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Paraquat (PQ)-induced acute kidney injury (AKI) might show the role for reactive oxygen species (ROS) in AKI. The purpose of this study was to investigate the characteristics of early urinary biomarkers in patients with acute PQ poisoning. We prospectively investigated changes in urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in acute PQ intoxication.From May 2008 to September 2008, 20 patients were included. Urine KIM-1, NGAL, and 8-hydroxy-2-deoxyguanosine (8-OH-dG) were measured at 6, 12, 24, 48, 72, and 120 h after ingestion. The serum creatinine was measured also at the same intervals.AKI was diagnosed in 11 out of 20 patients. There was a significant difference in the creatinine at 12 h between patients with AKI and those without AKI (0.50 +/- 0.15 vs. 1.04 +/- 0.53 mg/dL, p = 0.01). Urinary NGAL was higher in patients with AKI compared to patients without AKI at 24 h (2.84 vs. 0.96 ng/mL). Urinary KIM-1 was not different in comparisons between patients with AKI and those without AKI. Regardless of the AKI, the NGAL and KIM-1 were increased at between 24 and 48 h.PQ is a very potent stimulant of NGAL-1 and KIM-1. Therefore, the NGAL might reflect reactive oxygen species-induced kidney injury.

Comparison of the ocular surface changes following the use of two different prostaglandin F2α analogues containing benzalkonium chloride or polyquad in rabbit eyes

The aim of this study is to compare the effect of prostaglandin analogues preserved with either 0.015% or 0.001% benzalkoium chloride (BAK); or 0.001% polyquad (PQ) on the ocular surface of rabbit eyes.Forty white rabbits were randomized to receive four-times daily instillation of either 0.0015% tafluprost (TF) preserved with 0.001% BAK (TF-BAK); 0.004% travoprost (TR) with 0.015% BAK (TR-BAK) or 0.001% PQ (TR-PQ); or preservative-free artificial tears in one eye for a 4-week period. Tear samples collected from the 40 rabbits were analyzed by enzyme-linked immunosorbent assays (ELISA) to identify the presence of inflammatory cytokines: interleukin (IL)-1β and IL-6 on day 14. Subsequently, harvested cornea and bulbar conjunctiva were evaluated using light and transmission electron microscopy (TEM).IL-6 was significantly increased in TF-BAK and TR-BAK groups compared to controls and TR-PQ group (p = 0.005); however, IL-1β level was not significantly different among four groups (p = 0.360). Rabbits treated with TR-BAK showed decreased goblet cell density of bulbar conjunctiva and increased pyknotic change and vacuolization of corneal epithelial cells on light microscopy; similar change occurred but was less severe in TF-BAK group. The TR-PQ group showed similar results as the controls. The destruction of the microvillar architecture of bulbar conjunctiva and cornea was most prominent in the TR-BAK group.Preservatives included in the anti-glaucoma eye-drops showed different ocular surface changes according to the concentration and type in the rabbits. Prostaglandin analogues preserved with higher level of BAK may cause more harmful effects on the ocular surface than PQ-preserved medications.

BAT3-soluble : un nouveau biomarqueur au cours du syndrome des antisynthétases

Posted by Hervier B, Ouaras S, Gilardin L, et al. on 2016-12-13 00:58:35

Abstract

Introduction
Le syndrome des antisynthétases (SAS) est une myopathie inflammatoire (MI) fréquemment associée à une pneumopathie infiltrante diffuse (PID) et différents auto-anticorps anti-ARNt-synthétases. Les mécanismes auto-immuns concourant au SAS sont actuellement mal compris. Récemment, l’infiltration des tissus cibles par des cellules natural killer (NK) a été rapportée. De plus, une diminution spécifique du nombre de cellules NK circulantes exprimant le récepteur activateur NCR3/NKp30 a été mise en évidence chez les patients actifs : elle se traduit par une baisse de fonctionnalité des cellules NK. Ceci suggère donc leur implication dans la pathogénicité du SAS. Chez certains patients atteints de néoplasie, une diminution de NCR3/NKp30 a également été rapportée et corrélée avec une expression anormale des ligands de ce récepteur, dénommés B7-H6 et BAT3. Ces deux molécules de stress sont également exprimés et/ou sécrétées par les monocytes/macrophages. Dans la présente étude, nous avons évalué l’impact possible des formes solubles de B7-H6 et BAT3 au cours du SAS.

Patients et méthodes
De 2013 à 2016, 53 patients recevant ou non un traitement spécifique ont été inclus (15 hommes = 28 % ; âge médian 48 ans, extrêmes 18–77 ; dont 40 présentant un anticorps anti-Jo-1 = 75 %) et regroupés selon caractère actif (n = 27, 51 %) ou inactif (n = 26, 49 %) de la maladie. Ces patients ont été comparés à 17 sujets sains (2 hommes = 12 % ; âge médian 29, extrêmes 22-44) et 20 patients présentant une MI active mais non associée à des anticorps anti-ARNt-synthétases. (8 hommes = 40 % ; âge médian 48, extrêmes 25–78 ; incluant 12 dermatomyosites = 60 %, 7 myopathies nécrosantes auto-immunes = 35 % et 1 MI de chevauchement = 5 %). Les taux sériques d’interleukine (IL)-2 & IL-15 ont été quantifiés par test Elisa (R&D systems) tout comme les taux solubles de BAT3 (sBAT3) et B7-H6 (EIAab & Cusabio, respectivement). Les tests statistiques appropriés étaient considérés comme significatifs lorsque p < 0,05.

