23 research outputs found
Endothelial dysfunction and tendinopathy: how far have we come?
none9noSymptomatic tendon tears are one of the most
important causes of pain and joint dysfunction. Among the
intrinsic causes, vascularization recently gained a major
role. Endothelial function is indeed a key factor, as well as
vascular tone and thrombotic factors, in the regulation of
vascular homeostasis and the composition of vascular wall.
In this review, we studied systematically whether there is a
relationship between endothelial dysfunction and tendinopathy.
A literature search was performed using the isolated
or combined keywords endothelial dysfunction and
tendon,â ânitric oxide (NO) and tendinopathy,â and âendothelial
dysfunction in tendon healing.â We identified 21
published studies. Of the selected studies, 9 were in vivo
studies, 2 focusing on animals and 7 on humans, while 12
reported about in vitro evaluations, where 7 were carried
out on humans and 5 on animals. The evidence about a
direct relationship between tendinopathy and endothelial
dysfunction is still poor. As recent studies have shown,
there is no significant improvement in clinical and functional
assessments after treatment with NO in patients
suffering from tendinopathy in different locations. No
significant differences were identified in the outcomes
reported for experiment group when compared with controls
treated with conventional surgical procedures or
rehabilitation programs. Nitric oxide could be a marker to
quantify the response of the endothelium to mechanical
stress or hypoxia indicating the final balance between vasodilatating
and vasoconstricting factors and their effects,
but more ad stronger evidence is still needed to fully
support this practice.openR. Papalia;L. Moro;F. Franceschi;E. Albo;S. DâAdamio;A. Di Martino;G. VadalĂ ;C. Faldini;V. DenaroR. Papalia;L. Moro;F. Franceschi;E. Albo;S. DâAdamio;A. Di Martino;G. VadalĂ ;C. Faldini;V. Denar
Correction to: Abolishing Tau cleavage by caspases at Aspartate421 causes memory/synaptic plasticity deficits and pre-pathological Tau alterations (Translational Psychiatry, (2017), 7, 8, (e1198), 10.1038/tp.2017.165)
© 2018, The Author(s). This article was originally published under Nature Researchâs License to Publish, but has now been made available under a CC BY 4.0 license. The PDF and HTML versions of the article have been modified accordingly
Total synthesis of hyacinthacines B3, B4, and B 5 and purported hyacinthacine B7, 7-epi-hyacinthacine B7, and 7a-epi-hyacinthacine B3 from a common precursor
The total synthesis of hyacinthacines B3, B4, and B5 and purported hyacinthacine B7, 7-epi-hyacinthacine B7, and 7a-epi-hyacinthacine B3 from a common anti-1,2-amino alcohol precursor is described. These syntheses confirmed that the proposed structures and absolute configurations of hyacinthacines B3, B4, and B5 were correct and disclosed that the proposed structure of hyacinthacine B7 was incorrect. Our synthetic and spectroscopic studies suggest that the natural hyacinthacines B5 and B7 are the same compounds; however, without access to authentic samples this cannot be unequivocally proven
Accumulation of Cytoplasmic Glucocorticoid Receptor Is Related to Elevation of FKBP5 in Lymphocytes of Depressed Patients
We have previously shown that patients with the major depressive disorder (MDD) exhibited elevated phosphorylation of the lymphocyte glucocorticoid receptor (GR) at serine 226 (S226). Here, we further analyse potential alterations of GR signalization in lymphocytes of MDD patients, i.e. the cytoplasmic/nuclear distribution of GR, levels of FK506-binding protein 5 (FKBP5) and glucocorticoid-induced leucine zipper (GILZ). The FKBP5 acts as an important regulator of GR activation, by decreasing ligand binding and impeding translocation of the receptor to the nucleus, while GILZ mediates glucocorticoid anti-inflammatory effects. Our result showed that the depressed patients had significantly higher GR levels in the cytoplasm compared to controls, which was accompanied by higher FKBP5 levels. Linear regression model demonstrated significantly higher correlation between FKBP5 and cytoplasmic GR than the presence of MDD itself or phosphorylation of nuclear GR at S226. There were no differences in the levels of GILZ isoforms. Therefore, the results suggest that accumulation of the GR in cytoplasm is related to the elevation of FKBP5, adding one more step in understanding altered GR signalling in lymphocytes, and potentially brain tissue, of MDD patients