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BACKGROUND: Anemia is strongly associated with late-life depression (LLD), however, few studies have investigated the relationship between anemia and suicide attempts in LLD patients. It is still challenging to predict suicide risk in patients with depression. Therefore, there is growing interest in potential biomarkers of depressive disorders and suicidal behavior, which may play a significant role in the early diagnosis and treatment of depression. This study aimed to compare serum ferritin, folate, vitamin B12, and erythrocyte parameter levels in patients with LLD with those in healthy older adults, and the relationship between serum ferritin, folate, vitamin B12, and suicide attempts in patients. METHODS: Serum ferritin, folate, vitamin B12, and erythrocyte parameter levels were measured in 66 hospitalized LLD patients (30 without suicide attempt, 36 with suicide attempt) and 47 healthy individuals. All participants were surveyed for basic conditions and suicide attempts, and depression was assessed in LLD patients. RESULTS: Serum ferritin, folate, vitamin B12, red blood cell count, hemoglobin, hematocrit, mean platelet volume and plateletcrit levels were significantly lower in LLD patients compared with healthy older adults (P < 0.05). Further analysis of the relationship between serum ferritin, folate, and vitamin B12 levels and LLD patients' suicide attempts and showed a significant negative association between serum folate and vitamin B12 and suicide attempts (P < 0.05). CONCLUSIONS: Serum ferritin, folate, vitamin B12, red blood cell count, hemoglobin, hematocrit, mean platelet volume and plateletcrit levels were significantly lower in LLD patients than in healthy older adults. In addition, reduced serum folate and vitamin B12 levels in patients may have some effect on suicide attempts. More mechanistic studies are needed to further explain this association.
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Anemia , Pacientes Internos , Humanos , Anciano , Intento de Suicidio , Depresión/diagnóstico , Depresión/epidemiología , Anemia/diagnóstico , Anemia/epidemiología , Ácido Fólico , Vitamina B 12 , Hemoglobinas , Ferritinas , VitaminasRESUMEN
PURPOSE: To compare the postoperative rehabilitation of femoral neck fractures treated with robot-assisted nailing and freehand nailing. METHODS: We systematically searched the PubMed, EMBASE, Cochrane, China National Knowledge Infrastructure(CNKI), WanFang database, China Science and Technology Journal Database (VIP) and Web of Science databases to identify potentially eligible articles. Indispensable data such as the year of publication, country, study type, robot type, age, number of patients, sex distribution, study design, and outcome indicators were extracted. The outcome indicators of interest included healing rate, length of healing time, Harris score, operation time, frequency of X-ray fluoroscopy, frequency of guide pin insertion, and intraoperative blood loss. RevMan 5.4.1 was used for the meta-analysis. RESULTS: Fourteen studies with 908 participants were included in this meta-analysis. The results showed that in terms of healing rate (SMD = 2.75, 95% CI, 1.03 to 7.32, P = 0.04) and Harris score (SMD = 2.27, 95% CI, 0.79 to 3.75, P = 0.003), robot-assisted screw placement technique scores were higher than the traditional freehand technique. Additionally, operative time (SMD = -12.72, 95% CI, -19.74 to -5.70, P = 0.0004), healing time (SMD = -13.63, 95% CI, -20.18 to -7.08, P < 0.0001), frequency of X-ray fluoroscopy (SMD = - 13.64, 95% CI, - 18.32 to - 8.95, P < 0.00001), frequency of guide pin insertion (SMD = - 7.95, 95% CI, - 10.13 to - 5.76, P < 0.00001), and intraoperative blood loss (SMD = - 17.33, 95% CI, - 23.66 to - 11.00, P < 0.00001) were lower for patients who underwent robotic-assisted screw placement than those for patients who underwent the conventional freehand technique. CONCLUSION: Compared to the freehand nailing technique, robot-assisted nailing helps improve postoperative healing rates in patients with femoral neck fractures; shortens healing times; better restores hip function; reduces the number of intraoperative fluoroscopies, guides pin placements; reduces intraoperative bleeding; and increases perioperative safety.
