In Situ Formation of Heterojunction in Composite Lithium Anode Facilitates Fast and Uniform Interfacial Ion Transport.

Lithium metal is a highly promising anode for next-generation high-energy-density rechargeable batteries. Nevertheless, its practical application faces challenges due to the uncontrolled lithium dendrites growth and infinite volumetric expansion during repetitive cycling. Herein, a composite lithium anode is designed by mechanically rolling and pressing a cerium oxide-coated carbon textile with lithium foil (Li@CeO2/CT). The in situ generated cerium dioxide (CeO2) and cerium trioxide (Ce2O3) form a heterojunction with a reduced lithium-ion migration barrier, facilitating the rapid lithium ions migration. Additionally, both CeO2 and Ce2O3 exhibit higher adsorbed energy with lithium, enabling faster and more distributed interfacial transport of lithium ions. Furthermore, the high specific surface area of 3D skeleton can effectively reduce local current density, and alleviate the lithium volumetric changes upon plating/stripping. Benefiting from this unique structure, the highly compact and uniform lithium deposition is constructed, allowing the Li@CeO2/CT symmetric cells to maintain a stable cycling for over 500 cycles at an exceptional high current density of 100 mA cm-2. When paired with LiNi0.91Co0.06Mn0.03O2 (NCM91) cathode, the cell achieves 74.3% capacity retention after 800 cycles at 1 C, and a remarkable capacity retention of 81.1% after 500 cycles even at a high rate of 4  C.

MicroRNA-532-5p is implicated in the regulation of osteoporosis by forkhead box O1 and osteoblast differentiation.

BACKGROUND: MicroRNAs (miRNAs) are critical regulators in osteogenesis and cartilage formation. This study was designed to investigate whether miR-532-5p plays a role in the regulation of osteoporosis. METHODS: Osteoporotic fractures (OP group, n = 10) or osteoarthritis without osteoporosis (control group, n = 10) were selected as subjects in this study. Quantitative analysis of gene expression was performed by RT-PCR. Western blot was used to determine the expression levels of protein forkhead O1 (FOXO1). Bioinformatics analyses and luciferase reporter assay were used to verify the downstream target of miR-532-5p. RESULTS: Compared with the non-osteoporotic controls, miR-532-5p was upregulated in osteoporotic samples, and expression of miR-532-5p was downregulated in the osteogenic C2C12 cell model. Overexpression of miR-532-5p resulted in decreased expression levels of key osteoblast markers, including alkaline phosphatase (ALP), osteocalcin (OC), and collagen type I alpha 1 (COL1A1). The inhibitory results of miR-532-5p were reversed. MiR-532-5p contained a putative FOXO1 binding site. Moreover, miR-532-5p inhibited the expression of FOXO1, and overexpression of FOXO1 inhibited the effect of miR-532-5p on osteoblast markers. CONCLUSIONS: MiR-532-5p can provide references to osteoporosis by regulating the expression of FOXO1 and osteoblast differentiation. MiR-532-5p might serve as a therapeutic target for osteoporosis.

p63 protects chondrosarcoma malignancies mainly by enhancing the expression of PTEN.

Abnormal expression of p63 has been well identified in multiple malignancies. However, little study has been done on the association between p63 and chondro sarcoma. In the current study, we mainly explored the expression of p63 in different grades of chondrosarcoma. Our data showed that p63 was significantly decreased in grade II and III chondrosarcoma compared with that of grade I chondrosarcoma and normal control. As the characteristic of grade II and III chondrosarcoma is metastasis, we then searched the function of p63 chondrosarcoma. In vitro study showed that overexpression of p63 significantly suppressed chondrosarcoma cell viability, migration and invasion. Meanwhile, upregualtion of p63 induced chondrosarcoma cell apoptosis. Furthermore, we showed that overexpression of p63 could significantly increase the protein expression of PTEN. In contrast, silencing of PTEN markedly reduced the protein levels of Bax, and enhanced the expression of PCNA and p27, even in cells transfected with p-p63. These data showed that p63 was a tumor suppressor mainly through regulating PTEN in chondrosarcoma cells. In summary, reduction of p63 in grade II and III chondrosarcoma enhances the malignant phenotype mainly through modulating the expression of PTEN.

Reprogramming of ovarian aging epigenome by resveratrol.

