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Breast milk DHA proportion was positively associated with maternal aquatic product intake and DHA supplement use, and negatively associated with postpartum depression status.

To evaluate the clinical performance of an artificial intelligence (AI)-based motion correction (MC) reconstruction algorithm for cerebral CT.A total of 53 cases, where motion artifacts were found in the first scan so that an immediate rescan was taken, were retrospectively enrolled. While the rescanned images were reconstructed with a hybrid iterative reconstruction (IR) algorithm (reference group), images of the first scan were reconstructed with both the hybrid IR (motion group) and the MC algorithm (MC group). Image quality was compared in terms of standard deviation (SD), signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), the mean squared error (MSE), peak signal-to-noise ratio (PSNR), structural similarity index (SSIM), and mutual information (MI), as well as subjective scores. The diagnostic performance for each case was evaluated accordingly by lesion detectability or the Alberta Stroke Program Early CT Score (ASPECTS) assessment.Compared with the motion group, the SNR and CNR of the MC group were significantly increased. The MSE, PSNR, SSIM, and MI with respect to the reference group were improved by 44.1%, 15.8%, 7.4%, and 18.3%, respectively (all p0.001). Subjective image quality indicators were scored higher for the MC than the motion group (p0.05). Improved lesion detectability and higher AUC (0.817 vs 0.614) in the ASPECTS assessment were found for the MC to the motion group.The AI-based MC reconstruction algorithm has been clinically validated for reducing motion artifacts and improving diagnostic performance of cerebral CT.• An artificial intelligence-based motion correction (MC) reconstruction algorithm has been clinically validated in both qualitative and quantitative manner. • The MC algorithm reduces motion artifacts in cerebral CT and increases the diagnostic confidence for brain lesions. • The MC algorithm can help avoiding rescans caused by motion and improving the efficiency of cerebral CT in the emergency department.

Accumulating evidence suggests that vitamin D deficiency increases the risk of adverse perinatal outcomes. However, the dose-response relationship between maternal vitamin D status and adverse birth outcomes remains unclear. Focusing on prospective observational studies, we aimed to explore the dose-response relationship of vitamin D status with the risk of low birth weight (LBW), macrosomia (MA), preterm birth (PTB), small for gestational age (SGA), and intrauterine growth restriction (IUGR).Databases including PubMed, Embase, Scopus, and Web of Science were used up to 19 January 2021 to search for observational studies that fulfilled criteria as follows: cohort studies, case-cohort studies, or nested case-control studies. Random-effects models were used to pool relative risks (RRs) and 95% confidence intervals (CIs) in the observational studies.A total of 72 publications were included in this systematic review and 71 in the meta-analysis. Maternal 25-hydroxyvitamin D (25(OH)D) concentrations were inversely associated with the risk of LBW (RR: 0.65; 95% CI 0.48-0.86), PTB (RR: 0.67; 95% CI 0.57-0.79), and SGA (RR: 0.61; 95% CI 0.49-0.76) in the highest versus lowest meta-analysis, but not associated with MA and IUGR. Linear dose-response analysis showed that each 25 nmol/L increase in 25(OH)D was associated with a 6% and 10% reduction in the risk of PTB (RR: 0.94; 95% CI 0.90-0.98) and SGA (RR: 0.90; 95% CI 0.84-0.97), respectively.Our study suggests that a sufficient vitamin D status during pregnancy is protective against the risk of LBW, PTB, and SGA.

Under relatively mild conditions (240 °C and 0.4 MPa H2), Ru/Ti–SiO2 exhibited higher activity for C–O bond cleavage compared with both Ru/SiO2 and Ru/TiO2 catalysts, and achieved high guaiacol conversion (83.6%) and phenol selectivity (70.4%).

Brønsted acid sites rather than Lewis acid sites play an important role in controlling the product selectivity in the hydrodeoxygenation of n-C11H23COOCH3 over supported Ru catalysts.