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Fracturas del Cuello Femoral , Procedimientos Quirúrgicos Robotizados , Humanos , Pérdida de Sangre Quirúrgica , Tornillos Óseos , Fracturas del Cuello Femoral/rehabilitación , Fracturas del Cuello Femoral/cirugía , Estudios Retrospectivos , Procedimientos Quirúrgicos Robotizados/métodos , Resultado del TratamientoRESUMEN
Parkinson's disease (PD) is currently the fastest growing disabling neurological disorder worldwide, with motor and non-motor symptoms being its main clinical manifestations. The primary pathological features include a reduction in the number of dopaminergic neurons in the substantia nigra and decrease in dopamine levels in the nigrostriatal pathway. Existing treatments only alleviate clinical symptoms and do not stop disease progression; slowing down the loss of dopaminergic neurons and stimulating their regeneration are emerging therapies. Preclinical studies have demonstrated that transplantation of dopamine cells generated from human embryonic or induced pluripotent stem cells can restore the loss of dopamine. However, the application of cell transplantation is limited owing to ethical controversies and the restricted source of cells. Until recently, the reprogramming of astrocytes to replenish lost dopaminergic neurons has provided a promising alternative therapy for PD. In addition, repair of mitochondrial perturbations, clearance of damaged mitochondria in astrocytes, and control of astrocyte inflammation may be extensively neuroprotective and beneficial against chronic neuroinflammation in PD. Therefore, this review primarily focuses on the progress and remaining issues in astrocyte reprogramming using transcription factors (TFs) and miRNAs, as well as exploring possible new targets for treating PD by repairing astrocytic mitochondria and reducing astrocytic inflammation.
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Astrocitos , Enfermedad de Parkinson , Humanos , Astrocitos/metabolismo , Dopamina/metabolismo , Enfermedad de Parkinson/metabolismo , Neuronas Dopaminérgicas/metabolismo , Inflamación/metabolismoRESUMEN
BACKGROUND: Cutaneous squamous cell carcinoma (CSCC) is the second largest nonmelanoma skin cancer in humans; effective treatment options for metastatic CSCC are still in short. In this study, we aimed to explore the function of T-box transcription factor 2 (TBX2) in CSCC. METHODS: The expression level of TBX2 was determined in CSCC samples and cell lines. Programmed death ligand 1 (PD-L1) expression was also analyzed in human CSCC samples. Furthermore, SCC13 cells were transfected with TBX2-DN (loss of function) or normal TBX2 to check its role in regulating PD-L1. RESULTS: The expression level of TBX2 was positively correlated with the stage of CSCC. CSCC tumor cell lines have significantly higher expression levels of TBX2 than normal skin cell lines, and SCC13 cells showed the highest expression. PD-L1 expressions were upregulated during the progression of CSCC, and positively correlated with TBX2. Furthermore, PD-L1 expression increased in SCC13 cells overexpressing TBX2. However, TBX2 did not regulate the activation of IFNγ signal, but mediated the expression of interferon regulatory factor 1 (IRF1) and PD-L1 in both SCC13 and PDV cells. CONCLUSION: TBX2 could mediate antitumor immune response in CSCC by regulating the expression of PD-L1 through IRF1. It might be a prognostic marker in CSCC and synergistic target for PD-1 immunotherapy.