Resveratrol is an antiaging, antioxidant, and anti-inflammatory natural polyphenolic compound. Growing evidence indicates that resveratrol has potential therapeutic effects for improving aging ovarian function. However, the mechanisms underlying prolonged reproductive longevity remain elusive. We found that resveratrol ameliorates ovarian aging transcriptome, some of which are associated with specific changes in methylome. In addition to known aging transcriptome of oocytes and granulosa cells such as decline in oxidoreductase activity, metabolism and mitochondria function, and elevated DNA damage and apoptosis, actin cytoskeleton are notably downregulated with age, and these defects are mostly rescued by resveratrol. Moreover, the aging-associated hypermethylation of actin cytoskeleton is decreased by resveratrol. In contrast, deletion of Tet2, involved in DNA demethylation, abrogates resveratrol-reprogrammed ovarian aging transcriptome. Consistently, Tet2 deficiency results in additional altered pathways as shown by increased mTOR and Wnt signaling, as well as reduced DNA repair and actin cytoskeleton with mouse age. Moreover, genes associated with oxidoreductase activity and oxidation-reduction process were hypermethylated in Tet2-deficient oocytes from middle-age mice treated with resveratrol, indicating that loss of Tet2 abolishes the antioxidant effect of resveratrol. Taking together, our finding provides a comprehensive landscape of transcriptome and epigenetic changes associated with ovarian aging that can be reprogrammed by resveratrol administration, and suggests that aberrantly increased DNA methylation by Tet2 deficiency promotes additional aging epigenome that cannot be effectively restored to younger state by resveratrol.

Posterior pilon fracture treated by opening the fibula fracture gap.

BACKGROUND: Posterior pilon fracture is a relatively common clinical fracture involving the posterior articular surface of the distal tibia. Currently, this form of fracture is receiving increasing attention. The surgical approach and technique for the treatment of posterior pilon fractures are still controversial. The purpose of this retrospective study was to compare the clinical and imaging outcomes of pilon fractures after treatment with the open fibula fracture line (OFFL) surgical technique versus the traditional posterolateral approach (TPL). METHODS: A retrospective analysis of patients with posterior pilon fractures treated using the open fibula fracture line technique and the traditional posterolateral approach between January 2015 and March 2020. Thirty-one cases were included in the open fibula fracture line technique group and twenty-eight cases were included in the traditional posterolateral approach group. We used the Burwell-Charnley scale to assess the effectiveness of surgical repositioning. The clinical outcomes were evaluated using American Orthopaedic Foot & Ankle Society ankle-hind foot score (AOFAS) and visual analog score (VAS). RESULTS: The overall anatomic reduction rate was slightly better in the open fibula fracture line group than in the conventional posterolateral group (81% vs. 71%, p = 0.406), but there was no statistically significant difference between the two groups. There were no statistically significant differences between the two groups in terms of fracture healing time and time to full weight bearing (p > 0.05). At the final follow-up, the AOFAS functional score of the open fibula fracture line group was statistically superior to that of the conventional posterolateral group (p < 0.05). However, there was no statistical difference between the two groups in VAS pain scores at rest, during activity, and under weight bearing (p > 0.05). CONCLUSION: The trans-fibular fracture approach provides a better surgical option for specific types of posterior pilon fractures with a high rate of anatomic repositioning and a good near-term outcome. TRIAL REGISTRATION: Retrospective registration.

Frequency-dependent functional alterations in people living with HIV with early stage of HIV-associated neurocognitive disorder.

Background: HIV enters the brain soon after seroconversion and causes HIV-associated neurocognitive disorder (HAND). However, the pathogenesis of this insidious impairment at an early stage remains unclear. Objectives: To explore functional integration and segregation changes at the early stages of HAND, voxel-level indices of regional homogeneity (ReHo), the amplitude of low-frequency fluctuations (ALFF), and voxel-mirrored homotopic connectivity (VMHC) under two different frequency bands (slow-5: 0.01-0.027 Hz; slow-4: 0.027-0.073 Hz) were analyzed. Methods: Ninety-eight people living with HIV (PLWH) and 44 seronegative controls underwent resting-state functional magnetic resonance imaging. Furthermore, all PLWHs underwent neuropsychological and daily functioning tests. The main effect of the group and the interaction between the group and frequency band were investigated. Finally, the relationship between the altered indices and the cognitive domains was explored. Results: A significant group-by-frequency interaction was demonstrated in the right thalamus for ReHo; for VMHC, the interaction was observed in the bilateral precuneus and paracentral gyrus. The post hoc Bonferroni test indicated that the alteration of ReHo and VMHC could only be detected in slow-5. PLWH showed significantly reduced ALFF in both the frequency bands in the right occipital gyrus and right calcarine. Moreover, some altered functional integration and segregation indices are related to impaired cognitive function. Conclusion: People living with HIV displayed aberrant functional integration and segregation at the early stages of HAND, which is linked to cognitive function. The frequency band of slow-5 might be more sensitive for detecting insidious damage at an early stage.

