Effect of exercise on neurotrophic factor levels.

<p>Tissue and serum levels of GDNF, IGF-1 and BDNF were measured at 6 weeks after nerve repair. In all cases, except serum BDNF, exercised group had higher levels of all three neurotrophic factors in muscle, serum and distal nerve as measured by ELISA. Control is uninjured animals with no exercise program. Exercise and no exercise groups denote animals undergoing median nerve repair and regeneration. (* Denotes statistically significant difference compared to no-exercise group, P>0.05).</p

Effect of exercise on evoked motor response in nerve conduction study.

<p>Exercise improved both the amplitude of the evoked CMAP response (<b>A</b>) and distal latency (<b>B</b>) 6 weeks after median nerve repair. (* Denotes statistically significant difference, P>0.05).</p

Effect of exercise on neurotrophic factor levels.

<p>Tissue and serum levels of GDNF, IGF-1 and BDNF were measured at 6 weeks after nerve repair. In all cases, except serum BDNF, exercised group had higher levels of all three neurotrophic factors in muscle, serum and distal nerve as measured by ELISA. Control is uninjured animals with no exercise program. Exercise and no exercise groups denote animals undergoing median nerve repair and regeneration. (* Denotes statistically significant difference compared to no-exercise group, P>0.05).</p

Effect of exercise on muscle mass.

<p>Exercise resulted in larger myofiber size as shown in (<b>B</b>) compared to uninjured control (<b>A</b>) or no-exercise group (<b>C</b>). This is quantified in (<b>D</b>). There was also a difference in total muscle weight between the exercise and no-exercise groups (<b>E</b>). (* Denotes statistically significant difference compared to no-exercise group, P>0.05).</p

Effect of exercise on functional outcomes.

<p>Exercise improved both grip strength (<b>A</b>) and time on the inverted holding test (<b>B</b>) in mice with median nerve repair over 6 weeks. (* Denotes statistically significant difference, P>0.05).</p

Data_Sheet_1_Genomic surveillance of genes encoding the SARS-CoV-2 spike protein to monitor for emerging variants on Jeju Island, Republic of Korea.pdf

IntroductionThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has been fueled by new variants emerging from circulating strains. Here, we report results from a genomic surveillance study of SARS-CoV-2 on Jeju Island, Republic of Korea, from February 2021 to September 2022.MethodsA total of 3,585 SARS-CoV-2 positive samples were analyzed by Sanger sequencing of the gene encoding the spike protein before performing phylogenetic analyses.ResultsWe found that the Alpha variant (B.1.1.7) was dominant in May 2021 before being replaced by the Delta variant (B.1.617.2) in July 2021, which was dominant until December 2021 before being replaced by the Omicron variant. Mutations in the spike protein, including N440K and G446S, have been proposed to contribute to immune evasion, accelerating the spread of Omicron variants.DiscussionOur results from Juju Island, Republic of Korea, are consistent with and contribute to global surveillance efforts crucial for identifying new variants of concern of SARS-CoV-2 and for monitoring the transmission dynamics and characteristics of known strains.</p

Comparison of synaptic and map plasticity at different ages.

<p>Both synaptic (i.e., LTP) and map plasticity (i.e., map expansion following tone exposure) are observed in early window, and only in WT mice but not in <i>Fmr1</i> KO mice. Map plasticity data adapted from a previous report <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0104691#pone.0104691-Kim1" target="_blank">[12]</a>. Error bars represent SEM. *, <i>p</i><0.05.</p

Comparison of synaptic and map plasticity at different ages.

<p>Both synaptic (i.e., LTP) and map plasticity (i.e., map expansion following tone exposure) are observed in early window, and only in WT mice but not in <i>Fmr1</i> KO mice. Map plasticity data adapted from a previous report <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0104691#pone.0104691-Kim1" target="_blank">[12]</a>. Error bars represent SEM. *, <i>p</i><0.05.</p

Destabilization of LTP in Fmr1 KO mice.

<p><b>A</b>. Average synaptic potentiation shown in different time windows (15, 30 and 60 min). <b>B</b>. Decay slope in four groups (WT early, WT late, KO early and KO late). Note the steeper decay in early and late window of Fmr1 KO mice compared to those in early and late window of Fmr1 WT mice. *, <i>p</i><0.05; **, <i>p</i><0.01; n.s, not significant.</p

Differential LTP expression in early- (P16-20) and late-age (P27-31) windows.

<p><b>Ai</b>. A schematic of experimental setup. S, stimulus (black dot); R, recording (Layer III/IV). <b>Aii</b>. Field potential responses in the presence of NBQX and/or TTX. <b>Aiii</b>. Field potential amplitude measured at the peak latency (see dashed vertical line in <b>Aii</b>) was reduced by 80% by NBQX, and was completely abolished by further TTX application. <b>B</b>. Average responses in early- and late-age groups. Note the significant LTP in the early-age group but not in the late-age group. LTP in the early-age group was completely blocked by MPEP application. Insets show overlapping field potential traces before (black) and 60 min after (gray) LTP induction. Arrows indicate three consecutive tetanic stimulations. *, p<0.05.</p