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Carcinoma de Células Escamosas , Neoplasias Cutáneas , Humanos , Carcinoma de Células Escamosas/patología , Antígeno B7-H1/metabolismo , Neoplasias Cutáneas/patología , Inmunidad , Factores de TranscripciónRESUMEN
BACKGROUND: Circadian disturbance is a common nonmotor complaint in Parkinson's disease (PD). The molecular basis underlying circadian rhythm in PD is poorly understood. Neuroinflammation has been identified as a key contributor to PD pathology. In this study, we explored the potential link between the core clock molecule Rev-erbα and the microglia-mediated NLR family pyrin domain-containing 3 (NLRP3) inflammasome in PD pathogenesis. METHODS: We first examined the diurnal Rev-erbα rhythms and diurnal changes in microglia-mediated inflammatory cytokines expression in the SN of MPTP-induced PD mice. Further, we used BV2 cell to investigate the impacts of Rev-erbα on NLRP3 inflammasome and microglial polarization induced by 1-methyl-4-phenylpyridinium (MPP+) and αsyn pre-formed fibril. The role of Rev-erbα in regulating microglial activation via NF-κB and NLRP3 inflammasome pathway was then explored. Effects of SR9009 against NLRP3 inflammasome activation, microgliosis and nigrostriatal dopaminergic degeneration in the SN and striatum of MPTP-induced PD mice were studied in detail. RESULTS: BV2 cell-based experiments revealed the role of Rev-erbα in regulating microglial activation and polarization through the NF-κB and NLRP3 inflammasome pathways. Circadian oscillation of the core clock gene Rev-erbα in the substantia nigra (SN) disappeared in MPTP-induced PD mice, as well as diurnal changes in microglial morphology. The expression of inflammatory cytokines in SN of the MPTP-induced mice were significantly elevated. Furthermore, dopaminergic neurons loss in the nigrostriatal system were partially reversed by SR9009, a selective Rev-erbα agonist. In addition, SR9009 effectively reduced the MPTP-induced glial activation, microglial polarization and NLRP3 inflammasome activation in the nigrostriatal system. CONCLUSIONS: These observations suggest that the circadian clock protein Rev-erbα plays an essential role in attenuating neuroinflammation in PD pathology, and provides a potential therapeutic target for PD treatment.
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Relojes Circadianos , Enfermedad de Parkinson , 1-Metil-4-fenil-1,2,3,6-Tetrahidropiridina/farmacología , Animales , Proteínas CLOCK/genética , Proteínas CLOCK/metabolismo , Citocinas/metabolismo , Inflamasomas/metabolismo , Ratones , Ratones Endogámicos C57BL , Microglía/metabolismo , FN-kappa B/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Enfermedades Neuroinflamatorias , Neuroprotección , Enfermedad de Parkinson/patologíaRESUMEN
The microRNA miR-30a has been reported to mitigate podocyte damage and resist injurious factors in lupus nephritis (LN), but the precise molecular mechanisms underlying these effects remain elusive. We hypothesized that miR-30a can ameliorate podocyte injury by downregulating the Notch1 signaling pathway and investigated the role of miR-30a in the pathogenesis of podocyte-treated with Immunoglobulin G from patients with LN (IgG-LN). The study enrolled 30 patients from new-onset systemic lupus erythematosus and 28 healthy individuals, then evaluated the levels of their serum miR-30a using RT-qPCR. Additionally, MPC5 cells were transfected with NICD-vector to overexpress Notch1, then with miR-30a mimics or inhibitors to determine miR-30a effects on Notch1. Analysis of function and regulatory mechanisms were performed with RT-qPCR, Western blotting, and CCK8 assays. Furthermore, we verified the candidate sequence targeted by miR-30a using a luciferase reporter gene assay. We observed a significant decrease in the serum miR-30a levels in patients with LN. Also, in IgG-LN-treated podocytes, miR-30a decreased and Notch1 expression was elevated. Bioinformatic analysis and transfection experiments revealed that Notch1 is a direct target of miR-30a. Further supporting this finding, miR-30a upregulation appeared to alleviate IgG-LN-treated podocyte injury, and Notch1 overexpression reversed this effect. To conclude, miR-30a can ameliorate podocyte injury via suppression of the Notch1 signaling pathway.
