Thyroid cancer and cardiovascular diseases: a Mendelian randomization study.

Background: Multiple observational studies have shown associations between thyroid cancer (TC) and cardiovascular diseases (CVDs). However, the results were inconsistent, and the potential causal genetic relationship remains unclear. Methods: The genetic instruments of TC and CVDs were derived from data obtained through genome-wide association studies (GWAS). We performed the two-sample Mendelian randomization(MR) methods to investigate the causality of TC on CVDs. Summary-level statistics for CVDs, including heart failure (HF), atrial fibrillation (AF), coronary artery disease (CAD), myocardial infarction (MI), ischemic stroke (IS) and venous thromboembolism (VTE). The primary method employed in this MR analysis was the Inverse Variance Weighted (IVW) approach, and four additional algorithms were used: MR-Egger, weighted median, simple mode, and weighted mode. Additionally, we assessed the reliability of the causal relationship through pleiotropy, heterogeneity and leave-one-out sensitivity analysis. Results: In this MR analysis, we only detected causality of genetically predicted TC on HF (IVW method, odds ratio (OR) = 1.00134, 95% confidence interval (CI): 1.00023-1.00244, p = 0.017). However, There were no causal associations of TC with CAD, MI, AF, IS, and VTE. Conclusion: Our results confirmed the causal association between TC and HF. It is crucial to closely monitor the incidence of HF in TC patients and give comprehensive clinical intervention based on conventional treatment.

Cardiometabolic characteristics of people with metabolically healthy and unhealthy obesity.

There is considerable heterogeneity in the cardiometabolic abnormalities associated with obesity. We evaluated multi-organ system metabolic function in 20 adults with metabolically healthy obesity (MHO; normal fasting glucose and triglycerides, oral glucose tolerance, intrahepatic triglyceride content, and whole-body insulin sensitivity), 20 adults with metabolically unhealthy obesity (MUO; prediabetes, hepatic steatosis, and whole-body insulin resistance), and 15 adults who were metabolically healthy lean. Compared with MUO, people with MHO had (1) altered skeletal muscle biology (decreased ceramide content and increased expression of genes involved in BCAA catabolism and mitochondrial structure/function); (2) altered adipose tissue biology (decreased expression of genes involved in inflammation and extracellular matrix remodeling and increased expression of genes involved in lipogenesis); (3) lower 24-h plasma glucose, insulin, non-esterified fatty acids, and triglycerides; (4) higher plasma adiponectin and lower plasma PAI-1 concentrations; and (5) decreased oxidative stress. These findings provide a framework of potential mechanisms responsible for MHO and the metabolic heterogeneity of obesity. This study was registered at ClinicalTrials.gov (NCT02706262).

Impact of particulate-matter air pollution on 25-hydroxyvitamin D levels: a mendelian randomisation study.

OBJECTIVES: In observational studies, the 25-hydroxyvitamin D (25(OH)D) level in body has been found to be closely related to particulate matter (PM) air pollution. In this study, we used the two-sample mendelian randomisation (MR) method to investigate and discuss the potential causal relationship and mode of influence. STUDY DESIGN: MR study. METHODS: PM data (PM10, PM2.5-10, PM2.5, PM2.5 absorbance) came from the UK Biobank database, and 25(OH)D data came from European Bioinformatics Institute (EBI) database. The analysis was conducted utilising three prominent methods (inverse-variance-weighted [IVW], MR-Egger, weighted median, weighted mode, and simple mode). The primary emphasis was placed on IVW, accompanied by heterogeneity and horizontal pleiotropy tests. Furthermore, sensitivity analysis was undertaken. RESULTS: The MR analysis revealed a significant association between exposure to PM10 and a decrease in levels of 25(OH)D (odds ratio [OR]: 0.878, 95% confidence interval [CI]: 0.789-0.977). However, no significant relationship was observed between PM2.5 exposure and 25(OH)D (OR: 0.943, 95%CI: 0.858-1.037). Further analysis indicated that the main contributor to the decline in 25(OH)D levels is linked to PM2.5-10 exposure (OR: 0.840, 95%CI: 0.751-0.940) and PM2.5 absorbance (OR: 0.875, 95%CI: 0.824-0.929). No heterogeneity and horizontal pleiotropy existed. CONCLUSIONS: The MR results suggest that PM (PM10, PM2.5-10 and PM2.5 absorbance) exposure lowers vitamin D (VD) levels, but PM2.5 was not found to have a significant effect on VD in humans.