BACKGROUND: To investigate the relationship between fluid-attenuated inversion recovery (FLAIR) vascular hyperintensity (FVH), hemodynamics, and functional outcome in atherosclerotic middle cerebral artery (MCA) stenosis using a computational fluid dynamics (CFD) model based on magnetic resonance angiography (MRA), according to a modified Rankin Scale (mRS) at 3 months. METHODS: A total of 120 patients with 50–99% atherosclerotic MCA stenosis were included. The training and internal validation groups were composed of 99 participants and 21 participants, respectively. Demographic, imaging data, and functional outcome (mRS at 3 months) were collected. Hemodynamic parameters were obtained from the CFD model. The FVH score was based on the number of territories where FVH is positive, according to the spatial distribution in the Alberta Stroke Program Early Computed Tomography Score (ASPECTS). The prediction models were constructed according to clinical and hemodynamic parameters using multivariate logistic analysis. The DeLong test compared areas under the curves (AUCs) of the models. RESULTS: The multivariable logistic regression analysis showed that the National Institute of Health Stroke Scale (NIHSS) at admission, hypertension, hyperlipidemia, the ratio of wall shear stress before treatment (WSSR(before)), and difference in the ratio of wall shear stress (WSSR) were independently associated with functional outcome (all P

Ventilator-induced lung injury (VILI) may be caused by incorrect mechanical ventilation (MV), and its progression is mainly related to inflammatory reaction, apoptosis, and oxidative stress. The Wnt/β-catenin pathway can modulate inflammation and apoptosis; however, its role in VILI is unknown. This research aims to explore the role of the Wnt/β-catenin pathway in VILI. VILI models were established using rats and type II alveolar epithelial (ATII) cells. Glycogen synthase kinase 3β (GSK-3β), β-catenin, and cyclin D1 were determined using western blotting and immunofluorescence. Apoptosis of lung tissues was evaluated using TUNEL, flow cytometry, Bax, and Bcl2 protein. Interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). Lung pathological injury was evaluated through hematoxylin and eosin (H&E) staining. Lung permeability was evaluated by the ratio of dry to wet weight of lung tissue and the total protein level of bronchoalveolar lavage fluid (BALF). The results showed that GSK-3β expression was enhanced and β-catenin expression was diminished in lung tissue under MV. SB216763 increased β-catenin and cyclin D1 expression by inhibiting GSK-3β expression and inhibited the inflammatory response and apoptosis of lung, alleviated pulmonary edema and lung tissue permeability, and significantly mitigated lung injury. However, inhibition of β-catenin expression by MSAB attenuated the anti-inflammatory and antiapoptotic effects of SB216763 in VILI. Overall, the present study demonstrates that the Wnt/β-catenin pathway activation in MV may play an anti-inflammatory and antiapoptotic role, thereby alleviating lung injury and delaying VILI progression, which may be a key point of intervention in VILI.

Background: Mechanical Ventilationventilation (MV) is an essential life support mechanism in the clinic. It may also lead to ventilator-induced acute lung injury (VILI) due to local alveolar overstretching and/or repeated alveolar collapse. However, the pathogenesis of VILI is not completely clear, and its occurrence and development may be related to inflammatory reactions, oxidative stress, apoptosis and other physiological processes. Some studies have found that the apelin/APJ pathway is an endogenous antagonistic mechanism that is activated during Acute respiratory distress syndrome(ARDS), and it can counteract the injury response and prevent uncontrolled lung injury. To prove that apelin-13 plays a protective role in VILI, in this study, we established a rat VILI model to explore whether apelin-13 can attenuate VILI in rats by inhibiting inflammation, cell apoptosis and oxidative stress. Methods: SD rats were divided into four groups: the control group, high tidal volume group, high tidal volume+NS group, and high tidal volume+apelin-13 group. After tracheotomy, autonomous breathing was maintained in the rats. After tracheotomy, the other rats were connected to a small animal ventilator for 4 hours to establish the rat VILI model. The mRNA expression of apelin was measured by real-time quantitative polymerase chain reaction (qRT‒PCR), and the protein expression levels of APJ, the apoptotic protein Bax, Bcl-2 and Akt/P-Akt were measured by Western blotting (WB) and immunofluorescence. The degree of lung injury was evaluated by pathological staining of lung tissue and measuring the wet to dry ratio of lung tissue. The expression of inflammatory factors in alveolar lavage fluid was measured by enzyme-linked immunosorbent assay (ELISA), and the activity of myeloperoxidase (MPO) in lung tissue was measured to evaluate the degree of pulmonary inflammation. Results: The expression of apelin and the APJ receptor was upregulated under VILI conditions. After the rats were treated with apelin-13, the activation of the apelin-APJ signaling pathway, the pathological damage to lung tissues, the degree of cell apoptosis, and the levels of the inflammatory cytokines IL-1, IL-6 and TNF-α were reduced in the VILI model rats. The expression of MPO was decreased, and the activity of MPO was also decreased. Moreover, the Akt/P-Akt signaling pathway is associated with apoptosis. After treatment, the expression of Akt/P-Akt pathway-related proteins increased. Conclusion: During VILI, the apelin/APJ axis plays an endogenous role in ameliorating injury. Overexpression of apelin can significantly reduce the inflammatory response, cell apoptosis and oxidative stress in the lung tissues of VILI model rats and slow the occurrence and development of VILI.

