Achilles tendon assessment on quantitative MRI: Sources of variability and relationships to tendinopathy.

Quantitative MRI (qMRI) measures are useful in assessing musculoskeletal tissues, but application to tendon has been limited. The purposes of this study were to optimize, identify sources of variability, and establish reproducibility of qMRI to assess Achilles tendon. Additionally, preliminarily estimates of effect of tendon pathology on qMRI metrics and structure-function relationships between qMRI measures and ankle performance were examined.

Quantative MRI predicts tendon mechanical behavior, collagen composition, and organization.

Quantitative magnetic resonance imaging (qMRI) measures have provided insights into the composition, quality, and structure-function of musculoskeletal tissues. Low signal-to-noise ratio has limited application to tendon. Advances in scanning sequences and sample positioning have improved signal from tendon allowing for evaluation of structure and function.

Rehabilitation for Children With Dystonic Cerebral Palsy Using Haptic Feedback in Virtual Reality: Protocol for a Randomized Controlled Trial.

Background: Cerebral palsy (CP) is the most common developmental motor disorder in children. Individuals with CP demonstrate abnormal muscle tone and motor control. Within the population of children with CP, between 4% and 17% present dystonic symptoms that may manifest as large errors in movement tasks, high variability in movement trajectories, and undesired movements at rest.

Dance and rehabilitation in cerebral palsy: a systematic search and review.

Aim: To conduct a review of research literature on the use of dance and movement with music (rhythmic auditory stimulation [RAS]) in the neurorehabilitation of children and adults with cerebral palsy (CP).

Method: We conducted a systematic search and quality appraisal of the research literature on dance and RAS in CP. Additionally, we linked the research outcomes to the International Classification of Functioning, Disability and Health (ICF) framework.

Tissue bioavailability of anthocyanins from whole tart cherry in healthy rats.

Our aim was to confirm and identify the presence of tart cherry anthocyanins in several target tissues of healthy rats. Liquid chromatography-mass spectrometry analysis was employed for detection and characterisation of anthocyanin metabolites. It was shown that four native anthocyanins, namely cyanidin 3-glucosylrutinoside, cyanidin 3-rutinoside, cyanidin 3-rutinoside 5-β-D-glucoside, and peonidin 3-rutinoside were differentially distributed among targeted tissues of rats.

Differential effects of opioid peptides on myocardial ischemic tolerance.

Background: Opioid peptides, which can induce mammalian hibernation, may provide protection against subcellular and molecular changes during hypothermic myocardial ischemia. This study examined the differential effects of the three known myocyte opioid receptors, Mu (micro), Delta (delta), and Kappa (kappa), in augmenting myocardial ischemic tolerance.

Methods: Control hearts (CH) were compared to hearts pretreated with either the micro-agonist, fentanyl, the delta-agonist, DADLE, or delta-antagonist, NTB, or the kappa-agonist, U50488H (U50), or kappa-antagonist, nor-BNI.

Relative contribution of endogenous opioids to myocardial ischemic tolerance.

Background: Opioid preconditioning by exogenous opioids experimentally protects the myocardium against ischemia/reflow injury. Additionally, endogenous opioid peptides released during ischemia also enhance ischemic tolerance. Promiscuous opioid receptor agonists conceal the differential contribution of the mu, delta, and kappa opioid subtypes.

Prolonged lipopolysaccharide inhibits leukotriene synthesis in peritoneal macrophages: mediation by nitric oxide and prostaglandins.

Resident rat peritoneal macrophages synthesize a variety of prostanoids and leukotrienes from arachidonic acid. Overnight treatment with lipopolysaccharide (LPS) induces the synthesis of cyclooxygenase-2 (COX-2) and an altered prostanoid profile that emphasizes the preferential conversion of arachidonic acid to prostacyclin and prostaglandin E2. In these studies, we report that exposure to LPS also caused a strong suppression of 5-lipoxygenase but not 12-lipoxygenase activity, indicated by the inhibition of synthesis of both leukotriene B4 and 5-hydroxyeicosatetraenoic acid (5-HETE), but not of 12-HETE.