Potential causal associations of PM2.5 and osteoporosis: a two-sample mendelian randomization study.

Background: Observational studies suggest a potential association between atmospheric particulate matter 2.5 (PM2.5) and osteoporosis, but a causal association is unclear due to the presence of confounding factors. Methods: We utilized bone mineral density indices at four specific sites to represent osteoporosis: femoral neck (FN-BMD), lumbar spine (LS-BMD), forearm (FA-BMD), and heel (HE-BMD). The PM2.5 data was obtained from the UK Biobank database, while the datasets for FN-BMD, LS-BMD, and FA-BMD were obtained from the GEFOS database, and the dataset for HE-BMD was obtained from the EBI database. A two-sample Mendelian randomization analysis was conducted using mainly the inverse variance weighted method, horizontal pleiotropy and heterogeneity were also assessed. Results: The results indicated that PM2.5 was not correlated with a decrease in FN-BMD (ß: -0.305, 95%CI: -0.762, 0.153), LS-BMD (ß: 0.134, 95%CI: -0.396, 0.666), FA-BMD (ß: -0.056, 95%CI: -1.172,1.060), and HE-BMD (ß: -0.084, 95%CI: -0.261,0.093). Additionally, acceptable levels of horizontal pleiotropy and heterogeneity were observed. Conclusion: In contrast to most observational studies, our research did not discover a potential causal relationship between PM2.5 and the development of osteoporosis.

Cholesterol 25-hydroxylase mediates neuroinflammation and neurodegeneration in a mouse model of tauopathy.

Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles, in addition to neuroinflammation and changes in brain lipid metabolism. 25-Hydroxycholesterol (25-HC), a known modulator of both inflammation and lipid metabolism, is produced by cholesterol 25-hydroxylase encoded by Ch25h expressed as a "disease-associated microglia" signature gene. However, whether Ch25h influences tau-mediated neuroinflammation and neurodegeneration is unknown. Here, we show that in the absence of Ch25h and the resultant reduction in 25-HC, there is strikingly reduced age-dependent neurodegeneration and neuroinflammation in the hippocampus and entorhinal/piriform cortex of PS19 mice, which express the P301S mutant human tau transgene. Transcriptomic analyses of bulk hippocampal tissue and single nuclei revealed that Ch25h deficiency in PS19 mice strongly suppressed proinflammatory signaling in microglia. Our results suggest a key role for Ch25h/25-HC in potentiating proinflammatory signaling to promote tau-mediated neurodegeneration. Ch25h may represent a novel therapeutic target for primary tauopathies, AD, and other neuroinflammatory diseases.

Potential causal association between leisure sedentary behaviors and osteoporosis: A two-sample Mendelian randomization analysis.

Previous observational studies have observed a correlation between sedentary behavior and osteoporosis. However, conclusions from these studies have been contradictory. To explore the potential causal relationship between sedentary behavior and osteoporosis, we conducted a Mendelian randomization analysis. A two-sample Mendelian randomization was adopted to explore the causal relationship of leisure sedentary behavior with osteoporosis. We employed 5 methods to estimate the causal associations between leisure sedentary behavior and osteoporosis. Univariable Mendelian randomization results provided evidence for the causal relationship of the time spent on computer-use with the bone mineral density estimated by heel quantitative ultrasound (eBMD) (inverse variance weighted [IVW]: ß (95% confidence interval [CI]) - 0.150 (-0.270 to -0.031), P = .013; weighted median: ß (95%CI) - 0.195 (-0.336 to -0.055), P = .006). Similar associations were observed in the driving forearm bone mineral density (FABMD) (IVW: ß (95%CI) - 0.933 (-1.860 to -0.007), P = .048) and driving lumbar spine bone mineral density (IVW: ß (95%CI) - 0.649 (-1.175 to -0.124), P = .015). However, we did not find a significant causal relationship between the time spent on watching TV and bone mineral density. Research showed that there was a causal relationship between the time spent on computer use and driving time and eBMD, FABMD, and lumbar spine bone mineral density.

Synthesis of carbon quantum dots/porous aromatic frameworks (CQDs/PAF-45) composites and their enhanced photocatalytic performance.