BACKGROUND In this study we aimed to establish a new transfer learning model based on noncontrast and thin-layer computed tomography (CT) scans to distinguish between malignant and benign solid lung nodules. MATERIAL AND METHODS CT images from 202 patients with 210 lesions (malignant: 127, benign: 83) manifesting as solid lung nodules from January 2016 to December 2020 from 3 institutions were retrospectively collected, and each nodule was histopathologically confirmed. Two experienced thoracic radiologists reviewed all images and determined the regions of interest (ROIs) in the three-dimensional (3D) images layer-by-layer. We divided the lesions and images into training and testing sets at a ratio of 7: 3. The Inception V3 model was pretrained by the training dataset. Five-fold cross-validation was used to choose the optimal model. Receiver operator characteristic curves (ROC curves) for methods to evaluate the performance of the models were drafted. RESULTS In the validation set, the AUC, accuracy, sensitivity, and specificity of Inception V3 model (lesion-level) were 0.999, 0.989, 0.983, and 1.0, respectively, which is higher than the image-level (0.997, 0.933, 0.922, and 0.948, respectively). The Inception V3 model (lesion-level) performed better than the image-level but there was no significant difference between the models (P0.05). The ResNet50 model based on image level achieved AUC, accuracy, sensitivity, and specificity of 0.963, 0.926, 0.916, and 0.944, respectively, which is lower than that of Inception V3. CONCLUSIONS Our study developed a novel deep learning model based on noncontrast and thin-layer CT scans to classify benign vs malignant lung nodules, and the Inception V3 model greatly improved the differentiation accuracy and specificity.

Background Epigenetic mark such as DNA methylation plays pivotal roles in regulating ripening of both climacteric and non-climacteric fruits. However, it remains unclear whether mRNA m6A methylation, which has been shown to regulate ripening of the tomato, a typical climacteric fruit, is functionally conserved for ripening control among different types of fruits. Results Here we show that m6A methylation displays a dramatic change at ripening onset of strawberry, a classical non-climacteric fruit. The m6A modification in coding sequence (CDS) regions appears to be ripening-specific and tends to stabilize the mRNAs, whereas m6A around the stop codons and within the 3′ untranslated regions is generally negatively correlated with the abundance of associated mRNAs. We identified thousands of transcripts with m6A hypermethylation in the CDS regions, including those of NCED5, ABAR, and AREB1 in the abscisic acid (ABA) biosynthesis and signaling pathway. We demonstrate that the methyltransferases MTA and MTB are indispensable for normal ripening of strawberry fruit, and MTA-mediated m6A modification promotes mRNA stability of NCED5 and AREB1, while facilitating translation of ABAR. Conclusion Our findings uncover that m6A methylation regulates ripening of the non-climacteric strawberry fruit by targeting the ABA pathway, which is distinct from that in the climacteric tomato fruit.

The selective hydrodeoxygenation of lignin-derived guaiacol to value-added products, especially phenol, under relatively mild reaction conditions remains an important challenge. A Cl-modified Ru/TiO₂ catalyst exhibited higher phenol selectivity compared with an unmodified one in the conversion of guaiacol in 1,4-dioxane at 240 °C and 1 MPa H₂. Unlike Ru/TiO₂, the modified catalyst exhibited a modest activity of demethoxylation producing phenol but an inferior ability of hydrogenation of its aromatic ring, resulting in much slower consumption of phenol. The Cl species were likely localized at the metal–support interface and on the surface of metal particles, and these modified both Ru and Ti species electronically. It is presumed that electron-enriched Ru inhibits the ring hydrogenation reaction, and the defects on the TiO₂ surface promote the deoxygenation reaction.

