bluuebunny/crossref_metadata_2025_split huggingface dataset:
ATATÜRK ÜNİVERSİTESİ DİŞ HEKİMLİĞİ FAKÜLTESİ ÖĞRENCİLERİNİN PROTETİK DİŞ TEDAVİSİ UZMANLIĞI HAKKINDAKİ GÖRÜŞLERİNİN DEĞERLENDİRİLMESİ
Authors: KAPTI Yakup , ÖZDOĞAN Alper 
Published: April 2021

Amaç: Bu çalışmanın amacı Atatürk Üniversitesi Diş Hekimliği Fakültesi’nde 2018/2019 akademik döneminde eğitim gören öğrencilerin Protetik Diş Tedavisi uzmanlığı hakkındaki görüşlerini değerlendirmektir.Gereç ve Yöntemler:22 sorudan oluşan bir anket 1-5. sınıfta eğitim gören 491 öğrenciye uygulandı. Anket soruları Protetik Diş Tedavisinin preklinik, klinik ve teorik eğitimine yönelik sorular ve bazı faktörlere göre diğer uzmanlık dallarına göre sıralama isteyen sorulardan oluşmaktadır. Verilerin istatistiksel analizinde deskriptif, frekans analizleri, crosstabs ve independent sample t testi kullanıldı.Bulgular:Protetik Diş Tedavisi uzmanlığı ile ilgili görüşlerin öğrencilerin yaş, cinsiyet, eğitim dönemine göre farklılık göstermediği görüldü (p &gt;0.05). Protetik Diş Tedavisinin tüm faktörler eşliğinde değerlendirildiğinde tercih sırasının ortalama olarak 3.11 olduğu bulundu. Sonuç: Protetik Diş Tedavisi uzmanlığı ile ilgili düşüncelerin genel olarak olumlu ve tercih edilme durumunun iyi bir yerde olduğu sonucuna varıldı.Sonuçlar:Anahtar Kelimeler:Diş Hekimliği, Protetik Diş Tedavisi, Uzmanlık.
Cardiovascular response to physical exercise and the risk of Internet addiction in 15–16-year-old adolescents
Authors: Poskotinova Liliya V. , Krivonogova Olga V. , Zaborsky Oleg S. 
Published: April 2021

AbstractBackground and aimSubjective symptoms of Internet addiction (IA), such as interpersonal and health-related problems (IH-RP), do not correlate with objective physiological parameters. This study aimed to investigate the cardiovascular reactivity after physical exercise in 15–16-year-old adolescents showing different severities of symptoms of health-related problems due to Internet overuse.MethodsThis study included 20 healthy adolescents (boys, 15–16 years) with different risks of IA (by the Chen internet addiction scale [CIAS]). The physical exercise test was to perform a standing broad jump three times. The arterial blood pressures and heart rates were recorded before, immediately after, and at 4 minutes of rest after exercise.Results and discussionThe total sample of adolescents was divided into two groups, that is, those with IH-RP scores of 12 or less (Group I, n = 12) and those scoring more than 12 points (Group II, n = 8). The diastolic blood pressure significantly increased after exercise in group II, whereas it remained stable in group I. The heart rate in group I tended to increase, but the changes were not statistically significant. Group II adolescents showed significant increases in heart rate, and at rest, this parameter was significantly higher than the baseline value.ConclusionsAdolescents with a risk of IA and severe symptoms of interpersonal and health-related problems had increased sympathetic activity during and after speed-strength physical exercise compared to those without the aforementioned symptoms.
Intercalated Cell Subtypes in Connecting Tubule and Cortical Collecting Duct of Rat and Mouse
Authors: KIM JIN , KIM YOUNG-HEE , CHA JUNG-HO , TISHER C. CRAIG , MADSEN KIRSTEN M. 
Published: April 2021