Modification and functionalization of porous aromatic framework (PAF) materials have emerged as crucial research directions in various fields. In this study, we employed a hydrothermal method to synthesize a carbon quantum dots (CQDs) solution. By loading different amounts of CQDs onto the surface of PAF-45 material through ultrasonic and hydrothermal treatments, we successfully formed CQDs/PAF-45 composite materials. The introduction of CQDs effectively transformed the hydrophobic nature of PAF-45 into a hydrophilic material, thereby overcoming the challenge of achieving efficient contact between PAF catalysts and reactants in aqueous solutions. In the photocatalytic degradation experiments of Rhodamine B (RhB), tetracycline, CQDs/PAF-45 composite materials surpassed that of the pristine PAF-45 material. Notably, the 1 wt% CQDs/PAF-45 composite material exhibited the highest photocatalytic activity, with degradation efficiencies for Rhodamine B, tetracycline, and phenol approximately 1.4 times, 1.5 times and 1.5 times higher than those of the PAF-45 material, respectively.

Lei's formula attenuates osteoarthritis mediated by suppression of chondrocyte senescence via the mTOR axis: in vitro and in vivo experiments.

Lei's formula (LSF), a traditional Chinese herbal remedy, is recognized for its remarkable clinical effectiveness in treating osteoarthritis (OA). Despite its therapeutic potential, the exact molecular mechanisms underlying LSF's action in OA have remained enigmatic. Existing research has shed light on the role of the mTOR signaling pathway in promoting chondrocyte senescence, a central factor in OA-related cartilage degeneration. Consequently, targeting mTOR to mitigate chondrocyte senescence presents a promising avenue for OA treatment. The primary objective of this study is to establish LSF's chondroprotective potential and confirm its anti-osteoarthritic efficacy through mTOR inhibition. In vivo assessments using an OA mouse model reveal substantial articular cartilage degeneration. However, LSF serves as an effective guardian of articular cartilage, evidenced by reduced subchondral osteosclerosis, increased cartilage thickness, improved surface smoothness, decreased OARSI scores, elevated expression of cartilage anabolic markers (Col2 and Aggrecan), reduced expression of catabolic markers (Adamts5 and MMP13), increased expression of the chondrocyte hypertrophy marker (Col10), and decreased expression of chondrocyte senescence markers (P16 and P21). In vitro findings demonstrate that LSF shields chondrocytes from H2O2-induced apoptosis, inhibits senescence, enhances chondrocyte differentiation, promotes the synthesis of type II collagen and proteoglycans, and reduces cartilage degradation. Mechanistically, LSF suppresses chondrocyte senescence through the mTOR axis, orchestrating the equilibrium between chondrocyte anabolism and catabolism, ultimately leading to reduced apoptosis and decelerated OA cartilage degradation. LSF holds significant promise as a therapeutic approach for OA treatment, offering new insights into potential treatments for this prevalent age-related condition.

Plasma and cerebrospinal fluid proteomic signatures of acutely sleep-deprived humans: an exploratory study.

Study Objectives: Acute sleep deprivation affects both central and peripheral biological processes. Prior research has mainly focused on specific proteins or biological pathways that are dysregulated in the setting of sustained wakefulness. This exploratory study aimed to provide a comprehensive view of the biological processes and proteins impacted by acute sleep deprivation in both plasma and cerebrospinal fluid (CSF). Methods: We collected plasma and CSF from human participants during one night of sleep deprivation and controlled normal sleep conditions. One thousand and three hundred proteins were measured at hour 0 and hour 24 using a high-scale aptamer-based proteomics platform (SOMAscan) and a systematic biological database tool (Metascape) was used to reveal altered biological pathways. Results: Acute sleep deprivation decreased the number of upregulated and downregulated biological pathways and proteins in plasma but increased upregulated and downregulated biological pathways and proteins in CSF. Predominantly affected proteins and pathways were associated with immune response, inflammation, phosphorylation, membrane signaling, cell-cell adhesion, and extracellular matrix organization. Conclusions: The identified modifications across biofluids add to evidence that acute sleep deprivation has important impacts on biological pathways and proteins that can negatively affect human health. As a hypothesis-driving study, these findings may help with the exploration of novel mechanisms that mediate sleep loss and associated conditions, drive the discovery of new sleep loss biomarkers, and ultimately aid in the identification of new targets for intervention to human diseases.

Causal relationship between breakfast skipping and bone mineral density: a two-sample Mendelian randomized study.

