Protective effects of sinomenine against dextran sulfate sodium-induced ulcerative colitis in rats via alteration of HO-1/Nrf2 and inflammatory pathway.

BACKGROUND: Dextran Sulfate Sodium (DSS) induces ulcerative colitis (UC), a type of inflammatory bowel disease (IBD) that leads to inflammation, swelling, and ulcers in the large intestine. The aim of this experimental study is to examine how sinomenine, a plant-derived alkaloid, can prevent or reduce the damage caused by DSS in the colon and rectum of rats. MATERIAL AND METHODS: Induction of ulcerative colitis (UC) in rats was achieved by orally administering a 2% Dextran Sulfate Sodium (DSS) solution, while the rats concurrently received oral administrations of sinomenine and sulfasalazine. The food, water intake was estimated. The body weight, disease activity index (DAI), colon length and spleen index estimated. Antioxidant, cytokines, inflammatory parameters and mRNA expression were estimated. The composition of gut microbiota was analyzed at both the phylum and genus levels in the fecal samples obtained from all groups of rats. RESULTS: Sinomenine treatment enhanced the body weight, colon length and reduced the DAI, spleen index. Sinomenine treatment remarkably suppressed the level of NO, MPO, ICAM-1, and VCAM-1 along with alteration of antioxidant parameters such as SOD, CAT, GPx, GR and MDA. Sinomenine treatment also decreased the cytokines like TNF-α, IL-1, IL-1ß, IL-6, IL-10, IL-17, IL-18 in the serum and colon tissue; inflammatory parameters viz., PAF, COX-2, PGE2, iNOS, NF-κB; matrix metalloproteinases level such as MMP-1 and MMP-2. Sinomenine significantly (P < 0.001) enhanced the level of HO-1 and Nrf2. Sinomenine altered the mRNA expression of RIP1, RIP3, DRP3, NLRP3, IL-1ß, caspase-1 and IL-18. Sinomenine remarkably altered the relative abundance of gut microbiota like firmicutes, Bacteroidetes, F/B ratio, Verrucomicrobia, and Actinobacteria. CONCLUSION: The results clearly indicate that sinomenine demonstrated a protective effect against DSS-induced inflammation, potentially through the modulation of inflammatory pathways and gut microbiota.

ZSM-5@ceramic foam composite catalyst derived from spent bleaching clay for continuous pyrolysis of waste oil to produce monocyclic aromatic hydrocarbons.

Spent bleaching clay, a solid waste generated during the refining process of vegetable oils, lacks an efficient treatment solution. In this study, spent bleaching clay was innovatively employed to fabricate ceramic foams. The thermal stability analysis, microstructure, and crystal phase composition of the ceramic foams were characterized by TG-DSC, SEM, and XRD. An investigation into the influence of Al2O3 content on the ceramic foams was conducted. Results showed that, as the Al2O3 content increased from 15 wt% to 30 wt%, there was a noticeable decrease in bulk density and linear shrinkage, accompanied by an increase in compressive strength. Additionally, the ceramic foams were used as catalyst supports, to synthesize ZSM-5@ceramic foam composite catalysts for pyrolysis of waste oil. The open pores of the ZSCF catalyst not only reduced diffusion path length but also facilitated the exposure of more acid sites, thereby increasing the utilization efficiency of ZSM-5 zeolite. This, in turn, engendered a significant enhancement in monocyclic aromatic hydrocarbons content from 39.15 % (ZSM-5 powder catalyst) to 78.96 %. Besides, a larger support pore size and a thicker ZSM-5 zeolite coating layer led to an increase in monocyclic aromatic hydrocarbons content. As the time on stream was extended to 56 min, the monocyclic aromatic hydrocarbon content obtained with the composite catalyst remained 12.41 % higher than that of the ZSM-5 powder catalyst. These findings validate the potential of the composite catalyst. In essence, this study advances the utilization of spent bleaching clay and introduces a novel concept for ceramic foam fabrication. Furthermore, it contributes to the scaling up of catalytic pyrolysis technology.

