Pulsed electromagnetic field therapy for management of osteoarthritis-related pain, stiffness and physical function: clinical experience in the elderly.

BACKGROUND: Pulsed electromagnetic field (PEMF) therapy has shown promising therapeutic effectiveness on bone- and cartilage-related pathologies, being also safe for management of knee osteoarthritis. AIM: The aim of this study was to investigate the clinical efficacy of a PEMF device for management of knee osteoarthritis in elderly patients. MATERIALS AND METHODS: A 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. RESULTS: Changes 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. CONCLUSION: The present study shows that PEMF therapy improves pain, stiffness and physical function in elderly patients affected by knee osteoarthritis.

The feasibility of a fiber optic laser approach to relieving lymphedematous syndrome: a case report.

Here we report a case of successful fiber optic laser treatment of lymphedema in a swollen arm post mastectomy. At the moment, this procedure has only anecdotal evidence to justify its use, but in our experience is a feasible, minimally invasive day-stay procedure which has been demonstrated to be safe and effective. Further nonhomogeneous case pooling and follow-up would enable guidelines and definite surgical protocols for its use to be implemented.

Real time measurements of water flow in amphibian gastric glands: modulation via the extracellular Ca2+-sensing receptor.

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. Water movement was measured by recording changes in the concentration of impermeant TEA(+) ions ([TEA(+)](gl)) with TEA(+)-sensitive microelectrodes inserted in the lumen of individual gastric glands. Glandular K(+) (K(+)(gl)) and H(+) (pH(gl)) were also measured by using K(+)- and H(+)-sensitive microelectrodes, respectively. Stimulation with histamine significantly decreased [TEA](gl), indicating net water flow toward the gland lumen. This response was inhibited by the H(+)/K(+)-ATPase inhibitor, SCH 28080. Histamine also elicited a significant and reversible increase in [K(+)](gl) that was blocked by chromanol 293B, a blocker of KCQN1 K(+) channels. Histamine failed to induce net water flow in the presence of chromanol 293B. In the "resting state," stimulation of CaR with diverse agonists resulted in significant increase in [TEA](gl). CaR activation also significantly reduced histamine-induced water secretion and apical K(+) transport. Our data validate the strong link between histamine-stimulated acid secretion and water transport. We also show that cAMP-dependent [K(+)](gl) elevation prior to the onset of acid secretion generates the osmotic gradient initially driving water into the gastric glands and that CaR activation inhibits this process, probably through reduction of intracellular cAMP levels.

Fatty acid ethyl esters cause pancreatic calcium toxicity via inositol trisphosphate receptors and loss of ATP synthesis.

BACKGROUND & AIMS: Fatty acid ethyl esters are ethanol metabolites inducing sustained, toxic elevations of the acinar cytosolic free calcium ion concentration ([Ca(2+)](C)) implicated in pancreatitis. We sought to define the mechanisms of this elevation. METHODS: Isolated mouse pancreatic acinar cells were loaded with fluorescent dyes for confocal microscopy to measure [Ca(2+)](C) (Fluo 4, Fura Red), endoplasmic reticulum calcium ion concentration ([Ca(2+)](ER), Mg Fluo 4), mitochondrial membrane potential (TMRM), ADP:ATP ratio (Mg Green), and NADH autofluorescence in response to palmitoleic acid ethyl ester and palmitoleic acid (10-100 micromol/L). Whole-cell patch clamp was used to measure the calcium-activated chloride current and apply ethanol metabolites and/or ATP intracellularly. RESULTS: Intracellular delivery of ester induced oscillatory increases of [Ca(2+)](C) and calcium-activated currents, inhibited acutely by caffeine (20 mmol/L), but not atropine, indicating involvement of inositol trisphosphate receptor channels. The stronger effect of extracellular ester or acid caused depletion of [Ca(2+)](ER), not prevented by caffeine, but associated with depleted ATP, depleted NADH autofluorescence, and depolarized mitochondria, suggesting calcium-ATPase pump failure because of lack of ATP. Intracellular ATP abolished the sustained rise in [Ca(2+)](C), although oscillatory signals persisted that were prevented by caffeine. Inhibition of ester hydrolysis markedly reduced its calcium-releasing effect and consequent toxicity. CONCLUSIONS: Fatty acid ethyl ester increases [Ca(2+)](C) through inositol trisphosphate receptors and, following hydrolysis, through calcium-ATPase pump failure from impaired mitochondrial ATP production. Lowering cellular fatty acid substrate concentrations may reduce cell injury in pancreatitis.

Extracellular calcium acts as a "third messenger" to regulate enzyme and alkaline secretion.

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+.