Somatosensory Information in Lifting Objects While Applying Contralateral Finger Touch to the Target Arm

We have observed that the magnitude of grip force used to lift and transport a hand-held object could be reduced if a light finger touch is provided by the contralateral arm to the target arm. In the current study, we investigate if different types of somatosensory information formulate parallel modulation of grip force when perform similar functional experimental task. Nine healthy individuals performed the same task of lifting and transporting an insrumented cup with contrlalateral index finger touch to the wrist, elbow and shoulder, in addition to no touch condition. Movement of the contralateral arm was produced when touch to the wrist and elbow; while touching the shoulder involve no movement of contralateral arm. But a relative movement between finger tip and the touch location can be found with application of finger touch to the shoulder. Grip force was reduced approximately the same amount in all touch conditions (wrist, elbow, shoulder) as compared to no touch condition. This outcome suggest that proprioceptive information from the muscle and joint receptors of the contralateral arm is used in control of grip force when a finger touch applied to wrist and elbow and cutaneous information is utilized when touch became available to the shoulder. It needs to be highlighted that different neural mechanisms are employed while lifting a hand-held object with a self contralateral finger touch. The results of the study also provided additional evidence to support the use of a second arm in the performance of activities of daily living and stress the importance of future studies investigating contralateral arm sensory input in grip force control

Control of Vertical Posture During Dual-Task Performance

People frequently perform daily activities that involve multitasking. For example, we maintain posture while holding a cup of coffee or a cell phone. It is not uncommon to experience a perturbation during such a task performance. In this dissertation, we study control of vertical posture in the presence of postural instability and holding an object in one hand. Successful completion of these tasks depends on efficient interaction of two components of the task: maintenance of vertical posture (postural component) and stabilization of the object (focal component). While each component was studied extensively in the past, investigating the interaction between the postural and focal components received much lesser attention in the prior literature. As such, a series of studies were conducted in order to examine the interplay between the postural and focal components. In the first study (chapter 3), we investigated the effect of postural asymmetry induced by performing a secondary motor task on control of vertical posture. Participants (N=9) were asked to stand on the force platform and hold an object in one hand that induced body asymmetry. In addition, the subjects stood with feet apart and feet together (narrow base of support) and were subjected to perturbationa applied to their shoulders. In this study and following studies the side of holding an object will be referred as a target side and the other side of body will be referred as a contralateral side. Reciprocal activation of muscles on the target side and co-contraction of muscles on the contralateral side were seen when standing in asymmetrical stance and being subjected to external perturbation. Decreased magnitudes of muscle activation were seen in the APA phase while standing with narrow base of support. In the second study (chapter 4), we investigated motor control perspectives of coordinating maintenance of posture and application of grip force when holding an object and being perturbed. In this study, participants (N=10) were asked to stand on the force platform holding an instrumented cup while being perturbed at the shoulders. Gripping task demands were manipulated by positioning a slippery cap on top of the cup. Onsets of grip force were seen before the onsets of the center of pressure (COP) displacement and initiation of the movements of the cup during the anticipatory postural adjustments (APAs) phase of postural control, while the onsets of maximum grip force preceded the maximum COP displacement. When the task demands increased by holding an instrumented cup with the slippery cap, participants tended to generate grip force earlier and of a smaller magnitude. Moreover, the COP displacement in the APA phase when holding the cup with the slippery cap was smaller as compared to the holding the cup only. In the third study (chapter 5), we studied APAs and CPAs people use to maintain balance while standing on a sliding board that was either unlocked (and as such unstable) or locked (and as such stable) and performing voluntary arm movements. Nine subjects were enrolled in the study. Larger EMG integrals were seen in the muscles of the lower extremity in both APA and CPA phases of postural control when standing on the unstable surface (unlocked sliding board). No significant difference was observed in the trunk muscles. Larger maximum COP displacement was seen when participants stood on the stable surface (locked sliding board). The results also demonstrated that the CNS modified activation of the lower extremity muscles rather than trunk muscles when standing on a free to move sliding board and performing bilateral arm flexion. In the forth study (chapter 6), we studied the role of a secondary task (holding an object) in maintenance of vertical posture in the presence of postural instability. Participants (N=12) were asked to stand on a free to move sliding board while holding an instrumented cup (with and without a slippery cap) and being perturbed. Reciprocal activation of muscles of the shank on both target and contralateral sides and co-contraction of muscles on both sides of the trunk was seen in the APAs phase. Decreased magnitudes of muscle activation in the target side were seen when standing and holding a cup with the slippery cap. The results of the study support the suggestion that the CNS employs dual-process for controlling postural and motor components when balance is jeopardized