Objective: To explore the causal association between breakfast skipping and bone mineral density (BMD) through two-sample Mendelian randomisation (MR) analysis. Methods: A two-sample MR approach was adopted to explore the causal relationship of breakfast skipping with BMDs (across three skeletal sites and five age groups). Publicly available genome-wide association study summary data were used for MR analysis. We used five methods to estimate the causal associations between breakfast skipping and BMDs: inverse-variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode. IVW was used for the main analysis and the remaining four methods were used as supplementary analyses. The heterogeneity of the MR results was determined using IVW and MR-Egger methods. The pleiotropy of the MR results was determined using MR-Egger intercept. Furthermore, a leave-one-out test was performed to determine whether the MR results were affected by a single nucleotide polymorphism. Results: With the IVW method, we did not find any causal relationship between breakfast skipping and forearm, femoral neck, and lumbar spine BMD. Subsequently, when we included BMD data stratified by five different age groups in the analysis, the results showed that there was no apparent causal effect between breakfast skipping and age-stratified BMD. This finding was supported by all four supplementary methods (P > 0.05 for all methods). No heterogeneity or horizontal pleiotropy was detected in any of the analyses (P > 0.05). The leave-one-out tests conducted in the analyses did not identify any single nucleotide polymorphism that could have influenced the MR results, indicating the reliability of our findings. Conclusion: No causal effect was found between breakfast skipping and BMD (across three skeletal sites and five age groups).

Reference values of gait parameters in healthy Chinese university students: A cross-sectional observational study.

BACKGROUND: Gait is influenced by race, age, and diseases type. Reference values for gait are closely related to numerous health outcomes. To gain a comprehensive understanding of gait patterns, particularly in relation to race-related pathologies and disorders, it is crucial to establish reference values for gait in daily life considering sex and age. Therefore, our objective was to present sex and age-based reference values for gait in daily life, providing a valuable foundation for further research and clinical applications. AIM: To establish reference values for lower extremity joint kinematics and kinetics during gait in asymptomatic adult women and men. METHODS: Spatiotemporal, kinematics and kinetics parameters were measured in 171 healthy adults (70 males and 101 females) using the computer-aided soft tissue foot model. Full curve statistical parametric mapping was performed using independent and paired-samples t-tests. RESULTS: Compared with females, males required more time (cycle time, double-limb support time, stance time, swing time, and stride time), and the differences were statistically significant. In addition, the step and stride lengths of males were longer. Compared to males, female cadence was faster, and statures-per-second and stride-per-minute were higher. There were no statistical differences in speed and stride width between the two groups. After adjusting for height, it was observed that women walked significantly faster than men, and they also had a higher cadence. However, in terms of step length, stride length, and stride width, both genders exhibited similarities. CONCLUSION: We established reference values for gait speed and spatiotemporal gait parameters in Chinese university students. This contributes to a valuable database for gait assessment and evaluation of preventive or rehabilitative programs.

Nickel-catalysed asymmetric hydromonofluoromethylation of 1,3-enynes for enantioselective construction of monofluoromethyl-tethered chiral allenes.

An unprecedented nickel-catalysed enantioselective hydromonofluoromethylation of 1,3-enynes is developed, allowing the diverse access to monofluoromethyl-tethered axially chiral allenes, including the challenging deuterated monofluoromethyl (CD2F)-tethered ones that are otherwise inaccessible. It represents the first asymmetric 1,4-hydrofunctionalization of 1,3-enynes using low-cost asymmetric nickel catalysis, thus opening a new avenue for the activation of 1,3-enynes in reaction development. The utility is further verified by its broad substrate scope, good functionality tolerance, mild conditions, and diversified product elaborations toward other valuable fluorinated structures. Mechanistic experiments and DFT calculations provide insights into the reaction mechanism and the origin of the enantioselectivity.

Comparative bioactivity of S-methoprene and novel S-methobutene against mosquitoes (Diptera: Culicidae).

Mosquitoes and mosquito-borne illnesses significantly impact public health and human well-being. To address this concern, environmentally compatible larvicides have become a critical component of integrated mosquito management. However, the number of available larvicides is at a historical low. Currently, larvicides that harness microbials and insect growth regulators account for most products. Screening of new active ingredients (AIs) or improvement of existing AIs is thus necessary to augment the capacity for mosquito control. S-methoprene possesses a similar molecular structure and identical function to mosquito juvenile hormone and has been one of the main targets for research and development. The efficacy and safety of S-methoprene have been well documented since the late 1960s, and numerous products have been commercialized to combat pests of economic importance. However, S-methoprene is vulnerable to environmental factors that lead to its degradation, which has created challenges in formulation development, particularly where extended efficacy is desired. A derivative of S-methoprene, namely S-methobutene, with molecular modification has become available. This derivative has demonstrated an enhanced activity of inhibition of emergence (IE) against species across the Aedes, Anopheles, and Culex genera at IE10, IE50, and IE90. Furthermore, S-methobutene consistently outperformed S-methoprene during a 120-day aging process against the southern house mosquito Cx. quinquefasciatus, where the IE% in S-methobutene was significantly higher than that in S-methoprene on most aging intervals. The former had significantly longer residual activity than the latter. The potential of S-methobutene for further development and application is discussed in consideration of its enhanced activity and stability.