BackgroundDeoxythymidylate kinase (DTYMK) is a rate-limiting enzyme in pyrimidine metabolism. Crucially, it is overexpressed in a variety of tumors and is associated with poor prognosis in liver cancer. The role of DTYMK in lung adenocarcinoma remains poorly understood, particularly with respect to immune infiltration. MethodsThe present study aimed to compare the expression of DTYMK between normal tissues, lung adenocarcinoma, and other cancer types using data obtained via The Cancer Genome Atlas, Tumor Immune Estimation Resource 2.0, Gene Expression Database of Normal and Tumor Tissues 2, and Gene Expression Profiling Interactive Analysis (GEPIA). The prognostic value of DTYMK in patients with lung adenocarcinoma was evaluated using GEPIA and Kaplan–Meier plotter. STRING and GeneMANIA were employed to assess protein and gene interaction with DTYMK. R software and TISIDB were used to analyze the correlation between DTYMK expression and immune infiltration. Finally, we validated DTYMK protein expression in lung adenocarcinoma using the UALCAN and HPA databases. ResultsDTYMK expression was significantly increased in various cancer and lung adenocarcinoma tissues (p < 0.05), and was associated with poor prognosis (p < 0.05) in patients with lung adenocarcinoma. In addition, DTYMK was negatively associated with the vast majority of immune cells in lung adenocarcinoma.ConclusionsIncreased expression of DTYMK is associated with poor prognosis in lung adenocarcinoma patients. DTYMK may serve as a potential prognostic biomarker in lung adenocarcinoma. In addition, DTYMK may influence the progression and prognosis of lung adenocarcinoma by influencing the immune microenvironment of tumors.

Globally, Mechanical ventilation is the most commonly used short-term life support technology. Ventilator-induced lung injury (VILI) is an inflammatory injury caused by mechanical ventilation. MicroRNAs (miRNAs) are considered as new gene regulators that play an important role in lung injury and inflammation. However, the role and mechanism of action of miR-9a-5p in VILI remain unclear.Herein, a rat model of VILI was established. To determine the expression levels of miR-9a-5p and CXCR4 mRNA, real-time quantitative polymerase chain reactions (qRT-PCR) were conducted. As well as western blot (WB) and immunofluorescence analyses, we determined the expression of CXCR4, SDF-1 and MAPK signaling pathway-related kinases. Hematoxylin and eosin (HE) staining and the wet-dry ratio of the lung tissue were used to evaluate organ injury. An enzyme-linked immunosorbent assay (Elisa) and myeloperoxidase (MPO) activity measurements were performed to evaluate the inflammatory response. In addition, double luciferase reporter assays were used to verify the association between miR-9a-5p and CXCR4.The expression of miR-9a-5p was low, whereas that of CXCR4 was high in the lung tissues of VILI rats. The overexpression of miR-9a-5p alleviated the degree of pathological injury in the lung tissues of rats with VILI, downregulating inflammatory cytokine expression and MPO activity. In the VILI rat model, miR-9a-5p targeted the negative regulation of CXCR4, and CXCR4 overexpression to reverse the lung-protective and anti-inflammatory effects of miR-9a-5p overexpression in VILI rats. miR-9a-5p also inhibited the phosphorylation of extracellular signal receptor-activated kinase (ERK), a protein related to the MAPK signaling pathway, by downregulating CXCR4 expression.miR-9a-5p can hinder the activation of the MAPK/ERK signaling pathway and reduce inflammatory reactions and lung injury in VILI rats through the targeted regulation of CXCR4 expression. Therefore, miR-9a-5p could serve as an intervention target to supply a new strategy for the care of VILI.

Pancreatic cancer is a fatal disease with a high mortality rate and poor prognosis worldwide. The aberrant expression of microRNAs (miRs) is associated with cancer development and progression. The present study aimed to evaluate the functional role of miR‑142‑5p in migration and invasion, and investigated its underlying molecular mechanism in pancreatic cancer cells. First, it was identified that miR‑142‑5p expression was downregulated in pancreatic cancer tissues and cell lines by reverse transcription‑quantitative polymerase chain reaction. Furthermore, phosphoinositide‑3‑kinase catalytic subunit α (PIK3CA) was identified as a target of miR‑142‑5p. The expression of PIK3CA was upregulated in tumor tissues and its expression was negatively regulated by miR‑142‑5p expression. Notably, overexpression of miR‑142‑5p inhibited the proliferation, migration and invasion of PanC1 cells, while PIK3CA reversed this inhibition. In addition, miR‑142‑5p suppressed the expression of focal adhesion kinase (FAK) and matrix metalloproteinase (MMP)9, as well as phosphorylated protein kinase B (AKT) protein level, while PIK3CA reversed the suppression induced by miR‑142‑5p. In conclusion, miR‑142‑5p functions as a tumor suppressor, which inhibits the migration and invasion of pancreatic cancer by suppressing the expression of FAK and MMP9, as well as the phosphatidylinositol 3‑kinase/AKT signaling pathway by targeting PIK3CA. These findings suggest that miR‑142‑5p may be a novel therapeutic target for the treatment of pancreatic cancer.