Abstract.
At least two populations of intercalated cells, type A and type B, exist in the connecting tubule (CNT), initial collecting tubule (ICT), and cortical collecting duct (CCD). Type A intercalated cells secrete protons via an apical H+ - ATPase and reabsorb bicarbonate by a band 3-like Cl-/HCO3
- exchanger, AE1, located in the basolateral plasma membrane. Type B intercalated cells secrete bicarbonate by an apical Cl-/HCO3
- exchanger that is distinct from AE1 and remains to be identified. They express H+ -ATPase in the basolateral plasma membrane and in vesicles throughout the cytoplasm. A third type of intercalated cell with apical H+ -ATPase, but no AE1, has been described in the CNT and CCD of both rat and mouse. The prevalence of the third cell type is not known. The aim of this study was to characterize and quantify intercalated cell subtypes, including the newly described third non A-non B cell, in the CNT, ICT, and CCD of the rat and mouse. A triple immunolabeling procedure was developed in which antibodies to H+ -ATPase and band 3 protein were used to identify subpopulations of intercalated cells, and segment-specific antibodies were used to identify distal tubule and collecting duct segments. In both rat and mouse, intercalated cells constituted approximately 40% of the cells in the CNT, ICT, and CCD. Type A, type B, and non A-non B intercalated cells were observed in all of the three segments, with type A cells being the most prevalent in both species. In the mouse, however, non A-non B cells constituted more than half of the intercalated cells in the CNT, 39% in the ICT, and 22% in the CCD, compared with 14, 7, and 5%, respectively, in the rat. In contrast, type B intercalated cells accounted for only 8 to 16% of the intercalated cells in the three segments in the mouse compared with 26 to 39% in the rat. It is concluded that striking differences exist in the prevalence and distribution of the different types of intercalated cells in the CNT, ICT, and CCD of rat and mouse. In the rat, the non A-non B cells are fairly rare, whereas in the mouse, they constitute a major fraction of the intercalated cells, primarily at the expense of the type B intercalated cells.
Can Renal Replacement Be Deferred by a Supplemented Very Low Protein Diet?
Authors: WALSER MACKENZIE , HILL SYLVIA 
Published: April 2021

Abstract.
Patients with chronic renal failure are commonly started on renal replacement therapy (RRT) as soon as (or, in some centers, before) the usual criteria for severity are met, i.e., GFR <10 ml/min for nondiabetic patients and <15 ml/min for diabetic patients. To determine whether RRT can safely be deferred beyond this point, adults with all types of chronic renal failure who met these criteria on presentation (23 patients) or who reached these levels of severity during treatment (53 patients) were managed conservatively until RRT was judged necessary by their chosen dialysis or transplantation team, without input into this decision from the present authors. Patients were prescribed a very low protein diet (0.3 g/kg) plus supplemental essential amino acids and/or ketoacids and followed closely. The intervals between the time at which GFR became less than 10 ml/min (15 ml/min in diabetic patients) and the date at which renal replacement therapy was started were used as estimates of renal survival on nutritional therapy. Kaplan—Meier analysis showed median renal survival of 353 d. Acidosis and hypercholesterolemia were both predictive of shorter renal survival. Signs of malnutrition did not develop. Final GFR averaged 5.6 ± 1.9 ml/min. Two patients died; thus, annual mortality was only 2.5%. Hospitalizations totaled 19 in 93 patient-years of treatment, or 0.2 per year. Thus, these well motivated patients with GFR <10 ml/min (<15 ml/min in diabetic patients) were safely managed by diet and close follow-up for a median of nearly 1 yr without dialysis. It is concluded that further study of this approach is indicated.
Dialysis Modality and Delayed Graft Function after Cadaveric Renal Transplantation
Authors: BLEYER ANTHONY J. , BURKART JOHN M. , RUSSELL GREGORY B. , ADAMS PATRICIA L. 
Published: April 2021