The second polar body contributes to the fate asymmetry in the mouse embryo.

The polar bodies (PBs) are extruded microcells during oocyte meiosis and generally regarded as inessentials for embryonic development. Therefore, PBs have been widely used as important materials for pre-implantation genetic diagnosis in human. Here we report that the second PB (PB2) in the mouse zygote may play roles in cell-fate specification and post-implantation development. A subset of mRNAs encoding pluripotency-related factors are enriched in PB2. Nascent proteins may be synthesized in PB2 after fertilization and transport from PB2 to the zygote before the two-cell stage. The PB2-attached blastomere (pbB) at the two-cell stage, compared to the other blastomere (npbB), likely contributes more descendants to the inner cell mass (ICM) lineage in the blastocyst. Removal of PB2 from the zygote or transient blockage of material exchange between PB2 and the zygote by nocodazole treatment appears to cause a loss of the ICM fate bias of pbB. PB2 removal or nocodazole treatment also results in abnormal post-implantation development. Injection of PB2 lysate into pbB of PB2-removed two-cell-stage embryos may reset the cell-fate preference and rescue post-implantation development. Our data collectively suggest that PB2 would demarcate the earliest cell-fate asymmetry of the mouse zygote and be required for post-implantation development.

Tet1 Deficiency Leads to Premature Ovarian Failure.

Tet enzymes participate in DNA demethylation and play critical roles in stem cell pluripotency and differentiation. DNA methylation alters with age. We find that Tet1 deficiency reduces fertility and leads to accelerated reproductive failure with age. Noticeably, Tet1-deficient mice at young age exhibit dramatically reduced follicle reserve and the follicle reserve further decreases with age, phenomenon consistent with premature ovarian failure (POF) syndrome. Consequently, Tet1-deficient mice become infertile by reproductive middle age, while age matched wild-type mice still robustly reproduce. Moreover, by single cell transcriptome analysis of oocytes, Tet1 deficiency elevates organelle fission, associated with defects in ubiquitination and declined autophagy, and also upregulates signaling pathways for Alzheimer's diseases, but down-regulates X-chromosome linked genes, such as Fmr1, which is known to be implicated in POF. Additionally, Line1 is aberrantly upregulated and endogenous retroviruses also are altered in Tet1-deficient oocytes. These molecular changes are consistent with oocyte senescence and follicle atresia and depletion found in premature ovarian failure or insufficiency. Our data suggest that Tet1 enzyme plays roles in maintaining oocyte quality as well as oocyte number and follicle reserve and its deficiency can lead to POF.

Molecular Features of Polycystic Ovary Syndrome Revealed by Transcriptome Analysis of Oocytes and Cumulus Cells.

Polycystic ovary syndrome (PCOS) is typically characterized by a polycystic ovarian morphology, hyperandrogenism, ovulatory dysfunction, and infertility. Furthermore, PCOS patients undergoing ovarian stimulation have more oocytes; however, the poor quality of oocytes leads to lower fertilization and implantation rates, decreased pregnancy rates, and increased miscarriage rates. The complex molecular mechanisms underlying PCOS and the poor quality of oocytes remain to be elucidated. We obtained matched oocytes and cumulus cells (CCs) from PCOS patients, compared them with age-matched controls, and performed RNA sequencing analysis to explore the transcriptional characteristics of their oocytes and CCs. Moreover, we validated our newly confirmed candidate genes for PCOS by immunofluorescence. Unsupervised clustering analysis showed that the overall global gene expression patterns and transposable element (TE) expression profiles of PCOS patients tightly clustered together, clearly distinct from those of controls. Abnormalities in functionally important pathways are found in PCOS oocytes. Notably, genes involved in microtubule processes, TUBB8 and TUBA1C, are overexpressed in PCOS oocytes. The metabolic and oxidative phosphorylation pathways are also dysregulated in both oocytes and CCs from PCOS patients. Moreover, in oocytes, differentially expressed TEs are not uniformly dispersed in human chromosomes. Endogenous retrovirus 1 (ERV1) elements located on chromosomes 2, 3, 4, and 5 are rather highly upregulated. Interestingly, these correlate with the most highly expressed protein-coding genes, including tubulin-associated genes TUBA1C, TUBB8P8, and TUBB8, linking the ERV1 elements to the occurrence of PCOS. Our comprehensive analysis of gene expression in oocytes and CCs, including TE expression, revealed the specific molecular features of PCOS. The aberrantly elevated expression of TUBB8 and TUBA1C and ERV1 provides additional markers for PCOS and may contribute to the compromised oocyte developmental competence in PCOS patients. Our findings may also have implications for treatment strategies to improve oocyte maturation and the pregnancy outcomes for women with PCOS.