Additional file 1 of The paradox of pandemic mitigation? Moderating role of pandemic severity on the impact of social distancing policies: a cultural value perspective

Additional file 1: Supplementary Material. Table 1. Descriptive statistics for study variables in the 57 countries. Table 2. Multilevel regression results for GSI on mobility. Table 3. Multilevel regression results for GSI*DNC on mobility. Figure 1. Conditional effect of GSI on mobility (RE) as a function of DNC. Figure 2. Average RE under GSI and DNC conditions in different periods. Table 4. Moderated moderation model of RE (the coefficients of the interaction terms). Figure 3. Conditional effect of GSI on RE as a function of DNC under different embeddedness values. Figure 4. Conditional effect of GSI on RE as a function of DNC under different autonomy values. Figure 5. Conditional effect of GSI on RE as a function of DNC under different hierarchy values. Figure 6. Conditional effect of GSI on RE as a function of DNC under different egalitarianism values. Figure 7. Conditional effect of GSI on RE as a function of DNC under different mastery values. Figure 8. Conditional effect of GSI on RE as a function of DNC under different harmony values

Geographic Origins of D. melanogaster Populations Screened in This Study

<p>Screens revealed zero to 14 <i>P</i> elements per population (indicated by the number of squares), distinctive by insertion location, in the proximal promoter regions of genes examined (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-t001" target="_blank">Table 1</a>). Colors of squares correspond to gene set (see Introduction). Inset: Percentages of distinctive <i>P</i> elements discovered in <i>Hsp70</i> genes and each of the three gene sets screened. A total of 161 <i>P</i> element insertions (the ten <i>P</i> elements in the coding sequence and the five non–<i>P</i> element insertions are not included in the figure). These tallies potentially under-report the actual number of <i>P</i> elements; see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#s2" target="_blank">Results</a>. F06 (Celera) is the strain whose genome has been sequenced [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-b025" target="_blank">25</a>] and is the reference strain for the present study. Populations F18, F50, and F52 (in light gray text) were removed from the analysis after screens failed for multiple genes and primer sets.</p

Data_Sheet_1_New insights into the genetic structure of the outbreak-prone bamboo grasshoppers.DOCX

IntroductionThe genetic structure of species is shaped by natural (e.g., terrain, climate) and non-natural (e.g., human activities) factors. Geographical isolation and natural barriers are important causes of genetic structure formation of species. Here, we explored this issue in bamboo grasshopper, Ceracris kiangsu, which is an important pest that feeds on bamboo in East and Southeastern Asia.MethodsBased on 186 newly sequenced and 286 previously sequenced mitochondrial COI fragments, and 8 nuclear microsatellite loci, we examined the genetic diversity and population genetic structure of C. kiangsu.ResultsThe degree of genetic differentiation among populations was also high, and Mantel test showed that it was significantly correlated with geographical distance. Principal coordinate analysis and STRUCTURE results revealed two genetically different groups, a South China (S-China) Group and a Southeast Asia (SE-Asia) Group. Climate variables partly explained the population genetic structure. The demographic history and ABC showed that the S-China Group experienced population expansion, whereas the SE-Asia Group was consistently stable.DiscussionOur study demonstrates an obvious population structure maintained in this migratory insect and reveals the potential effect of past climatic change, geographical isolation, and ecological factors on the evolution of their genetic structure.</p

The Hazard Ratio (HR) of TP53 mutation with the Overall Survival (OS) of different subtypes.

<p>HR > 1 implied worse OS for the TP53 mutated group.</p

Locations of <i>P</i> Elements Integrating into the Proximal Promoters of Heat-Shock Genes Other than <i>Hsp70</i> (Gene Set I)

