bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pengaruh Bimbingan Konseling dan Pembelajaran Akidah Akhlak Terhadap Perilaku Keberagamaan Siswa di Mts Ma’had Al-Zaytun Indramayu
Authors: Humaeroh Iis 
Published: April 2021

Class IX will soon graduate and continue to higher education. For this reason, scientific provisions in learning morals and counseling are needed to prepare graduates who are smart and have good morals. This study was to determine the effect of counseling guidance and learning akidah akhlak on students' religious behavior in MTs. Ma'had Al-Zaytun Indramayu. The object of this research is the students of class IX MTs Ma'had Al-Zaytun Indramayu. This research was conducted on 135 respondents using a quantitative descriptive approach. Methods of data collection using survey methods, with the research instrument is a questionnaire. The approach used in this research is SPSS. This study proves that counseling guidance has a positive and significant effect on students 'religious behavior, which means that counseling plays a role in improving students' religious behavior. Learning akidah akhlak also has a positive and significant effect on students 'religious behavior, which can be interpreted that learning akidah akhlak plays a role in improving students' religious behavior. So, counseling and learning of akidah akhlak together have a positive and significant effect on students' religious behavior.Keywords: Counseling Guidance, Learning Akidah Akhlak, Students' Religious Behavior ABSTRAKKelas IX akan segera lulus dan melanjutkan ke jenjang pendidikan yang lebih tinggi. Untuk itu bekal keilmuan dalam pembelajaran akidah akhlak dan bimbingan konseling sangat diperlukan untuk menyiapkan lulusan yang cerdas dan berakhlakul karimah. Penelitian ini untuk mengetahui pengaruh bimbingan konseling dan pembelajaran akidah akhlak terhadap perilaku keberagamaan siswa di MTs. Ma’had Al-Zaytun Indramayu. Objek penelitian ini adalah siswa kelas IX MTs. Ma’had Al-Zaytun Indramayu. Penelitian ini dilakukan terhadap 135 responden dengan menggunakan pendekatan deskriptif kuantitatif. Metode pengumpulan data menggunakan metode survey, dengan instrument penelitian adalah kuesioner. Pendekatan yang digunakan dalam penelitian ini adalah SPSS. Penelitian ini membuktikan bahwa bimbingan konseling berpengaruh positif dan signifikan terhadap perilaku keberagamaan siswa, yang mana dapat diartikan bahwa bimbingan konseling berperan dalam meningkatkan perilaku keberagamaan siswa. Pembelajaran akidah akhlak juga berpengaruh positif dan signifikan terhadap perilaku keberagamaan siswa, yang mana dapat diartikan bahwa Pembelajaran akidah akhlak berperan dalam meningkatkan perilaku keberagamaan siswa. Jadi, bimbingan konseling dan pembelajaran akidah akhlak secara bersama-sama berpengaruh positif dan signifikan terhadap perilaku keberagamaan siswa.Kata Kunci: Bimbingan Konseling, Pembelajaran Akidah Akhlak, Perilaku Keberagamaan Siswa
Calcitonin Induces 25-Hydroxyvitamin D3 1α-Hydroxylase mRNA Expression via Protein Kinase C Pathway in LLC-PK1 Cells
Authors: YOSHIDA NORIKO , YOSHIDA TADASHI , NAKAMURA AKIRA , MONKAWA TOSHIAKI , HAYASHI MATSUHIKO , SARUTA TAKAO 
Published: April 2021