Background:Camptothecin (CPT) is known as an anticancer drug in traditional Chinese medicine. However, due to the lack of targeting, low solubility, and instability of CPT, its therapeutic applications are hampered. Therefore, we synthesized a series of CPT-bile acid analogues that obtained a national patent to improve their tumour-targeting chemotherapeutic effects on liver or colon cancers. Among these analogues, the compound G2 shows high antitumor activity with enhanced liver targeting and improved oral absorption. It is significant to further investigate the possible anticancer mechanism of G2 for its further clinical research and application.Objective:We aimed to unearth the anticancer mechanism of G2 in HepG2 and HCT116 cells.Methods:Cell viability was measured using MTT assay; cell cycle, Mitochondrial Membrane Potential (MMP), and cell apoptosis were detected by flow cytometer; ROS was measured by Fluorescent Microplate Reader; the mRNA and protein levels of cell cycle-related and apoptosis-associated proteins were examined by RT-PCR and western blot, respectively.Results:We found that G2 inhibited cells proliferation of HepG2 and HCT116 remarkably in a dosedependent manner. Moreover, G2-treatment led to S and G2/M phase arrest in both cells, which could be elucidated by the change of mRNA levels of p21, p27 and Cyclin E and the increased protein level of p21. G2 also induced dramatically ROS accumulated and MMP decreased, which contributed to the apoptosis through activation of both the extrinsic and intrinsic pathways via changing the genes and proteins expression involved in apoptosis pathway in both of HepG2 and HCT116 cells.Conclusion:These findings suggested that the apoptosis in both cell lines induced by G2 was related to the extrinsic and intrinsic pathways.

In this paper, we propose a transfer learning-based dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) method for classifying fibroadenoma and invasive ductal carcinoma (IDC) in breast tumors. A total of 207 breast tumors from patients were collected and identified by pathologic diagnosis within 15 days after enhanced DCE-MRI examination; 119 patients (average age 50.52±10.33 years) had fibroadenomas, and 88 patients (average age 42.20±10.10 years) had IDCs. Two lesion-level models were built based on the InceptionV3 and VGG19 models, which were pretrained with the ImageNet dataset. The effects of different depths of transfer learning were examined. The network's performance was evaluated through five-fold cross validation. In the lesion-level models, the model based on Inception V3 obtained better results (area under the receiver operating characteristic curve (AUC) = 0.89) when the weights were frozen before layer-276. The other model based on VGG19 obtained better results (AUC = 0.87) when the weights were frozen before layer-13. Compared with the image-level models, both lesion-level models displayed better discrimination (accuracy increased by 13% and 14%) based on the VGG19 and Inception V3 models, respectively. Our research confirms that transfer learning can be utilized to classify fibroadenomas and IDCs in DCE-MRI images. Different depths of transfer learning result in different performances, and our proposed lesion-level model notably improves the classification accuracy.

The hydrodeoxygenation of a model compound, ethyl stearate, of biomass-derived resources into long chain alkanes was investigated with Re-modified Ru/TiO2 catalysts. A monometallic Ru(1)/TiO2 catalyst, in which Ru was loaded in 1 wt%, gave a selectivity of >95% to the long chain alkanes of n-octadecane and n-heptadecane at almost 100% conversion at 220 °C, while another monometallic Re(10)/TiO2 catalyst was less active in spite of its higher metal loading (10 wt%). It is interesting that the addition of less active Re species to Ru(1)/TiO2 not only enhanced the rate of hydrodeoxygenation and increased the ratio of n-octadecane/n-heptadecane, while the high total selectivity towards alkanes remained unchanged. The alkane ratio depended on the content of Re added, increasing significantly from 0.5 for Ru(1)/TiO2 to 3.2 for Ru(1)Re(10)/TiO2. The impacts of Re addition on the catalytic performance of Ru/TiO2 were discussed on the basis of physicochemical properties characterized for Re-modified and unmodified Ru/TiO2 catalysts. It is suggested that the improved hydrodeoxygenation activity of Re-modified catalysts depends on the presence of Lewis acid sites, and the weak acid sites are important for determining catalytic selectivity. In addition, reaction pathways in the hydrodeoxygenation of ethyl stearate to n-octadecane and n-heptadecane were examined by control reactions with possible intermediates such as 1-octadecanol and stearic acid. The Re-modified Ru/TiO2 catalysts were shown to be recyclable during repeated runs when the same mole ratio of catalyst to substrate was used.