A Multimodal Ultrasound Observation Study on the Effect of Vitamin D on Uterine Fibroids in Non-menopausal Women.

INTRODUCTION: It has been reported in the literature that Vitamin D can inhibit the growth of uterine fibroids, but the evaluation index is only the size of the uterine fibroids. The purpose of this study was to evaluate the effect of vitamin D on the size, hardness, and blood flow of uterine fibroids in premenopausal women by multimodal ultrasound. METHODS: A total of 64 pre-menopausal women with uterine fibroids complicated vitamin D deficiency were enrolled in this study and randomly divided into two groups: the vitamin D group (n=32) which received oral vitamin D (1600 IU/ day) and the control group (n=32) without vitamin D supplementation. After three months of intervention, the mean diameter of uterine fibroids, elastic strain ratio, and blood flow grade were evaluated by multimodal ultrasound, and the clinical symptoms of the two groups were evaluated by questionnaire. RESULTS: The vitamin D group reported a significant increment in the serum 25-hydroxyvitamin D (P < 0.001). In addition, there were significant reductions in the mean diameter, and elastic strain ratio of uterine fibroids (P =.043 and P =.038, respectively), but no significant difference in the blood flow grade of uterine fibroids was observed (P =.272). Compared with the control group, the vitamin D group achieved significant relief in dysmenorrhea and frequent urination, as well as improvement in heavy menstrual bleeding. CONCLUSION: The application of multimodal ultrasound provides a more comprehensive theoretical basis for vitamin on uterine fibroids. Vitamin D can effectively reduce the size of uterine fibroids in pre-menopausal women and relieve their symptoms. It is highly likely to be a promising, safe, effective, and inexpensive drug for uterine fibroids, which has good application value and promotion prospects.

The novel role of activating receptor KIR2DS5 in preeclampsia.

Preeclampsia (PE) is a serious complication of pregnancy. Decidual natural killer (dNK) cells were reported to participate in the remodeling of spiral arteries through producing a group of cytokines, including granulocyte-macrophage colony stimulating factor (GM-CSF). KIR2DS5 is an activating receptor of NK cells that specifically recognizes HLA-C2 on trophoblasts. Currently, there are no reports regarding the precise mechanism of KIR2DS5 in PE. This study included 30 PE patients and 30 healthy pregnant women. We found that the expressions of KIR2DS5 were significantly lower in PE deciduae compared to those of healthy pregnancies. By transfecting knockdown and overexpression lentivirus vectors of KIR2DS5 into dNK cells isolated from deciduae of early pregnancy, we altered the KIR2DS5 expression level in dNK cells. Then, these dNK cells and trophoblast cell lines were co-cultured as trophoblast-dNK cells. In the trophoblast-dNK cells, we examined the influence of KIR2DS5 on the biological manifestations of trophoblasts. As anticipated, overexpression of KIR2DS5 could facilitate cell proliferation, migration, and invasion. Furthermore, increased expression of KIR2DS5 inhibited cell apoptosis and enhanced the progression of cells from theG1 to theS stage. Further mechanistic study demonstrated a positive relationship between KIR2DS5 and GM-CSF in trophoblast-dNK cells. Accordingly, our observations indicated that a decrease in KIR2DS5 could reduce the expression of GM-CSF via the JAK2/STAT5 pathway, resulting in the failure of the activated signal to be transmitted to dNK cells and ultimately leading to the occurrence of PE. KIR2DS5 may be a new contributor for the prediction and diagnosis of PE.

The central role of natural killer cells in preeclampsia.