Abstract.
The biosynthesis of 1α, 25-dihydroxyvitamin D3 from 25-hydroxyvitamin D3 is catalyzed by 25-hydroxyvitamin D3 1α-hydroxylase (CYP27B1) in renal proximal tubules. It was recently demonstrated that LLC-PK1 cells express CYP27B1 mRNA, which is regulated by intracellular cAMP but not vitamin D3. To clarify the effect of calcitonin on vitamin D3 metabolism in vitro, LLC-PK1 cells were incubated with hormonal factors, and expression of CYP27B1 mRNA was measured by quantitative reverse transcription-PCR. Calcitonin at 100 nmol/L significantly increased CYP27B1 mRNA expression by 24 h (271 ± 21% of control). Incubation with calcitonin over a range of 1 μmol/L to 1 pmol/L resulted in a concentration-dependent increase in CYP27B1 mRNA levels. It is known that the calcitonin receptor has dual intracellular signaling pathways, via protein kinases A and C. Both 500 μmol/L 8-bromo-cAMP, a protein kinase A activator, and 100 nmol/L phorbol 12-myristate 13-acetate, a protein kinase C activator, increased CYP27B1 mRNA levels at 24 h (207 ± 54 and 246 ± 58% of control, respectively). However, calcitonin-induced CYP27B1 mRNA expression was only inhibited by the protein kinase C inhibitors staurosporine and calphostin C. The protein kinase A inhibitors Rp-cAMPS at 10 and 100 μmol/L and H-89 at 10 μmol/L had no effect on the action of calcitonin, in spite of cAMP-activation by calcitonin. The present data suggest that calcitonin upregulates CYP27B1 mRNA expression via the protein kinase C pathway in LLC-PK1 cells.
Chronic Reduction in Renal Mass in the Rat Attenuates Ischemia/Reperfusion Injury and Does Not Impair Tubular Regeneration
Authors: VERCAUTEREN SVEN R. , YSEBAERT DIRK K. , DE GREEF KATHLEEN E. , EYSKENS ERIK J. , DE BROE MARC E. 
Published: April 2021

Abstract.
It is not known whether a kidney with chronic structural and functional changes is more vulnerable to an acute renal insult, and whether its regeneration capacity after injury is altered. To study this question, Lewis rats were submitted 10 wk after 5/6 nephrectomy to an ischemic insult of 60 min (remnant kidney [RK] group). Functional and morphologic data of the RK group were compared with data obtained in 10-wk uninephrectomized (1K) and normal (2K) Lewis rats with unilateral and bilateral renal ischemia, respectively. The acute postischemic decrease in creatinine clearance was smallest in the RK group, followed by the 2K and 1K groups, respectively. At days 1 and 3, fewer proximal tubules in the outer stripe of the outer medulla of the RK and 2K groups had undergone acute tubular necrosis compared with the 1K group. The mean percentage of tubules with signs of regeneration was maximal at day 3 in the three experimental groups. At day 10, regeneration was almost complete in the three groups. The number of leukocytes (OX1+ cells) present in the RK before ischemia did not increase after ischemia/reperfusion injury (377 ± 146 cells/mm2 at day 0) in contrast to the 1K and 2K groups. In the latter groups, the number of leukocytes had increased gradually, reaching a maximum at day 15 (1K: 960 ± 308 cells/mm2) and day 10 (2K: 668 ± 164 cells/mm2), respectively. In conclusion, this study has shown that an RK exhibiting chronic morphologic changes of interstitial fibrosis and tubular atrophy is protected against ischemia/reperfusion injury, and that its regeneration capacity is preserved. The reperfusion injury is not followed by further accumulation of leukocytes, which were already present in the RK before ischemia.
The PlA2 Polymorphism of the Platelet Glycoprotein IIIA Gene as a Risk Factor for Acute Renal Allograft Rejection
Authors: SALIDO EDUARDO , MARTÍN BASILIO , BARRIOS YSAMAR , LINARES JOSÉ D. , HERNÁNDEZ DOMINGO , COBOS MARIAN , CHECA MARÍA D. , HORTAL LUIS , FERNÁNDEZ ANA , GARCÍA JOSÉ J. , TORRES ARMANDO 
Published: April 2021