Evaluation of phagocytosis and arachidonate metabolism by alveolar macrophages and recruited neutrophils from F344xBN rats of different ages.

The incidence of infectious respiratory diseases increases with aging. Resident alveolar macrophages (AMs) and recruited leukocytes (PMNL) mediate cellular defense against bacterial infections in the lung, and phagocytosis and lipid mediator synthesis are important components of their antimicrobial capacity. The objective of this study was to determine if either phagocytic capacity or lipid mediator generation declines with normal aging, in either AMs or PMNL recruited to a site of inflammation.

Co-localization of leukotriene a4 hydrolase with 5-lipoxygenase in nuclei of alveolar macrophages and rat basophilic leukemia cells but not neutrophils.

The synthesis of leukotriene B(4) from arachidonic acid requires the sequential action of two enzymes: 5-lipoxygenase and leukotriene A(4) hydrolase. 5-Lipoxygenase is known to be present in the cytoplasm of some leukocytes and able to accumulate in the nucleoplasm of others. In this study, we asked if leukotriene A(4) hydrolase co-localizes with 5-lipoxygenase in different types of leukocytes.

Arachidonic acid is preferentially metabolized by cyclooxygenase-2 to prostacyclin and prostaglandin E2.

The two cyclooxygenase isoforms, cyclooxygenase-1 and cyclooxygenase-2, both metabolize arachidonic acid to prostaglandin H2, which is subsequently processed by downstream enzymes to the various prostanoids. In the present study, we asked if the two isoforms differ in the profile of prostanoids that ultimately arise from their action on arachidonic acid. Resident peritoneal macrophages contained only cyclooxygenase-1 and synthesized (from either endogenous or exogenous arachidonic acid) a balance of four major prostanoids: prostacyclin, thromboxane A2, prostaglandin D2, and 12-hydroxyheptadecatrienoic acid.

Capacity for repeatable leukotriene generation after transient stimulation of mast cells and macrophages.

Leukotriene (LT) synthesis is initiated by the enzyme 5-lipoxygenase (5-LO). Prolonged cell stimulation causes the translocation of 5-LO to the nuclear envelope and the synthesis of LT, with subsequent inactivation and persistent membrane association of 5-LO. In this study, we examined whether persistent membrane association of 5-LO, as well as the inactivation of 5-LO, could be prevented by shortening the length of cell stimulation or by blocking LT synthesis.

Rapid import of cytosolic 5-lipoxygenase into the nucleus of neutrophils after in vivo recruitment and in vitro adherence.

5-Lipoxygenase catalyzes the synthesis of leukotrienes from arachidonic acid. The subcellular distribution of 5-lipoxygenase is known to be cell type-dependent and is cytosolic in blood neutrophils. In this study, we asked whether neutrophil recruitment into sites of inflammation can alter the subcellular compartmentation of 5-lipoxygenase.

Colchicine inhibits arachidonate release and 5-lipoxygenase action in alveolar macrophages.

Although colchicine is known to inhibit leukotriene synthesis in neutrophils, its effect on other aspects of arachidonic acid (AA) metabolism as well as its mechanism of action are unknown. To address these questions, we investigated the effects of colchicine on resident rat alveolar macrophages (AM), cells that generate a variety of lipoxygenase and cyclooxygenase products after stimulation. Pretreatment of AM with 10 microM colchicine for 1 h dramatically inhibited the synthesis of all 5-lipoxygenase (5-LO) metabolites from endogenous AA in ionophore A-23187-stimulated cells.

Effects of granulocyte-macrophage colony-stimulating factor on eicosanoid production by mononuclear phagocytes.

Granulocyte-macrophage CSF (GM-CSF) primes granulocytes for leukotriene (LT) synthesis. Here, we examined the effects of GM-CSF on arachidonic acid (AA) metabolism in rat alveolar macrophages (AM), peritoneal macrophages, and human peripheral blood monocytes. Pretreatment of AMs with GM-CSF for 24 h significantly increased the synthesis of immunoreactive LTB4 upon subsequent stimulation with calcium ionophore.

