Polymorphism of Genetic variability of gene in sheep

MUC1 gene encodes the polypeptide of a mucin present on the apical surface of the secreting mammary cells during lactation and on the surface of the milk fat globules (Mather, 2000). MUC1 contains a minisatellite region: the sequence, coding for the extracellular protein domain, consists mostly of a motif of 60 bp that in human, cattle and goat is tandemly repeated a variable number of times (VNTR polymorphism), giving rise to molecular variants of different size (Patton et al., 1995)

Intraoperative measurement of parathyroid hormone: A Copernican revolution in the surgical treatment of hyperparathyroidism

Intraoperative parathyroid hormone (PTH) monitoring in the setting of the operating room represents a valuable example of the rationale use of the laboratory diagnostic in a patient-oriented approach. Rapid intraoperative PTH (ioPTH) assay is a valid tool for an accurate evaluation of the success of parathyroid surgery. The reliability of the user-friendly portable systems as well as the collaboration between operators and surgical staff allow the one-site monitoring of the ioPTH decrements on the course of the surgical management of hyperparathyroidism.The rapid answer provided by an effective decrement of PTH during parathyroidectomy contributes dramatically to the efficacy of parathyroid surgery and the reduction of the number of re-operations. Therefore the dose of ioPTH is a valid and reliable support for the success of the intervention of parathyroidectomy at controlled costs

The Human Cytomegalovirus UL116 Glycoprotein Is a Chaperone to Control gH-Based Complexes Levels on Virions

Human cytomegalovirus (HCMV) relies in large part upon the viral membrane fusion glycoprotein B and two alternative gH/gL complexes, gH/gL/gO (Trimer) and gH/gL/UL128/UL130/UL131A (Pentamer) to enter into cells. The relative amounts of Trimer and Pentamer vary among HCMV strains and contribute to differences in cell tropism. Although the viral ER resident protein UL148 has been shown to interact with gH to facilitate gO incorporation, the mechanisms that favor the assembly and maturation of one complex over another remain poorly understood. HCMV virions also contain an alternative non-disulfide bound heterodimer comprised of gH and UL116 whose function remains unknown. Here, we show that disruption of HCMV gene UL116 causes infectivity defects of ∼10-fold relative to wild-type virus and leads to reduced expression of both gH/gL complexes in virions. Furthermore, gH that is not covalently bound to other viral glycoproteins, which are readily detected in wild-type HCMV virions, become undetectable in the absence of UL116 suggesting that the gH/UL116 complex is abundant in virions. We find evidence that UL116 and UL148 interact during infection indicating that the two proteins might cooperate to regulate the abundance of HCMV gH complexes. Altogether, these results are consistent with a role of UL116 as a chaperone for gH during the assembly and maturation of gH complexes in infected cells

Galectin-9 Regulates Monosodium Urate Crystal-Induced Gouty Inflammation Through the Modulation of Treg/Th17 Ratio

Gout is caused by depositing monosodium urate (MSU) crystals within the articular area. The infiltration of neutrophils and monocytes drives the initial inflammatory response followed by lymphocytes. Interestingly, emerging evidence supports the view that in situ imbalance of T helper 17 cells (Th17)/regulatory T cells (Treg) impacts the subsequent damage to target tissues. Galectin-9 (Gal-9) is a modulator of innate and adaptive immunity with both pro- and anti-inflammatory functions, dependent upon its expression and cellular location. However, the specific cellular and molecular mechanisms by which Gal-9 modulates the inflammatory response in the onset and progression of gouty arthritis has yet to be elucidated. In this study, we sought to comprehensively characterise the functional role of exogenous Gal-9 in an in vivo model of MSU crystal-induced gouty inflammation by monitoring in situ neutrophils, monocytes and Th17/Treg recruited phenotypes and related cyto-chemokines profile. Treatment with Gal-9 revealed a dose-dependent reduction in joint inflammation scores, knee joint oedema and expression of different pro-inflammatory cyto-chemokines. Furthermore, flow cytometry analysis highlighted a significant modulation of infiltrating inflammatory monocytes (CD11b+/CD115+/LY6-Chi) and Th17 (CD4+/IL-17+)/Treg (CD4+/CD25+/FOXP-3+) cells following Gal-9 treatment. Collectively the results presented in this study indicate that the administration of Gal-9 could provide a new therapeutic strategy for preventing tissue damage in gouty arthritic inflammation and, possibly, in other inflammatory-based diseases