bluuebunny/crossref_metadata_2025_split huggingface dataset:
Autoimmune thyroid disease correlates to islet autoimmunity on zinc transporter 8 autoantibody
Authors: Cai Yun , Yan Jieni , Gu Yong , Chen Heng , Chen Yang , Xu Xinyu , Zhang Mei , Yu Liping , Zheng Xuqin , Yang Tao 
Published: April 2021

Objective
The most common coexisting organ-specific autoimmune disease in patients with type 1 diabetes mellitus (T1DM) is autoimmune thyroid disease (AITD). However, there have been few clinical reports based on a large population about the prevalence of zinc transporter 8 autoantibody (ZnT8A) and other islet autoantibodies in AITD patients. We aimed to explore the presence of islet autoantibodies, ZnT8A, glutamic acid decarboxylase autoantibodies (GADA) and insulinoma-associated antigen 2 autoantibodies (IA-2A) compared with thyroid autoantibodies, thyroid peroxidase autoantibodies (TPOAb) and thyroglobulin autoantibodies (TGAb) and thyrotropin receptor autoantibodies (TRAb) in patients with Graves’ disease (GD), Hashimoto’s thyroiditis (HT) and T1DM patients with AITD.

Methods
Totally, 389 patients with GD, 334 patients with HT, 108 T1DM patients with AITD and 115 healthy controls (HC) were recruited in the study. Islet autoantibodies (ZnT8A, GADA and IA-2A) were detected by radioligand binding assay. Thyroid autoantibodies, TPOAb and TGAb were detected by chemiluminescence assay, and TRAb was detected by RIA.

Results
The prevalence of ZnT8A, GADA and IA-2A was higher in GD and HT patients than that of HC (ZnT8A: GD 8.48%, HT 10.8% vs HC 1.74%; GADA: GD 7.46%, HT 7.74% vs HC 0.870%; IA-2A: GD 4.88%, HT 3.59% vs HC 0%; All P < 0.05) but lower than that of T1DM subjects with AITD (ZnT8A: 42.6%; IA-2A: 44.4%; GADA: 74.1%; all P < 0.0001).

Conclusions
An increased prevalence of ZnT8A as well as GADA and IA-2A was found in both GD and HT patients, indicating that there is a potential link between thyroid autoimmunity and islet autoimmunity.
PERİODONTAL HASTALIK VE KARDİYOVASKÜLER HASTALIKLAR
Authors: SÜME KEŞİR Siddika Selva , KARŞIYAKA HENDEK Meltem , OLGUN Ebru 
Published: April 2021

Periodontal ve kardiyovasküler hastalıklar patogenezinde
enflamasyonun rol oynadığı durumlardır. Yakın dönemde yapılan çalışmalar,
periodontal hastalığın kardiyovasküler hastalık oluşumu ve ilerlemesi üzerine
etkili olabileceğini ortaya koymuştur. Aterom lezyonlarında tespit edilen oral
patojenler iki hastalık arasındaki olası ilişkiyi kuvvetlendirmektedir. İltihaplı
ve ülsere dişeti epiteli yolu ile periodontal patojenlerin sistemik dolaşıma
infiltrasyonu olası mekanizma olarak kabul edilmektedir. Bakteriyel
infiltrasyon sonucunda vasküler dokuları etkileyen oral patojenlerin, sistemik
dolaşımda ilerleyerek kardiyovasküler sistem için zararlı reaksiyonları
başlattıkları düşünülmektedir. Ayrıca, ülsere dişetinden proenflamatuvar
sitokin/kemokin sızıntısı akut faz proteinlerinin sentezine neden
olabilir. Kronik bakteriyemi kazanılmış bağışıklık cevabını uyarabilmektedir.
Periodontal patojenlere cevap olarak üretilen antikorlar endotel hücreleri ve
modifiye lipidler arasındaki çapraz reaksiyonları uyarabilmektedir. Bu
reaksiyonların damar duvarında lipid yoğunluğunu arttırabileceği
düşünülmektedir. Bunlara ek olarak, bazı
antikorların ve enflamatuvar sitokinlerin T Yardımcı Hücre-1 cevabını uyararak
aterom içindeki makrofajların aktivasyonunu arttırdıkları savunulmaktadır. Tüm bu
mekanizmaların aterogenezin başlamasına ve ilerlemesine katkıda bulunduğu
düşünülmektedir. Bu derleme, periodontal hastalık ve kardiyovasküler hastalık arasındaki
ilişkide olası mekanizmalara değinmektedir.
Distress-driven impulsivity interacts with cognitive inflexibility to determine addiction-like eating
Authors: Liu Chang , Rotaru Kristian , Lee Rico S. C. , Tiego Jeggan , Suo Chao , Yücel Murat , Albertella Lucy 
Published: April 2021