Abstract.
Glycoprotein IIIa/IIb is a membrane receptor for fibrinogen and von Willebrand factor that plays an important role in platelet aggregation. The β integrin chain of this receptor, GPIIIa, is polymorphic, and the allele known as PlA2 has been associated with coronary thrombosis. The GPIIIa genotype of a cohort of 119 consecutive renal allograft recipients (46.3 ± 13 yr; 85 M/34 F; 24.4% diabetic patients) was determined by PCR-restriction fragment length polymorphism, and those patients were followed for at least 12 mo. From 119 patients with at least 1 yr of follow-up, those who suffered an acute rejection (n = 52) showed a lower proportion of HLA-DR β1 identity with the donor (7.7% versus 23.9%; P = 0.03), a higher proportion of cytomegalovirus-positive (CMV+) donors/CMV- recipients (21% versus 7.5%; P = 0.05), and the PlA2 allele was more frequent (48.1% versus 26.9%; P = 0.02) compared with patients free of acute rejection (n = 67). No other variable was associated with acute rejection in the univariate analysis. The impact of the three above-mentioned significant variables on acute rejection was analyzed by stepwise logistic regression. The presence of the PlA2 allele yielded an odds ratio of 2.75 (95% confidence interval, 1.01 to 7.93) and an HLA-DR β1 identity of 0.2 (95% confidence interval, 0.06 to 0.99) for suffering an acute rejection episode. In addition, the serum creatinine at discharge was higher in PlA2-positive versus PlA2-negative patients (2.2 ± 1.6 versus 1.5 ± 0.6 mg/dl, respectively; P = 0.01), and the prevalence of proteinuria > 1.5 g/d 1 yr after transplantation was significantly higher among patients showing the PlA2 allele (16% versus 3%; P = 0.02). Finally, in the entire cohort of patients, the 2-yr graft survival was significantly lower in PlA2-positive (n = 43) compared with PlA2-negative (n = 76) patients (85.7% versus 97.2%; P = 0.015). No differences were found in patient survival (95.2% versus 98.7%, respectively). Proportional hazards regression analysis (Cox regression model) confirmed that serum creatinine level at discharge is the best predictor of allograft survival, followed by CMV status, delayed graft function, and the glycoprotein IIIa/IIb genotype. The PlA2 polymorphism is an independent risk factor for acute renal graft rejection, affecting short-term graft survival. Future studies aimed at preventing the hemostatic imbalance favoring platelet aggregation associated with this polymorphism may be important in preventing acute rejection and its impact on chronic rejection.
Beneficial Effect of Serotonin 5-HT2-Receptor Antagonism on Renal Blood Flow Autoregulation in Cyclosporin-Treated Rats
Authors: VERBEKE MARLEEN , VAN DE VOORDE JOHAN , DE RIDDER LEO , LAMEIRE NORBERT 
Published: April 2021

Abstract.
Renal blood flow (RBF) autoregulation reappears in postischemic rat kidneys during serotonin (5-HT2) antagonism. The aim of the present study was to analyze whether 5-HT2 antagonism can ameliorate impaired RBF autoregulation in rats treated with 20 mg/kg per d cyclosporin A during 10 d. Autoregulation of RBF was assessed during stepwise lowering of renal perfusion pressure from 110 to 70 mmHg by gradual compression of the aorta. Autoregulation was lost in the cyclosporin A-treated rats. During administration of the 5-HT2 antagonist ritanserin (0.6 mg/kg intravenous bolus, followed by 1.2 mg/kg per h intravenous infusion during 1 h), autoregulation acutely reappeared. Intrarenal bolus injections of a selective 5-HT2-agonist, 2,5 dimethoxy-4-iodoamphetamine hydrochloride, elicited a significantly stronger renal vasocontraction in cyclosporin A-treated rats than in control rats. This finding was also observed with serotonin after nitric oxide-synthase blockade. These results (1) show the importance of 5-HT2-receptor-mediated vasoconstriction in the suppression of vasodilatory autoregulation of RBF in experimental cyclosporin A-induced renal dysfunction and (2) demonstrate that the complete loss of RBF autoregulation is not due to damage of the vascular smooth muscle cells.
Intrarenal Insulin-Like Growth Factor-1 Axis after Unilateral Nephrectomy in Rat
Authors: FERVENZA FERNANDO C. , TSAO TANNY , HSU FAY , RABKIN RALPH 
Published: April 2021

