## Σάββατο, 9 Ιουλίου 2016

### Purpose

The purposes of this experiment were to, first, document the effect of 45-kg thoracic loading on peak exercise responses and, second, the effects of systematic increases in thoracic load on physiological responses to submaximal treadmill walking at a standardized speed and grade.

### Methods

On separate days, 19 males (age 27 ± 5 years, height 180.0 ± 7.4 cm, mass 86.9 ± 15.1 kg) completed randomly ordered graded exercise tests to exhaustion in loaded (45 kg) and unloaded conditions. On a third day, each subject completed four randomly ordered, 10-min bouts of treadmill walking at 1.34 m s−1 and 4 % grade in the following conditions: unloaded, and with backpacks weighted to 15, 30, and 45 kg.

### Results

With 45-kg thoracic loading, absolute oxygen consumption ( $$\dot{V}{\text{O}}_{2}$$ ), minute ventilation, power output, and test duration were significantly decreased at peak exercise. End-inspiratory lung volume and tidal volume were significantly reduced with no changes in end-expiratory lung volume, breathing frequency, and the respiratory exchange ratio. Peak end-tidal carbon dioxide and the ratio of alveolar ventilation to carbon dioxide production were similar between conditions. The reductions in peak physiological responses were greater than expected based on previous research with lighter loads. During submaximal treadmill exercise, $$\dot{V}{\text{O}}_{2}$$ increased (P < 0.05) by 11.0 (unloaded to 15 kg), 14.5 (15–30 kg), and 18.0 % (30–45 kg) showing that the increase in exercise $$\dot{V}{\text{O}}_{2}$$ was not proportional to load mass.

### Conclusion

These results provide further insight into the specificity of physiological responses to different types of load carriage.

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### Academy News – July PM&R Journal

As the primary medical society for the specialty of PM&R, your Academy is focused on moving the specialty and you forward. Academy membership supports initiatives to assist our members with:

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### Spanish Translated Abstracts

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### Ethical, Legal, and Medical Challenges When a Patient Refuses a Transfer From Rehabilitation to Acute Medical Services

I have asked Preya S. Tarsney, JD, to guest edit this Ethical/Legal column on a specific type of informed refusal in the rehabilitation context. Ms Tarsney started her legal career in litigation and health law, and then specialized in clinical medical ethics, completing a postdoctoral fellowship at the University of Chicago's MacLean Center for Clinical Medical Ethics. She is currently a Bioethicist in the Donnelley Ethics Program of the Rehabilitation Institute of Chicago, a Lecturer in physical medicine and rehabilitation (PM&R) at Northwestern University Feinberg School of Medicine, and a Faculty Lecturer at the University of Chicago.

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### Driving Under the Influence of Opioids

A 45-year-old man presents to your clinic as a new patient. His medical history is negative; however, his surgical history reveals a history of an L4-S1 posterior decompression and fusion that was performed 5 years earlier. The fusion was performed for a well-established chronic left-sided L5 and S1 lumbar radiculopathy. The patient's low back pain and left lower extremity pain improved for 3 months and then returned to his presurgical level of 7/10. Postsurgical magnetic resonance imaging shows stable fusion structure without evidence of new disk herniations, with scar tissue surrounding the left-sided L5 and S1 nerve roots.

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### Abstract

The plant-specific expansin proteins constitute an ancient and major gene family known to have roles in regulating diverse biological processes in plants. Although the functions of many expansin genes have been identified in wheat and other species, little is known about the evolution and genomic locations of the expansin genes in wheat (Triticum aestivum). In this study, a total of 87 expansin genes were identified in the wheat genome, including 52 EXPAs, 42 EXPBs and 4 EXLAs. The EXLB gene was not found in the wheat genome. Phylogenetic tree and comparative analysis revealed amplification of the EXPBs in rice, maize and wheat. The predicted wheat expansins were distributed across 14 of 21 chromosomes with different densities, 3 tightly co-located clusters and 15 paralogous pairs, indicating that tandem duplication and segmental duplication events also played roles in the evolution of expansins in wheat. In addition, the gene structures and conserved protein domains of wheat expansins suggest high levels of conservation within the phylogenetic subgroups. Analysis of a published microarray database showed that most wheat expansin genes exhibit different expression levels in different tissues and developmental stages. To our knowledge, this is the first report of a genome-wide analysis of the wheat expansin gene family, which should provide valuable information for further elucidating the classification and putative functions of the entire gene family.