Abstract

Background
Researchers are only just beginning to understand the neurocognitive drivers of addiction-like eating behaviours, a highly distressing and relatively common condition. Two constructs have been consistently linked to addiction-like eating: distress-driven impulsivity and cognitive inflexibility. Despite a large body of addiction research showing that impulsivity-related traits can interact with other risk markers to result in an especially heightened risk for addictive behaviours, no study to date has examined how distress-driven impulsivity interacts with cognitive inflexibility in relation to addiction-like eating behaviours. The current study examines the interactive contribution of distress-driven impulsivity and cognitive inflexibility to addiction-like eating behaviours.

Method
One hundred and thirty-one participants [mean age 21 years (SD = 2.3), 61.8% female] completed the modified Yale Food Addiction Scale, the S-UPPS-P impulsivity scale, and a cognitive flexibility task. A bootstrap method was used to examine the associations between distress-driven impulsivity, cognitive inflexibility, and their interaction with addiction-like eating behaviours.

Results
There was a significant interaction effect between distress-driven impulsivity and cognitive flexibility (P = 0.03). The follow-up test revealed that higher distress-driven impulsivity was associated with more addiction-like eating behaviours among participants classified as cognitively inflexible only.

Conclusion
The current findings shed light on the mechanisms underlying addiction-like eating behaviours, including how traits and cognition might interact to drive them. The findings also suggest that interventions that directly address distress-driven impulsivity and cognitive inflexibility might be effective in reducing risk for addiction-like eating and related disorders.
Pressure Natriuresis in Nitric Oxide-Deficient Hypertensive Rats
Authors: FORTEPIANI LOURDES A. , RODRIGO ELENA , ORTÍZ M. CLARA , CACHOFEIRO VICTORIA , ATUCHA NOEMÍ M. , RUILOPE LUIS M. , LAHERA VICENTE , GARCÍA-ESTAN[Combining Tilde] JOAQUÍN 
Published: April 2021

Abstract.
Chronic inhibition of nitric oxide (NO) synthesis has been shown to result in arterial hypertension and an important blunting of the pressure diuresis and natriuresis response (PDN). The mechanisms mediating these abnormalities are not completely understood. In the present study, the role of several antihypertensive drugs to ameliorate these alterations was evaluated. The PDN relationships have been evaluated in rats chronically (8 wk) treated with the NO synthesis inhibitor N
G-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg per d in the drinking water). Appropriate groups of rats were simultaneously treated with the angiotensin II receptor blocker candesartan at a low (1.5 mg/kg per d) and high (2.5 mg/kg per d) dose, with the converting enzyme inhibitor captopril (60 mg/kg per d) and with the calcium channel blocker verapamil (100 mg/kg per d). Chronic treatment with L-NAME significantly elevated mean BP (163.6 ± 6.5 mmHg versus 105.1 ± 3.6 in controls), reduced GFR and renal blood flow (RBF), and shifted to the right the PDN responses. Chronic administration of low-dose candesartan, captopril, or verapamil prevented the arterial hypertension and improved renal hemodynamics, but these levels were not completely normalized. High-dose administration also improved renal hemodynamics but induced reduced BP below the levels of control animals. Despite the normalization of the elevated BP, the PDN responses of these hypertensive treated groups were not normalized, and the slopes of the respective diuretic or natriuretic responses were very similar to those of the hypertensive untreated rats. The results indicate that interruption or blockade of the reninangiotensin system and calcium channel blockade are effective treatments for the NO-deficient arterial hypertension and renal vasoconstriction. However, the PDN responses are not normalized, and this finding suggests that the antihypertensive treatment is not enough to overcome the renal alterations associated with the chronic deficiency of NO.
Mechanism of Inhibitory Effect of Warfarin on Mesangial Cell Proliferation
Authors: YANAGITA MOTOKO , ISHII KENJI , OZAKI HARUNOBU , ARAI HIDENORI , NAKANO TORU , OHASHI KAZUMASA , MIZUNO KENSAKU , KITA TORU , DOI TOSHIO 
Published: April 2021