Abstract.
It has been suggested that insulin-like growth factor-1 (IGF-1) may play a role in early compensatory renal growth. Since IGF-1 action is influenced by IGF binding proteins (IGFBP), this study was conducted to characterize the changes in gene expression not only of IGF-1 and its receptor, but also of IGFBP in the hypertrophying kidney of adult and weanling rats 1 wk after removal of the other kidney. At this time, there were distinct age-dependent changes in the renal IGF-1 axis. In the mature kidney, IGF-1 mRNA levels fell without a change in kidney IGF-1 peptide content. Likewise, although IGFBP-2, -3, and -5 mRNA levels fell, membrane-associated IGFBP did not change. IGF-1 receptor mRNA levels and IGF-1 receptor number both fell. In the weanling kidneys, IGF-1 mRNA and peptide levels and IGF-1 receptor binding were unaltered. However, IGFBP-3, -4, and -5 mRNA levels were increased, as were plasma membrane-associated IGFBP. Although these changes in the intrarenal IGF-1 axis were distinct, it is difficult to conceive how in either the mature or immature rat they could contribute to the ongoing compensatory renal growth that occurs 1 wk after loss of kidney mass unless IGF-1 were acting in a synergistic manner with other growth promoters.
cGMP-Dependent and -Independent Inhibition of a K+ Conductance by Natriuretic Peptides
Authors: HIRSCH JOCHEN R. , MEYER MARKUS , MÄGERT HANS-JURGEN , FORSSMANN WOLF-GEORG , MOLLERUP STEEN , HERTER PETER , WEBER GERHARD , CERMAK RAINER , ANKORINA-STARK IEVA , SCHLATTER EBERHARD , KRUHØFFER MOGENS 
Published: April 2021

Abstract.
In immortalized human kidney epithelial (IHKE-1) cells derived from proximal tubules, two natriuretic peptide receptors (NPR) were identified. In addition to NPR-A, which is bound by atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and urodilatin (URO), a novel form of NPR-B that might be bound by C-type natriuretic peptide (CNP) was identified using PCR. This novel splice variant of NPR-B (NPR-Bi) was also found in human kidney. Whereas ANP, BNP, and URO increased intracellular cGMP levels in IHKE-1 cells in a concentration-dependent manner, CNP had no effect on cGMP levels. To determine the physiologic responses to these agonists in IHKE-1 cells, the membrane voltage (V
m) was monitored using the slow whole-cell patch-clamp technique. ANP (10 nM), BNP (10 nM), and URO (16 nM) depolarized these cells by 3 to 4 mV (n = 47, 7, and 16, respectively), an effect that could be mimicked by 0.1 mM 8-Br-cGMP (n = 15). The effects of ANP and 8-Br-cGMP were not additive (n = 4). CNP (10 nM) also depolarized these cells, by 3 ± 1 mV (n = 28), despite the absence of an increase in cellular cGMP levels, indicating a cGMP-independent mechanism. In the presence of CNP, 8-Br-cGMP further depolarized V
m significantly, by 1.6 ± 0.3 mV (n = 5). The depolarizations by ANP were completely abolished in the presence of Ba2+ (1 mM, n = 4) and thus can be related to inhibition of a K+ conductance in the luminal membrane of IHKE-1 cells. The depolarizations attributable to CNP were completely blocked when genistein (10 μM, n = 6), an inhibitor of tyrosine kinases, was present. These findings indicate that natriuretic peptides regulate electrogenic transport processes via cGMP-dependent and -independent pathways that influence the V
m of IHKE-1 cells.
Mechanisms of Mitogen-Activated Protein Kinase Activation in Experimental Diabetes
Authors: AWAZU MIDORI , ISHIKURA KENJI , HIDA MARIKO , HOSHIYA MAKIKO 
Published: April 2021