Oral squamous cell carcinoma (OSCC) is the most predominant type of oral cancer, featured with poor prognosis and high mortality. Circular RNA (circRNA) exerts its function in a variety of human cancers, including OSCC. Circ_0005050, as a novel circRNA, has not been well explored in OSCC so far. This study centered on investigating the impact of circ_0005050 on OSCC cell growth and its molecular mechanism. RNA or protein expression was detected by RT-qPCR or western blot analysis. Functional assays were employed to uncover the changes of OSCC cell biological behaviors. Mechanistic assays were done to verify the underlying mechanism of circ_0005050 in OSCC cells. According to the collected data, circ_0005050 was significantly up-regulated in OSCC cells compared to normal cells. Circ_0005050 depletion hampered proliferative ability of OSCC cells while promoting cell apoptotic ability. As for mechanism analyses, circ_0005050 knockdown led to the reduction of STAT3 expression and JAK/STAT3 signaling pathway activity. Moreover, circ_0005050 competitively bound to miR-23a-3p and miR-625-5p to up-regulate STAT3, thus prompting malignant behaviors of OSCC cells. In conclusion, circ_0005050 regulates miR-23a-3p/miR-625-5p/STAT3 axis to activate JAK/STAT3 signaling pathway, consequently facilitating OSCC cell proliferation and inhibiting cell apoptosis.

Dynamic chemical modifications in eukaryotic messenger RNAs (mRNAs) constitute an essential layer of gene regulation, among which N

Mechanical ventilation is an important supportive treatment for acute respiratory distress syndrome (ARDS). However, improper mechanical ventilation can cause a "second hit" to the lung, that is, ventilator-induced lung injury (VILI), characterized by translocation of pulmonary inflammatory mediators into the bloodstream, aggravating systemic inflammatory response syndrome, and multiple organ failure. Although the current protective mechanical ventilation strategy plays an important role in supporting treatment, the mortality of ARDS with mechanical ventilation is still very high. Therefore, to explore the strategy of pulmonary protective ventilation has always been the key orientation of ARDS and has important clinical significance. This article reviews the application, advantages and disadvantages of assisted and non-assisted spontaneous respiration in ARDS patients undergoing mechanical ventilation, in order to provide a reference for research and development of new strategies for ARDS protective ventilation.

Epidemiological studies have investigated the associations between vitamin D and the risk of adverse pregnancy outcomes; however, the results are conflicting and dose-response relationships remain to be confirmed. This study aimed to summarize previous studies on the associations of vitamin D levels with the risk of gestational diabetes mellitus (GDM), pre-eclampsia (PE), gestational hypertension (GH), and caesarean section (C-section), and to clarify the dose-response trends. PubMed, Embase, Scopus, and Web of Science were searched to identify eligible articles. A total of 69 prospective observational studies including cohort studies, case-cohort studies, or nested case-control studies were included in the current systematic review, of which 68 studies were available for meta-analysis. Compared with the lowest level, the highest level of 25(OH)D was significantly associated with a lower risk of GDM (RR: 0.76; 95% CI: 0.66-0.87), PE (RR: 0.74; 95% CI: 0.60-0.90;), and GH (RR: 0.87; 95% CI: 0.79-0.97); however, no significant relationship was found for C-section (RR: 1.00; 95% CI: 0.90-1.12). There was significant between-study heterogeneity for GDM (I2 = 69.2%; Pheterogeneity < 0.001), PE (I2 = 52.0%; Pheterogeneity = 0.001), and C-section (I2 = 59.1%; Pheterogeneity < 0.001), while no heterogeneity was found for GH (I2 = 0.0%; Pheterogeneity = 0.676). For each 25 nmol L-1 increase in 25(OH)D, the pooled RR was 0.92 (95% CI: 0.86-0.97) for GDM and 0.89 (95% CI: 0.84-0.94) for PE, respectively. Notably, the dose-response analysis showed a non-linear relationship between maternal 25(OH)D levels and the risk of PE (Pnon-linearity = 0.009). Our meta-analysis provides further scientific evidence of the inverse association between 25(OH)D levels and the risk of GDM, PE, and GH, which may be useful for the prevention of pregnancy complications. However, more evidence from prospective studies is needed regarding the dietary intake of vitamin D during pregnancy.