Abstract.
Because proliferation of mesangial cells is a hallmark of glomerular diseases, understanding the regulatory mechanism of mesangial proliferation is important for the treatment. Warfarin has long been used to treat glomerular diseases, although its mechanism of effect on mesangial proliferation has remained unknown. Therefore, this study was conducted to examine whether warfarin can inhibit mouse mesangial cell proliferation by focusing on Gas6, which has been shown to be activated by vitamin K-dependent γ-carboxylation. In mesangial cells, Gas6 and its receptor Axl were expressed. In addition, exogenous Gas6 phosphorylated Axl, activated extracellular signal-regulated kinase, and stimulated [3H]-thymidine incorporation in mouse mesangial cells. This study also examined whether endogenous Gas6 stimulates mesangial proliferation. Conditioned medium (CM) from serum-starved mesangial cells could stimulate [3H]-thymidine incorporation and phosphorylate extracellular signal-regulated kinase, whereas CM in the presence of warfarin could not. Simultaneous administration of vitamin K could cancel the inhibitory effect of warfarin. These results suggest that vitamin K-dependent growth factors in the CM are critical for mesangial proliferation. Addition of the extracellular domain of Axl to the CM inhibited its mitogenic effect on mesangial cells, suggesting that this vitamin K-dependent growth factor is Gas6. It is concluded that Gas6 is an endogenous mitogen in mesangial cells, and warfarin inhibits mesangial proliferation possibly by inhibiting γ-carboxylation of Gas6. This study sheds light on the regulation of mesangial proliferation and may lead to a new therapeutic strategy for glomerular diseases.
Role for Interactions Between IP-10/Mig and CXCR3 in Proliferative Glomerulonephritis
Authors: ROMAGNANI PAOLA , BELTRAME CHIARA , ANNUNZIATO FRANCESCO , LASAGNI LAURA , LUCONI MICHAELA , GALLI GRAZIA , COSMI LORENZO , MAGGI ENRICO , SALVADORI MAURIZIO , PUPILLI CINZIA , SERIO MARIO 
Published: April 2021

Abstract.
The mechanisms responsible for mesangial cell proliferation in proliferative glomerulonephritis are only partially understood. This article reports the results of an immunohistochemical study showing high expression of the chemokine receptor CXCR3 by mesangial cells of patients with IgA nephropathy, membranoproliferative glomerulonephritis, or rapidly progressive glomerulonephritis. CXCR3 was also detectable by flow cytometry in cultured human mesangial cells, in which it appeared to be functionally active, as determined by the ability of its ligand, the (interferon-γ)-inducible protein of 10 kD (IP-10) to induce intracellular Ca2+ influx. Both IP-10 and the monokine induced by interferon-γ (Mig) were also effective in inducing proliferation of human mesangial cells. These data suggest that in patients with proliferative glomerulonephritis, the chemokines IP-10 and/or Mig not only may act as chemoattractants for infiltrating mononuclear cells in the inflamed tissue, but also may directly induce the proliferation of mesangial cells.
A Mouse Model for Liddle's Syndrome
Authors: PRADERVAND SYLVAIN , WANG QING , BURNIER MICHEL , BEERMANN FRIEDRICH , HORISBERGER JEAN DANIEL , HUMMLER EDITH , ROSSIER BERNARD C. 
Published: April 2021

