Association of N-terminal pro-brain natriuretic peptide level with adverse outcomes in patients with acute myocardial infarction: A meta-analysis.

Background: Studies evaluating the association of blood level of N-terminal pro-brain natriuretic peptide (NT-proBNP) with adverse prognosis have yielded conflicting results in patients with acute myocardial infarction (AMI). This meta-analysis sought to evaluate the prognostic value of blood level of NT-proBNP in patients with AMI.

Methods: Two authors independently searched articles in PubMed and Embase databases up to June 13, 2021.

Effects of thromboxane prostanoid receptor deficiency on diabetic nephropathy induced by high fat diet and streptozotocin in mice.

Diabetic nephropathy (DN), one of the main causes of end-stage renal disease, still remains as a challenge of clinical management. This study aimed to determine whether deficiency of the thromboxane (TX) prostanoid receptor (TP), which mediates the contractile activities of all prostanoids, alleviates the development of DN and if so, to examine the underlying mechanism(s). Diabetes was induced by high fat diet and streptozotocin injection in wild-type (WT) mice and those with TP deficiency (TP).

Prostaglandin E sequentially activates E-prostanoid receptor-3 and thromboxane prostanoid receptor to evoke contraction and increase in resistance of the mouse renal vasculature.

Although recognized to have an in vivo vasodepressor effect blunted by the vasoconstrictor effect of E-prostanoid receptor-3 (EP3), prostaglandin E (PGE ) evokes contractions of many vascular beds that are sensitive to antagonizing the thromboxane prostanoid receptor (TP). This study aimed to determine the direct effect of PGE on renal arteries and/or the whole renal vasculature and how each of these two receptors is involved in the responses. Experiments were performed on isolated vessels and perfused kidneys of wild-type mice and/or mice with deficiency in TP (TP ), EP3 (EP3 ), or both TP and EP3 (TP /EP3 ).

EP3 Blockade Adds to the Effect of TP Deficiency in Alleviating Endothelial Dysfunction in Atherosclerotic Mouse Aortas.

Endothelial dysfunction, which leads to ischemic events under atherosclerotic conditions, can be attenuated by antagonizing the thromboxane-prostanoid receptor (TP) that mediates the vasoconstrictor effect of prostanoids including prostacyclin (PGI). This study aimed to determine whether antagonizing the E prostanoid receptor-3 (EP3; which can also be activated by PGI) adds to the above effect of TP deficiency (TP) under atherosclerotic conditions and if so, the underlying mechanism(s). Atherosclerosis was induced in ApoE mice and those with ApoE and TP.

Expression Profiling of Notch Signalling Pathway and Gamma-Secretase Activity in the Brain of Ts1Cje Mouse Model of Down Syndrome.

Notch signalling pathway is involved in the proliferation of neural progenitor cells (NPCs), to inhibit neuronal cell commitment and to promote glial cell fate. Notch protein is cleaved by gamma-secretase, a multisubunit transmembrane protein complex that releases the Notch intracellular domain (NICD) and subsequently activates the downstream targets. Down syndrome (DS) individuals exhibit an increased number of glial cells (particularly astrocytes), and reduced number of neurons suggesting the involvement of Notch signalling pathway in the neurogenic-to-gliogenic shift in DS brain.

TP and/or EP3 receptors mediate the vasoconstrictor and pressor responses of prostaglandin F in mice and/or humans.

The vasoconstrictor and/or pressor effects of prostaglandin (PG)F participate in the development of vascular pathologies and limit the clinical use of the agent. This study aimed to determine the receptor types responsible for the vasoconstrictor activity of PGF and whether they mediate the pressor response evoked by the prostanoid under in vivo conditions. Experiments were performed on genetically altered mice and/or on vessels from these mice or humans.

Prostaglandin D evokes potent uterine contraction via the F prostanoid receptor in postpartum rats.

Prostaglandin (PG) D, a prostanoid known to have hypotensive effect, can evoke increased in vitro prepartum myometrial contraction resulting from up-regulation of the F prostanoid (FP) receptor. The present study further determined postpartum rat uterine responses to PGD to evaluate the possibility of the prostanoid becoming a therapeutic for postpartum uterine atony, a major cause of postpartum hemorrhage that can lead to maternal morbidity. In vitro and in vivo postpartum uterine responses to PGD were determined and compared to those of prepartum rats.