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### In memoriam: Professor Irena Hausmanowa-Petrusewicz (1917–2015)

Professor Irena Hausmanowa-Petrusewicz, one of the most distinguished Polish neurologists, a leader in the field of neuromuscular diseases and electromyography whose contribution was well recognized in international neurological society, passed away on July 7th, 2015.

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### Impact of Cognition on Burn Inpatient Rehabilitation Outcomes

A significant proportion of burn injury patients are admitted to inpatient rehabilitation facilities (IRFs). There is increasing interest in the use of functional variables, such as cognition, in predicting IRF outcomes. Cognitive impairment is an important cause of disability in the burn injury population, yet its relationship to IRF outcomes has not been studied.

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### Comparing the Course of Mental Health over the First Year after Stroke with Healthy Controls in Colombia, South America

Stroke is a primary cause of death and disability in upper-middle income countries such as Colombia. Given the lack of comprehensive rehabilitation for stroke patients in Colombia, there is a need to assess longitudinal mental health problems post-stroke in this region.

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### Refractive error and associated risk factors in 6-12 years school children

2016-07-09T07-31-30Z
Source: National Journal of Physiology, Pharmacy and Pharmacology
Umamaheswari Kannan, Anandhi Rajendiran, Dhanalakshmi Yeraballi, Karthik Shanmugavel, Nitin Ashok John, Senthamizhan Rene.
Background: Refractive error (RE) is one of the most common causes of visual impairment around the world and the second leading cause of treatable blindness. Lack of awareness about risk factors and complications that arise, are the reasons for an increasing trend an early age. Aims and Objectives: This study aimed at finding the influence of risk factors on RE among rural and urban schoolchildren and its prevalence. Materials and Methods: A total of 1300 schoolchildren in the age group of 6-12 years were screened for REs. Children with visual acuity

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### Abstract

We introduce a new analytic technique for the microsegmentation of high-density EEG to identify the discrete brain microstates evoked by the visual reversal checkerboard task. To test the sensitivity of the present analytic approach to differences in evoked brain microstates across experimental conditions, subjects were instructed to (a) passively view the reversals of the checkerboard (passive viewing condition), or (b) actively search for a target stimulus that may appear at the fixation point, and they were offered a monetary reward if they correctly detected the stimulus (active viewing condition). Results revealed that, within the first 168 ms of a checkerboard presentation, the same four brain microstates were evoked in the passive and active viewing conditions, whereas the brain microstates evoked after 168 ms differed between these two conditions, with more brain microstates elicited in the active than in the passive viewing condition. Additionally, distinctions were found in the active condition between a change in a scalp configuration that reflects a change in microstate and a change in scalp configuration that reflects a change in the level of activation of the same microstate. Finally, the bootstrapping procedure identified that two microstates lacked robustness even though statistical significance thresholds were met, suggesting these microstates should be replicated prior to placing weight on their generalizability across individuals. These results illustrate the utility of the analytic approach and provide new information about the spatiotemporal dynamics of the brain states underlying passive and active viewing in the visual checkerboard task.

