Recovery Following Peer and Text Messaging Support After Discharge From Acute Psychiatric Care in Edmonton, Alberta: Controlled Observational Study.

Background: Peer support is an emotional, social, and practical help provided by nonprofessionals to assist others in sustaining health behaviors. Peer support is valued in recovery-oriented models of mental health and is becoming increasingly implemented at the organizational level. Text messaging is a relatively low-cost, high-impact, and easily scalable program that uses existing technology, is devoid of geographic barriers, and is easily accessible to end users.

Suboptimal magnesium status in the United States: are the health consequences underestimated?

In comparison with calcium, magnesium is an "orphan nutrient" that has been studied considerably less heavily. Low magnesium intakes and blood levels have been associated with type 2 diabetes, metabolic syndrome, elevated C-reactive protein, hypertension, atherosclerotic vascular disease, sudden cardiac death, osteoporosis, migraine headache, asthma, and colon cancer. Almost half (48%) of the US population consumed less than the required amount of magnesium from food in 2005-2006, and the figure was down from 56% in 2001-2002.

Variation of trabecular architecture in proximal femur of postmenopausal women.

This investigation of microstructure in the human proximal femur probes the relationship between the parameters of the FRAX index of fracture risk and the parameters of bone microstructure. The specificity of fracture sites at the proximal femur raises the question of whether trabecular parameters are site-specific during post-menopause, before occurrence of fragility fracture. The donated proximal femurs of sixteen post-menopausal women in the sixth and seventh decades of life, free of metabolic pathologies and therapeutic interventions that could have altered the bone tissue, constituted the material of the study.

TNFalpha receptor knockout in mice reduces adverse effects of magnesium deficiency on bone.

Epidemiologic studies have linked low dietary magnesium (Mg) intake to osteoporosis. Dietary Mg restriction in animal models has demonstrated a decrease in bone mass and an increase in skeletal fragility. The exact mechanism for the decrease in bone mass is not clear but a decrease in osteoblast number and an increase in osteoclast number (Oc.

Skeletal and hormonal effects of magnesium deficiency.

Magnesium (Mg) is the second most abundant intracellular cation where it plays an important role in enzyme function and trans-membrane ion transport. Mg deficiency has been associated with a number of clinical disorders including osteoporosis. Osteoporosis is common problem accounting for 2 million fractures per year in the United States at a cost of over $17 billion dollars.

Reduction of dietary magnesium by only 50% in the rat disrupts bone and mineral metabolism.

Introduction: The objective of this study was to determine the effect of a moderate reduction of dietary magnesium [50% of nutrient requirement (50% NR)] on bone and mineral metabolism in the rat, and to explore possible mechanisms for the resultant reduced bone mass.

Methods: Female rats were 6 weeks of age at the start of study. Serum magnesium (Mg), calcium (Ca), parathyroid hormone (PTH), 1,25(OH)(2)-vitamin D, alkaline phosphatase, osteocalcin, and pyridinoline were measured during the study at 3- and 6-month time points in control (dietary Mg of 100% NR) and Mg-deficient animals (dietary Mg at 50% NR).

Immunolocalization of RANKL is increased and OPG decreased during dietary magnesium deficiency in the rat.

Background: Epidemiological studies have linked low dietary magnesium (Mg) to low bone mineral density and osteoporosis. Mg deficiency in animal models has demonstrated a reduction in bone mass and increase in skeletal fragility. One major mechanism appears to be an increase in osteoclast number and bone resorption.

Dietary magnesium reduction to 25% of nutrient requirement disrupts bone and mineral metabolism in the rat.

Low dietary magnesium (Mg) may be a risk factor for osteoporosis. In animals, severe Mg deficiency (0.04% of nutrient requirement [NR]) results in bone loss.

Magnesium deficiency in critical illness.

Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma.

Preservation of bone mineral density of the proximal femur following hemisurface arthroplasty.

Bone mineral density of the proximal femur was measured in six patients who underwent hemisurface replacement for osteonecrosis of the femoral head. Bone mineral density values in operated and contralateral nonoperated hips were compared. In four patients who had sequential examinations, bone mineral density was compared over time.

Magnesium deficiency and osteoporosis: animal and human observations.

Although osteoporosis is a major health concern for our growing population of the elderly, there continues to be a need for well-designed clinical and animal studies on the link between dietary magnesium (Mg) intake and osteoporosis. Relatively few animal studies have assessed the skeletal and hormonal impact of long-term low Mg intake; however, these studies have demonstrated that Mg deficiency results in bone loss. Potential mechanisms include a substance P-induced release of inflammatory cytokines as well as impaired production of parathyroid hormone and 1,25-dihydroxyvitamin D.

Alterations in growth plate and articular cartilage morphology are associated with reduced SOX9 localization in the magnesium-deficient rat.

Insufficient dietary magnesium (Mg) intake has been associated with low bone mass in humans,and recent basic science studies have indicated that this bone loss may be secondary to increased release of substance P and TNFc Much less is known about the effects of low Mg intake on cartilage. We have evaluated growth plate and articular cartilage in rats following a 6 month dietary Mg restriction. Histomorphometry demonstrated significantly decreased distal femur articular cartilage chondrocyte density and decreased tibial growth plate width in experimental animals compared to controls.

Alterations in osteoclast morphology following osteoprotegerin administration in the magnesium-deficient mouse.

In the present study, we used osteoprotegerin (OPG), which blocks osteoclastogenesis, to correct and thus explain the hypercalcemia that is seen during dietary Mg deficiency in the mouse. Control and Mg-deficient mice received injections for 12 days of either OPG or vehicle only. Serum Ca was similar in Mg-deficient mice treated with OPG and in control mice receiving OPG (9.

