Week and weekend day cadence patterns long-term post-bariatric surgery

Obesity can negatively influence walking cadence, reducing the overall intensity of daily activities and increasing the risk of weight gain. Purpose: Objectively describe the walking cadence of individuals’ long-term post-bariatric surgery. Methods: Fifty-eight participants, 51.2 ± 8.9 years old, with a BMI of 34.6 ± 10.1 kg/m2, 10.0 ± 3.1 years post-surgery wore an activPAL accelerometer for 7 consecutive days. Data was analyzed using participants’ current BMI, dichotomized by obesity status, < or ≥ 30 kg/m2. Results: On average, participants walked 5124 ± 2549 steps/day on weekdays and 6097 ± 2786 steps/day on weekend days (p = .003). Participants spent the majority (75%) of their daily steps at a slow-walking average cadence (non-obese: week = 65.3 ± 5.0 steps/min and weekend = 63.8 ± 6.7 steps/min; obese: week = 67.8 ± 8.2 steps/min and weekend = 63.3 ± 6.9 steps/min), with no difference between groups for week or weekend days (p = .153 and .774). The cadence of participants with obesity was significantly lower on weekends compared to weekdays for walking events > 30 s (p = .002) and > 60 s (p = .008) in duration. Weekday cadence of participants without obesity was similar to weekend day cadence across all walking event durations. The majority of walking events occurred below 30 s in duration for all participants. Conclusions: Long-term post-bariatric surgery, movement occurs in short duration bouts at a slow-walking cadence for the majority of movement. Individuals without obesity had similar movement patterns from week to weekend days while participants with obesity significantly lowered their cadence on weekend days

Long lasting pain hypersensitivity following ligation of the tendon of the masseter muscle in rats: A model of myogenic orofacial pain

<p>Abstract</p> <p>Background</p> <p>A major subgroup of patients with temporomandibular joint (TMJ) disorders have masticatory muscle hypersensitivity. To study myofacial temporomandibular pain, a number of preclinical models have been developed to induce myogenic pain of the masseter muscle, one of the four muscles involved in mastication. The currently used models, however, generate pain that decreases over time and only lasts from hours to weeks and hence are not suitable for studying chronicity of the myogenic pain in TMJ disorders. Here we report a model of constant myogenic orofacial pain that lasts for months.</p> <p>Results</p> <p>The model involves unilateral ligation of the tendon of the anterior superficial part of the rat masseter muscle (TASM). The ligation of the TASM was achieved with two chromic gut (4.0) ligatures via an intraoral approach. Nocifensive behavior of the rat was assessed by probing the skin site above the TASM with a series of von Frey filaments. The response frequencies were determined and an EF₅₀value, defined as the von Frey filament force that produces a 50% response frequency, was derived and used as a measure of mechanical sensitivity. Following TASM ligation, the EF₅₀of the injured side was significantly reduced and maintained throughout the 8-week observation period, suggesting the presence of mechanical hyperalgesia/allodynia. In sham-operated rats, the EF₅₀of the injured side was transiently reduced for about a week, likely due to injury produced by the surgery. Somatotopically relevant Fos protein expression was indentified in the subnucleus caudalis of the spinal trigeminal sensory complex. In the same region, persistent upregulation of NMDA receptor NR1 phosphorylation and protein expression and increased expression of glial markers glial fibrillary acidic protein (astroglia) and CD11b (microglia) were found. Morphine (0.4-8 mg/kg, s.c.) and duloxetine (0.4-20 mg/kg, i.p.), a selective serotonin-norepinephrine reuptake inhibitor, produced dose-dependent attenuation of hyperalgesia.</p> <p>Conclusions</p> <p>Ligation injury of the TASM in rats led to long-lasting and constant mechanical hypersensitivity of myogenic origin. The model will be particularly useful in studying the chronicity of myogenic pain TMJ disorders. The model can also be adapted to other regions of the body for studying pathology of painful tendinopathy seen in sports injury, muscle overuse, and rheumatoid arthritis.</p

The lower mass function of the young open cluster Blanco 1: from 30 Mjup to 3 Mo

We performed a deep wide field optical survey of the young (~100-150 Myr) open cluster Blanco1 to study its low mass population well down into the brown dwarf regime and estimate its mass function over the whole cluster mass range.The survey covers 2.3 square degrees in the I and z-bands down to I ~ z ~ 24 with the CFH12K camera. Considering two different cluster ages (100 and 150 Myr), we selected cluster member candidates on the basis of their location in the (I,I-z) CMD relative to the isochrones, and estimated the contamination by foreground late-type field dwarfs using statistical arguments, infrared photometry and low-resolution optical spectroscopy. We find that our survey should contain about 57% of the cluster members in the 0.03-0.6 Mo mass range, including 30-40 brown dwarfs. The candidate's radial distribution presents evidence that mass segregation has already occured in the cluster. We took it into account to estimate the cluster mass function across the stellar/substellar boundary. We find that, between 0.03Mo and 0.6Mo, the cluster mass distribution does not depend much on its exact age, and is well represented by a single power-law, with an index alpha=0.69 +/- 0.15. Over the whole mass domain, from 0.03Mo to 3Mo, the mass function is better fitted by a log-normal function with m0=0.36 +/- 0.07Mo and sigma=0.58 +/- 0.06. Comparison between the Blanco1 mass function, other young open clusters' MF, and the galactic disc MF suggests that the IMF, from the substellar domain to the higher mass part, does not depend much on initial conditions. We discuss the implications of this result on theories developed to date to explain the origin of the mass distribution.Comment: 18 pages, 15 figures and 5 tables accepted in A&

A Simple Iterative Model Accurately Captures Complex Trapline Formation by Bumblebees Across Spatial Scales and Flower Arrangements

PMCID: PMC3591286This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Phenotypic and molecular assessment of seven patients with 6p25 deletion syndrome: Relevance to ocular dysgenesis and hearing impairment

BACKGROUND: Thirty-nine patients have been described with deletions involving chromosome 6p25. However, relatively few of these deletions have had molecular characterization. Common phenotypes of 6p25 deletion syndrome patients include hydrocephalus, hearing loss, and ocular, craniofacial, skeletal, cardiac, and renal malformations. Molecular characterization of deletions can identify genes that are responsible for these phenotypes. METHODS: We report the clinical phenotype of seven patients with terminal deletions of chromosome 6p25 and compare them to previously reported patients. Molecular characterization of the deletions was performed using polymorphic marker analysis to determine the extents of the deletions in these seven 6p25 deletion syndrome patients. RESULTS: Our results, and previous data, show that ocular dysgenesis and hearing impairment are the two most highly penetrant phenotypes of the 6p25 deletion syndrome. While deletion of the forkhead box C1 gene (FOXC1) probably underlies the ocular dysgenesis, no gene in this region is known to be involved in hearing impairment. CONCLUSIONS: Ocular dysgenesis and hearing impairment are the two most common phenotypes of 6p25 deletion syndrome. We conclude that a locus for dominant hearing loss is present at 6p25 and that this locus is restricted to a region distal to D6S1617. Molecular characterization of more 6p25 deletion patients will aid in refinement of this locus and the identification of a gene involved in dominant hearing loss