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Lupus Eritematoso Sistémico , Nefritis Lúpica , MicroARNs , Podocitos , Humanos , Inmunoglobulina G/metabolismo , Lupus Eritematoso Sistémico/metabolismo , Nefritis Lúpica/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Podocitos/metabolismo , Podocitos/patología , Receptor Notch1/genética , Receptor Notch1/metabolismoRESUMEN
Increasing evidence suggests that microglial activation is strongly linked to the initiation and progression of Parkinson's disease. Cell-to-cell propagation of α-synuclein pathology is a highlighted feature of Parkinson's disease, and the focus of such research has been primarily on neurons. However, recent studies as well as the data contained herein suggest that microglia, the primary phagocytes in the brain, play a direct role in the spread of α-synuclein pathology. Recent data revealed that plasma exosomes derived from Parkinson's disease patients (PD-EXO) carry pathological α-synuclein and target microglia preferentially. Hence, PD-EXO are likely a key tool for investigating the role of microglia in α-synuclein transmission. We showed that intrastriatal injection of PD-EXO resulted in the propagation of exosomal α-synuclein from microglia to neurons following microglia activation. Toll-like receptor 2 (TLR2) in microglia was activated by exosomal α-synuclein and acted as a crucial mediator of PD-EXO-induced microglial activation. Additionally, partial microglia depletion resulted in a significant decrease of exogenous α-synuclein in the substantia nigra. Furthermore, exosomal α-synuclein internalization was initiated by binding to TLR2 of microglia. Excessive α-synuclein phagocytosis may induce the inflammatory responses of microglia and provide the seed for microglia-to-neuron transmission. Consistently, TLR2 silencing in microglia mitigated α-synuclein pathology in vivo. Overall, the present data support the idea that the interaction of exosomal α-synuclein and microglial TLR2 contribute to excessive α-synuclein phagocytosis and microglial activation, which lead to the further propagation and spread of α-synuclein pathology, thereby highlighting the pivotal roles of reactive microglia in α-synuclein transmission.
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Exosomas/metabolismo , Microglía/metabolismo , Enfermedad de Parkinson/metabolismo , Receptor Toll-Like 2/metabolismo , alfa-Sinucleína/metabolismo , Animales , Encéfalo/metabolismo , Encéfalo/patología , Femenino , Humanos , Masculino , Ratones , Ratones Endogámicos C57BL , Microglía/patología , Enfermedad de Parkinson/patología , Ratas , Ratas Sprague-DawleyRESUMEN
Bone microstructure governs microcrack propagation complexity. Current research, relying on linear elastic fracture mechanics, inadequately considers authentic multi-level structures, like cement lines and osteons, impacting stress intensity at cracks. This study, by constructing models encompassing single or multiple osteons, delves into the influence of factors like crack length, osteon radius, and modulus ratio on the stress intensity factor at the crack tip. Employing a fracture mechanics phase-field approach to simulate crack propagation paths, it particularly explores the role of cement lines as weak interfaces in crack extension. The aim is to comprehensively and systematically elucidate the critical factors of bone microstructure in the context of crack propagation.
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Hydroxyapatite (HAP) constitutes the primary mineral component of bones, and its crystal structure, along with the surface interaction with proteins, significantly influences the outstanding mechanical properties of bone. This study focuses on natural hydroxyapatite, constructing a surface model with calcium vacancy defects. Employing a representative model of aspartic acid residues, we delve into the adsorption mechanism on the crystal surface and scrutinize the adsorption forms of amino acid residues on HAP and calcium-deficient hydroxyapatite (CDHA) surfaces. The research also explores the impact of different environments on adsorption energy. Furthermore, a simplified sandwich structure of crystal-polypeptide-crystal is presented, analyzing the distribution of amino acid residue adsorption sites on the crystal surface of the polypeptide fragment. This investigation aims to elucidate how the stick-slip mechanism of polypeptide molecules on the crystal surface influences the mechanical properties of the system. By uncovering the interface mechanical behavior between HAP and osteopontin peptides, this article offers valuable theoretical insights for the construction and biomimetic design of biocomposites.
