A novel strategy combining magnetic particle hyperthermia pulses with enhanced performance binary ferrite carriers for effective in vitro manipulation of primary human osteogenic sarcoma cells.

The present study examines the heating efficiency of a combination of manganese or cobalt ferrites in a binary (Co- or Mn-) ferrite nanoparticle form with magnetite, covered with citric acid to improve biocompatibility. The nanoparticle synthesis is based on the aqueous co-precipitation of proper salts, a facile, low-cost, environmentally friendly and high yield synthetic approach. By detailed structural and magnetic characterisation, the direct influence of structural and magnetic features on magnetic hyperthermia concludes to optimum heating efficiency. At a second stage, best performing magnetic nanoparticles undergo in vitro testing in three cell lines: one cancer cell line and two reference healthy cell lines. Both binary ferrite (MnFe2O4/Fe3O4 and CoFe2O4/Fe3O4) appear to be internalised and well tolerated by the cells while a versatile hyperthermia protocol is attempted in an effort to further improve their in vitro performance. Within this protocol, hyperthermia sequences are split in two runs with an intermediate 48 h time interval cell incubation stage while in each run a variable field mode (single or multiple pulses) is applied. Single-pulse field mode represents a typical hyperthermia application scheme where cells undergo the thermal shock continuously. On the other hand multiple-pulses mode refers to multiple, much shorter in duration AC field changes (field ON/OFFs), at each hyperthermia run, resulting eventually in high heating rate and much more harmful cell treatment. Consequently, we propose a novel series of improved performance heat mediators based on ferrite structures which show maximum efficiency at cancer cells when combined with a versatile multiple-pulse hyperthermia module.

Oral calcium supplementation ambulatory blood pressure and relation to changes in intracellular ions and sodium-hydrogen exchange.

BACKGROUND: Calcium (Ca2+) supplementation has been shown paradoxically to reduce intracellular Ca2+ and induce vascular relaxation. The aim of the study was to assess 24-h blood pressure (BP) change after Ca2+ supplementation and to investigate its relation to changes in intracellular ions and the activity of the first isoform of sodium-hydrogen exchange (NHE-1) in subjects with hypertension and type 2 diabetes. METHODS: This parallel, randomized controlled, single-blinded trial, consisted of 31 patients with type 2 diabetes, and hypertension who were allocated to receive 1,500 mg of Ca2+ per day (n = 15) or no treatment (n = 16) for 8 weeks. RESULTS: In the Ca2+ group a decrease of 1.7 +/- 2.7 mm Hg (mean +/- SE) P = 0.52 for mean 24-h systolic BP (SBP) and 2.1 +/- 1.5 mm Hg, P = 0.19 for mean 24-h diastolic BP (DBP) was recorded. Whereas in the control group an increase of 1.4 +/- 2.7 mm Hg, P = 0.59 for mean 24-h SBP and 1.2 +/- 2.8 mm Hg, P = 0.83 for mean 24-h DBP was observed. Intraplatelet Ca2+ decreased whereas intraplatelet magnesium (Mg2+) and erythrocyte K+ increased in the intervention group. Change in mean 24-h SBP in the pooled group correlated with both change in intraplatelet Ca2+ (r = 0.49, P < 0.05) and NHE-1 activity (r = 0.6, P < 0.001). The contribution of intraplatelet Ca2+ was attenuated when both parameters were entered in a multivariate regression model. CONCLUSIONS: The present study shows a weak, statistically nonsignificant trend towards association of Ca2+ supplementation on 24-h BP in hypertensive subjects with type 2 diabetes. However, our results indicated an interrelation of [Ca2+]i levels and NHE-1 activity on BP in patients with hypertension and type 2 diabetes.

Hypophosphataemic osteomalacia due to de Toni-Debre-Fanconi syndrome in a 19-year old girl.

Osteomalacia associated with adult onset Fanconi syndrome is thought to result from hypophosphataemia due to renal phosphate loss and relative 1,25-dihydroxyvitamin D3 deficiency. In this disorder, the impaired renal phosphate uptake occurs as part of a generalized tubular defect in association with other features such as bicarbonuria, glycosuria and aminoaciduria. Fanconi syndrome is either hereditary--juvenile form--or is associated with various acquired or heritable diseases. In adults, the disease is similar to the juvenile form, but osteomalacia is a prominent feature. We report a sporadic, adult onset, hypophosphataemia in a 19-year old female patient who presented after puberty complaining of bone and joint pain and difficulty in walking following a minor fall. Radiological examination revealed numerous bilateral fractures of the ribs and pelvis while biochemical investigations showed combination of high phosphate clearance, low serum bicarbonate, glycosuria and glycinuria. Known causes of acquired renal tubular dysfunction were ruled out. The patient was diagnosed as having idiopathic Fanconi syndrome and started on vitamin D3 (Alfacalcidol 1 mg/day) and oral phosphorus (Joulie Solution, 1.5 g/day), which led to resolution of symptoms and an increase in serum phosphate (from 0,54 to 0,71 mmol/l) within few months following the initiation of therapy. However, radiological re-examination showed no signs of fracture healing.