Abstract.
Liddle's syndrome (or pseudoaldosteronism) is an autosomal dominant form of salt-sensitive hypertension, due to abnormal sodium transport by the renal tubule. To study the pathophysiology of salt sensitivity, a mouse model for Liddle's syndrome has been generated by Cre/loxP-mediated recombination. Under normal salt diet, mice heterozygous (L/+) and homozygous (L/L) for Liddle mutation (L) develop normally during the first 3 mo of life. In these mice, BP is not different from wild type despite evidence for increased sodium reabsorption in distal colon and low plasma aldosterone, suggesting chronic hypervolemia. Under high salt intake, the Liddle mice develop high BP, metabolic alkalosis, and hypokalemia accompanied by cardiac and renal hypertrophy. This animal model reproduces to a large extent a human form of salt-sensitive hypertension and establishes a causal relationship between dietary salt, a gene expressed in kidney and hypertension.
Early Experience with Dual Kidney Transplantation in Adults using Expanded Donor Criteria
Authors: REMUZZI GIUSEPPE , GRINYÒ JOSEP , RUGGENENTI PIERO , BEATINI MARCO , COLE EDWARD H. , MILFORD EDGAR L. , BRENNER BARRY M. 
Published: April 2021

Abstract.
Dual transplant of marginal kidneys otherwise not considered for single transplant may give access to an expanded pool of cadaveric organs without exposing recipients to the drawbacks of a limited nephron mass supply. This prospective, case-control study compares adverse events and graft outcome in 24 recipients of two marginal kidneys from donors who were >60 yr old or who had diabetes, hypertension, or non-nephrotic proteinuria (cases), with that of 48 age- and gender-matched control subjects who received single ideal grafts at the same center and were given the same immuno-suppressive therapy. Marginal kidneys with no macroscopic abnormalities were selected for the double transplant on the basis of a predefined score of histologic damage. Six-month patient and kidney survival was 100% with both of the procedures. Incidence (20.8% versus 20.8%) and median (range) duration of posttransplant anuria (5 [2 to 12] versus 7 [2 to 13] days) were comparable in cases and control subjects, respectively. Time to normal serum creatinine and mean serum creatinine values at each time visit were comparable as well, but with significantly lower levels in cases compared with control subjects from month 2 to last follow-up (1.56 ± 0.65 versus 1.74 ± 0.73 mg/dl, P = 0.04). Diastolic BP values averaged during the entire posttransplant period were significantly lower in cases than in control subjects (83.2 ± 11.5 versus 85.1 ± 12.5 mmHg, respectively, P = 0.008). Donor/recipient body weight ratio was the only covariate significantly associated at univariate (P = 0.002) and multivariate (P = 0.001) analysis with last available serum creatinine concentrations. Incidence of acute allograft rejections (20.8% versus 18.8%) and of major surgical complications was comparable in the two groups. No renal artery or vein thrombosis was reported in either group. Dual transplants of marginal kidneys are as safe and tolerated as single transplants, and possibly offer an improved filtration power without exposing the recipient to enhanced risk of delayed renal function recovery, acute allograft rejection, or major surgical complications.
Micropuncture Analysis of Tubuloglomerular Feedback Regulation in Transgenic Mice
Authors: SCHNERMANN JURGEN 
Published: April 2021