Induction of meiosis by embryonic gonadal somatic cells differentiated from pluripotent stem cells.

BACKGROUND: Depletion of oocytes leads to ovarian aging-associated infertility, endocrine disruption and related diseases. Excitingly, unlimited oocytes can be generated by differentiation of primordial germ cell like cells (PGCLCs) from pluripotent stem cells. Nevertheless, development of oocytes and follicles from PGCLCs relies on developmentally matched gonadal somatic cells, only available from E12.5 embryos in mice. It is therefore imperative to achieve an in vitro source of E12.5 gonadal somatic cells. METHODS: We explored to identify small molecules, which can induce female embryonic stem cells (ESCs) into gonadal somatic cell like cells. RESULTS: Using RNA-sequencing, we identified signaling pathways highly upregulated in E12.5_gonadal somatic cells (E12.5_GSCs). Through searching for the activators of these pathways, we identified small-molecule compounds Vitamin C (Vc) and AM580 in combination (V580) for inducing differentiation of female embryonic stem cells (ESCs) into E12.5_GSC-like cells (E12.5_GSCLCs). After V580 treatment for 6 days and sorted by a surface marker CD63, the cell population yielded a transcriptome profile similar to that of E12.5_GSCs, which promoted meiosis progression and folliculogenesis of primordial germ cells. This approach will contribute to the study of germ cell and follicle development and oocyte production and have implications in potentially treating female infertility. CONCLUSION: ESCs can be induced into embryonic gonadal somatic cell like cells by small molecules.

Tet1 Deficiency Leads to Premature Reproductive Aging by Reducing Spermatogonia Stem Cells and Germ Cell Differentiation.

Ten-eleven translocation (Tet) enzymes are involved in DNA demethylation, important in regulating embryo development, stem cell pluripotency and tumorigenesis. Alterations of DNA methylation with age have been shown in various somatic cell types. We investigated whether Tet1 and Tet2 regulate aging. We showed that Tet1-deficient mice undergo a progressive reduction of spermatogonia stem cells and spermatogenesis and thus accelerated infertility with age. Tet1 deficiency decreases 5hmC levels in spermatogonia and downregulates a subset of genes important for cell cycle, germ cell differentiation, meiosis and reproduction, such as Ccna1 and Spo11, resulting in premature reproductive aging. Moreover, Tet1 and 5hmC both regulate signaling pathways key for stem cell development, including Wnt and PI3K-Akt, autophagy and stress response genes. In contrast, effect of Tet2 deficiency on male reproductive aging is minor. Hence, Tet1 maintains spermatogonia stem cells with age, revealing an important role of Tet1 in regulating stem cell aging.

Functional Oocytes Derived from Granulosa Cells.

The generation of genomically stable and functional oocytes has great potential for preserving fertility and restoring ovarian function. It remains elusive whether functional oocytes can be generated from adult female somatic cells through reprogramming to germline-competent pluripotent stem cells (gPSCs) by chemical treatment alone. Here, we show that somatic granulosa cells isolated from adult mouse ovaries can be robustly induced to generate gPSCs by a purely chemical approach, with additional Rock inhibition and critical reprogramming facilitated by crotonic sodium or acid. These gPSCs acquired high germline competency and could consistently be directed to differentiate into primordial-germ-cell-like cells and form functional oocytes that produce fertile mice. Moreover, gPSCs promoted by crotonylation and the derived germ cells exhibited longer telomeres and high genomic stability like PGCs in vivo, providing additional evidence supporting the safety and effectiveness of chemical induction, which is particularly important for germ cells in genetic inheritance.

Biomechanical Comparison of Modified TARP Technique Versus Modified Goel Technique for the Treatment of Basilar Invagination: A Finite Element Analysis.

