL) is a critical component of the counter-current multiplication mechanism. In this study, two new antibodies raised to ROMK were used to investigate changes in the renal abundance of ROMK with treatments known to strongly promote TAL function. These antibodies specifically recognized protein of the predicted size of 45 kD in immunoblots of rat kidney or COS cells transfected with ROMK cDNA. Infusion of 1-deamino-(8-D-arginine)-vasopressin (dDAVP), a vasopressin V2 receptor-selective agonist, for 7 d into Brattleboro rats resulted in dramatic increases in apical membrane labeling of ROMK in the TAL of dDAVP-treated rats, as assessed by immunocytochemical analyses. Using immunoblotting, a more than threefold increase in immunoreactive ROMK levels was observed in the outer medulla after dDAVP infusion. Restriction of water intake to increase vasopressin levels also significantly increased TAL ROMK immunolabeling and abundance in immunoblots. In addition, dietary Na+ levels were varied to determine whether ROMK abundance was also affected under other conditions known to alter TAL transport. Rats fed higher levels of sodium, as either NaCl or NaHCO3 (8 mEq/250 g body wt per d), exhibited significantly increased density of the 45-kD band, compared with the respective control animals. Moreover, in rats fed a low-NaCl diet (0.25 mEq/250 g body wt per d), a 50% decrease in band density for the 45-kD band was observed (relative to control rats fed 2.75 mEq/250 g body wt per d of NaCl). These results demonstrate that long-term adaptive changes in ROMK abundance occur in the TAL with stimuli that enhance transport by this segment.
P-Glycoprotein-Mediated Drug Secretion in Mouse Proximal Tubule Perfused In Vitro
Authors: TSURUOKA SHUICHI , SUGIMOTO KOH-ICHI , FUJIMURA AKIO , IMAI MASASHI , ASANO YASUSHI , MUTO SHIGEAKI 
Published: May 2021

Abstract.
To examine the functional significance of durg-transporting P-glycoprotein (P-gp), studies were conducted in the isolated and perfused proximal tubule S2 segment from mice disrupting both mdr1a and mdr1b genes [mdr1a/1b(—)(—)] and their wild-type mice. Efflux of the intracellular fluorescence of rhodamine 123, a fluorescence substrate of P-gp, into the lumen was measured, and the decay half-time of the intracellular fluorescence (T1/2) as an index of the drug-transporting P-gp activity was regarded. In the wild-type mice, the T1/2 was 34 ± 4 s (n = 36) at the basal period and was increased to 434 ± 41 s by the addition of luminal verapamil, a P-gp inhibitor. In the mdr1a/1b(—)(—) mice, the T1/2 was 407 ± 16 s (n = 10) at the basal period and was no longer affected by the luminal addition of verapamil. The digoxin content in the kidney after a repeated administration of the drug was markedly elevated in the mdr1a/1b(—)(—) mice. In conclusion, P-gp—mediated drug efflux capacity indeed exists in the apical membrane of proximal tubule cells from the wild-type mice, whereas it is absent in that of the mdr1a/1b(—)(—) mice.
Epidermal Growth Factor Activates Store-Operated Calcium Channels in Human Glomerular Mesangial Cells
Authors: MA RONG , SANSOM STEVEN C. 
Published: May 2021