Abstract.
Micropuncture methods have been used widely as a means to define the function of single tubules and study the functional connection between tubules and afferent arterioles (so-called tubuloglomerular feedback [TGF]). Transgenic mouse strains have become a new research tool with the potential of shedding new light on the role of specific gene products in renal tubular and vascular function. The micropuncture approach has therefore been adapted to studies in the mouse kidney. Although the data presented here support the feasibility of using this technique in the mouse, technical improvements are desirable in the areas of anesthesia, ureteral urine collections, blood collections, volume replacement, and functional stability for extended time periods. During ketamine/inactin anesthesia, TGF responses could regularly be elicited in wild-type mice. In contrast, changes in loop flow did not alter stop-flow pressure in angiotensin II type 1A receptor and angiotensin-converting enzyme knockout mice. Infusion of angiotensin II in subpressor doses partially restored TGF responsiveness in angiotensin-converting enzyme knockout animals. Normal TGF responses compared to wild type were found in nitric oxide synthase I and thromboxane receptor knockout mice. Using free-flow micropuncture techniques, the proximal-distal single-nephron GFR difference was found to be augmented in aquaporin-1 and Na/H exchanger-3 knockout mice, suggesting TGF activation in these strains of mice. These results support an essential role of angiotensin II in TGF regulation mediated through the angiotensin II type 1A receptor. Chronic nitric oxide synthase I and thromboxane receptor deficiency did not change TGF responsiveness. Aquaporin-1 and Na/H exchanger-3 deficiency enhances TGF suppression of TGF probably by volume depletion-mediated TGF sensitization. The use of micropuncture methodology in transgenic mice combines old and new research tools in a way that promises to yield important new insights into single-nephron function in physiologic and pathophysiologic conditions.
Apical Proteins Stimulate Complement Synthesis by Cultured Human Proximal Tubular Epithelial Cells
Authors: TANG SYDNEY , SHEERIN NEIL S. , ZHOU WUDING , BROWN ZARIN , SACKS STEVEN H. 
Published: April 2021

Abstract.
There is increasing evidence to suggest that the renal tubular epithelium is important in the pathogenesis of progressive renal failure resulting from persistent proteinuria. The role of complement in the progression of chronic renal failure is not well defined. The purpose of this study was to characterize the production of complement by human proximal tubular epithelial cells exposed to serum proteins at the apical surface. Complement C3 gene expression was analyzed by reverse transcription and PCR. C3 protein biosynthesis was confirmed by metabolic labeling followed by immunoprecipitation and quantified by enzyme-linked immunosorbent assay. In the quiescent state, proximal tubular epithelial cells grown on permeable membrane supports secreted C3 predominantly into the apical medium. The addition of 5 mg/ml serum proteins led to an 8.9-fold increase in basolateral C3 secretion and a 2.1-fold increase in apical C3 secretion, altering the ratio of basolateral: apical C3 secretion from 0.44 ± 0.16 to 1.87 ± 0.52. C3 mRNA expression was also upregulated in a time- and dose-dependent manner. Serum fractionation demonstrated that the stimulant responsible for these effects was in the molecular weight range 30 to 100 kD. The observed phenomenon was not reproduced when purified human albumin alone was used as the stimulant. These findings could provide a possible mechanism for the link between proteinuria and interstitial fibrosis. This may have potential implications for strategies directed against complement in retarding the progression of chronic renal failure.
Hypertrophy of Intramyocardial Arteriolar Smooth Muscle Cells in Experimental Renal Failure
Authors: TÖRNIG JOHANNES , GROSS MARIE-LUISE , SIMONAVICIENE AURELIA , MALL GERHARD , RITZ EBERHARD , AMANN KERSTIN 
Published: April 2021

Abstract.
Wall thickening of intramyocardial arteries in patients with chronic renal failure may contribute to the increased susceptibility of the uremic heart to ischemic injury. In this context, the following questions arise: (1) Is intramyocardial wall thickening in experimental renal failure due to hypertrophy, hyperplasia or both? (2) Which stimuli trigger wall thickening? Using novel stereologic techniques (Nucleator, Selector), intramyocardial arteries were examined in sham-operated and subtotally nephrectomized (SNX) Sprague Dawley rats with moderate renal failure of 8 wk duration. Systolic BP during the experiment was not significantly different in both groups. Absolute and relative left ventricular weight, wall thickness (5.69 ± 1.11 μm versus 4.42 ± 0.99 μm), and wall-to-lumen ratio of intramyocardial arteries (0.117 ± 0.03 μm/μm versus 0.089 ± 0.01 μm/μm) were significantly greater in SNX than in sham-operated rats. The mean cell and nuclear volume of intramyocardial arteriolar smooth muscle cells was significantly increased in SNX rats (650 ± 230 μm3
versus 430 ± 90 μm3 and 26 ± 4.5 versus 19.9 ± 2.2 μm3, respectively). In parallel, the total arteriolar wall volume was significantly greater in the left ventricle of SNX (+ 58%) compared with sham rats. In contrast, the total length of all left ventricular arteries was comparable in both groups. The increase in mean cell volume without significant change in cell number indicates that arteriolar wall thickening in the heart of SNX rats is explained by hypertrophy rather than hyperplasia of arterial smooth muscle cells. This finding in a nonhypertensive experimental model of chronic renal failure contrasts with findings in spontaneously hypertensive rats. Independent of BP and left ventricular hypertrophy, specific growth signals must act on cardiac arteriolar smooth muscle cells.
Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor
Authors: FANESTIL DARRELL D. , HYDE RONALD H. , BLAKELY PATRICIA , VAUGHN DUKE A. 
Published: April 2021