STUDY DESIGN: A finite element analysis. OBJECTIVE: The aim of this study was to determine the biomechanical differences between atlantoaxial fusion cage combined with transoral atlantoaxial reduction plate fixation (TARP + Cage, modified TARP technique) and that combined with C1 lateral mass screw and C2 pedicle screw fixation (C1LS + C2PS + Cage, modified Goel technique) in the treatment of basilar invagination (BI) by finite element analysis. SUMMARY OF BACKGROUND DATA: Clinical studies have shown that transoral anterior atlantoaxial release followed by TARP fixation can achieve reduction, decompression, fixation, and fusion of C1-C2 through a transoral-only approach. Although cage has been used to reduce the BI through posterior approach, there are no studies referred to the cage combined with TARP for C1-C2 fusion. METHODS: A finite element model was used to investigate and compare the stability between TARP + Cage fixation and C1LS + C2PS + Cage fixation in the treatment of BI. Vertical load of 40  N was applied on the C0, to simulate head weight, and 1.5  Nm torque was applied to the C0 to simulate flexion, extension, lateral bending, and rotation. RESULTS: In comparison with the C1LS + C2PS + Cage model, the TARP + Cage model reduced the ROM by 44.7%, 30.0%, and 10.5% in extension, lateral bending, and axial rotation, while the TARP + Cage model increased the ROM by 30.0% in flexion, and the TARP + Cage model also led to lower screw stress in all motions with one exception (anterior C2PS stress in extension). CONCLUSION: Our results indicate that the TARP + Cage fixation may offer higher stability to C1LS + C2PS + Cage in extension, lateral bending, and axial rotation but lower stability in flexion. Compared with modified Goel technique, the modified TARP technique not only has the capability of transferring the load and distributing the stress but also can provide neural decompression, stabilization and fusion, and restore C1-C2 normal fusion angle. LEVEL OF EVIDENCE: N/A.

miR-135a modulates tendon stem/progenitor cell senescence via suppressing ROCK1.

Tendon stem/progenitor cell (TSPC) senescence may lead to age-related tendon disorders and impair tendon regeneration and replacement capacity in humans. However, the mechanisms governing TSPC aging and degeneration remain obscure. Recently, it has been reported that Rho-associated coiled-coil protein kinase 1 (ROCK1) might be a key player in TSPC aging process. miRNAs are also involved in cellular senescence. In this study, whether miRNAs modulate senescence of TSPCs through targeting ROCK1 was evaluated. We found that miR-135a, which directly binds to the 3'-untranslated region of ROCK1, is significantly downregulated in aged compared with young TSPCs. Overexpression of miR-135a in young TSPCs suppresses senescence, promotes proliferation, and induces migration and tenogenic differentiation, whereas suppression of miR-135a in aged TSPCs has the opposite effects. By gain-of-function and loss-of-function studies, we confirmed that ROCK1 mediates the effects of miR-135a in TSPCs. Taken together, our data suggest that miR-135a plays an important role in TSPC senescence via targeting ROCK1.

A comparison of primary and delayed wound closure in severe open tibial fractures initially treated with internal fixation and vacuum-assisted wound coverage: a case-controlled study.

The ideal timing of wound closure for open tibial fractures is debatable. This study aimed to compare outcomes of primary and delayed wound closure in severe open tibial fractures initially treated with internal fixation and vacuum-assisted wound coverage (VAC). Data of 80 patients with Gustilo-Anderson type IIIA and IIIB open tibial fractures treated with primary internal fixation, VAC, either primary wound closure (PWC) or delayed wound closure (DWC), and external fixation were reviewed retrospectively, and outcomes and complications compared. Patients were divided into three groups, including a PWC group (n = 27), DWC group (n = 22), and a control group (n = 31) that had received external fixation. Among all patients, the median age was 38 years (IRQ 32-47 years), and 67.5% were male. Injuries included 33 Gustilo-Anderson type IIIA and 47 type IIIB. Among injuries, 83% (66/80) were high-energy trauma, 63.8% were contaminated and median injury severity score (ISS) was 14 points. Significant differences were found between groups in fixation methods (p < 0.001). No significant differences were observed between groups in rates of deep infection, osteomyelitis, amputation and nonunion at 6 and 12 months (all p > 0.05), although all rates were markedly lower in the PWC group. The outcomes of PWC performed in conjunction with primary internal fixation and VAC for the treatment of Gustilo-Andersen type IIIA and IIIB open tibial fractures are similar to or better than those of DWC with primary internal fixation and VAC.