Preeclampsia (PE) is a disease that is unique to pregnancy and affects multiple systems. It can lead to maternal and perinatal mortality. The precise etiology of PE is unclear. Patients with PE may have systemic or local immune abnormalities. A group of researchers has proposed that the immune communication between the fetus and mother is primarily moderated by natural killer (NK) cells as opposed to T cells, since NK cells are the most abundant immune cells in the uterus. This review examines the immunological roles of NK cells in the pathogenesis of PE. Our aim is to provide obstetricians with a comprehensive and updated research progress report on NK cells in PE patients. It has been reported that decidual NK (dNK) cells contribute to the process of uterine spiral artery remodeling and can modulate trophoblast invasion. Additionally, dNK cells can stimulate fetal growth and regulate delivery. It appears that the count or proportion of circulating NK cells is elevated in patients with or at risk for PE. Changes in the number or function of dNK cells may be the cause of PE. The Th1/Th2 equilibrium in PE has gradually shifted to an NK1/NK2 equilibrium based on cytokine production. An improper combination of killer cell immunoglobulin-like receptor (KIR) and human leukocyte antigen (HLA)-C may lead to insufficient activation of dNK cells, thereby causing PE. In the etiology of PE, NK cells appear to exert a central effect in both peripheral blood and the maternal-fetal interface. To maintain immune equilibrium both locally and systemically, it is necessary to take therapeutic measures directed at NK cells.

Early postsurgical lethal outcome due to splenic littoral cell angioma: A case report.

BACKGROUND: Littoral cell angioma (LCA) is a rare benign vascular tumor of the spleen. Given its rarity, standard diagnostic and therapeutic recommendations have yet to be developed for reported cases. Splenectomy is the only method of obtaining a pathological diagnosis and providing treatment to obtain a favorable prognosis. CASE SUMMARY: A 33-year-old female presented with abdominal pain for one month. Computed tomography and ultrasound revealed splenomegaly with multiple lesions and two accessory spleens. The patient underwent laparoscopic total splenectomy and accessory splenectomy, and splenic LCA was confirmed by pathology. Four months after surgery, the patient presented with acute liver failure, was readmitted, rapidly progressed to multiple organ dysfunction syndrome and died. CONCLUSION: Preoperative diagnosis of LCA is challenging. We systematically reviewed online databases to identify the relevant literature and found a close relationship between malignancy and immunodysregulation. When a patient suffers from both splenic tumors and malignancy or immune-related disease, LCA is possible. Due to potential malignancy, total splenectomy (including accessory spleen) and regular follow-up after surgery are recommended. If LCA is diagnosed after surgery, a comprehensive postoperative examination is needed.

Triptonide inhibits growth and metastasis in HCC by suppressing EGFR/PI3K/AKT signaling.

Liver cancer represents one of the deadliest cancers, with a rising incidence worldwide. Triptonide is found in the traditional Chinese medicinal plant Tripterygium wilfordii Hook. This study aimed to examine the anticancer properties of triptonide in human hepatocellular carcinoma (HCC). HCC cells were administered with triptonide at various levels, and CCK-8 and colony formation assays were carried out for detecting HCC cell proliferation. Then, cell apoptosis and cell cycle distribution were evaluated by flow cytometry. Tumor growth was monitored noninvasively by ultrasound imaging. Cell migration and invasion were quantitated by wound healing and Transwell assays. A metastasis model was established via tail vein injection of HCC cells in nude mice. Immunoblot was performed to quantitate the expression of proteins involved in the EGFR/PI3K/AKT signaling and its downstream effectors. Triptonide repressed cell proliferation and induced cell cycle arrest and apoptosis in cultured HCC cells, and suppressed tumor growth in vivo. In addition, triptonide inhibited EMT, migration and invasion in cultured HCC cells, and lung metastasis in nude mice. Mechanistically, triptonide acted by inhibiting the EGFR/PI3K/AKT signaling and regulated its downstream effectors, e.g., the cell cycle-associated protein cyclin D1, the apoptosis-related protein Bcl-2, the EMT marker E-cadherin, and the invasion-related protein MMP-9. Triptonide suppresses proliferation, EMT, migration and invasion, and promotes apoptosis and cell cycle arrest by repressing the EGFR/PI3K/AKT signaling. Therefore, triptonide might be considered for liver cancer treatment.