Abstract.
The purpose of this investigation was to compare outcomes in the immediate posttransplant period for hemodialysis (HD) and peritoneal (PD) dialysis patients who received cadaveric renal transplantation. Data were obtained from the United Network of Organ Sharing on all cadaveric graft recipients who were dialysis-dependent at the time of transplantation between April 1994 and December 1995. Baseline characteristics were compared between groups, and multivariate logistic regression was performed with outcome measures including urine production in the first 24 h posttransplantation (U24), requirement for dialysis in the first week posttransplant (FWDIAL), and treatment for acute rejection during the initial hospitalization. The odds of oliguria (not producing urine in the first 24 h) were 1.49 (1.28 to 1.74) times higher in HD versus PD patients. After adjustment for other comorbid conditions including age, gender, race, HLA mismatch, time on dialysis, panel-reactive antibodies, and cold and warm ischemia time, the odds of oliguria were 1.60 (1.14 to 2.25) times higher in black HD patients compared with PD patients and 1.29 (1.06 to 1.57) times higher in white HD patients. In a similar manner, after adjustment for significant comorbid conditions, the odds of requiring dialysis in the first week were 1.56 (1.22 to 2.0) times higher in black HD patients versus PD patients and 1.40 (1.21 to 1.60) times higher in white HD patients. The rate of acute rejection was similar during the first hospitalization. These results suggest that there is an association between hemodialysis and delayed graft function. Differences in biocompatibility between the two modalities could potentially be responsible.
QT Dispersion Before and After Hemodialysis
Authors: MORRIS SCOTT T. W. , GALIATSOU EFTYCHIA , STEWART GRAHAM A. , RODGER R. STUART C. , JARDINE ALAN G. 
Published: April 2021

Abstract.
Sudden cardiac death is common in patients on hemodialysis, and may occur in the immediate postdialysis period, when ventricular premature complexes are common. Elevated QT dispersion (Maximum — Minimum QT interval on standard 12-lead electrocardiogram) is associated with increased risk of ventricular arrhythmias following myocardial infarction, but has not previously been assessed in patients with chronic renal failure. We studied electrocardiograms recorded in 50 patients before and after a single hemodialysis session, and in 20 control subjects. QT dispersion was significantly higher in patients (63.1 ± 20.6 ms) compared with control subjects (36.0 ± 13.7 ms; P < 0.001) and rose significantly after hemodialysis to levels comparable to those seen following myocardial infarction (76.6 ± 27.0 ms; P < 0.01). Because QT dispersion reflects nonhomogeneous recovery of ventricular excitability, hemodialysis patients may be at significantly greater risk of reentrant arrhythmias and sudden death in the postdialysis period.
YB-1 Regulation of the Human and Rat Gelatinase A Genes via Similar Enhancer Elements
Authors: MERTENS PETER R. , ALFONSO-JAUME MARIA ALEXANDRA , STEINMANN KARIN , LOVETT DAVID H. 
Published: April 2021

Abstract.
Experimental and clinical studies strongly suggest that gelatinase A plays a central role in the evolution of glomerular injury and sclerosis. The sequences of the 5′ flanking regions of the human and rat gelatinase A genes do not share similarities with other members of the matrix metallo-proteinase gene family and are regulated in a distinctive manner. The human and rat gelatinase A genes include regions of significant homology (r2 human; RE-1 rat), which have been shown to act as potent cis-activators of transcription. The rat RE-1 sequence interacts specifically with the developmentally regulated transcription factors AP2 and YB-1, resulting in a synergistic activation of gelatinase A transcription. Although the human r2 sequence specifically interacts with AP2 (Mol Cell Biol 10: 6524-6532, 1990), there is no clear evidence for the presence of a canonical YB-1 binding site (Y-box) within this sequence. This study demonstrates, despite the absence of a canonical Y-box sequence in the r2 element, that YB-1 and AP2 specifically interact with r2, yielding synergistic transactivation of the human gelatinase A gene. It is concluded that the r2 element is the conserved functional analog of the RE-1 element, and that interactions of AP2 and YB-1 govern human gelatinase A gene expression.
Renal Vascular Reactivity in Mice
Authors: RUAN XIAOPING , OLIVERIO MICHAEL I. , COFFMAN THOMAS M. , ARENDSHORST WILLIAM J. 
Published: April 2021