Résultats
Alors que la concentration sérique médiane de sB7-H6 était similaire chez les patients et les contrôles, les titres de sBAT3 étaient significativement augmentés chez les patients avec SAS (250 vs. 134 pg/mL, p = 0,0002). De plus, sBAT3 corrélait avec l’activité du SAS : la concentration médiane de sBAT3 atteignant 340 pg/mL chez les patients actifs vs. 160 pg/mL chez les inactifs (p < 0,0001). Par ailleurs, pour les patients actifs bénéficiant d’un second dosage longitudinal, une diminution de sBAT3 était constatée sous traitement (de 472 à 259 pg/mL, p = 0,06) était constatée 5/6 fois (83 %). L’augmentation de sBAT3 était très spécifique du SAS, puisque retrouvée supérieure à deux fois la norme seulement chez 1/20 patients (5 %) avec MI active non associée aux anti-ARNt-synthétases (concentration médiane = 178 pg/mL, p < 0,0001). Les mécanismes résultant en une augmentation de sBAT3 restent inconnus mais sBAT3 ne corrélait pas avec les concentrations sériques des cytokines pro-inflammatoires IL2 et IL15.

Conclusion
L’augmentation significative et spécifique de sBAT3 chez les patients avec SAS actif et sa diminution sous traitement suggèrent que cette molécule de stress soit impliquée dans la pathogénicité du SAS et puisse être considérée comme un biomarqueur de la maladie.

 

Increased ANGPTL3, 4 and ANGPTL8/betatrophin expression levels in obesity and T2D

Posted by Abu-Farha M, Al-Khairi I, Cherian P, et al. on 2016-12-12 23:15:10

Abstract

Background
Hypertriglyceridemia is associated with increased risk for cardiovascular diseases and type 2 diabetes (T2D). Angiopoietin like proteins particularly 3, 4 and recently 8 are well established regulators of plasma triglyceride level through regulating the activity of lipoprotein lipase. Plasma level and association between ANGPTL3, 4 and 8 is not well established in human subjects. This study was designed to establish the level of these proteins in plasma and adipose tissues and investigate the association between ANGPTL8 with ANGPTL3 and 4 in T2D and non-diabetics subjects.

Methods
A total of 235 subjects were enrolled in this study, 144 non-diabetics and 91 T2D. ANGPTL 3, 4 and 8 levels were measured in plasma by ELISA and using real time RT-PCR in adipose tissues.

Results
In this study, we showed that ANGPTL3, 4 and 8 were higher in T2D subjects. Dividing the non-diabetic subjects according to their BMI showed higher level of ANGPTL3, 4 and 8 in obese subjects compared to non-obese subjects. No significant difference was observed between the T2D subjects. ANGPTL8 was showed positive correlation with ANGPTL3 in the non-diabetic subjects in the non-obese (r = 0.2437, p-Value = 0.0543) and obese subjects (r = 0.418, p-Value = 0.0125). No association was observed in the T2D subjects. On the other hand, ANGPTL4 was positively associated with the obese subjects in both the non-diabetics (r = 0.3322, p-Value = 0.0316) and the obese T2D subjects (r = 0.3161, p-Value = 0.0211).

Conclusion
In conclusion, our data shows that ANGPTL3, 4 and 8 are increased in obesity and T2D. ANGPTL8 associates with ANGPTL3 in the non-diabetic subjects while it associated more with ANGPTL4 in the obese and T2D subjects. Taken together, this data highlight the role of these proteins in metabolic diseases and how they interact with each other’s under different physiological and pathophysiological conditions.

 

 

Estimation of Ellagic acid and/or Repaglinide Effects on Insulin Signaling, Oxidative Stress and Inflammatory Mediators of Liver, Pancreas, Adipose Tissue and Brain in Insulin Resistant/Type 2 Diabetic Rats

ABSTRACT

Even though ellagic acid was valued before in many models of cancer, so far its full mechanistic effect has not been deeply elucidated, which is the goal of this study. For that reason, we observed its 2 weeks influence of ellagic acid (10mg/kg, p.o b.wt.) and/or repaglinide (0.5mg/kg, p.o b.wt.) on insulin resistant/type 2 diabetic albino rats induced by high fat fructose diet (HFFD) diet for 2 months. On the serum biochemical level, ellagic acid challenged the HFFD consequence, where it showed a significant improvement in the glucose/insulin balance, liver enzymes, lipid profile, inflammatory cytokines, redox level, adepokines, ammonia and manganese. While in the tissue level (Liver, Pancreas, Adipose Tissue and Brain), it revealed a significant enhancement in insulin signaling, auto phosphorylation process, adiponectin receptors, glucose transporters, inflammatory mediators and apoptotic markers. Additionally, ellagic acid mitigated also the decreased locomotor activity. Amazingly, combined treatment of both ellagic acid and repaglinide displayed a more pronounced effect which overrides that of either treatment alone. These outcomes give a new insight into the promising molecular mechanisms by which ellagic acid modulates numerous factors induced in the progression of diabetes.

 

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