Evaluating glioma-associated microRNA by complementation on a biological nanosensor.

Glioma is a tumor in the brain and spinal cord originating in the glial cells that surround the nerve cells. Among several microRNAs reported, miRNA-363 is associated with human glioma. Based on miRNA-363 levels, the development and progression of glioma can be monitored. The current study used an interdigitated electrode sensor to monitor microRNA-363 levels, which indeed reflects the severity of glioma. The interdigitated electrode was generated using a photolithography technique followed by surface chemical modification carried out to insert miRNA-363 complementary oligo as the probe complexed with gold nanoparticles. The proposed sensor works based on the dipole moment between two electrodes, and when molecular immobilization or interaction occurs, the response by the signal output changes. The changes in the target microRNA-363 sequence were standardized to identify glioma. The limit of detection of miRNA-363 was 10 fM with an R2 value of 0.996 on the linear coefficient regression ranges between 1 fM and 100 pM. Furthermore, unrelated sequences failed to increase the response of the current with the complementary probe, indicating specific miRNA-363 detection on the interdigitated electrode. This study demonstrates the platform to be used for determining the presence of microRNA-363 in glioma and as the basis for other biomarker analyses.

Multifunctional Drug-Loaded Phase-Change Nanoparticles Inhibit the Epithelial-Mesenchymal Transition of Hepatocellular Carcinoma by Affecting the Activity of Activated Hepatic Stellate Cells.

Objectives. Preparation of a multifunctional drug-loaded phase-change nanoparticle (NP), pirfenidone perfluoropentane liposome NPs (PPL NPs), and combined with low-intensity focused ultrasound (LIFU) to influence epithelial mesenchymal transition (EMT) for hepatocellular carcinoma (HCC) by inhibiting the activity of activated Hepatic Stellate Cells (a-HSCs). Methods. PPL NPs were prepared by the thin film dispersion method. The appearance, particle size, zeta potential, encapsulation efficiency, drug loading rate, drug release in vitro, and stability of PPL NPs were tested. The role of a-HSCs in HCC metastasis was studied by CCK-8, colony formation assay, apoptosis, cellular uptake assay, wound healing assay, and Transwell assay. Western blot was used to detect the related protein expression levels. In vitro and vivo, the acoustic droplet vaporization (ADV) of PPL NPs was tested at different times and LIFU intensities. Biosafety of the PPL NPs was assessed by measuring nude mouse body weight and hematoxylin and eosin (H&E) staining. Results. The results showed that the PPL NPs had good biosafety, with an average particle size of 346.6 ± 62.21 nm and an average zeta potential of -15.23 mV. When the LIFU power is 2.4 W/cm2, it can improve the permeability of cells, further promote the uptake of drugs by cells, and improve the toxicity of drugs. In vitro experiments showed that PPL NPs could inhibit the proliferation of a-HSCs cells, thereby affecting the metastasis of HCC, and were related to the TGFß-Smad2/3-Snail signaling pathway. Both in vivo and in vitro PPL NPs enhanced ultrasound imaging by LIFU-triggered ADV. Conclusion. The PPL NPs designed and prepared in this study combined with LIFU irradiation could significantly alter the EMT of HCC by inhibiting LX2. Clinically, PPL NPs will also be considered a promising contrast agent due to their ultrasound imaging capabilities.

CCL2-targeted ginkgolic acid exerts anti-glioblastoma effects by inhibiting the JAK3-STAT1/PI3K-AKT signaling pathway.

