Effects of low-fat dairy intake on blood pressure, endothelial function, and lipoprotein lipids in subjects with prehypertension or stage 1 hypertension.

Objective: This randomized crossover trial assessed the effects of 5 weeks of consuming low-fat dairy (one serving/day each of 1% fluid milk, low-fat cheese, and low-fat yogurt) versus nondairy products (one serving/day each of apple juice, pretzels, and cereal bar) on systolic and diastolic blood pressures (SBP and DBP), vascular function (reactive hyperemia index [RHI] and augmentation index), and plasma lipids.

Methods: Patients were 62 men and women (mean age 54.5 years, body mass index 29.

Phospholipase Cε hydrolyzes perinuclear phosphatidylinositol 4-phosphate to regulate cardiac hypertrophy.

Phospholipase Cε (PLCε) is a multifunctional enzyme implicated in cardiovascular, pancreatic, and inflammatory functions. Here we show that conditional deletion of PLCε in mouse cardiac myocytes protects from stress-induced pathological hypertrophy. PLCε small interfering RNA (siRNA) in ventricular myocytes decreases endothelin-1 (ET-1)-dependent elevation of nuclear calcium and activation of nuclear protein kinase D (PKD).

Dairy and blood pressure: a fresh look at the evidence.

The Dietary Guidelines for Americans, 2010 indicated there is moderate evidence for an association between the consumption of dairy foods and lower blood pressure in adults; however, it also stated that more evidence was needed, especially in clinical trials, to fully delineate a causal relationship. The purpose of this review is to provide background by examining the historical literature and the evidence reviewed by the 2010 Dietary Guidelines Advisory Committee, to examine the gaps in knowledge indicated by that committee, and to determine if recently published evidence is sufficient to elucidate or dismiss an association between dairy foods and blood pressure maintenance. Examination of the newly published literature, together with evaluation of the evidence as a whole, shows that the preponderance of evidence indicates dairy foods are beneficially associated with blood pressure; however, additional research is necessary to identify the mechanism of action of dairy foods.

The association between dairy product consumption and cognitive function in the National Health and Nutrition Examination Survey.

The present cross-sectional study sought to determine the potential relationships between the intake of dairy foods (total dairy products, milk and cheese) and cognitive function through information garnered in the National Health and Nutrition Examination Surveys (1988-94 and 1999-2002). Cognitive measures of vasomotor speed, coding speed and immediate memory recall were assessed from a simple reaction time task (SRTT), symbol-digit substitution test (SDST) and serial digit learning task, respectively, in adults 20-59 years of age. A summation of the percentile rank scores on each of the three tests provided a measure of overall cognitive function.

Vitamin D intake and status are associated with lower prevalence of metabolic syndrome in U.S. adults: National Health and Nutrition Examination Surveys 2003-2006.

Background: Previous reports have shown that metabolic syndrome and some metabolic syndrome components are associated with serum 25-hydroxyvitamin D [25(OH)D].

Methods: Using the National Health and Nutrition Examination Surveys (NHANES), 2003-2006, we evaluated the associations of vitamin D intake (n=3543) and vitamin D status [25(OH)D; n=3529], with the prevalence of metabolic syndrome and its components in adults 20 years and older. Exclusion criteria included nonfasted subjects, those pregnant and/or lactating, and, for intake analyses, those with unreliable 24-h recall records.

Influence of dairy product and milk fat consumption on cardiovascular disease risk: a review of the evidence.

Although evidence has linked the consumption of saturated fat (SF) to increased LDL levels and an increased risk of the development of cardiovascular disease (CVD), recent findings have indicated that the link between CVD and SF may be less straightforward than originally thought. This may be due to the fact that some food sources high in SF contain an array of saturated and unsaturated fatty acids, each of which may differentially affect lipoprotein metabolism, as well as contribute significant amounts of other nutrients, which may alter CVD risk. The purpose of this review is to examine the published research on the relationship between milk fat containing dairy foods and cardiovascular health.

Tumor necrosis factor-alpha mediated signaling in neuronal homeostasis and dysfunction.

Tumor necrosis factor-alpha (TNF-alpha) is a potent pro-inflammatory molecule, which upon engagement with its cognate receptors on target cells, triggers downstream signaling cascades that control a number of cellular processes related to cell viability, gene expression, ion homeostasis, and synaptic integrity. In the central nervous system (CNS), TNF-alpha is produced by brain-resident astrocytes, microglia, and neurons in response to numerous intrinsic and extrinsic stimuli. This review will summarize the key events that lead to TNF-alpha elaboration in the CNS, and the effects that these inflammatory signals impart on neuronal signaling in the context of homeostasis and neuropathology.

Impaired TNF-alpha control of IP3R-mediated Ca2+ release in Alzheimer's disease mouse neurons.

The misguided control of inflammatory signaling has been previously implicated in the pathogenesis of several neurological disorders, including Alzheimer's disease (AD). Induction of tumor necrosis factor-alpha (TNF-alpha), a central mediator of neuroinflammation, occurs commensurate with the onset of early disease in 3xTg-AD mice, which develop both amyloid plaque and neurofibrillary tangle pathologies in an age- and region-dependent pattern. Herein, we describe regulation inherent to 3xTg-AD neurons, which results in the loss of TNF-alpha mediated enhancement of inositol 1,4,5 trisphosphate (IP3R)-mediated Ca2+ release.

Tumor necrosis factor-alpha-mediated regulation of the inositol 1,4,5-trisphosphate receptor promoter.

Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, has been implicated as a central mediator in multiple homeostatic and pathologic processes. Signaling cascades downstream of its cellular cognate receptors, as well as the resultant transcriptional responses have received intense interest in regards to how such signals impact cellular physiology. Notably, TNF-alpha was shown to potentiate neuronal Ca(2+) signaling by enhancing type-1 inositol 1,4,5-trisphosphate receptor (IP(3)R) steady-state mRNA levels.

Chronic neuron-specific tumor necrosis factor-alpha expression enhances the local inflammatory environment ultimately leading to neuronal death in 3xTg-AD mice.

Inflammatory mediators, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta, appear integral in initiating and/or propagating Alzheimer's disease (AD)-associated pathogenesis. We have previously observed a significant increase in the number of mRNA transcripts encoding the pro-inflammatory cytokine TNF-alpha, which correlated to regionally enhanced microglial activation in the brains of triple transgenic mice (3xTg-AD) before the onset of overt amyloid pathology. In this study, we reveal that neurons serve as significant sources of TNF-alpha in 3xTg-AD mice.

Tumor necrosis factor-alpha potentiates intraneuronal Ca2+ signaling via regulation of the inositol 1,4,5-trisphosphate receptor.

Inflammatory events have long been implicated in initiating and/or propagating the pathophysiology associated with a number of neurological diseases. In addition, defects in Ca2+-handling processes, which shape membrane potential, influence gene transcription, and affect neuronal spiking patterns, have also been implicated in disease progression and cognitive decline. The mechanisms underlying the purported interplay that exists between neuroinflammation and Ca2+ homeostasis have yet to be defined.