Insertion of glaucoma drainage devices has become a mainstay in the surgical management of multiple forms of glaucoma, and the indications for this procedure continue to expand. A unique clinical challenge in the postoperative care of these devices is the hypertensive phase, a period of postoperative intraocular pressure elevation in the first three months after surgery. We discuss the influence of a variety of factors on the development of the hypertensive phase after glaucoma drainage implantation, including type of device, device material, and device surface area. Furthermore, several intraoperative and postoperative interventions are investigated as attempts to mitigate this phenomenon. Included among these are the use of antimetabolites, collagen matrix, and a variety of approaches to postoperative inflammation and intraocular pressure control. We provide an overview of our current knowledge of the etiology and management of the hypertensive phase.

Some well-established immunotherapy, radiotherapy, postoperation, anticancer drugs such as anthracyclines, antimetabolites, human epidermal growth factor receptor 2 blockers, tyrosine kinase inhibitors, alkylating agents, checkpoint inhibitors, and angiogenesis inhibitors, are significantly linked to cardiotoxicity. Cardiotoxicity is a common complication of several cancer treatments. Some studies observed complications of cardiac arrhythmia associated with the treatment of cancer, including atrial fibrillation (AF), supraventricular arrhythmias, and cardiac repolarization abnormalities. AF increases the risk of cardiovascular morbidity and mortality; it is associated with an almost doubled risk of mortality and a nearly 5-fold increase in the risk of stroke. The occurrence of AF is also usually researched in patients with advanced cancer and those undergoing active cancer treatments. During cancer treatments, the incidence rate of AF affects the prognosis of tumor treatment and challenges the treatment strategy. The present article is mainly focused on the cardiotoxicity of cancer treatments. In our review, we discuss these anticancer therapies and how they induce AF and consequently provide information on the precaution of AF during cancer treatment.

In this study is reported a simple and inexpensive method for concurrent determination of taurine and choline in different supplementary nutrient samples using dual-channeled capillary electrophoresis (CE) instrument with capacitively coupled contactless conductivity detection (C4D). The objective of the work is to propose a tool for food control activities that allows screening of different target compounds (having different characteristics) in a single run for high throughput and can be realizable even with modest infrastructure. Taurine was analyzed in the first CE channel using the background electrolyte (BGE) composed of 150 mM tris(hydroxymethyl)aminomethane/lactic acid (pH 8.96) whereas choline was simultaneously separated in the second CE channel using a BGE containing 150 mM tris(hydroxymethyl)aminomethane/acetic acid (pH 9.5). The best achieved detection limit was 0.27 mg/L and 0.45 mg/L for taurine and choline, respectively, using the developed CE-C4D method. Good agreement between results obtained from CE-C4D and those with the standard confirmation methods (HPLC-DAD for taurine and LC/MS for choline) was achieved, with the result deviation for the two pairs of data being less than 12%.

Introduction The use of paclitaxel in pregnant cancer patients is feasible in terms of fetal safety, but little is known about the effects of paclitaxel on the placenta. Using three experimental models, we aimed to assess the effects of paclitaxel on the expression of placental drug transporters. Methods In the in vitro model (human primary trophoblast culture), trophoblasts were isolated from normal term placentas and subsequently exposed to paclitaxel. The transcriptional regulation of 84 genes encoding for drug transporters, and the protein expression of ABCB1/P-gp and ABCG2/BCRP were assessed. In the in vivo model, placental tissues isolated from pregnant cancer patients treated with paclitaxel were analyzed to assess the protein expression of ABCB1/P-gp and ABCG2/BCRP. The same parameters were assessed in extracts from human placental cotyledons perfused ex vivo with paclitaxel. Results In the in vitro model, the expression of twelve drug-transporters genes was found to be significantly down-regulated after exposure to paclitaxel, including ABCC10, SLC28A3, SLC29A2, and ATP7B (involved in the transport of taxanes, antimetabolites, and cisplatin, respectively). The protein expression of ABCB1/P-gp increased by 1.3-fold after paclitaxel administration. Finally, the protein expression of ABCB1/P-gp and ABCG2/BCRP was higher in cotyledons from mothers treated with multiple doses of paclitaxel during pregnancy than in cotyledons perfused with a single dose of paclitaxel. Discussion Paclitaxel modulates the expression of placental drug transporters involved in the disposition of various anticancer agents. Further studies will be needed to assess the impact of repeated or prolonged exposure to paclitaxel on the expression and function of placental drug transporters.

Drug combination represents one of the most accredited strategies of cancer therapy able to improve drug efficacy and possibly overcome drug resistance. Among the agents used to complement conventional chemotherapy, carbonic anhydrase IX (CAIX) inhibitors appear as one of the most suitable, as markers of hypoxic and acidic cancer cells which do not respond to chemo- and radiotherapy. We performed preclinical in vitro assays to evaluate whether the SLC-0111 CAIX inhibitor co-operates and potentiates the cytotoxic effects of conventional chemotherapeutic drugs in A375-M6 melanoma cells, MCF7 breast cancer cells, and HCT116 colorectal cancer cells. Here, we demonstrate that the SLC-0111 CAIX inhibitor potentiates cytotoxicity of Dacarbazine and Temozolomide currently used for advanced melanoma treatment. SLC-0111 also increases breast cancer cell response to Doxorubicin and enhances 5-Fluorouracil cytostatic activity on colon cancer cells. These findings disclose the possibility to extend the use of CAIX inhibitors in the combination therapy of various cancer histotypes.