AIMS: Glioblastoma (GBM) with aggressive nature and poor prognosis has become the most common intracranial tumor. Most clinical chemotherapeutic drugs fail to achieve the anticipated therapeutic outcome. This study identified the anti-GBM effects of ginkgolic acids (GAs) and elucidated the potential molecular mechanisms, exploiting the significant antitumor effects of GAs, which are widely present in the outer bark of Ginkgo biloba. MATERIALS AND METHODS: Two GBM cell lines, U251 and T98G, were selected for in vitro experiments to evaluate the antitumor effects of GA. Cell viability and proliferation were examined by MTT and colony formation assay. The effect of GA on apoptosis and the cell cycle was examined by flow cytometry. Scratch and Transwell assays reflected the migration and invasion ability. The molecular mechanisms were explored by using immunoblot analysis, RNA sequencing and bioinformatics. In the nude mouse transplantation tumor model, preclinical treatment effects were assessed by ultrasound and MRI. KEY FINDINGS: The present study showed that GA inhibited the proliferation, migration, invasion, stemness, epithelial-to-mesenchymal transition (EMT) of GBM cells and induced apoptosis by inhibiting CCL2, affecting the JAK-STAT and PI3K-AKT signaling pathways, and inhibiting the EMT regulators Snail and Slug. Finally, GA showed significant control of tumors in a GBM xenograft model. SIGNIFICANCE: GA inhibits the progression of GBM cells by targeting CCL2, affecting the JAK-STAT and PI3K-AKT signaling pathways, and inhibiting the EMT regulators Snail and Slug. The outstanding antitumor properties of GA provide a novel strategy for the GBM therapy.

Resveratrol alleviates Ang II-induced vascular smooth muscle cell senescence by upregulating E2F1/SOD2 axis.

Background: Vascular smooth muscle cells (VSMCs) senescence is a crucial factor relevant to accelerate cardiovascular diseases. Resveratrol (RES) has been reported that could obstruct vascular senescence. However, the detailed molecular mechanisms of RES in VSMCs senescence are still indistinct and deserve further investigations. Methods and Results: In this study, VSMCs were treated with 100 nM angiotensin II (Ang II) for 3 days and then followed with a range of different concentrations of RES (0.5, 5, 15, 25, 35, 50 µM), and 25 µM of RES was chose for following experiments. We found that the E2F1 and SOD2 expressions were reduced in Ang II-induced VSMCs. RES treatment impeded Ang II-induced oxidative stress and mitochondrial dysfunction through elevating E2F1 and SOD2 expression, thereby alleviating VSMCs senescence. Additionally, E2F1 knockdown reversed the protective effects of RES on VSMCs senescence caused by Ang II administration. Ch-IP assay and dual luciferase reporter gene assay validated that E2F1 could bind to the promoter region of SOD2. Furthermore, E2F1 or SOD2 overexpression blocked Ang II-induced on VSMCs senescence. Conclusion: In conclusion, RES mitigated Ang II-induced VSMCs senescence by suppressing oxidative stress and mitochondrial dysfunction through activating E2F1/SOD2 axis. Our study disclosed that RES might be a potential drug and the axis of its regulatory mechanism might be therapeutic targets for postponing vascular senescence.

Targeting the TREM1-positive myeloid microenvironment in glioblastoma.

Background: Tumor cellular and molecular heterogeneity is a hallmark of glioblastoma and underlies treatment resistance and recurrence. This manuscript investigated the myeloid-derived microenvironment as a driver of glioblastoma heterogeneity and provided a pharmacological pathway for its suppression. Methods: Transcriptomic signatures of glioblastoma infiltrated myeloid-derived cells were assessed using R2: genomic platform, Ivy Glioblastoma Spatial Atlas, and single-cell RNA-seq data of primary and recurrent glioblastomas. Myeloid-derived cell prints were evaluated in five PDX cell lines using RNA-seq data. Two immunocompetent mouse glioblastoma models were utilized to isolate and characterize tumor-infiltrated myeloid-derived cells and glioblastoma/host cell hybrids. The ability of an inhibitor of HuR dimerization SRI42127 to suppress TREM1+-microenvironment and glioblastoma/myeloid-derived cell interaction was assessed in vivo and in vitro. Results: TREM1+-microenvironment is enriched in glioblastoma peri-necrotic zones. TREM1 appearance is enhanced with tumor grade and associated with poor patient outcomes. We confirmed an expression of a variety of myeloid-derived cell markers, including TREM1, in PDX cell lines. In mouse glioblastoma models, we demonstrated a reduction in the TREM1+-microenvironment and glioblastoma/host cell fusion after treatment with SRI42127. In vitro assays confirmed inhibition of cell fusion events and reduction of myeloid-derived cell migration towards glioblastoma cells by SRI42127 and TREM1 decoy peptide (LP17) versus control treatments. Conclusions: TREM1+-myeloid-derived microenvironment promulgates glioblastoma heterogeneity and is a therapeutic target. Pharmacological inhibition of HuR dimerization leads to suppression of the TREM1+-myeloid-derived microenvironment and the neoplastic/non-neoplastic fusogenic cell network.