Bone loss induced by dietary magnesium reduction to 10% of the nutrient requirement in rats is associated with increased release of substance P and tumor necrosis factor-alpha.

Dietary Mg intake has been linked to osteoporosis. Previous studies have demonstrated that severe Mg deficiency [0.04% of nutrient requirement (NR)] results in osteoporosis in rodent models.

Magnesium deficiency: effect on bone mineral density in the mouse appendicular skeleton.

Background: Dietary magnesium (Mg) deficiency in the mouse perturbs bone and mineral homeostasis. The objective of the present study was to evaluate bone mineral density of the femur in control and Mg-deficient mice.

Methods: BALB/c mice aged 28 days at study initiation were maintained on a normal or Mg deficient (0.

Magnesium deficiency: effect on bone and mineral metabolism in the mouse.

Insufficient dietary magnesium (Mg) intake has been associated in humans with low bone mass. Mg deficiency in the rat has suggested bone loss is due to increased bone resorption and/or inadequate bone formation during remodeling. The purpose of this study was to assess the effect of a low Mg diet on bone and mineral metabolism in the young and mature BALB/c mouse and explore the hypothesis that inflammatory cytokines may contribute to Mg deficiency-induced osteoporosis.

Bone mineral density screening: assessment of influence on prevention and treatment of osteoporosis.

Objective: To assess the effect of bone mineral density (BMD) screening on the decision to initiate preventive or therapeutic measures for osteoporosis.

Methods: We offered low-cost BMD screening by dual-energy x-ray absorptiometry of the lumbar spine and proximal femur in conjunction with National Osteoporosis Week. In an effort to assess whether the availability of the BMD measurements resulted in any medical action by the participants of the screening, we conducted a retrospective telephone survey 9 to 12 months after the screening.

Genetic heterogeneity in familial renal magnesium wasting.

Isolated hereditary renal magnesium (Mg) wasting may result from mutations in the renal tubular epithelial cell tight junction protein paracellin-1 gene or the tubular Na(+),K(+)-ATPase gamma-subunit gene FXYD2. The FXYD2 gene mutation was discovered in two Dutch families as an autosomal dominant disorder. It is characterized by isolated renal Mg wasting with resultant symptomatic hypomagnesemia.

Beneficial antithrombotic effects of the association of pharmacological oral magnesium therapy with aspirin in coronary heart disease patients.

The use of magnesium in the treatment of acute myocardial infarction remains controversial despite preliminary experimental evidence that magnesium plays a beneficial role as a regulator of thrombosis. The aim of our study was to determine whether oral magnesium treatment inhibits platelet-dependent thrombosis (PDT) in stable patients with coronary artery disease (CAD). In a randomized prospective, double-blind, cross-over and placebo controlled study, 42 patients with stable CAD (37 men, 5 women, mean age 68 +/- 9 years) on aspirin received either magnesium oxide tablets (800-1,200 mg/day) or placebo for 3 months (Phase 1) followed by a 4-week washout period, and the cross-over treatment for 3 months (Phase 2).

Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease.

Background: Although reduced intracellular levels of magnesium have been described in patients with acute myocardial infarction, its significance as a regulator of thrombosis remains unknown.

Methods And Results: To determine whether reduced intracellular levels of magnesium enhance platelet-dependent thrombosis, we evaluated 42 patients with coronary artery disease (CAD) by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 minutes by using an ex vivo perfusion (Badimon) chamber. Baseline analysis demonstrated significant associations between intracellular levels of magnesium, platelet-dependent thrombosis (P =.

Magnesium deficiency-induced osteoporosis in the rat: uncoupling of bone formation and bone resorption.

Magnesium (Mg) intake has been linked to bone mass and/or rate of bone loss in humans. Experimental Mg deficiency in animal models has resulted in impaired bone growth, osteopenia, and increased skeletal fragility. In order to assess changes in bone and mineral homeostasis that may be responsible, we induced dietary Mg deficiency in adult Simonsen albino rats for 16 weeks.

Oral magnesium supplementation inhibits platelet-dependent thrombosis in patients with coronary artery disease.

The use of magnesium in the treatment of acute myocardial infarction remains controversial despite preliminary experimental evidence that magnesium plays a beneficial role as a regulator of thrombosis. This study examines whether oral magnesium treatment inhibits platelet-dependent thrombosis (PDT) in patients with coronary artery disease (CAD). In a randomized prospective, double-blind, crossover, and placebo-controlled study, 42 patients with CAD (37 men, 5 women, mean age 68 +/- 9 years) on aspirin received either magnesium oxide tablets (800 to 1,200 mg/day) or placebo for 3 months (phase 1) followed by a 4-week wash-out period, and the crossover treatment for 3 months (phase 2).

Combined effect of vitamin D3 analogs and paclitaxel on the growth of MCF-7 breast cancer cells in vivo.

Vitamin D3 analogs and paclitaxel (Taxol) are able to inhibit the in vitro growth of a variety of malignant cells including breast cancer cells. These two compounds decrease growth by different mechanisms and they have nonoverlapping toxicities. We examined the abilities of three vitamin D3 compounds to inhibit growth of a human mammary cancer (MCF-7) in BNX triple immunodeficient mice either alone or with Taxol.

Intracellular magnesium predicts functional capacity in patients with coronary artery disease.

To determine whether increased intracellular levels of magnesium ([Mg]i) are associated with enhanced functional capacity, we performed symptom-limited exercise treadmill testing on 42 stable coronary artery disease (CAD) patients (37 men, 5 women, mean age 68 +/- 9 years). [Mg]i was found to be an independent and significant predictor of exercise duration (R = 0.31, p = 0.