BackgroundPulsed electromagnetic field (PEMF) therapy has shown promising therapeutic effectiveness on bone- and cartilage-related pathologies, being also safe for management of knee osteoarthritis.AimThe aim of this study was to investigate the clinical efficacy of a PEMF device for management of knee osteoarthritis in elderly patients.Materials and methodsA total of 33 patients were screened, and 28 patients, aged between 60 and 83 and affected by bilateral knee osteoarthritis, were enrolled in this study. They received PEMF therapy on the right leg for a total of three 30-minute sessions per week for a period of 6 weeks, while the left leg did not receive any treatment and served as control. An intravenous drip containing ketoprofen, sodium clodronate, glucosamine sulfate, calcitonin, and ascorbic acid, for a total volume of 500 mL, was administered during PEMF therapy. At baseline and 3 months post-PEMF therapy, Visual Analog Scale (VAS) was used to assess knee pain and Western Ontario McMaster Universities Osteoarthritis Index (WOMAC) was used to measure knee pain, stiffness and physical function.ResultsChanges in VAS and WOMAC scores were calculated for both knees as baseline minus post-treatment. A two sample Student’s t-test, comparing change in knee-related VAS pain for PEMF-treated leg (49.8 ± 2.03) vs control leg (11 ± 1.1), showed a significant difference in favor of PEMF therapy (P < 0.001). A two sample Student’s t-test comparing change in knee-related WOMAC pain, stiffness, and physical function for PEMF-treated leg (8.5 ± 0.4, 3.5 ± 0.2, 38.5 ± 2.08, respectively) vs control leg (2.6 ± 0.2; 1.6 ± 0.1; 4.5 ± 0.5 respectively), also showed a significant difference in favor of PEMF therapy (P < 0.001). No adverse reactions to therapy were observed.ConclusionThe present study shows that PEMF therapy improves pain, stiffness and physical function in elderly patients affected by knee osteoarthritis.
It is generally assumed that the functional consequences of stimulation with Ca2+-mobilizing agonists are derived exclusively from the second messenger action of intracellular Ca2+, acting on targets inside the cells. However, during Ca2+ signaling events, Ca2+ moves in and out of the cell, causing changes not only in intracellular Ca2+, but also in local extracellular Ca2+. The fact that numerous cell types possess an extracellular Ca2+ “sensor” raises the question of whether these dynamic changes in external [Ca2+] may serve some sort of messenger function. We found that in intact gastric mucosa, the changes in extracellular [Ca2+] secondary to carbachol-induced increases in intracellular [Ca2+] were sufficient and necessary to elicit alkaline secretion and pepsinogen secretion, independent of intracellular [Ca2+] changes. These findings suggest that extracellular Ca2+ can act as a “third messenger” via Ca2+ sensor(s) to regulate specific subsets of tissue function previously assumed to be under the direct control of intracellular Ca2+.
The mechanisms for the formation of the osmotic gradient driving water movements in the gastric gland and its modulation via the extracellular Ca 2؉ -sensing receptor (CaR) were investigated. Real time measurements of net water flux in the lumen of single gastric glands of the intact amphibian stomach were performed using ion-selective double-barreled microelectrodes.
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