Synthesis, characterization, and evaluation of microwave-assisted fabricated selenylation Astragalus polysaccharides.

Selenylation Astragalus polysaccharides (Se-APS) was fabricated by an optimized microwave-assisted method. Their physicochemical properties, antioxidant capacities and selenium (Se) release rate under gastrointestinal conditions were determined. Se-APS with the highest Se content (18.8 mg/g) was prepared in 0.4 % nitric acid, under the microwave conditions of 90 min and 80 °C. FTIR and XPS spectra indicated that Se was bound to the polysaccharide chain in the form of O-Se-O and O-H···Se, and most of Se+4 was reduced to Se0. Meanwhile, the micromorphology of Se-APS became clusters, loose and porous, which decreased its hydrodynamic particle size and negative surface charges. Besides, Se-APS displayed strong scavenging capacities towards ABTS and superoxide anion free radicals than Na2SeO3, and showed higher Se release rate (12.52 ± 0.31 %) under intestinal fluid comparing with gastric fluid (3.14 ± 0.38 %) during 8 h in vitro digestion. The results provided efficient preparation method references for selenylation polysaccharides, and broaden the application fields of APS.

Inhibition of the RNA Regulator HuR by SRI-42127 Attenuates Neuropathic Pain After Nerve Injury Through Suppression of Neuroinflammatory Responses.

Microglial activation with the production of pro-inflammatory mediators such as IL-6, TNF-α, and IL-1ß, is a major driver of neuropathic pain (NP) following peripheral nerve injury. We have previously shown that the RNA binding protein, HuR, is a positive node of regulation for many of these inflammatory mediators in glia and that its chemical inhibition or genetic deletion attenuates their production. In this report, we show that systemic administration of SRI-42127, a novel small molecule HuR inhibitor, attenuates mechanical allodynia, a hallmark of NP, in the early and chronic phases after spared nerve injury in male and female mice. Flow cytometry of lumbar spinal cords in SRI-42127-treated mice shows a reduction in infiltrating macrophages and a concomitant decrease in microglial populations expressing IL-6, TNF-α, IL-1ß, and CCL2. Immunohistochemistry, ELISA, and qPCR of lumbar spinal cord tissue indicate suppression of these cytokines and other inflammatory mediators. ELISA of plasma samples in the acute phase also shows attenuation of inflammatory responses. In summary, inhibition of HuR by SRI-42127 leads to the suppression of neuroinflammatory responses and allodynia after nerve injury and represents a promising new direction in the treatment of NP.

Theoretical study of extremely narrow plasmonic surface lattice resonances observed by MIM nanogratings under normal incidence in asymmetric environments.

Nanoarray structures can support plasmonic surface lattice resonances (SLRs) with extremely narrow linewidths and huge electric field enhancement features, which are attractive applications in nanolasers, biochemical sensors, and nonlinear optics. However, current nanoarray structures located in an asymmetric dielectric environment with a refractive index contrast of 1.00/1.52 of the superstrate/substrate excite much poorer SLRs under normal incidence, which largely limits their application range. In this work, we report extremely narrow SLRs supported by one-dimensional metal-insulator-metal nanograting in asymmetric dielectric environments. The simulation results show that an SLRs with linewidth of 3.26 nm and quality factor of 233.2 can be excited under normal incidence. This high-quality SLRs is attributed to the interference formation between the out-of-plane dipole resonance mode and the out-of-plane quadrupole resonance mode. We also show that the resonance wavelength and quality factor can be tuned by changing the structure geometry and period, and we calculate the normal incidence SLRs quality factor to be up to 248 in 1.33/1.52 and 250 in 1.45/1.52. We expect the SLRs of this work to find potential applications in asymmetric dielectric environments.