Translocation and leukotriene synthetic capacity of nuclear 5-lipoxygenase in rat basophilic leukemia cells and alveolar macrophages.

Leukotriene (LT) synthesis involves the translocation of enzymatically active 5-lipoxygenase (5-LO) from a soluble site to a bound site, where it interacts with 5-lipoxygenase-activating protein (FLAP). In human polymorphonuclear leukocytes (PMNs), 5-LO moves from the cytosol to the nuclear envelope (NE) to interact with FLAP. However, 5-LO has recently been found within the nucleus, as well as the cytosol, of rat basophilic leukemia (RBL) cells and alveolar macrophages (AMs).

Redistribution of 5-lipoxygenase and cytosolic phospholipase A2 to the nuclear fraction upon macrophage activation.

Both the cytosolic phospholipase A2 and 5-lipoxygenase enzymes redistribute from the high-speed supernatant to a particulate fraction upon cell activation with associated leukotriene synthesis, but the subcellular site to which these enzymes translocate is not known. In this study, we disrupted resting and ionophore A23187-stimulated rat peritoneal macrophages by N2 cavitation and separated lysates into nuclear, cytosolic, and crude membrane fractions; these were then examined by immunoblot analysis for their contents of immunoreactive cytosolic phospholipase A2, 5-lipoxygenase, and 5-lipoxygenase activating protein. 5-Lipoxygenase activating protein was localized predominantly in the nuclear fraction of both resting and activated cells, while both cytosolic phospholipase A2 and 5-lipoxygenase redistributed from the cytosol fraction in resting cells to the nuclear fraction in activated cells.

Basal activation of protein kinase C in rat alveolar macrophages: implications for arachidonate metabolism.

Alveolar macrophages (AM) exhibit numerous functional differences from other mononuclear phagocyte populations, even though they are derived from a common circulating monocytic precursor. Yet no differences in fundamental signaling mechanisms uniquely expressed by AM have been elucidated to date. Protein kinase C (PKC) is one signal transduction mechanism thought to have an important role in regulating macrophage function and about which little information exists for AM.

Diminished protein kinase C-activated arachidonate metabolism accompanies rat macrophage differentiation in the lung.

Alveolar macrophages (AM) differ from other macrophage (m phi) populations in their profile of eicosanoids synthesized from arachidonic acid (AA)3. Little information is available regarding possible differences in the regulation of AA metabolism among various m phi populations. In our study, we compared the ability of cultured resident rat AM and peritoneal m phi (PM) to release and metabolize AA in response to exogenous activators of protein kinase C (PKC).

Alterations in the pattern of arachidonate metabolism accompany rat macrophage differentiation in the lung.

The present study was undertaken to investigate the changes in arachidonic acid (AA) metabolism which accompany rat macrophage (m phi) differentiation in the lung in order to determine whether these changes occur in the alveolar space or in the pulmonary interstitium, as well as the mechanisms responsible for such changes. Metabolism of endogenous and exogenous AA by cultured m phi obtained from the peritoneum (PM), the pulmonary interstitium (IM), and the alveolar spaces (AM) was examined by using HPLC and RIA. Although PM and AM released similar amounts of endogenous AA in response to both ionophore A23187 and the particulate zymosan, PM metabolized AA predominantly to cyclooxygenase (CO) products, whereas AM produced predominantly 5-lypoxygenase (5-LO) metabolites.

Acute nephrotoxicities and hepatotoxicities of 1,2-dibromo-3-chloropropane and 1,2-dibromoethane in male and female F344 rats.

Four consecutive intraperitoneal (i.p.) injections with 40 mg/kg of 1,2-dibromo-3-chloropropane (DBCP) reduced the in vitro accumulation of p-aminohippurate (PAH) and tetraethylammonium (TEA) by slices of renal cortex and increased blood urea nitrogen (BUN) concentration in both male and female rats, but elevated serum glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) activities in females only.