Abstract.
The present study describes methodology and its application to evaluate renal reactivity in acute studies on anesthetized mice. Renal blood flow (RBF) was measured using an ultrasonic transit-time flowmeter and a non-cannulating V-shaped probe. An intrarenal artery injection technique established feasibility and reproducibility of studies of renal vascular reactivity to angiotensin II (AngII) in adult wild-type mice. The study also examined whether AngII would affect RBF in mice lacking AT1A receptors due to gene targeting. Mean arterial pressure averaged 83 and 62 mmHg, respectively, in mice with and without AT1A receptors. The RBF was similar in both groups, averaging 7 ml/min per g kidney wt. AngII injection (10-μl bolus) into the renal artery produced transient, dose-dependent, selective reductions in RBF in AT1A knockout mice as well as wild-type mice. The response was considerably greater in mice with AT1A receptors: 10% for 0.1 ng, 30% for 1 ng, and 45% for 5 ng AngII in control animals versus respective decreases of 6, 15, and 17% in knockout mice. In other studies, angiotensin-converting enzyme (captopril) or renin (CP-71362-14) was inhibited. During inhibition of AngII formation, renal vascular reactivity to AngII increased twofold in both groups. Coadministration of the AT1 receptor antagonist losartan (1 to 1000 ng) elicited dose-dependent inhibition of AngII effects, with near maximum blockage of 80 to 90% in both groups of mice. The putative AT2 receptor antagonist PD 123319 inhibited 30 to 40% of AngII-induced vasoconstriction, whereas CGP 42112 had no effect in either group. In conclusion, AngII can elicit renal vasoconstriction, albeit attenuated, in AT1A knockout mice. The weaker RBF effects are most likely due to the absence of the AT1A receptor. Inhibition of the response by AT1 receptor antagonist suggests mediation by the AT1B receptor in these animals. The residual constrictor effect observed during AT1 receptor blockade and sensitive to PD 123319 appears to be mediated by a non-AT1 receptor.
The Dysregulated Podocyte Phenotype
Authors: BARISONI LAURA , KRIZ WILHELM , MUNDEL PETER , D'AGATI VIVETTE 
Published: April 2021

Abstract.
Podocytes are highly differentiated, postmitotic cells, whose function is largely based on their complex cytoarchitecture. The differentiation of podocytes coincides with progressive expression of maturity markers, including WT-1, CALLA, C3b receptor, GLEPP-1, podocalyxin, and synaptopodin. In collapsing forms of focal segmental glomerulosclerosis (FSGS), including idiopathic FSGS and HIV-associated nephropathy, podocytes undergo characteristic, irreversible ultrastructural changes. This study analyzes the expression pattern of the above differentiation markers and of the proliferation marker Ki-67 in collapsing idiopathic FSGS and HIV-associated nephropathy compared with minimal change disease, membranous glomerulopathy, as well as normal adult and fetal human kidney. In minimal change disease and membranous glomerulopathy, all mature podocyte markers were retained at normal levels despite severe proteinuria and foot process fusion; no cell proliferation was observed. In contrast, in collapsing idiopathic FSGS and HIV-associated nephropathy, there was disappearance of all markers from all collapsed glomeruli and of synaptopodin from 16% of noncollapsed glomeruli. This phenotypic dysregulation of podocytes was associated with cell proliferation in both diseases. It is concluded that the loss of specific podocyte markers defines a novel dysregulated podocyte phenotype and suggests a common pathomechanism in collapsing FSGS, whether idiopathic or HIV-associated.
Elevated Myocardial Cytosolic Calcium Impairs Insulin-Like Growth Factor-1-Stimulated Protein Synthesis in Chronic Renal Failure
Authors: QING DAVID PEIYUAN , DING HU , VADGAMA JAY , WU YAN YUAN , KOPPLE JOEL D. 
Published: April 2021