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Huesos , Durapatita , Osteopontina , Durapatita/química , Huesos/metabolismo , Huesos/química , Osteopontina/química , Osteopontina/metabolismo , Adsorción , Péptidos/química , Péptidos/metabolismo , Humanos , Modelos Moleculares , Unión Proteica , Cristalización , Propiedades de Superficie , Calcio/metabolismo , Calcio/químicaRESUMEN
Circadian rhythms are involved in the regulation of many aspects of the body, including cell function, physical activity and disease. Circadian disturbance often predates the typical symptoms of neurodegenerative diseases and is not only a non-motor symptom, but also one of the causes of their occurrence and progression. Glial cells possess circadian clocks that regulate their function to maintain brain development and homeostasis. Emerging evidence suggests that the microglial circadian clock is involved in the regulation of many physiological processes, such as cytokine release, phagocytosis, and nutritional and metabolic support, and that disruption of the microglia clock may affect multiple aspects of Parkinson's disease, especially neuroinflammation and α-synuclein processes. Herein, we review recent advances in the circadian control of microglia function in health and disease, and discuss novel pharmacological interventions for microglial clocks in neurodegenerative disorders.
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Relojes Circadianos , Enfermedades Neurodegenerativas , Enfermedad de Parkinson , Humanos , Enfermedad de Parkinson/metabolismo , Microglía/metabolismo , Enfermedades Neurodegenerativas/metabolismo , Ritmo Circadiano/fisiologíaRESUMEN
GPR84 is a promising therapeutic target and biomarker for a range of diseases. In this study, we reported the discovery of BINOL phosphate (BINOP) derivatives as GPR84 antagonists. By investigating the structure-activity relationship, we identified 15S as a novel GPR84 antagonist. 15S exhibits low nanomolar potency and high selectivity for GPR84, while its enantiomer 15R is less active. Next, we rationally designed and synthesized a series of GPR84 fluorogenic probes by conjugating Nile red and compound 15S. The leading hybrid, probe F8, not only retained GPR84 activity but also exhibited low nonspecific binding and a turn-on fluorescent signal in an apolar environment. F8 enabled visualization and detection of GPR84 in GPR84-overexpressing HEK293 cells and lipopolysaccharide-stimulated neutrophils. Furthermore, we demonstrated that F8 can detect upregulated GPR84 protein levels in mice models of inflammatory bowel disease and acute lung injury. Thus, compound F8 represents a promising tool for studying GPR84 functions.
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Colorantes Fluorescentes , Receptores Acoplados a Proteínas G , Receptores Acoplados a Proteínas G/antagonistas & inhibidores , Receptores Acoplados a Proteínas G/metabolismo , Humanos , Colorantes Fluorescentes/química , Colorantes Fluorescentes/síntesis química , Animales , Células HEK293 , Relación Estructura-Actividad , Ratones , Ratones Endogámicos C57BL , Descubrimiento de Drogas , Lipopolisacáridos/farmacologíaRESUMEN
INTRODUCTION: Microglia are the main phagocytes in the brain and can induce neuroinflammation. Moreover, they are critical to alpha-synuclein (α-syn) aggregation and propagation. Plasma exosomes derived from patients diagnosed with Parkinson's disease (PD-exo) reportedly evoked α-syn aggregation and inflammation in microglia. In turn, microglia internalized and released exosomal α-syn, enhancing α-syn propagation. However, the specific mechanism through which PD-exo influences α-syn degradation remains unknown. METHODS: Exosomes were extracted from the plasma of patients with PD by differential ultracentrifugation, analyzed using electron microscopy (EM) and nanoparticle flow cytometry, and stereotaxically injected into the unilateral striatum of the mice. Transmission EM was employed to visualize lysosomes and autophagosomes in BV2 cells, and lysosome pH was measured with LysoSensor Yellow/Blue DND-160. Cathepsin B and D, lysosomal-associated membrane protein 1 (LAMP1), ATP6V1G1, tumor susceptibility gene 101 protein, calnexin, α-syn, ionized calcium binding adaptor molecule 1, and NLR family pyrin domain containing 3 were evaluated using quantitative polymerase chain reaction or western blotting, and α-syn, LAMP1, and ATP6V1G1 were also observed by immunofluorescence. Small interfering ribonucleic acid against V1G1 was transfected into BV2 cells and primary microglia using Lipofectamine® 3000. A PD mouse model was established via injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into mice. A lentiviral-mediated strategy to overexpress ATP6V1G1 in the brain of MPTP-treated mice was employed. Motor coordination was assessed using rotarod and pole tests, and neurodegeneration in the mouse substantia nigra and striatum tissues was determined using immunofluorescence histochemical and western blotting of tyrosine hydroxylase. RESULTS: PD-exo decreased the expression of V1G1, responsible for the acidification of intra- and extracellular milieu. This impairment of lysosomal acidification resulted in the accumulation of abnormally swollen lysosomes and decreased lysosomal enzyme activities, impairing lysosomal protein degradation and causing α-syn accumulation. Additionally, V1G1 overexpression conferred the mice neuroprotection during MPTP exposure. CONCLUSION: Pathogenic protein accumulation is a key feature of PD, and compromised V-type ATPase dysfunction might participate in PD pathogenesis. Moreover, V1G1 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which may provide opportunities to develop novel therapeutic interventions for PD treatment.