Effect of minimally invasive percutaneous plates versus interlocking intramedullary nailing in tibial shaft treatment for fractures in adults: a meta-analysis.

OBJECTIVE: The aim of this article was to determine the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults. METHOD: Literature searches of the Cochrane Library, PubMed, EMBASE, the Chinese Biomedical Literature database, the CNKI database, Wanfang Data, and the Weipu Journal database were performed up to August 2013. Only randomized and quasi-randomized controlled clinical trials comparing the use of percutaneous plates and interlocking intramedullary nails for tibial shaft fractures were included. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. RESULTS: Eleven trials were included. Compared with interlocking intramedullary nailing, minimally invasive percutaneous plates shortened fracture healing time and resulted in lower rates of postoperative delayed union and pain. There was no significant difference between the two methods with regard to the rates of excellent and good Johner-Wruh scoring, the rate of reoperation, and other complications. CONCLUSIONS: Overall, insufficient evidence exists regarding the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults. Low-quality evidence suggests that minimally invasive percutaneous plates could shorten fracture healing time, decrease the rate of postoperative delayed union, and decrease pain levels compared with interlocking intramedullary nailing. There is no significant difference between the two groups in terms of functional recovery scores, reoperation, and other complications. Further research that includes high-quality randomized controlled, multicenter trials is required to compare the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults.

Clinical effectiveness analysis of dextran 40 plus dexamethasone on the prevention of fat embolism syndrome.

This study aims to investigate the clinical efficacy of Dextran 40 plus dexamethasone on the prevention of fat embolism syndrome (FES) in high-risk patients with long bone shaft fractures. According to the different preventive medication, a total of 1837 cases of long bone shaft fracture patients with injury severity score (ISS) > 16 were divided into four groups: dextran plus dexamethasone group, dextran group, dexamethasone group and control group. The morbidity and mortality of FES in each group were analyzed with pairwise comparison analysis. There were totally 17 cases of FES and 1 case died. The morbidity of FES was 0.33% in dextran plus dexamethasone group and significantly lowers than that of other groups (P < 0.05). There was no significant difference among other groups (P > 0.05). Conclusion from our data is dextran 40 plus dexamethasone can effectively prevent long bone shaft fractures occurring in high-risk patients with FES.

miR-16 inhibits cell proliferation by targeting IGF1R and the Raf1-MEK1/2-ERK1/2 pathway in osteosarcoma.

Several miRNAs have been implicated in the development and progression of osteosarcoma (OS). In this study, we found that miR-16 is downregulated in OS cell lines and tissues. Overexpression of miR-16 suppresses OS cell proliferation and tumor growth in nude mice. Furthermore, we confirmed that IGF1R is a direct target of miR-16. Mechanistic investigation revealed that miR-16 overexpression inhibits the Raf1-MEK1/2-ERK1/2 pathway. In clinical specimens, IGF1R levels inversely correlate with miR-16 expression. Our results provide significant clues regarding the role of miR-16 as a tumor suppressor by targeting IGF1R in OS.

Effect of minimally invasive percutaneous plates versus interlocking intramedullary nailing in tibial shaft treatment for fractures in adults: A meta-analysis

OBJECTIVE: The aim of this article was to determine the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults. METHOD: Literature searches of the Cochrane Library, PubMed, EMBASE, the Chinese Biomedical Literature database, the CNKI database, Wanfang Data, and the Weipu Journal database were performed up to August 2013. Only randomized and quasi-randomized controlled clinical trials comparing the use of percutaneous plates and interlocking intramedullary nails for tibial shaft fractures were included. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. RESULTS: Eleven trials were included. Compared with interlocking intramedullary nailing, minimally invasive percutaneous plates shortened fracture healing time and resulted in lower rates of postoperative delayed union and pain. There was no significant difference between the two methods with regard to the rates of excellent and good Johner-Wruh scoring, the rate of reoperation, and other complications. CONCLUSIONS: Overall, insufficient evidence exists regarding the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults. Low-quality evidence suggests that minimally invasive percutaneous plates could shorten fracture healing time, decrease the rate of postoperative delayed union, and decrease pain levels compared with interlocking intramedullary nailing. There is no significant difference between the two groups in terms of functional recovery scores, reoperation, and other complications. Further research that includes high-quality randomized controlled, multicenter trials is required to compare the effects of minimally invasive percutaneous plates versus interlocking intramedullary nailing in the treatment of tibial shaft fractures in adults. .