Serum Proteomic Analysis of Peripartum Cardiomyopathy Reveals Distinctive Dysregulation of Inflammatory and Cholesterol Metabolism Pathways.

BACKGROUND: The pathophysiology of peripartum cardiomyopathy (PPCM) and its distinctive biological features remain incompletely understood. High-throughput serum proteomic profiling, a powerful tool to gain insights into the pathophysiology of diseases at a systems biology level, has never been used to investigate PPCM relative to nonischemic cardiomyopathy. OBJECTIVES: The aim of this study was to characterize the pathophysiology of PPCM through serum proteomic analysis. METHODS: Aptamer-based proteomic analysis (SomaScan 7K) was performed on serum samples from women with PPCM (n = 67), women with nonischemic nonperipartum cardiomyopathy (NPCM) (n = 31), and age-matched healthy peripartum and nonperipartum women (n = 10 each). Serum samples were obtained from the IPAC (Investigation of Pregnancy-Associated Cardiomyopathy) and IMAC2 (Intervention in Myocarditis and Acute Cardiomyopathy) studies. RESULTS: Principal component analysis revealed unique clustering of each patient group (P for difference <0.001). Biological pathway analyses of differentially measured proteins in PPCM relative to NPCM, before and after normalization to pertinent healthy controls, highlighted specific dysregulation of inflammatory pathways in PPCM, including the upregulation of the cholesterol metabolism-related anti-inflammatory pathway liver-X receptor/retinoid-X receptor (LXR/RXR) (P < 0.01, Z-score 1.9-2.1). Cardiac recovery by 12 months in PPCM was associated with the downregulation of pro-inflammatory pathways and the upregulation of LXR/RXR, and an additional RXR-dependent pathway involved in the regulation of inflammation and metabolism, peroxisome proliferator-activated receptor α/RXRα signaling. CONCLUSIONS: Serum proteomic profiling of PPCM relative to NPCM and healthy controls indicated that PPCM is a distinct disease entity characterized by the unique dysregulation of inflammation-related pathways and cholesterol metabolism-related anti-inflammatory pathways. These findings provide insight into the pathophysiology of PPCM and point to novel potential therapeutic targets.

Ability of lactulose breath test results to accurately identify colorectal polyps through the measurement of small intestine bacterial overgrowth.

BACKGROUND: While colorectal polyps are not cancerous, some types of polyps, known as adenomas, can develop into colorectal cancer over time. Polyps can often be found and removed by colonoscopy; however, this is an invasive and expensive test. Thus, there is a need for new methods of screening patients at high risk of developing polyps. AIM: To identify a potential association between colorectal polyps and small intestine bacteria overgrowth (SIBO) or other relevant factors in a patient cohort with lactulose breath test (LBT) results. METHODS: A total of 382 patients who had received an LBT were classified into polyp and non-polyp groups that were confirmed by colonoscopy and pathology. SIBO was diagnosed by measuring LBT-derived hydrogen (H) and methane (M) levels according to 2017 North American Consensus recommendations. Logistic regression was used to assess the ability of LBT to predict colorectal polyps. Intestinal barrier function damage (IBFD) was determined by blood assays. RESULTS: H and M levels revealed that the prevalence of SIBO was significantly higher in the polyp group than in the non-polyp group (41% vs 23%, P < 0.01; 71% vs 59%, P < 0.05, respectively). Within 90 min of lactulose ingestion, the peak H values in the adenomatous and inflammatory/hyperplastic polyp patients were significantly higher than those in the non-polyp group (P < 0.01, and P = 0.03, respectively). In 227 patients with SIBO defined by combining H and M values, the rate of IBFD determined by blood lipopolysaccharide levels was significantly higher among patients with polyps than those without (15% vs 5%, P < 0.05). In regression analysis with age and gender adjustment, colorectal polyps were most accurately predicted with models using M peak values or combined H and M values limited by North American Consensus recommendations for SIBO. These models had a sensitivity of ≥ 0.67, a specificity of ≥ 0.64, and an accuracy of ≥ 0.66. CONCLUSION: The current study made key associations among colorectal polyps, SIBO, and IBFD and demonstrated that LBT has moderate potential as an alternative noninvasive screening tool for colorectal polyps.

Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a lethal muscle disease caused by absence of the protein dystrophin, which acts as a structural link between the basal lamina and contractile machinery to stabilize muscle membranes in response to mechanical stress. In DMD, mechanical stress leads to exaggerated membrane injury and fiber breakdown, with fast fibers being the most susceptible to damage. A major contributor to this injury is muscle contraction, controlled by the motor protein myosin. However, how muscle contraction and fast muscle fiber damage contribute to the pathophysiology of DMD has not been well characterized. We explored the role of fast skeletal muscle contraction in DMD with a potentially novel, selective, orally active inhibitor of fast skeletal muscle myosin, EDG-5506. Surprisingly, even modest decreases of contraction (<15%) were sufficient to protect skeletal muscles in dystrophic mdx mice from stress injury. Longer-term treatment also decreased muscle fibrosis in key disease-implicated tissues. Importantly, therapeutic levels of myosin inhibition with EDG-5506 did not detrimentally affect strength or coordination. Finally, in dystrophic dogs, EDG-5506 reversibly reduced circulating muscle injury biomarkers and increased habitual activity. This unexpected biology may represent an important alternative treatment strategy for Duchenne and related myopathies.

Highly Enantioselective Construction of Multifunctional Silicon-Stereogenic Silacycles by Asymmetric Enamine Catalysis.

We report the first highly enantioselective construction of silicon-stereocenters by asymmetric enamine catalysis. An unprecedented desymmetric intramolecular aldolization of prochiral siladials was thus developed for the facile access of multifunctional silicon-stereogenic silacycles in high to excellent enantioselectivity. With an enal moiety, these adducts could be readily elaborated for the diverse synthesis of silicon-stereogenic compounds, and for late-stage modification.

Nickel-catalyzed regio- and enantio-selective Markovnikov hydromonofluoroalkylation of 1,3-dienes.

A highly enantio- and regio-selective Markovnikov hydromonofluoro(methyl)alkylation of 1,3-dienes was developed using redox-neutral nickel catalysis. It provided a facile strategy to construct diverse monofluoromethyl- or monofluoroalkyl-containing chiral allylic molecules. Notably, this represents the first catalytic asymmetric Markovnikov hydrofluoroalkylation of olefins. The practicability of this methodology is further highlighted by its broad substrate scope, mild base-free conditions, excellent enantio- and regio-selectivity, and diversified product elaborations to access useful fluorinated building blocks.

Me2(CH2Cl)SiCF3 Facilitated Tandem Synthesis of Oxasilacycles Featuring a Trifluoromethyl Group.

An unprecedented tandem trifluoromethylsilylation/intramolecular SN2 substitution sequence was realized by using bifunctional reagent Me2(CH2Cl)SiCF3, allowing efficient construction of valuable trifluoromethylated oxasilacyclohexanes that are difficult to access by known methods. Initial attempts into developing asymmetric variant reveal that using cinchonine-derived dimeric PTC catalyst could afford chiral oxasilacyclohexanes in up to 92% enantiomeric excess.

Comparison of flexible fixation and screw fixation for isolated Lisfranc ligament injuries: A protocol for a meta-analysis of comparative studies.

BACKGROUND: The frequency of isolated Lisfranc ligament (ILL) injuries has been increasing recently with the increase in low-energy trauma resulting from sports injuries. For ILL injuries, the optimal method of fixation still remains controversial. The traditional fixation method is achieved by trans-articular screws, but recently, dorsal bridge plates and suture button (SB) fixation have become alternatives. Some biomechanical studies have showed that SB fixation can provide adequate strength compared to trans-articular screws. Therefore, a meta-analysis is imperative to provide evidence on whether flexible fixation is comparable to screw fixation for treatment of ILL injuries. METHODS: We will conduct a comprehensive literature search in PubMed, Cochrane Library, EMBASE and Web of Science databases and for comparative studies. We will apply the risk-of-bias tool of the Cochrane Collaboration for Randomized Controlled Trials to assess the methodological quality. Risk-of-Bias Assessment Tool for Non-randomized Studies was used to evaluate the quality of comparative studies. Statistical analysis will be conducted using RevMan 5.4 software (Cochrane Collaboration, London, England). RESULTS: This systematic review will evaluate the functional outcomes and radiographic results of flexible fixation for treatment of ILL injuries. CONCLUSION: The conclusion of this study will provide evidence for judging whether flexible fixation is superior to screw fixation for treatment of ILL injuries.