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Exosomas , Ratones Endogámicos C57BL , Microglía , Enfermedad de Parkinson , ATPasas de Translocación de Protón Vacuolares , alfa-Sinucleína , Anciano , Animales , Femenino , Humanos , Masculino , Ratones , Persona de Mediana Edad , alfa-Sinucleína/metabolismo , Exosomas/metabolismo , Lisosomas/metabolismo , Microglía/metabolismo , Microglía/patología , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/patología , ATPasas de Translocación de Protón Vacuolares/metabolismo , ATPasas de Translocación de Protón Vacuolares/genéticaRESUMEN
The intricate functional interactions between mitochondria and lysosomes play a pivotal role in maintaining cellular homeostasis and proper cellular functions. This dynamic interplay involves the exchange of molecules and signaling, impacting cellular metabolism, mitophagy, organellar dynamics, and cellular responses to stress. Dysregulation of these processes has been implicated in various neurodegenerative diseases. Additionally, mitochondrial-lysosomal crosstalk regulates the exosome release in neurons and glial cells. Under stress conditions, neurons and glial cells exhibit mitochondrial dysfunction and a fragmented network, which further leads to lysosomal dysfunction, thereby inhibiting autophagic flux and enhancing exosome release. This comprehensive review synthesizes current knowledge on mitochondrial regulation of cell death, organelle dynamics, and vesicle trafficking, emphasizing their significant contributions to neurodegenerative diseases. Furthermore, we explore the emerging field of nanomedicine in the management of neurodegenerative diseases. The review provides readers with an insightful overview of nano strategies that are currently advancing the mitochondrial-lysosome-extracellular vesicle axis as a therapeutic approach for mitigating neurodegenerative diseases.
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Vesículas Extracelulares , Lisosomas , Mitocondrias , Enfermedades Neurodegenerativas , Humanos , Lisosomas/metabolismo , Vesículas Extracelulares/metabolismo , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neurodegenerativas/patología , Mitocondrias/metabolismo , Animales , Nanomedicina Teranóstica/métodosRESUMEN
Current treatments for orthopaedic illnesses frequently result in poor prognosis, treatment failure, numerous relapses, and other unpleasant outcomes that have a significant impact on patients' quality of life. Cell-free therapy has emerged as one of the most promising options in recent decades for improving the status quo. As a result, using exosomes produced from various cells to modulate ferroptosis has been proposed as a therapeutic method for the condition. Exosomes are extracellular vesicles that secrete various bioactive chemicals that influence disease treatment and play a role in the genesis and progression of orthopaedic illnesses. Ferroptosis is a recently defined kind of controlled cell death typified by large iron ion buildup and lipid peroxidation. An increasing number of studies indicate that ferroptosis plays a significant role in orthopaedic illnesses. Exosomes, as intercellular information transfer channels, have been found to play a significant role in the regulation of ferroptosis processes. Furthermore, accumulating research suggests that exosomes can influence the course of many diseases by regulating ferroptosis in injured cells. In order to better understand the processes by which exosomes govern ferroptosis in the therapy of orthopaedic illnesses. This review discusses the biogenesis, secretion, and uptake of exosomes, as well as the mechanisms of ferroptosis and exosomes in the therapy of orthopaedic illnesses. It focuses on recent research advances and exosome mechanisms in regulating iron death for the therapy of orthopaedic illnesses. The present state of review conducted both domestically and internationally is elucidated and anticipated as a viable avenue for future therapy in the field of orthopaedics.
