25 research outputs found

    Additional suture augmentation to anterior cruciate ligament reconstruction with hamstring autografts bring no benefits to clinical results, graft maturation and graft-bone interface healing

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    Abstract Background From the perspective of graft protection and early rehabilitation during the maturation and remodeling phases of graft healing, suture augmentation (SA) for anterior cruciate ligament reconstruction (ACLR) has attracted more and more attention. Study Design Retrospective study. Purpose To determine whether the additional SA affects clinical results, graft maturation and graft-bone interface healing during two years follow-up after ACLR. Methods 20 ACLRs with additional SA (ACLR-SA group) and 20 ACLRs without additional SA (ACLR group) were performed between January 2020 and December 2021 by the same surgeon and were retrospectively analyzed. Pre- and postoperative International Knee Documentation Committee (IKDC) scores, Lysholm scores, graft failure and reoperation were evaluated. The signal/noise quotient (SNQ) of autografts and the signal intensity of graft-bone interface were analyzed. All 40 patients in ACLR-SA group and ACLR group completed 2-years follow-up. Results There was no patient in the two cohorts experienced graft failure and reoperation. The postoperative IKDC and Lysholm scores have been significantly improved compared with preoperative scored in both ACLR-SA group and ACLR group, however, there was no significant difference between two groups. The SNQ of proximal graft of ACLR-SA group (14.78 ± 8.62 vs. 8.1 ± 5.5, p = 0.041) was significantly greater while the grades of graft-bone interface healing of posterior tibial was significantly lower than that of ACLR group at 1-year postoperatively (p = 0.03), respectively. There were no significant differences between the two groups of the SNQ of proximal, distal medial graft segments, and the graft-bone interface healing grades of anterior femoral, posterior femoral, anterior tibial and posterior tibial at other time points (p>0.05). Conclusions The additional SA in ACLR had no effect on IKDC scores, Lysholm scores, graft maturation and graft-bone interface healing at 2-year postoperatively. Our research does not support the routine use of SA in ACLR

    The microrna 17-92 cluster in neural progenitor cells is required for stroke-induced neurogenesis and gliogenesis

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    Background: Molecular mechanisms underlying stroke-induced neurogenesis have not been fully investigated. The microRNA 17-92 cluster (miR17-92) regulates proliferation and differentiation of adult neural progenitor cells (NPCs). The present study investigated whether the miR17-92 cluster in NPCs is required for stroke-induced neurogenesis. Methods and Results: Mice with inducible and conditional knockdown of the miR17-92 cluster in nestin lineage NPCs (nestin-CreERT2/miR17-92-/-, 17-92-cKO, n=9) and wild-type litters (WT, n=9) were treated by tamoxifen. Administration of tamoxifen resulted in more than 60% reduction of individual members of the miR-17-92 cluster (miR-17: 1.0 vs 0.4; miR-19a: 1.0 vs 0.3; miR-19b: 1.0 vs 0.2; miR-20a: 1.0 vs 0.4; miR- 92a: 1.0 vs 0.4 fold in WT, p\u3c0.05) in NPCs localized to the subventricular zone (SVZ). Two days after termination of tamoxifen treatment, these mice were subjected to permanent right middle cerebral artery occlusion (MCAO) and sacrificed 28 days post-MCAo. Compared to WT mice, 17-92-cKO mice exhibited significant (p\u3c0.05) reduction of proliferation of NPCs measured by the number of Ki67+ cells (226±43 vs 471±100 cells/mm2) and the number of DCX+ neuroblasts (11±2% vs 24±4% ) in the ischemic SVZ. Cultured NPCs harvested from ischemic cKO mice showed significant (p\u3c0.05) reduction of BrdU+ cells (37±2% vs 61±4% WT , n=3/group), Tuj1+ neuroblasts (5±0.2% vs 9±0.4% ), GFAP+ cells (33±3% vs 53±2%), and NG2+ oligodendrocyte progenitor cells (OPCs, 3±0.1% vs 5±0.5%). These in vivo and in vitro data indicate that reduction of the miR17-92 cluster suppresses stroke-induced neurogenesis and gliogenesis. Western blot analysis showed that miR17-92 cKO significantly (p\u3c0.05) increased and reduced a cytoskeleton-associated protein, Enigma homolog1 (ENH1, 1.6 vs 1.0 fold), and its down-stream transcription factor, inhibitor of differentiation1 (ID1, 1.0 vs 0.6 fold), respectively. ENH1 is a putative target of the miR17-92 cluster.Conclusion: Our data indicate that the miR17-92 cluster in adult nestin lineage NPCs is required for stroke-induced neurongenesis and gliogenesis, and that the miR17-92 cluster possibly targets ENH1/ID1 signaling

