[Study on the use of multi-compartment compliance aids to improve blood pressure values in hypertensive patients].

Objectives: To analyse the improvement of adherence in non-adherent patients with uncontrolled HT, polymedicated and older than 55 years after the use, or not, of Multicompartment compliance aids (MCA).

Design: Longitudinal research (6 month). Levels of adherence to treatment were analysed using an adapted version of Morisky-Green test, counting of returned medication (MCA group) and blood pressure (BP) values.

Intracellular prostaglandin E2 contributes to hypoxia-induced proximal tubular cell death.

Proximal tubular cells (PTC) are particularly vulnerable to hypoxia-induced apoptosis, a relevant factor for kidney disease. We hypothesized here that PTC death under hypoxia is mediated by cyclo-oxygenase (COX-2)-dependent production of prostaglandin E (PGE), which was confirmed in human proximal tubular HK-2 cells because hypoxia (1% O)-induced apoptosis (i) was prevented by a COX-2 inhibitor and by antagonists of prostaglandin (EP) receptors and (ii) was associated to an increase in intracellular PGE (iPGE) due to hypoxia-inducible factor-1α-dependent transcriptional up-regulation of COX-2. Apoptosis was also prevented by inhibitors of the prostaglandin uptake transporter PGT, which indicated that iPGE contributes to hypoxia-induced apoptosis (on the contrary, hypoxia/reoxygenation-induced PTC death was exclusively due to extracellular PGE).

Comprehensive metabolomic study of the response of HK-2 cells to hyperglycemic hypoxic diabetic-like milieu.

Diabetic nephropathy (DN) is the leading cause of chronic kidney disease. Although hyperglycaemia has been determined as the most important risk factor, hypoxia also plays a relevant role in the development of this disease. In this work, a comprehensive metabolomic study of the response of HK-2 cells, a human cell line derived from normal proximal tubular epithelial cells, to hyperglycemic, hypoxic diabetic-like milieu has been performed.

Time-series proteomic study of the response of HK-2 cells to hyperglycemic, hypoxic diabetic-like milieu.

During diabetes, renal proximal tubular cells (PTC) are exposed to a combination of high glucose and hypoxic conditions, which plays a relevant role in the development of diabetic kidney disease (DKD). In this work, a time-series proteomic study was performed to analyse the effect of a diabetic-like microenvironment induced changes on HK-2 cells, a human cell line derived from normal proximal tubular epithelial cells. Cells simultaneously exposed to high glucose (25 mM) and hypoxia (1% O2) were compared to cells in control conditions for up to 48 h.

Author Correction: Mechanism and Consequences of The Impaired Hif-1α Response to Hypoxia in Human Proximal Tubular HK-2 Cells Exposed to High Glucose.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Retinoic acid receptor-beta prevents cisplatin-induced proximal tubular cell death.

Cisplatin's toxicity in renal tubular epithelial cells limits the therapeutic efficacy of this antineoplastic drug. In cultured human proximal tubular HK-2 cells (PTC) a prostaglandin uptake transporter (PGT)-dependent increase in intracellular prostaglandin E (iPGE) mediates cisplatin's toxicity (i.e.

Mechanism and Consequences of The Impaired Hif-1α Response to Hypoxia in Human Proximal Tubular HK-2 Cells Exposed to High Glucose.

Renal hypoxia and loss of proximal tubular cells (PTC) are relevant in diabetic nephropathy. Hypoxia inhibits hypoxia-inducible factor-1α (HIF-1α) degradation, which leads to cellular adaptive responses through HIF-1-dependent activation of gene hypoxia-responsive elements (HRE). However, the diabetic microenvironment represses the HIF-1/HRE response in PTC.

Apoptosis and cell proliferation in proximal tubular cells exposed to apoptotic bodies. Novel pathophysiological implications in cisplatin-induced renal injury.

The therapeutic efficacy of the antineoplastic drug cisplatin is limited by its nephrotoxicity, which affects particularly to proximal tubular cells (PTC). Cisplatin-induced cytotoxicity appears to be multifactorial and involves inflammation, oxidative stress as well as apoptosis. We have recently shown that the cyclo-oxygenase-2 (COX-2)/intracellular prostaglandin E (iPGE)/EP receptor pathway mediates the apoptotic effect of cisplatin on human proximal tubular HK-2 cells.

[Information quality and health risks in Spanish-language retail websites for Chinese herbal medicine].

Objective: The growing use of purchase online via Internet retailers favours the access to potentially toxic natural products. It also contributes to the quick dissemination of the claims made by the retailers on efficacy and safety, these claims being not always based upon reliable information. Here, we have conducted an online search to find Spanish-language retail websites for Chinese herbal medicine and we have analysed them for the quality of product information and the potential health risks.

The effect of the European traditional use directive on the register of herbal medicinal products in Spain.

Background: Directive 2004/24/EC, which came into force in 2011, created new regulatory requirements for traditional herbal medicines (THM). This study compared the Spanish THM registry before and after the Directive came fully into force in 2011.

Methods: We consulted the herbal medicinal plant and drug catalogues (General Council of the Official Colleges of Pharmacists), the website of the European Medicines Agency (EMA), and retail web sites.