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Exosomas , Ferroptosis , Ferroptosis/fisiología , Humanos , Exosomas/metabolismo , Animales , Hierro/metabolismoRESUMEN
BACKGROUND: Mild cognitive impairment (MCI) is the prodromal stage of dementia. In this stage, reasonable intervention measures can help to delay the decline of cognitive function. Supplementation of n-3 polyunsaturated fatty acids (n-3PUFAs) may be beneficial to delay the decline of cognitive function in the elderly. OBJECTIVE: To investigate the effectiveness of docosapentaenoic acid (DHA) or/and eicosapentaenoic acid (EPA) supplements in the elderly with MCI. METHODS: Eight electronic databases, PubMed, Cochrane Library, Embase, VIP, SinoMed, Web of Science, CNKI, and WANFANG DATA, were searched for related articles from inception until January 2022. Subgroup analyses and sensitivity analyses were performed to detect confounding variables. Standardized mean differences (SMD) with 95% confidence intervals (CI) were determined. Heterogeneity was evaluated by I2 statistics. Publication bias was detected using funnel plots. Stata12.0 was used for Begg's and Egger's test to quantify whether publication bias. Linear relationship between global cognition and covariates was examined in meta-regression analysis. RESULTS: Twelve studies (nâ=â1,124) were included. The methodological quality of research is mostly medium. Compared with placebo, n-3PUFAs supplements have benefits on global cognition [SMDâ=â0.51, 95% CI(0.12, 0.91), pâ=â0.01]. No significant differences were observed between intervention group and placebo on language fluency, executive functions, and depression. CONCLUSION: Our findings indicated DHA and/or EPA supplements have benefits on global cognition, and it may also reduce the level of blood amyloid-ß (Aß)-related biomarkers (e.g., Aß 40, Aß 42) and inflammatory factors (e.g., 1L-6, 1L-10). Since there are only two relative articles, more research is needed in the future to clarify the relationship.
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A 5-nm-thick artificial solid electrolyte interface (SEI) was engineered for the hard carbon anodes of sodium-ion batteries. Benefiting from the artificial SEI, the hard carbon anode shows a significantly improved initial Coulombic efficiency of 94% and superior rate performance with a reversible capacity of 247 mA h g-1 after 800 cycles at 1C, 220 mA h g-1 after 400 cycles at 6C.
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STUDY DESIGN: Meta-analysis and systematic review. BACKGROUND: Robot-assisted pedicle screw placement technique offers greater accuracy than the traditional freehand screw placement technique. However, it is controversial whether there is a difference between the two procedures in terms of improved clinical outcomes. MATERIALS AND METHODS: We systematically searched PubMed, EMBASE, Cochrane, and Web of Science to identify potentially eligible articles. Indispensable data such as the year of publication, study type, age, number of patients, sex distribution, and outcomes were extracted. The outcome indicators of interest included Oswestry disability index (ODI), visual analog scale (VAS) score, operative time, intraoperative blood loss, and post-operative length of stay. RevMan 5.4.1 was used for the meta-analysis. RESULTS: A total of eight studies with 508 participants were included. Eight were related to ΔVAS, six were related to ΔODI, seven were related to operative time, five were related to intraoperative blood loss, and seven were related to the length of hospitalization. The results showed that, in terms of ΔVAS (95% CI, -1.20 to -0.36, P = 0.0003) and ΔODI (95% CI, -2.50 to -0.48, P = 0.004), robot-assisted pedicle screw placement technique scored higher than traditional freehand technique. Additionally, the intraoperative blood loss (95% CI, -140.34 to -10.94, P = 0.02) and the length of hospitalization (95% CI, -2.59 to -0.31, P = 0.01) for patients who underwent robotic-assisted pedicle screw placement were less than that of those who underwent the conventional freehand screw placement. No significant difference was found between robot-assisted techniques and conventional freehand techniques in pedicle screw placement in surgical time (95% CI, -2.24 to 26.32, P = 0.10). CONCLUSIONS: Robot-assisted technique helps improve short-term clinical outcomes, reduce intraoperative blood loss and patient suffering, and shorten recovery time compared to the freehand technique.
