Abstract The purpose of this study was to investigate differences in ankle plantar flexion proprioception and lower extremity function between Achilles tendinopathy (AT) patients and healthy controls. 17 patients with midportion AT (age 22.0 ± 3.0, 7 females, and 10 males) and 17 healthy controls (age 21.5 ± 2.1, 7 females, and 10 males) were recruited. The following tests were performed randomly: the ankle plantar flexion active movement extent discrimination assessment (AMEDA), weight‐bearing lunge test (WBLT), single leg hop test, figure‐of‐eight hop test, Y Balance Test (YBT), and lower extremity functional test (LEFT). Group comparisons were made between the AT and healthy groups, and receiver operator characteristic (ROC) curves were used to analyze the ability of tests to differentiate between participants with and without AT. Results showed that the AT group performed significantly worse in the ankle proprioception test ( p = 0.016), single leg hop test ( p = 0.001), figure‐of‐eight hop test ( p < 0.001), unilateral LEFT ( p = 0.001), and LEFT injury risk score ( p = 0.001) than healthy controls. No significant between group difference was found in WBLT and YBT. Diagnostic analysis showed that the AMEDA ( p = 0.018), single leg hop test ( p = 0.003), figure‐of‐eight hop test ( p = 0.002), and LEFT ( p = 0.001) could differentiate between patients with AT and the healthy individuals. The current study demonstrated that ankle proprioception and functional performance involving explosive jump are impaired in patients with AT, suggesting poorer dynamic neuromuscular function and a higher risk of lower limb injury in this population, and furthermore, these tests should be considered in the assessment for AT.
Proprioception plays an important role in joint stability, and ankle sprains usually happen involving plantarflexion, internal rotation, and inversion. However, ankle 3D movement proprioception has never been measured in weight-bearing. Accordingly, the active 3-dimensional movement extent discrimination apparatus (AMEDA-3D) was developed and its reliability and validity were investigated. A total of 58 subjects volunteered for this trial, with 12 subjects with chronic ankle instability (CAI) and 12 healthy controls in the test-retest reliability study. There were 17 subjects with CAI and 17 healthy controls in the validity study. An intraclass correlation coefficient (ICC) and Minimum Detectable Change at the 90% confidence interval (MDC
RNase H1 has been acknowledged as an endoribonuclease specializing in the internal degradation of the RNA moiety within RNA-DNA hybrids, and its ribonuclease activity is indispensable in multifaceted aspects of nucleic acid metabolism. However, the molecular mechanism underlying RNase H1-mediated hybrid cleavage remains inadequately elucidated. Herein, using single-molecule approaches, we probe the dynamics of the hybrid cleavage by Saccharomyces cerevisiae RNase H1. Remarkably, a single RNase H1 enzyme displays 3'-to-5' exoribonuclease activity. The directional RNA degradation proceeds processively and yet discretely, wherein unwinding approximately 6-bp hybrids as a prerequisite for two consecutive 3-nt RNA excisions limits the overall rate within each catalytic cycle. Moreover, Replication Protein A (RPA) reinforces RNase H1's 3'-to-5' nucleolytic rate and processivity and stimulates its 5'-to-3' exoribonuclease activity. This stimulation is primarily realized through the pre-separation of the hybrids and consequently transfers RNase H1 to a bidirectional exoribonuclease, further potentiating its cleavage efficiency. These findings unveil unprecedented characteristics of an RNase and provide a dynamic view of RPA-enhanced processive hybrid cleavage by RNase H1.
Adv. Sci. 2021, 8, 2002794 DOI: 10.1002/advs.202002794 In the original published article, the previous forward and reverse primers of Cidea in Table S1 (Supporting Information) were reversed. Now these two primers of Cidea have been exchanged. Please find the correct Table S1 below. The authors apologize for any inconvenience caused.
It has been demonstrated in a number of studies that high levels of uric acid can cause crystal deposition in the tendons of the lower extremities, which in turn can impair the Achilles tendon. This study aimed to interpret whether hyperuricemia is relevant with Achilles tendon rupture. Patients diagnosed with Achilles tendon rupture at the same institution between 2013 and 2022 were included in the case group. Healthy subjects who had physical examinations during the same period were included in the control group. Propensity score matching was used to match in a 1:1 ratio. Demographic and clinical characteristics of patients in both groups were compared. Five hundred and fourteen patients were included in the study (ATR=257; Control group=257). The proportion of individuals with hyperuricemia varied significantly between the 2 groups (Achilles tendon rupture group=43.6%; control group=27.6%; p<0.001). The Achilles tendon rupture and hyperuricemia were linked by conditional logistic regression (p<0.001; OR=2.036; 95CI%=1.400-2.961). Compared with healthy subjects, patients with hyperuricemia have a higher risk of Achilles tendon rupture. Further studies are required to verify the effects of hyperuricemia and monosodium urate crystals on Achilles tendon structure.
Abstract Type V-F CRISPR-Cas12f is a group of hypercompact RNA-guided nucleases that present a versatile in vivo delivery platform for gene therapy. Upon target recognition, Acidibacillus sulfuroxidans Cas12f (AsCas12f1) distinctively engenders three DNA break sites, two of which are located outside the protospacer. Combining ensemble and single-molecule approaches, we elucidate the molecular details underlying AsCas12f1-mediated DNA cleavages. We find that following the protospacer DNA unwinding and non-target strand (NTS) DNA nicking, AsCas12f1 surprisingly carries out bidirectional exonucleolytic cleavage from the nick. Subsequently, DNA unwinding is extended to the out-of-protospacer region, and AsCas12f1 gradually digests the unwound DNA beyond the protospacer. Eventually, the single endonucleolytic target-strand DNA cleavage at 3 nt downstream of the protospacer readily dissociates the ternary AsCas12f1-sgRNA–DNA complex from the protospacer adjacent motif-distal end, leaving a staggered double-strand DNA break. The coupling between the unwinding and cleavage of both protospacer and out-of-protospacer DNA is promoted by Mg2+. Kinetic analysis on the engineered AsCas12f1-v5.1 variant identifies the only accelerated step of the protospacer NTS DNA trimming within the sequential DNA cleavage. Our findings provide a dynamic view of AsCas12f1 catalyzing DNA unwinding-coupled nucleolytic cleavage and help with practical improvements of Cas12f-based genome editing tools.
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