Abstract.
Rats and humans with chronic renal failure (CRF) are reported to have resistance to recombinant human insulin-like growth factor-1 (rhIGF-1). Because basal cytosolic calcium ([Ca2+]i), a second messenger, may be increased in CRF, this study was conducted to examine whether elevated basal [Ca2+]i may cause resistance to IGF-1. Cardiomyocytes from four groups of rats were studied: untreated CRF, CRF with parathyroidectomy (PTX), CRF with the calcium channel blocker felodipine (F), and sham operation of the kidney (SO). CRF was created by ligation of two-thirds of the left renal artery and contralateral nephrectomy. Rats from each group were pair-fed the same diet for 20 to 22 d. Basal [Ca2+]i in cardiomyocytes (nM) in the CRF rats (102.0 ± 2.8; SEM), was significantly higher than in each of the CRF-PTX, CRF-F, and SO groups (65.2 ± 1.9, 63.8 ± 2.6, and 63.5 ± 2.0, respectively; P < 0.01). rhIGF-1 increased cardiomyocyte [Ca2+]i in all four groups of rats. The rise in [Ca2+]i was significantly diminished in the CRF rats (P < 0.05) and did not differ among the CRF-PTX, CRF-F, and SO rats. Protein synthesis after incubation with 0, 50, 100, 200, or 400 ng/ml rhIGF-1 was lower in cardiomyocytes from CRF rats than in each of the other three groups (P < 0.05) and was significantly less in the CRF-F rats compared with SO animals. IGF-1 receptor mRNA and IGF-1 receptor number and affinity were not different among the four groups. These findings suggest that cardiomyocytes from CRF rats display elevated basal [Ca2+]i and attenuated rhIGF-1-induced increase in [Ca2+]i; basal protein synthesis is decreased, and IGF-1-stimulated protein synthesis is impaired; elevated basal [Ca2+]i seems to contribute to this diminished response to rhIGF-1.
Angiotensin II-Stimulated Nitric Oxide Release from Porcine Pulmonary Endothelium Is Mediated by Angiotensin IV
Authors: HILL-KAPTURCZAK NATHALIE , KAPTURCZAK MATTHIAS H. , BLOCK EDWARD R. , PATEL JAWAHARLAL M. , MALINSKI TADEUSZ , MADSEN KIRSTEN M. , TISHER C. CRAIG 
Published: April 2021

Abstract.
In this study, a nitric oxide (NO) sensor was used to examine the ability of angiotensin II (AngII), AngIV, and bradykinin (Bk) to stimulate NO release from porcine pulmonary artery (PPAE) and porcine aortic endothelial (PAE) cells and to explore the mechanism of the AngII-stimulated NO release. Physiologic concentrations of AngII, but not Bk, caused release of NO from PPAE cells. In contrast, Bk, but not AngII, stimulated NO release from PAE cells. AngII-stimulated NO release from PPAE cells required extracellular L-arginine and was inhibited by L-nitro-arginine methyl ester. AT1 and AT2 receptor inhibition had no affect on AngII-mediated NO release or activation of NO synthase (NOS). AngIV, and AngII metabolite with binding sites that are pharmacologically distinct from the classic AngII receptors, stimulated considerably greater NO release and greater endothelial-type constitutive NOS activity than the same amount of AngII. The AngIV receptor antagonist, divalinal AngIV, blocked both AngII- and AngIV-mediated NO release as well as NOS activation. The results demonstrate that AngIV and the AngIV receptor are responsible, at least in part, for AngII-stimulated NO release and the associated endothelium-dependent vasorelaxation. Furthermore, these results suggest that differences exist in both AngII- and Bk-mediated NO release between PPAE and PAE cells, which may reflect important differences in response to these hormones between vascular beds.
Role of Xanthine Oxidase in Passive Heymann Nephritis in Rats
Authors: GWINNER WILFRIED , PLASGER JENS , BRANDES RALF P. , KUBAT BIRGIT , SCHULZE MATTHIAS , REGELE HEINZ , KERJASCHKI DONTSCHO , OLBRICHT CHRISTOPH J. , KOCH KARL-MARTIN 
Published: April 2021

