Effect of Combined Electromagnetic Field and Plantar Flexion Resistance Exercise on Wound Healing in Patients with Venous Leg Ulcers: A Randomized Controlled Trial

Background and Objectives: Venous ulcers are recognized to be more painful and resistant to therapy than ulcers of other etiologies. Various methods have been used for the conservative treatment of venous ulcers, such as pulsed electromagnetic field (PEMF) and plantar exercise, which promote wound healing due to a range of physiological effects. The study aimed to examine the effect of combined pulsed electromagnetic field therapy and plantar flexion resistance exercise (PRE) on patients with venous leg ulcers (VLUs). Materials and Methods: The study was a prospective, randomized controlled trial. A total of 60 patients between the ages of 40 and 55 with venous ulcers were randomly assigned to 1 of 3 groups. For up to 12 weeks, the first group received PEMF therapy and plantar flexion resistance exercise (PRE) therapy in addition to conservative ulcer treatment for up to 12 weeks. The second group received only PEMF therapy in addition to conservative ulcer treatment, while the third group served as the control and received only conservative ulcer treatment. Results: At the four-week follow-up, the two experimental groups revealed a considerable variation in ulcer surface area (USA) and ulcer volume (UV), with no significant change in the control group. At the 12-week follow-up, there were significant differences between the three groups, while group A underwent the most significant changes, with mean differences at [95% confidence interval] of (−4.75, −3.82, −0.98) for USA and (−12.63, −9.55, −2.45) for UV, respectively. Conclusions: On a short-term basis, adding a plantar resistance exercise to the PEMF had no appreciable short-term effects on ulcer healing; however, their combination had more pronounced medium-term effects

Effect of hydrophobic extension of aryl enaminones and pyrazole-linked compounds combined with sulphonamide, sulfaguanidine, or carboxylic acid functionalities on carbonic anhydrase inhibitory potency and selectivity

AbstractDesign and synthesis of three novel series of aryl enaminones (3a–f and 5a–c) and pyrazole (4a-c) linked compounds with sulphonamides, sulfaguanidine, or carboxylic acid functionalities were reported as carbonic anhydrase inhibitors (CAIs) using the “tail approach” strategy in their design to achieve the most variable amino acids in the middle/outer rims of the hCAs active site. The synthesised compounds were assessed in vitro for their inhibitory activity against the following human (h) isoforms, hCA I, II, IX, and XII using stopped-flow CO2 hydrase assay. Enaminone sulphonamide derivatives (3a–c) potently inhibited the target tumour-associated isoforms hCA IX and hCA XII (KIs 26.2–63.7 nM) and hence compounds 3a and 3c were further screened for their in vitro cytotoxic activity against MCF-7 and MDA-MB-231 cancer cell lines under normoxic and hypoxic conditions. Derivative 3c showed comparable potency against both MCF-7 and MDA-MB-231 cancer cell lines under both normoxic ((IC50 = 4.918 and 12.27 µM, respectively) and hypoxic (IC50 = 1.689 and 5.898 µM, respectively) conditions compared to the reference drug doxorubicin under normoxic (IC50 = 3.386 and 4.269 µM, respectively) and hypoxic conditions (IC50 = 1.368 and 2.62 µM, respectively). Cell cycle analysis and Annexin V-FITC and propidium iodide double staining methods were performed to reinforce the assumption that 3c may act as a cytotoxic agent through the induction of apoptosis in MCF-7 cancer cells

Effect of hydrophobic extension of aryl enaminones and pyrazole-linked compounds combined with sulphonamide, sulfaguanidine, or carboxylic acid functionalities on carbonic anhydrase inhibitory potency and selectivity

Design and synthesis of three novel series of aryl enaminones (3a–f and 5a–c) and pyrazole (4a-c) linked compounds with sulphonamides, sulfaguanidine, or carboxylic acid functionalities were reported as carbonic anhydrase inhibitors (CAIs) using the “tail approach” strategy in their design to achieve the most variable amino acids in the middle/outer rims of the hCAs active site. The synthesised compounds were assessed in vitro for their inhibitory activity against the following human (h) isoforms, hCA I, II, IX, and XII using stopped-flow CO2 hydrase assay. Enaminone sulphonamide derivatives (3a–c) potently inhibited the target tumour-associated isoforms hCA IX and hCA XII (KIs 26.2–63.7 nM) and hence compounds 3a and 3c were further screened for their in vitro cytotoxic activity against MCF-7 and MDA-MB-231 cancer cell lines under normoxic and hypoxic conditions. Derivative 3c showed comparable potency against both MCF-7 and MDA-MB-231 cancer cell lines under both normoxic ((IC50 = 4.918 and 12.27 µM, respectively) and hypoxic (IC50 = 1.689 and 5.898 µM, respectively) conditions compared to the reference drug doxorubicin under normoxic (IC50 = 3.386 and 4.269 µM, respectively) and hypoxic conditions (IC50 = 1.368 and 2.62 µM, respectively). Cell cycle analysis and Annexin V-FITC and propidium iodide double staining methods were performed to reinforce the assumption that 3c may act as a cytotoxic agent through the induction of apoptosis in MCF-7 cancer cells. </p