Abstract.
Various growth factors and vasoactive substances are implicated in the pathogenesis of renal growth seen in early diabetes mellitus (DM). Mitogen-activated protein kinase (MAPK) is an important mediator of these extracellular stimuli. Protein kinase C (PKC), an enzyme known to be stimulated in DM, also activates MAPK. Thus, MAPK activity was examined in glomeruli from streptozotocin-induced DM rats. MAPK activity, measured as myelin basic protein kinase, was elevated by approximately 50% in DM versus controls (CON). Increased protein contents of p42mapk and p44mapk, as well as increased tyrosine phosphorylation and mobility shift of p42mapk, were also observed in DM. Tyrosine dephosphorylation of pp42mapk, on the other hand, assessed by incubating glomerular membrane with or without sodium orthovanadate (vanadate), was significantly diminished in DM. Protein expression of MAPK phosphatase-1 (MKP-1), a dual specificity phosphatase that inactivates MAPK, was approximately 60% of CON. Reduction in MKP-1 was reproduced in cultured mesangial cells grown under high glucose (30 mM; HG). The suppression of MKP-1 was PKC-dependent since incubation of HG cells with phorbol 12-myristate 13-acetate for 24 h abolished it. Furthermore, calcium ionophore A23187 reversed the suppression, suggesting that blunted Ca2+ signalling, characteristic of HG cells secondary to PKC stimulation, may be the cause. These results demonstrate that glomerular MAPK is activated in DM by multiple mechanisms i.e., increases in protein contents, increased phosphorylation, and decreased dephosphorylation of the enzyme due to suppression of MKP-1. These alterations may have an implication in the pathogenesis of diabetic nephropathy.
Cloning of Porcine 25-Hydroxyvitamin D3 1α-Hydroxylase and Its Regulation by cAMP in LLC-PK1 Cells
Authors: YOSHIDA TADASHI , YOSHIDA NORIKO , NAKAMURA AKIRA , MONKAWA TOSHIAKI , HAYASHI MATSUHIKO , SARUTA TAKAO 
Published: April 2021

Abstract.
The 25-hydroxyvitamin D3 1α-hydroxylase, also referred to as CYP27B1, is a mitochondrial cytochrome P450 enzyme that catalyzes the biosynthesis of 1α, 25-dihydroxyvitamin D3 (1α,25(OH)2D3) from 25-hydroxyvitamin D3 in renal proximal tubular cells. Recently, human, mouse, and rat CYP27B1 cDNA have been cloned, however the gene regulation has not been fully elucidated. In the present study, porcine CYP27B1 cDNA was cloned, and the effects of cAMP and vitamin D3 on the regulation of CYP27B1 mRNA expression in LLC-PK1 cells were examined. PCR cloning revealed that porcine CYP27B1 cDNA consisted of 2316 bp, encoding a protein of 504 amino acids. The deduced amino acid sequence showed over 80% identity to the human, mouse, and rat enzyme. LLC-PK1 cells were incubated with humoral factors, and expression of CYP27B1 mRNA was measured by a quantitative reverse transcription-PCR. At the completion of 3-, 6-, 12-, and 24-h incubations, 500 μmol/L 8-bromo-cAMP had significantly increased CYP27B1 mRNA expression (260 to 340%). The adenylate cyclase activator forskolin at 50 μmol/L also had a stimulatory effect at 6 h (190%). Moreover, the protein kinase A inhibitor H-89 reduced the cAMP effect. On the other hand, 1α,25(OH)2D3 had no effect on CYP27B1 mRNA expression at 10 and 100 nmol/L, whereas expression of 25-hydroxyvitamin D3 24-hydroxylase (CYP24) mRNA was markedly increased by 1α,25(OH)2D3. These findings suggest that LLC-PK1 cells express CYP27B1 mRNA, and that cAMP is an upregulating factor of the CYP27B1 gene in vitro.
In Chronic Nephropathies Prolonged ACE Inhibition Can Induce Remission
Authors: RUGGENENTI PIERO , PERNA ANNALISA , BENINI ROBERTO , BERTANI TULLIO , ZOCCALI CARMINE , MAGGIORE QUIRINO , SALVADORI MAURIZIO , REMUZZI GIUSEPPE 
Published: April 2021