Abstract.
A cellular influx of Ca2+ is critical for initiating and maintaining growth in a variety of cell types. Experiments were performed to determine whether epidermal growth factor (EGF), which is known to initiate a proliferative response in mesangial cells, could regulate by intracellular signal transduction the store-operated Ca2+ channels (SOC) of human mesangial cells (HMC) in culture. The cell-attached patch configuration was used to monitor the activity of SOC, with 90 mM Ba2+ in the pipette and physiologic saline solution in the bath. Under control conditions, the mean NP
o value was 1.06 at a holding potential of -80 mV. When 100 nM EGF was added to the bath, SOC were activated by 53%. The EGF-evoked response was dose-dependent, with a half-maximal activation concentration of 4.8 nM. An inhibitor of tyrosine kinase, i.e., tyrphostin A23 (100 μM), completely abolished EGF-evoked channel activation. EGF combined with the inactive control compound tyrphostin A1 (100 μM) elicited significant (85%) activation of SOC. Calphostin C, an inhibitor of protein kinase C (PKC), did not affect the baseline activity of SOC but abolished the EGF-evoked enhancement of SOC activity. The PKC activator phorbol-12-myristate-13-acetate (PMA) significantly activated SOC. However, the effects of PMA were duplicative rather than additive or potentiating with maximal concentrations (100 nM) of EGF, suggesting that PMA and EGF activate SOC through a common PKC pathway. In addition, downregulation of PKC via incubation of HMC with PMA for 1 to 20 h depressed both basal activity and EGF-induced activation of SOC. It is concluded that EGF stimulates SOC in HMC through an intracellular signaling mechanism involving tyrosine kinase and PKC.
Oral Administration of Glomerular Basement Membrane Prevents the Development of Experimental Autoimmune Glomerulonephritis in the WKY Rat
Authors: REYNOLDS JOHN , PUSEY CHARLES D. 
Published: May 2021

Abstract.
Experimental autoimmune glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (WKY) rats by a single injection of collagenase-solubilized rat glomerular basement membrane (GBM) in adjuvant. EAG is characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing glomerulonephritis with crescent formation. The inhibitory effect of orally administered antigens has been reported in various animal models of autoimmunity but not in EAG in the rat. The effects of feeding rat GBM by gavage, at total doses of 0.5, 2.5, or 5 mg, before immunization were examined. A dose-dependent effect was observed on the development of EAG. A dose of 0.5 mg of GBM had no effect on disease, 2.5 mg resulted in a moderate reduction in the severity of nephritis but no change in anti-GBM antibody production, and 5 mg resulted in a marked reduction in circulating and deposited anti-GBM antibodies, albuminuria, deposits of fibrin in the glomeruli, severity of glomerular abnormalities, and numbers of infiltrating T cells and macrophages. Animals that were fed 5 mg of GBM showed a significant reduction in IgG2a but not IgG1, anti-GBM antibody levels, suggesting downregulation of Th1 responses. There was also a dose-dependent reduction in the proliferative responses of splenic T cells from treated animals to GBM antigen in vitro. These results clearly demonstrate that mucosal tolerance can be induced by oral administration of GBM antigen and that this approach is effective in preventing EAG.
Dodatek kwartalny
Authors: Uryszek Tomasz , Zimny Artur , Witczak Radosław , Zygmunt Michał 
Published: May 2021

„Ryzyko walutowe długu Skarbu Państwa w Polsce”
„Koniunktura w sektorze przedsiębiorstw niefinansowych w 3. kwartale 2014 r.”
„Koniunktura giełdowa”
„Zmiany w świecie finansów (podatków)”
„Sytuacja gospodarcza w Polsce po czwartym kwartale 2014 r.”
Students’ entrepreneurial behaviour – An eight-construct scale validation: A scale adaptation study
Authors: Soba Mustafa , Yildiz Ezgi Pelin , Ersoy Yusuf 
Published: May 2021

Entrepreneurship, especially among university students, measuring perception/tendency has been very popular in recent years due to reasons such as the importance of the subject, research applicability, reaching the target audience and relatively low research costs. In this context, it emphasises that the willingness, determination and predisposition of young people who will enter the business life to make a new venture and do their own business and their career planning are also important for entrepreneurial tendencies. In the context of this study, an adaptation study of the relevant scale developed by Schmidt Bohnenberger, Panizzon, Marcon, Toivonen and Lampinen into Turkish was carried out in order to determine undergraduate students’ entrepreneurial behaviour. The validity and reliability studies of the scale were carried out with the participation of 185 undergraduate students studying in different departments. Exploratory factor analysis was used to serve structure validity. At the end of the study, a seven-dimensional scale consisting of 40 items explaining 89.62% of the total variance was obtained. The internal consistency coefficient of the scale calculated with Cronbach’s alpha was 0.95. As a result, it contributed to the field by introducing a scale with proven reliability and validity.

Keywords: Entrepreneurship behaviour, undergraduate students, scale adaptation, validity–reliability.