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### Abstract

Congenital talipes equinovarus (CTEV) is one of the most common musculoskeletal disorders. Genetic factors have been suggested to be an important contributor to its pathogenesis. Some genes, including PITX1, TBX4, and RBM10, have been associated with CTEV. We aimed to determine the disease-causing mutations in Chinese patients with isolated CTEV. Genomic DNA was extracted from peripheral blood samples of a three-generation pedigree and 53 sporadic patients with CTEV. Whole-exome sequencing and Sanger sequencing were used to identify and validate disease-causing mutations, respectively. A putative pathogenic mutation c.4717G>T (p.D1573Y) in the filamin B (FLNB) gene, which co-segregated with CETV, was identified in the pedigree. Two additional novel missense mutations in the same gene [c.1897A>G (p.M633V) and c.2195A>G (p.Y732C)] were identified from the 53 sporadic patients. Plasmids expressing wild-type or mutant constructs were transfected into HEK293T cells to determine whether these amino acid substitutions affect protein activity. All three (M633V, Y732C, and D1573Y) affected FLNB protein expression and led to cytoplasmic focal accumulation. Our results provide evidence for the involvement of FLNB in the pathogenesis of isolated CTEV and have expanded the clinical spectrum of FLNB mutations.

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### Abstract

Atherosclerotic plaques are populated with smooth muscle cells (SMCs) and macrophages. SMCs are thought to accumulate in plaques because fully-differentiated, contractile SMCs reprogram into a 'synthetic' migratory phenotype, so-called phenotypic modulation, whilst plaque macrophages are thought to derive from blood-borne myeloid cells. Recently, these views have been challenged, with reports that SMC phenotypic modulation may not occur during vascular remodelling and that plaque macrophages may not be of haematopoietic origin. Following the fate of SMCs is complicated by the lack of specific markers for the migratory phenotype and direct demonstrations of phenotypic modulation are lacking. Therefore, we employed long-term, high-resolution, time-lapse microscopy to track the fate of unambiguously identified, fully-differentiated, contractile SMCs in response to the growth factors present in serum. Phenotypic modulation was clearly observed. The highly-elongated, contractile SMCs initially rounded up, for 1–3 days, before spreading outwards. Once spread, the SMCs became motile and displayed dynamic cell-cell communication behaviours. Significantly, they also displayed clear evidence of phagocytic activity. This macrophage-like behaviour was confirmed by their internalisation of 1 μm fluorescent latex beads. However, migratory SMCs did not uptake acetylated low-density lipoprotein or express the classic macrophage marker CD68. These results directly demonstrate that SMCs may rapidly undergo phenotypic modulation and develop phagocytic capabilities. Resident SMCs may provide a potential source of macrophages in vascular remodelling.

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### Abstract

The possible role of store operated calcium entry (SOCE) through the Orai1 channel in the formation and functions of dendritic spines was studied in cultured hippocampal neurons. In calcium store-depleted neurons a transient elevation of extracellular calcium concentration ([Ca2+]o) caused a rise in [Ca2+]i that was mediated by activation of the SOCE. The store depletion resulted in an increase in STIM2 (an endoplasmic calcium sensor) association with Orai1 in dendritic spines. The response to the rise in [Ca2+]o was larger in spines endowed with a cluster of Orai1 molecules than in spines devoid of Orai1. Transfection of neurons with a dominant negative Orai1 resulted in retarded maturation of dendritic spines, a reduction in synaptic connectivity with afferent neurons and a reduction in ability to undergo morphological changes following induction of chemical LTP. Likewise, siRNA-treated neurons had fewer mature dendritic spines, and lower rates of mEPSCs compared to scrambled control siRNA treated neurons. Thus, influx of calcium through Orai1 channels facilitates maturation of dendritic spines and formation of functional synapses in central neurons.

