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Objective: The aim of this study was to compare the laeverin level in maternal serum from first trimester (11–14 weeks) of pregnancy between normal pregnancies and pregnancies that later developed preeclampsia (PE).

Material and methods: This was a case-cohort study. The laeverin concentration was measured in cases with preterm PE (n = 55), term PE (n = 95), and a reference group of randomly selected women with normal pregnancy outcome (n = 200) in stored serum samples collected from the double-test as part of the combined first trimester trisomy 21 screening program. The samples were thawed and analyzed for laeverin. The median gestational age at blood sampling was 77 days (range 57–96 days). Multiple regression analysis was performed to establish a normal median. Concentrations were converted to multiples of the median (MoM) and groups were compared using the Mann–Whitney U-test.

Results: In the reference group, laeverin was significantly correlated with gestational age (r = 0.18, p = .01) and its concentration ranged from 41–393 µg/L. No significant differences in the median laeverin MoM were found between the reference group (1.01 MoM) and cases with preterm PE (0.98 MoM) or term PE (0.96 MoM).

Conclusions: First trimester maternal serum laeverin level cannot be used to predict preeclampsia.


Background and Purpose

Microglia phenotype and phagocytic activity are deregulated in Parkinson disease (PD). Peroxisome proliferator-activated receptor gamma (PPAR gamma) agonists are neuroprotective in experimental PD, but their role in regulating microglial phenotype and phagocytosis has been poorly investigated. We addressed it by using the PPAR gamma agonist MDG548.

Experimental Approach

Murine microglial cell line MMGT12 was stimulated with LPS and/or MDG548 and their effect on phagocytosis of fluorescent microspheres or necrotic neurons was investigated by flow cytometry. Cytokines and markers of microglia phenotype such as Mannose Receptor C-Type 1 (MRC1), Ym1 and CD68 were measured by ELISA and fluorescent immunohistochemistry. Levels of Beclin-1, recently shown to play a role in microglial phagocytosis, were measured by western blotting. In the In vivo MPTP-probenecid (MPTPp) model of PD in mice, MDG548 was tested on motor impairment, nigral neurodegeneration, microglial activation and phenotype.

Key Results

MDG548, applied to LPS-stimulated microglia, increased the phagocytosis of both latex beads and necrotic cells, upregulated the expression of MRC1, CD68 and to a lesser extent IL-10, while counteracted the LPS-induced increase of TNF-alpha and iNOS. MDG548 also caused the induction of Beclin-1. The chronic MPTPp treatment in mice downregulated MRC1 and TGF-beta and upregulated TNF-alpha and IL-1beta immunoreactivity in activated CD11bpositive microglia, causing the death of nigral dopaminergic neurons. MDG548 arrested the MPTPp-induced cell death, enhanced MRC1 and restored cytokines levels.

Conclusion and Implications

This study adds a novel mechanism for PPAR gamma-mediated neuroprotection in PD, and suggests that boosting the phagocytic activity and anti-inflammatory markers may represent an effective disease-modifying approach.

Insights into the role of estrogen-related receptors α, β and γ in tumor Leydig cells

Posted by M Kotula-Balak, A Milon, P Pawlicki, et al. on 2018-04-22 19:52:35


In this study, we demonstrate, for the first time, estrogen-related receptor (ERR) regulation of the physiological and biochemical status of testicular tumor Leydig cells.

In a mouse tumor Leydig cells, ERRs (alpha, beta, and gamma) were silenced via siRNA. Cell morphology and cell physiology (proliferation and observation of monolayer formation) were observed by inverted phase-contrast microscope. Leydig cell functional markers (steroid receptors and signaling molecules) were examined by immunofluorescence and Western blotting. Additionally, progesterone secretion was assessed. Mitochondrial mass and membrane potential were analyzed by flow-cytometry while cGMP and Ca2+ concentrations were analyzed using immunoenzymatic and colorimetric assays, respectively.

These results revealed, ERRs indirectly regulate Leydig cell proliferation while ERRalpha and beta affect cell monolayer formation. ERRs interact with canonical and membrane estrogen receptors (ERalpha, ERbeta, and GPER), androgen receptor, metalloproteinase (MMP 9), protein kinase A (PKA), extracellular-regulated kinase (ERK), and neurogenic locus notch homolog protein 2 (Notch2). Depending on the type of ERR knocked down, coupled with estradiol treatment, changes in progesterone concentration and cGMP and Ca2+ concentrations constitute a microenvironment that may effect tumor Leydig cell characteristics. ERRs should be considered important factors in developing of innovating approaches that target pathological processes of testicular Leydig cells.

Relation of locus 1p13 rs646776 polymorphism with the risk of preeclampsia

Posted by R H. Emam, M H. Ghattas, N M. Mesbah, et al. on 2018-03-26 19:07:44


Objective: This study aimed to assess the relation of locus 1p13 rs646776 (T/C) polymorphism with preeclampsia in Egyptian women.

Methods: The study included 100 healthy pregnant female subjects and 100 preeclampsia patients. The genotypes of the polymorphisms were assessed. Endothelin-1 level was determined in plasma.

Results: The major T allele of the 1p13.3 genomic region rs646776 polymorphism had a higher frequency in preeclampsia patients. Carriers of C allele had significantly lower endothelin-1 levels, lower systolic and diastolic blood pressure, decreased proteinuria, and increased HDL-C in the patients.

Conclusion: The rare C allele of rs646776 polymorphism in chromosomal locus 1p13.3 is associated with decreased risk of preeclampsia.


Esophageal squamous cell carcinoma (ESCC) is one of the most malignant tumors in China with a poor prognosis. Most ESCC patients were diagnosed at advanced stages, losing the opportunity for surgical excision. Hence, it remains a pressing work to identify biomarkers for early detection, prognosis prediction and targeting therapies in ESCC. Interferon-stimulated gene 15 (ISG15) encodes a 15-kDa protein, and is involved in the post-translational modification (PTMs) of multiple proteins. However, the molecular functions of ISG15 in ESCC remain unclear. In this work, we found that ISG15 was aberrantly expressed in ESCC tissues and cell lines. Enhanced protein level of ISG15 promoted cellular malignant phenotypes including proliferation, migration, invasion and tumor formation in vivo. Consistently, reduction of ISG15 attenuated the cellular malignant phenotype in ESCC cell lines. Furthermore, gene-expression profiles suggested that the differentially expressed ISG15 affected the expression of a panel of genes enriched in the cell adherens junction, such as c-MET. Notably, as a secreted protein, the concentration of ISG15 was elevated in ESCC plasma than healthy individuals, acting as a potential diagnostic marker. Taken together, our results suggested a tumor promotion role of ISG15 in ESCC via c-MET/Fyn/beta-catenin pathway.

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