    Differentiation between bipolar disorder and major depressive disorder in adolescents: from clinical to biological biomarkers

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    BackgroundMood disorders are very common among adolescents and include mainly bipolar disorder (BD) and major depressive disorder (MDD), with overlapping depressive symptoms that pose a significant challenge to realizing a rapid and accurate differential diagnosis in clinical practice. Misdiagnosis of BD as MDD can lead to inappropriate treatment and detrimental outcomes, including a poorer ultimate clinical and functional prognosis and even an increased risk of suicide. Therefore, it is of great significance for clinical management to identify clinical symptoms or features and biological markers that can accurately distinguish BD from MDD. With the aid of bibliometric analysis, we explore, visualize, and conclude the important directions of differential diagnostic studies of BD and MDD in adolescents.Materials and methodsA literature search was performed for studies on differential diagnostic studies of BD and MDD among adolescents in the Web of Science Core Collection database. All studies considered for this article were published between 2004 and 2023. Bibliometric analysis and visualization were performed using the VOSviewer and CiteSpace software.ResultsIn total, 148 publications were retrieved. The number of publications on differential diagnostic studies of BD and MDD among adolescents has been generally increasing since 2012, with the United States being an emerging hub with a growing influence in the field. Boris Birmaher is the top author in terms of the number of publications, and the Journal of Affective Disorders is the most published journal in the field. Co-occurrence analysis of keywords showed that clinical characteristics, genetic factors, and neuroimaging are current research hotspots. Ultimately, we comprehensively sorted out the current state of research in this area and proposed possible research directions in future.ConclusionThis is the first-ever study of bibliometric and visual analyses of differential diagnostic studies of BD and MDD in adolescents to reveal the current research status and important directions in the field. Our research and analysis results might provide some practical sources for academic scholars and clinical practice

    Ablation of the microRNA-17-92 cluster in neural stem cells diminishes adult hippocampal neurogenesis and cognitive function

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    Impairment of adult neurogenesis in the hippocampus causes cognitive deficits; however, the underlying molecular mechanisms have not been fully elucidated. microRNAs (miRNAs) regulate neural stem cell (NSC) function. With the use of a transgenic mouse line with conditional ablation of the miR-17-92 cluster in nestin lineage NSCs, we tested the hypothesis that the miR-17-92 cluster regulates adult neurogenesis and cognitive function in vivo. Compared with wild-type mice, ablation of the miR-17-92 cluster significantly reduced the number of proliferating NSCs and neuroblasts and neuronal differentiation in the dentate gyrus (DG) of the hippocampus and significantly impaired hippocampal-dependent learning and memory, as assayed by social recognition memory, novel object recognition, and Morris water-maze tests. Statistical analysis showed a highly significant correlation between newly generated neuroblasts in the DG and cognition deficits in miR-17-92 knockout (KO) mice. Western blot analysis showed that conditional KO of the miR-17-92 cluster significantly increased and reduced a cytoskeleton-associated protein, Enigma homolog 1 (ENH1), and its downstream transcription factor, inhibitor of differentiation 1 (ID1), respectively, as well as increased phosphatase and tensin homolog gene. These proteins are related to neuronal differentiation. Our study demonstrates that the miR-17-92 cluster in NSCs is critical for cognitive and behavioral function and regulates neurogenesis and that the miR-17-92 cluster may target ENH1/ID1 signaling.-Pan, W. L., Chopp, M., Fan, B., Zhang, R., Wang, X., Hu, J., Zhang, X. M., Zhang, Z. G., Liu, X. S. Ablation of the microRNA-17-92 cluster in neural stem cells diminishes adult hippocampal neurogenesis and cognitive function

    Investigate the Glass Transition Temperature of Hyperbranched Copolymers with Segmented Monomer Sequence

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    Hyperbranched copolymers with segmented structures were synthesized using a chain-growth copper-catalyzed azide–alkyne cycloaddition (CuAAC) polymerization via sequential monomer addition in one pot. Three AB2-type monomers that contained one alkynyl group (A), two azido groups (B), and one dangling group, either benzyl or oligo­(ethylene oxide) (EOx, x = 3 and 7.5), were used in these CuAAC reactions. Varying the addition sequences and feed ratios of the monomers produced a variety of hyperbranched copolymers with tunable compositions, molecular weights, segmented structures, and consequently glass transition temperature (Tg). It was found that the Tg of hyperbranched copolymers was little affected by the polymer molecular weights when Mn ≥ 5000. However, the values of Tg were significantly determined by the compositions of the terminal groups and the outermost segment of the hyperbranched copolymers. The last added AB2 monomer in the polymerization formed an outermost “shell” and shielded the contribution of inner segments to the glass transition of the copolymers, reflecting a chain sequence effect of hyperbranched polymers on the thermal properties
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