Abstract.
The Ramipril Efficacy in Nephropathy Core and Follow-Up Study found that ≥36 mo of continued ramipril therapy decreased substantially the risk of end-stage renal failure (ESRF) in patients with chronic nephropathies and a urinary protein excretion rate ≥3 g/24 h. This study investigates the time-dependent changes in GFR in these patients and in control subjects who were randomized to conventional therapy during the Core period and switched to ramipril during the Follow-Up study. Analyses included 150 patients (continued ramipril: n = 74; switched to ramipril: n = 76) who had at least three GFR measurements (including baseline) during the whole observation period and a subgroup of 43 patients (continued ramipril: n = 26; switched to ramipril: n = 17) who had at least six GFR measurements, including at least three on the Core and at least three on the Follow-Up study. Ramipril (1.25 to 5 mg/d) and conventional therapy were targeted at achieving a diastolic BP below 90 mmHg. The main efficacy variables were GFR and ESRF (need for dialysis). Analysis was by intention to treat. Throughout the study, the mean ± SEM rate of GFR decline (ΔGFR) was significantly lower in patients continued on ramipril compared to those switched to ramipril (0.51 ± 0.09 versus 0.76 ± 0.10 ml/min per 1.73 m2 per mo, P < 0.03). In patients on continued ramipril who had at least six GFR measured—but not in control subjects—ΔGFR progressively improved with time and, in the cohort with the longest follow-up, decreased from (in ml/min per 1.73 m2 per mo): 0.16 ± 0.12 (at 18 mo) to 0.10 ± 0.05 (at 60 mo). This rate was about 10-fold slower compared to patients on conventional therapy during the REIN Core study. Analyses of the individual slopes found that at the end of the follow-up, 10 of 26 patients on continued ramipril therapy had a positive ΔGFR and another 10 patients had an improvement of ΔGFR while on ramipril therapy. ΔGFR significantly improved in parallel with a significant reduction in proteinuria. Changes in ΔGFR (P = 0.0001) and proteinuria (P = 0.04) were significantly different in the two groups. Baseline characteristics and changes in systolic and diastolic BP and 24-h urine urea and sodium excretion were comparable. The present results offer evidence that in chronic nephropathies, the tendency of GFR to decline with time can be effectively halted, even in patients with remarkably severe disease.
Calcitonin Stimulates Lysosomal Enzyme Release and Uptake in LLC-PK1 Cells
Authors: GOTO MASAKO , MIZUNASHI KAZUTOSHI 
Published: April 2021

Abstract.
Renal tubular targeted hormones increase urinary excretion of a lysosomal enzyme, N-acetyl-β-D-glucosaminidase (NAG). To elucidate the mechanism of this event, the calcitonin effect on NAG handling by LLC-PK1 cells was examined. Calcitonin (1 nM to 1 μM), phorbol myristate (10 nM to 1 μM), and ionomycin (1 to 10 μM) promoted NAG release without any increase in lactate dehydrogenase release or any reduction of mitochondrial dehydrogenase activity. Treatment with 100 nM calphostin C or 50 μM KN-93 partially reversed the calcitonin effect on NAG release. Calcitonin promoted secretion of fluorescence ceramide, a reporter of protein transport from Golgi apparatus to cell surface. Calcitonin-stimulated NAG release was partially inhibited by 10 μg/ml brefeldin A, a blocker of protein transport through the Golgi apparatus. Calcitonin accelerated cellular uptake of exogenous NAG, which was inhibited by low temperature, 0.1 mM monodansyl cadaverine (receptor-mediated endocytosis inhibitor), and 10 mM mannose-6-phosphate. Furthermore, calcitonin promoted progression of intracellular membranes stained by a fluorescence membrane marker, styryl pyridinium dye, from cell periphery to perinuclear regions (commonly referred to as recycling vesicles) and increased dye release from preloaded cells. Fluorescence release from the cells preloaded with FITC-labeled NAG or albumin was also stimulated by calcitonin. These calcitonin effects on endocytotic and re-exocytotic pathways were inhibited by 100 nM cytochalasin D, 100 nM nocodazole, 0.1 to 1 μM bafilomycin A1, or 0.1 mM monodansyl cadaverine. Increased urinary NAG excretion has been considered to reflect renal tubular damage. However, it was demonstrated here that stimulation of secretory and recycling pathways may be an alternative mechanism for calcitonin-induced enzymuria, which will become a new indicator of renal tubular response to this hormone.