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### Abstract

The enterochromaffin (EC) cell in GI epithelium is the source of nearly all systemic serotonin (5-hydroxytryptamine, 5-HT), which is an important neurotransmitter and endocrine, autocrine and paracrine hormone. The EC cell is a specialized mechanosensor, and it is well known that it releases 5-HT in response to mechanical forces. However, the EC cell mechanotransduction mechanism is unknown. The aim of this work was to determine whether Piezo2 is involved in EC cell mechanosensation. Piezo2 mRNA was expressed in human jejunum and mouse mucosa from all segments of small bowel. Piezo2 immunoreactivity localized specifically within EC cells of human and mouse small bowel epithelium. The EC cell model released 5-HT in response to stretch, and had Piezo2 mRNA & protein, and a mechanically-sensitive inward non-selective cation current characteristic of Piezo2. Both inward currents and 5-HT release were inhibited by Piezo2 siRNA and antagonists (Gd3+ and D-GsMTx4). Jejunum mucosal pressure increased 5-HT release and short circuit current via submucosal 5HT3 and 5HT4 receptors. Pressure-induced secretion was inhibited by the mechanosensitive ion channel antagonists Gd3+, ruthenium red and D-GsMTx4. We conclude that the EC cells in human and mouse small bowel GI epithelium selectively express the mechanosensitive ion channel Piezo2, and activation of Piezo2 by force leads to inward currents, 5-HT release and an increase in mucosal secretion. Therefore, Piezo2 is critical to EC cell mechanosensitivity and downstream physiologic effects.

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### Abstract

Serotonergic (5-HT) pathways to the spinal cord are implicated in the control of locomotion based on studies using 5-HT7 receptor agonists and antagonists and 5-HT7 receptor knockout mice. Blockade of these receptors is thought to interfere with the activity of coordinating interneurons, a conclusion derived primarily from in vitro studies on isolated spinal cord of neonatal rats and mice. Developmental changes in the effects of 5-HT on spinal neurons have recently been described, and there is increasing data on control of sensory input by 5-HT7 receptors on dorsal root ganglion cells and/or dorsal horn neurons, leading us to determine the effects of 5-HT7 receptor blockade on voluntary overground locomotion and on locomotion without afferent input from the moving limb (fictive locomotion) in adult animals. Intrathecal injections of the selective 5-HT7 antagonist SB269970 in adult intact rats suppressed locomotion by partial paralysis of hindlimbs. This occurred without a direct effect on motoneurons as revealed by an investigation of reflex activity. The antagonist disrupted intra- and interlimb coordination during locomotion in all intact animals but not during fictive locomotion induced by stimulation of the mesencephalic locomotor region (MLR). MLR evoked fictive locomotion was transiently blocked, then the amplitude and frequency of rhythmic activity was reduced by SB269970, consistent with the notion that the MLR activates 5-HT neurons, leading to excitation of CPG neurons with 5-HT7 receptors. Effects on coordination in adults required the presence of afferent input, suggesting a switch to 5-HT7 receptor mediated control of sensory pathways during development.

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### Aims

To explore the association between plasma concentrations of brain-derived neurotrophic factor (BDNF) and the occurrence of emergence agitation (EA) in the elderly after gastrointestinal surgery.

### Methods

Seventy-two patients were recruited, who received gastrointestinal surgery and general anesthesia. BDNF level of blood was detected by ELISA before anesthesia (baseline), 10 min after tracheal intubation before the start of surgery, at skin closure, 10 min after tracheal extubation, and 24 h postoperatively. Patients with a Ricker Sedation-Agitation Scale (RSAS) score ≥5 at any time in the post anesthesia care unit were considered to have emergence agitation.

### Results

The incidence of EA in this population was 40 % (29/72). The EA group had higher plasma BDNF levels at skin closure (497.86 ± 69.65 vs. 307.86 ± 51.91, p < 0.05) and especially at 10 min after tracheal extubation (900 ± 224.6 vs. 476.28 ± 107.15, p < 0.001). Moreover, the levels of plasma BDNF at skin closure, 10 min after tracheal extubation and postoperative pain, were positively related with RSAS scores.

### Conclusions

Our results suggest that plasma BDNF is associated with the occurrence of emergence agitation after gastrointestinal surgery.

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