<p>Data are plotted as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g002" target="_blank">Figure 2</a> except as follows: F-numbers in columns refer to natural populations with transposons integrating at identical sites. Primer sets used in the screens amplified regions 3′ to transcription start site of different length; <i>P</i> elements discovered upstream of the initiator are plotted (pale), but not included in comparative analyses (i.e., in <i>Hsp22</i> in population F31, <i>Hsp68</i> in F05, and in <i>Hsrω</i> in F14). In <i>Hsrω</i>, numerous <i>P</i> elements were discovered in one region (box); a randomly chosen subset of these were localized (by sequencing) within that region (see enlargement). Several putative deletions were also discovered, and are plotted. For population codes see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g001" target="_blank">Figure 1</a>. <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-st001" target="_blank">Table S1</a> provides additional information about Gene Set I and relevant sources for the organization of promoter regions.</p

Number of Natural <i>P</i> Element Insertions (161 Total) Distinctive by Population and Location into the “Proximal Promoter Region” of Each of the Screened Genes (Table 1)

<p>Genes without any such insertions are not represented in the main figure. These tallies and estimates are conservative in three ways: (1) <i>P</i> elements inserting within 1,000 bp of the transcription start site of <i>Bsg25D</i> and <i>CG6396</i> are included although they actually insert into neighboring genes (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g004" target="_blank">Figure 4</a>); (2) The tally for <i>Hsp70</i> excludes non–<i>P</i> elements and those previously discovered (<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g002" target="_blank">Figure 2</a>), and divides the remaining total (44, light gray bar in background) by five, the <i>Hsp70</i> copy number for natural populations [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-b017" target="_blank">17</a>]; and (3) Re-screening of a subset of insertions implies an underestimation of the tally at the 161 <i>P</i> insertion sites (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#s2" target="_blank">Results</a> and <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g007" target="_blank">Figure 7</a>). Inset: frequencies of genes in each Gene Set (I, including <i>Hsp70,</i> II, and III) in which 0, 1, or >1 <i>P</i> elements had inserted.</p

Locations of <i>P</i> Elements Integrating into the Proximal Promoters of Non–Heat-Shock Genes Resembling Heat-Shock Genes in Relevant Features of Their Proximal Promoters (Gene Set II), and in Genes Dissimilar to Heat-Shock Genes (Gene Set III)

<p>Data are plotted as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g002" target="_blank">Figure 2</a> except as follows: Primer sets used in the screens amplified regions 3′ to transcription start site of different length; <i>P</i> elements discovered upstream of the initiator are plotted (pale), but not included in comparative analyses (i.e., in <i>su(s)</i> in population F17, in <i>Act5C</i> in F03 and F31, and in <i>Elf</i> in F43 and F54). Note that in Gene Set III, the two <i>P</i> elements discovered are not clearly associated with their focal genes, integrating into or just upstream of genes neighboring the focal genes. For population codes, see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-g001" target="_blank">Figure 1</a>. <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0020165#pgen-0020165-t001" target="_blank">Table 1</a> provides additional information about the gene sets.</p

TP53 mutation predicts the poor prognosis of non-Hodgkin lymphomas: Evidence from a meta-analysis

<div><p>Non-Hodgkin lymphoma (NHL) is a group of malignant hematologic disorders with high heterogeneity. The diagnosis, clinical manifestations, classification, and prognosis of this condition differ among numerous NHL subgroups. The prognostic significance of the mutation of TP53, a tumor suppressor gene involved in cell cycle regulation, should be confirmed in NHL. In this study, our searching strategy and inclusion criteria were implemented, and the pooled hazard ratios (HRs) of the included studies were calculated directly or indirectly. A total of 1,851 patients were enrolled in 22 studies. A meta-analysis was then performed using STATA version 12.0 to confirm the correlation between the status of TP53 mutation and the survival time of patients with NHL. Statistical heterogeneity was assessed with a chi-square-based Q statistical test and Inconsistency index (<i>I</i>²) statistic. Sensitivity analysis and publication bias were also evaluated. A total of 22 studies were included in our meta-analysis. The pooled HR of the overall survival from 20 studies was 2.30 (95% CI: 1.92–2.76, p = 0.001) with heterogeneity (I² 30.2% p = 0.099). The pooled HR of the progression free survival provided in 5 articles was 2.28 (95% CI: 1.78–2.93, p = 0.001) with heterogeneity (I² 39.8% p = 0.156). No publication bias was found among the included studies, and sensitivity analysis suggested that the combined HRs were stable after any of the studies was excluded from our meta-analysis. This study identified the prognostic significance of TP53 mutation that varied in different NHL subgroups. The group with a mutated TP53 was significantly associated with poor prognosis in patients with NHL. This parameter is a valuable basis for accurate individual therapeutic regimens.</p></div