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Galectin

About: Galectin is a research topic. Over the lifetime, 2076 publications have been published within this topic receiving 103409 citations. The topic is also known as: IPR001079 & Galectin.


Papers
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Journal ArticleDOI
TL;DR: Galectin-9 maternal serum levels were not significantly correlated with pPROM, however, in order to investigate gal-1 and gal-9 levels as potential, promising markers of pPRom, further clinical studies on larger groups are required.
Abstract: Preterm prelabor rupture of membranes (pPROM) accounts for nearly half of premature births. Although several risk factors have been identified, no markers allowing for effective prevention have been discovered. In this study, we investigated how the maternal serum levels of galectin-1 and galectin-9 change in patients with pPROM in comparison to uncomplicated pregnancies. A total of 75 patients were enrolled to both study and control group (37 vs. 38, respectively). The serum concentration of galectin-1 and galectin-9 were assayed in duplicate using an enzyme-linked immunoassay. All analyses were performed using PQ Stat v. 1.8.4 software. Galectin-1 levels were significantly higher in the controls (13.32 vs. 14.71 ng/mL, p = 0.02). Galectin-9 levels were similar in both groups (13.31 vs. 14.76 ng/mL, p = 0.30). Lower galectin levels were detected for early pPROM (before 32nd GW) in comparison to late pPROM and the controls (8.85 vs. 14.45 vs. 14.71 ng/mL, p = 0.0004). Similar trend was observed in galectin-9 levels, although no statistical significance was found (11.57 vs. 14.25 vs. 14.76 ng/mL, p = 0.26). Low galectin-1 maternal serum level is associated with the incidence of preterm prelabor rupture of membranes. Galectin-9 maternal serum levels were not significantly correlated with pPROM. However, in order to investigate gal-1 and gal-9 levels as potential, promising markers of pPROM, further clinical studies on larger groups are required.

2 citations

Journal ArticleDOI
TL;DR: This work reviews the regulatory mechanisms of galectins in normal and pathological pregnancies and has implications for clinicians in the prevention, diagnosis and treatment of pregnancy-related diseases.
Abstract: Galectins (Gal) are characterized by their affinity for galactoside structures on glycoconjugates. This relationship is mediated by carbohydrate recognition domains, which are multifunctional regulators of basic cellular biological processes with high structural similarity among family members. They participate in both innate and adaptive immune responses, as well as in reproductive immunology. Recently, the discovery that galectins are highly expressed at the maternal–fetal interface has garnerd the interest of experts in human reproduction. Galectins are involved in a variety of functions such as maternal–fetal immune tolerance, angiogenesis, trophoblast invasion and placental development and are considered to be important mediators of successful embryo implantation and during pregnancy. Dysregulation of these galectins is associated with abnormal and pathological pregnancies (e.g., preeclampsia, gestational diabetes mellitus, fetal growth restriction, preterm birth). Our work reviews the regulatory mechanisms of galectins in normal and pathological pregnancies and has implications for clinicians in the prevention, diagnosis and treatment of pregnancy-related diseases.

2 citations

Patent
19 Jan 2017
TL;DR: In this article, the authors described methods for the treatment of diseases and conditions relating to galectin 3 using a modified pectin (e.g., GCS-100).
Abstract: The invention provides methods for the treatment of diseases and conditions relating to galectin 3 using a galectin-3 inhibitor, such as a modified pectin (e.g., GCS-100). Also described are methods for conjoint therapy, and methods for assessing and/or monitoring the effects of a galectin-3 inhibitor, e.g., to adapt the dosing regimen of the inhibitor during therapy.

2 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023182
2022176
2021107
2020120
201995
2018119