Abstract.
This study reports for the first time a relationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by saturation binding with 3H-metolazone). Ion-selective electrodes measured plasma ionized magnesium (PMg+ +), calcium (PCa + +), and potassium (PK +). Restricting dietary Mg for 1 wk decreased PMg + + 18%, TZR 25%, and renal excretion of magnesium (UMg) and calcium (UCa) more than 50% without changing PCa + +, PK +, or plasma aldosterone. A low Mg diet for 1 d significantly decreased PMg + +, TZR, UMg and UCa. Return of dietary Mg after 5 d of Mg restriction restored PMg + + and TZR toward normal. In the control, Mg-deficient, and Mg-repleting animals, TZR correlated with PMg + + (r = 0.86) and with UMg (r = 0.87) but not UCa (r = 0.09). Increasing oral intake of Mg for 1 wk increased PMg + + 14%, TZR 32%, UMg 74%, and UCa more than fourfold without changing PCa + + or PK +. In contrast, increasing dietary Ca content from 0.02% to 1.91% did not change TZR, but increased UCa fivefold without changing PCa + +. Hormonal mediators (if any) involved in the relationship between dietary Mg and TZR remain to be elucidated, as does the relationship between TZR and tubular reabsorption of Mg.
Regulation of Aquaporin mRNA Expression in Rat Kidney by Water Intake
Authors: MURILLO-CARRETERO MARIA I. , ILUNDÁIN ANUNCIACIÓN A. , ECHEVARRIA MIRIAM 
Published: April 2021

Abstract.
Three aquaporins (AQP) are present in the membrane of the principal collecting duct cells. On the apical side, the levels of AQP2 protein are increased in response to both arginine vasopressin and water deprivation. However, whether this change parallels changes in the abundance of AQP3 and AQP4 in the basolateral membrane is less well known. This study evaluates the effect of either dehydration or water loading on the rat kidney mRNA expression of AQP2, AQP3, and AQP4. Poly(A+)RNA was prepared from renal cortex and medulla of control, water-deprived, well hydrated, and water-deprived rats treated with OPC31260, a V2 receptor antagonist. Northern blots were done and mRNA levels were quantified using a PhosphorImager system. Relative to control, water deprivation increased the expression of cortical AQP2, -3, and -4, whereas water loading decreased the cortical and medullar expression of AQP2, -3, and -4. Therefore, in addition to AQP2 and -3, AQP4 expression is also regulated by water intake. Treatment with OPC31260 (40 mg/kg of weight per d) inhibited up to 20 to 30% the upregulation of AQP-mRNA induced by water deprivation. Blood values of arginine vasopressin and aldosterone were significantly increased by water deprivation, whereas they were unchanged by water overloading. Taken together, these results indicate that renal AQP2, -3, and -4 expression is regulated in a coordinated manner. Simultaneous up- or downregulation of the three transcripts occurred upon either water deprivation or water loading of animals, respectively. However, the signaling mechanism for the two longterm adaptive processes may be different, and, in addition to arginine vasopressin, other factors may be involved in the transcriptional regulatory processes.