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Tornillos Pediculares , Procedimientos Quirúrgicos Robotizados , Robótica , Fusión Vertebral , Humanos , Pérdida de Sangre Quirúrgica , Procedimientos Quirúrgicos Robotizados/métodos , Fusión Vertebral/métodos , Estudios Retrospectivos , Vértebras Lumbares/cirugíaRESUMEN
Objective: To review the research progress of design of bone scaffolds with different single cell structures. Methods: The related literature on the study of bone scaffolds with different single cell structures at home and abroad in recent years was extensively reviewed, and the research progress was summarized. Results: The single cell structure of bone scaffold can be divided into regular cell structure, irregular cell structure, cell structure designed based on topology optimization theory, and cell structure designed based on triply periodic minimal surface. Different single cell structures have different structural morphology and geometric characteristics, and the selection of single cell structure directly determines the mechanical properties and biological properties of bone scaffold. It is very important to choose a reasonable cell structure for bone scaffold to replace the original bone tissue. Conclusion: Bone scaffolds have been widely studied, but there are many kinds of bone scaffolds at present, and the optimization of single cell structure should be considered comprehensively, which is helpful to develop bone scaffolds with excellent performance and provide effective support for bone tissue.
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Huesos , Andamios del TejidoRESUMEN
Objective: To summarize the influence of microstructure on performance of triply-periodic minimal surface (TPMS) bone scaffolds. Methods: The relevant literature on the microstructure of TPMS bone scaffolds both domestically and internationally in recent years was widely reviewed, and the research progress in the imfluence of microstructure on the performance of bone scaffolds was summarized. Results: The microstructure characteristics of TPMS bone scaffolds, such as pore shape, porosity, pore size, curvature, specific surface area, and tortuosity, exert a profound influence on bone scaffold performance. By finely adjusting the above parameters, it becomes feasible to substantially optimize the structural mechanical characteristics of the scaffold, thereby effectively preempting the occurrence of stress shielding phenomena. Concurrently, the manipulation of these parameters can also optimize the scaffold's biological performance, facilitating cell adhesion, proliferation, and growth, while facilitating the ingrowth and permeation of bone tissue. Ultimately, the ideal bone fusion results will obtain. Conclusion: The microstructure significantly and substantially influences the performance of TPMS bone scaffolds. By deeply exploring the characteristics of these microstructure effects on the performance of bone scaffolds, the design of bone scaffolds can be further optimized to better match specific implantation regions.
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Ingeniería de Tejidos , Andamios del Tejido , Andamios del Tejido/química , Ingeniería de Tejidos/métodos , Huesos , PorosidadRESUMEN
To advance the understanding of the dynamic relationship between brain activities and emotional experiences, we examined the neural patterns of tension, a unique emotion that highly depends on how an event unfolds. Specifically, the present study explored the temporal relationship between functional connectivity patterns within and between different brain functional modules and the fluctuation in tension during film watching. Due to the highly contextualized and time-varying nature of tension, we expected that multiple neural networks would be involved in the dynamic tension experience. Using the neuroimaging data of 546 participants, we conducted a dynamic brain analysis to identify the intra- and inter-module functional connectivity patterns that are significantly correlated with the fluctuation of tension over time. The results showed that the inter-module connectivity of cingulo-opercular network, fronto-parietal network, and default mode network is involved in the dynamic experience of tension. These findings demonstrate a close relationship between brain functional connectivity patterns and emotional dynamics, which supports the importance of functional connectivity dynamics in understanding our cognitive and emotional processes.