P ostural misalignment of head on trunk (e.g., forward head posture) is associated with complaints of pain in the neck and shoulder region 1-5 and temporomandibular joint dysfunction 6,7 , but is also observed in asymptomatic individuals 8-10 . Attempts to correct this misalignment towards an ideal posture using a combination of strengthening, stretching, and behavioral/biofeedback training represent a significant component of the physical intervention provided to clients with painful neck and/or Abstract: Forward head posture (FHP) is most often described as excessive anterior positioning of the head in relation to a vertical reference line, involving increased cervical spine lordosis (head forward, middle cervical spine extended, lower cervical spine flexed) and rounded shoulders with thoracic kyphosis. Although exercise is routinely used to improve FHP, relatively little data exists on efficacy. The present study was designed to examine the impact of a 10-week targeted and progressive home exercise program on improving FHP. As improvement through exercise of postural alignment depends upon participants adhering to the program, we also looked at issues related to exercise compliance. Seventeen control (C) and 23 exercise (E) participants with a FHP deviation were part of this program. Pre-and post-exercise postural measurements of FHP were obtained from the sagittal plane using the Biotonix TM Postural Analysis System; in addition neck flexion range of motion was measured. Participants were randomly assigned to C or E groups. The E group performed neck extensor and pectoralis major stretches and deep neck flexor and shoulder retractor strengthening exercises for the 10-week period. Two-factor (group, pre-test/post-test) analysis of variance models were used to test main effects and interactions. There were no significant differences (p>0.05) between groups on any pre-test measure. For the E group, there were significant differences and interactions (p<0.05) between pre-and post-tests and also between the E and C groups at post-test for range of motion and one postural measurement. The results demonstrate that a short, home-based targeted exercise program can improve postural alignment related to FHP. These results provide a foundation for further development of postural improvement programs that include an exercise component.
Wasting of lean tissue as a consequence of metabolic acidosis is a serious problem in patients with chronic renal failure. A possible contributor is inhibition by low pH of the System A (SNAT2) transporter, which carries the amino acid L-glutamine (L-Gln) into muscle cells. The aim of this study was to determine the effect of selective SNAT2 inhibition on intracellular amino acid profiles and amino acid-dependent signaling through mammalian target of rapamycin in L6 skeletal muscle cells. Inhibition of SNAT2 with the selective competitive substrate methylaminoisobutyrate, metabolic acidosis (pH 7.1), or silencing SNAT2 expression with small interfering RNA all depleted intracellular L-Gln. SNAT2 inhibition also indirectly depleted other amino acids whose intracellular concentrations are maintained by the L-Gln gradient across the plasma membrane, notably the anabolic amino acid L-leucine. Consequently, SNAT2 inhibition strongly impaired signaling through mammalian target of rapamycin to ribosomal protein S6 kinase, ribosomal protein S6, and 4E-BP1, leading to impairment of protein synthesis comparable with that induced by rapamycin. It is concluded that even though SNAT2 is only one of several L-Gln transporters in muscle, it may determine intracellular anabolic amino acid levels, regulating the amino acid signaling that affects protein mass, nucleotide/nucleic acid metabolism, and cell growth.
This study examined the role of pain catastrophizing, fear of movement and depression as determinants of repetition-induced summation of activity-related pain. The sample consisted of 90 (44 women and 46 men) work-disabled individuals with chronic low back pain. Participants were asked to lift a series of 18 canisters that varied according to weight (2.9kg, 3.4kg, 3.9kg) and distance from the body. The canisters were arranged in a 3x6 matrix and the weights were distributed such that each 'column' of three canisters was equated in terms of physical demands. Participants rated their pain after each lift, and in a separate trial, estimated the weight of each canister. Mean activity-related pain ratings were computed for each Column of the task. An index of repetition-induced summation of pain was derived as the change in pain ratings across the six 'columns' of the task. Pain catastrophizing, fear of movement and depression were significantly correlated with condition-related pain (e.g., MPQ) and activity-related pain ratings. Women rated their pain as more intense than men, and estimated weights to be greater than men. A repetition-induced summation of pain effect was observed where pain ratings increased as participants lifted successive canisters. Fear of movement, but not pain catastrophizing or depression, was associated with greater repetition-induced summation of pain. The findings point to possible neurophysiological mechanisms that could help explain why fear of pain is a robust predictor of pain-related disability. Mechanisms of repetition-induced summation of activity-related pain are discussed.
The similarity of changes in response to MeAIB and acid implies that these share a common intracellular signalling pathway triggered by inhibition of System A. Even though System A is only a minor contributor to total Gln influx in L6 cells, it is suggested that blockade of System A with acid or MeAIB induces a catabolic state by denying Gln access to a key intracellular regulatory site.
Indoleamine 2,3-dioxygenase (IDO) is the first enzyme in the kynurenine pathway. The kynurenines formed in this pathway chemically modify proteins and cause apoptosis in cells. Evidence suggests that kynurenines and their protein modifications are involved in cataract formation, but this has yet to be directly demonstrated. We generated transgenic mouse lines (Tg) that overexpress human IDO in the lens. Homozygous Tg (homTg) lenses had higher IDO immunoreactivity, ~4.5 times greater IDO mRNA, and ~8 times higher IDO activity compared to lenses from hemizygous Tg animals (hemTg). The kynurenine content was 3-fold higher in homTg than hemTg but was not detected in Wt lenses. Kynurenine-modifications were ~2.6 times greater in homTg than hemTg or Wt. HomTg lenses had vacuoles in the epithelium and cortical fiber cells. Kynurenine-modifications coincided with apoptosis in the secondary fiber cells of homTg lenses. Caspase-3 and -9 activities were markedly higher in homTg than in hemTg and Wt. The GSH content was ~36% lower in homTg compared to hemTg and Wt lenses. HomTg animals also developed bilateral cataracts within 3 months of birth. Together these data demonstrate that IDO-mediated production of kynurenines results in defects in fiber cell differentiation and their apoptosis and suggest that IDO activity is kept low in the lens to prevent deleterious effects by kynurenines.
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