Abstract.
Passive Heymann nephritis (PHN) in rats is a model of human membranous nephropathy characterized by formation of subepithelial immune deposits in the glomerular capillary wall and complement activation. Oxygen radicals have been implicated in the subsequent glomerular damage which leads to proteinuria. This study examines the involvement of xanthine oxidase in this process. Xanthine oxidase activity was increased nearly twofold in glomeruli isolated 1 and 12 d after induction of PHN, and this was associated with increased glomerular superoxide anion generation. Analysis of glomerular samples by Northern and Western blotting revealed no quantitative changes in xanthine oxidoreductase expression in PHN, suggesting conversion of xanthine dehydrogenase to the oxidase form as the cause of increased activity. Treatment of rats with tungsten, an inhibitor of xanthine oxidase, before induction of PHN resulted in a marked decrease in glomerular xanthine oxidase activity and superoxide anion generation, and decreased proteinuria by 80% (day 12: 423 ± 245 mg/d in PHN versus 78 ± 53 mg/d in tungsten-treated PHN animals, P < 0.01). These findings point to a pivotal role of xanthine oxidase in the pathophysiology of PHN and could be of importance in the therapy of human membranous nephropathy.
α1β1 Integrin-Mediated Collagen Matrix Remodeling by Rat Mesangial Cells Is Differentially Regulated by Transforming Growth Factor-β and Platelet-Derived Growth Factor-BB
Authors: KAGAMI SHOJI , KONDO SHUJI , LÖSTER KLEMENS , REUTTER WERNER , KUHARA TAKASHI , YASUTOMO KOJI , KURODA YASUHIRO 
Published: April 2021

Abstract.
Pathologic remodeling of mesangial matrix after glomerular injury is the central biologic feature of glomerular scarring (sclerosis). Transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF)-BB have been implicated in the development of glomerular scarring in rat and human glomerulonephritis. To clarify molecular and cellular mechanisms involved in abnormal mesangial remodeling, this study focused on the role of α1β1 integrin, a collagen/laminin receptor, in rat mesangial cells, using collagen gel contraction as an experimental model of in vivo collagen matrix remodeling and scar formation. In addition, the influence of TGF-β and PDGF-BB on mesangial cell (MC)-mediated collagen gel contraction in association with the α1β1 integrin expression was evaluated. Integrin function blocking studies using anti-α1, β1 subunit antibodies indicated that MC-α1β1 integrin is essentially required not only for collagen-dependent adhesion/migration, but also for gel contraction. Protein synthesis and mRNA analysis experiments demonstrated that TGF-β, but not PDGF-BB, increases the expression of α1β1 integrin in mesangial cells cultured on plastic surface and in collagen gels. The upregulation of α1β1 integrin expression by TGF-β correlated with increases in gel contraction and collagen-dependent adhesion but not migration of mesangial cells. On the other hand, PDGF-BB enhanced MC-mediated gel contraction and migration without affecting cell adhesion to collagen I. Growth factor-induced collagen-dependent adhesion, migration, and gel contraction were significantly attenuated by incubation with anti-α1, β1 subunit antibodies. Thus, these data indicate that α1β1 integrin-mediated collagen matrix remodeling can be modulated by TGF-β and PDGF-BB via different mechanisms. α1β1 integrin-mediated mesangial matrix remodeling induced by TGF-β or PDGF-BB may be a pathogenic mechanism leading to glomerular scarring.