Is Clostridioides difficile toxins detection necessary when the glutamate dehydrogenase enzyme is detected?

Introduction: Clostridioides difficile causes diarrhea and pseudomembranous colitis. Its diagnosis is made with glutamate dehydrogenase (GDH) or toxins A and B detection and is confirmed with nucleic acid amplification tests.

Objective: To define if GDH determination is redundant to that of toxins.

Leptin in embryos from control and diabetic rats during organogenesis: a modulator of nitric oxide production and lipid homeostasis.

Background: Leptin is involved in many metabolic and reproductive events and its levels are altered by the diabetic pathology. In this study, leptin concentrations and leptin effects on both nitric oxide (NO) and lipid concentrations were investigated in embryos from control and diabetic rats.

Methods: Diabetes was induced by neonatal streptozotocin administration (90 mg/kg).

Leptin modulates nitric oxide production and lipid metabolism in human placenta.

Leptin has significant effects on appetite, energy expenditure, lipid mobilisation and reproduction. During pregnancy, leptin is produced in the placenta, a tissue in which leptin receptors are highly expressed, suggesting autocrine/paracrine functions for this hormone. In the present study, a putative role of leptin as a regulator of nitric oxide (NO) production and lipid metabolism was evaluated in term human placenta.

Oxidative stress promotes the increase of matrix metalloproteinases-2 and -9 activities in the feto-placental unit of diabetic rats.

Maternal diabetes increases the risk of congenital malformations, placental dysfunction and diseases in both the neonate and the offspring's later life. Oxidative stress has been involved in the etiology of these abnormalities. Matrix metalloproteases (MMPs), involved in multiple developmental pathways, are increased in the fetus and placenta from diabetic experimental models.

Modulatory effect of leptin on nitric oxide production and lipid metabolism in term placental tissues from control and streptozotocin-induced diabetic rats.

Leptin production by placental tissues contributes to its circulating levels and functions. The diabetic pathology induces alterations in leptin levels. In the present study, leptin levels were evaluated in placental tissue from control and neonatal streptozotocin-induced (n-STZ) diabetic rats during late gestation.

Lipid metabolism in the embryos of diabetic rats during early organogenesis: modulatory effect of prostaglandin E2.

The purpose of this work was to evaluate de novo lipid biosynthesis and the lipid profile, and to study the effect of prostaglandin E2 (PGE2; prostaglandin has previously been found to be involved in diabetes embryopathy) on lipid metabolism in embryos from control and streptozotocin-induced diabetic rats during organogenesis. Increased levels of triacylglycerols were found in embryos of diabetic rats compared with controls, whereas no differences were detected in the levels of cholesterol, cholesterylester, phosphatidylcholine and phosphatidylethanolamine. When the de novo synthesis of lipids in the embryo was studied using [14C]acetate as a tracer, a diminished rate of incorporation of [14C]acetate into the evaluated lipid classes was detected in the diabetic embryo compared with controls.

Metalloproteinase 2 activity and modulation in uterus from neonatal streptozotocin-induced diabetic rats during embryo implantation.

Matrix metalloproteinases (MMPs) are responsible for the remodelling of the uterine extracellular matrix during embryo implantation. Nitric oxide (NO) production is increased at the time when implantation begins. Abnormal tissue levels of MMPs are present in diabetes; elevated NO levels in tissues and an increased oxidative stress are also found.

Nitric oxide induces gelatinase A (matrix metalloproteinase 2) during rat embryo implantation.

Objective: To evaluate a reciprocal signaling interaction initiated by embryo-derived nitric oxide (NO) to facilitate implantation by increased production of gelatinase A (matrix metalloproteinase 2, MMP2) in uterine stroma.

Design: Experimental animal studies.

Setting: Reproductive-physiology research laboratory.

Levels of endothelin-1 in embryos from control and neonatal streptozotocin-induced diabetic rats, and their relationship with nitric oxide generation.

Endothelin-1 (ET-1), a potent vasoconstrictor peptide and modulator of vasoactive substances such as prostanoids and nitric oxide (NO), plays an important role during embryo and fetal development. In this work, ET-1, nitrate and nitrite, and prostaglandin E2 (PGE2) levels in embryos from control and neonatal streptozotocin-induced (n-stz) diabetic rats were assessed, and the modulatory pathways regulating the generation of these vasoactive agents investigated. Endothelin-1 concentrations were found to be increased in embryos from n-stz diabetic rats when compared with controls.

Oxidative stress and altered prostanoid production in the placenta of streptozotocin-induced diabetic rats.

The oxidative stress in placental tissues during late pregnancy, as well as the relationship between reactive oxygen species (ROS) and the arachidonic acid (AA) pathway was evaluated in a neonatal streptozotocin (STZ)-induced diabetic rat model. Lipoperoxide levels are increased in diabetic tissues compared with control tissues (P<0.001) and they seem to increase throughout the development of gestation both in control (P<0.

Streptozotocin-pancreatic damage in the rat: modulatory effect of 15-deoxy delta12,14-prostaglandin j(2) on nitridergic and prostanoid pathway.

15-deoxy-delta (12,14)prostaglandin J(2) (15d-PGJ(2)) has been identified as a natural ligand of the PPARgamma subtype. PPAR activation in nonadipose tissues seems to inhibit iNOS and COX2 expression. Vasoactive compounds like nitric oxide and prostaglandins are increased in pancreatic tissue from streptozotocin-diabetic rats.