The Evaluation of Gait and Balance for Patients with Early Diabetic Peripheral Neuropathy: A Cross-Sectional Study.

Objective: Falls often occur in patients with diabetic neuropathy due to biomechanical alternation. The implication of diabetic peripheral neuropathy (DPN) on gait and balance remains poorly understood. Methods: A total of 11 dynamic gait, balance and electrophysiological parameters were evaluated in 176 participants. The biomechanical parameters were compared between groups. Results: Stride length and stride velocity were significantly lower in all subgroups of DPN compared with healthy subjects (p<0.05). Stance phase and double support phase were significantly higher, but swing phase were significantly lower across all subgroups of DPN than healthy subjects (p<0.05). Under eyes-open standing, the ML and AP range parameters of CoM sway, ankle sway and hip sway, CoM sway index, ankle swing index in both subclinical and confirmed DPN patients were all significantly higher compared to healthy subjects (p<0.05). Under eyes-closed standing, AP range parameters of CoM sway in subclinical DPN and confirmed DPN patients were significantly higher than healthy subjects (p<0.05). The hip sway areas in diabetics were significantly higher compared to healthy subjects (p<0.05). Conclusion: The abnormal biomechanical parameters existed in the early stages of patients with DPN. The static balance under eyes-open and eye-closed condition is maintained by ankle joint compensation strategy and hip joint protection strategy. An early evaluation and better risk management is essential for diabetic patients with a history of more than 5 years even without DPN clinical symptoms and signs. Clinical Trial Registration Number: No. ChiCTR1800019179, www.chictr.org.cn.

A Review of Roles of Uterine Artery Doppler in Pregnancy Complications.

The invasion of trophoblasts into the uterine decidua and decidual vessels is critical for the formation of placenta. The defects of placentation are related to the etiologies of preeclampsia (PE), fetal growth restriction (FGR), and small-for-gestational age (SGA) neonates. It is possible to predict significant vascular events during pregnancy through uterine artery Doppler (UAD). From the implantation stage to the end of pregnancy, detecting changes in uterine and placental blood vessels can provide a favorable diagnostic instrument for pregnancy complications. This review aims to collect literature about the roles of UAD in pregnancy complications. We consider all relevant articles in English from January 1, 1983 to October 30, 2021. Predicting pregnancy complications in advance allows practitioners to carry out timely interventions to avoid or lessen the harm to mothers and neonates. Administering low-dose aspirin daily before 16 weeks of pregnancy can significantly reduce the incidence of pregnancy complications. From early pregnancy to late pregnancy, UAD can combine with other maternal factors, biochemical indicators, and fetal measurement data to identify high-risk population. The identification of high-risk groups can also lessen maternal mortality. Besides, through moderate risk stratification, stringent monitoring for high-risk pregnant women can be implemented, decreasing the incidence of adversities.

The role of plasminogen activator inhibitor-1 in gynecological and obstetrical diseases: An update review.

In a normal pregnancy, maternal circulatory system presents a hypercoagulable state due to the effect of hormone secretion. Even minor variations in fibrinolytic system could lead to hyper- or hypofibrinolysis, affecting placental formation, and causing adverse pregnancy outcomes. Plasminogen activator inhibitor-1 (PAI-1) restrains the fibrinolysis cascade. A controversial relationship exists regarding the role of PAI-1 in gynecological and obstetrical diseases. In this review, the authors focused on discussing the sophisticated roles of PAI-1 gene in adverse pregnancy complications and gynecological conditions, which include recurrent pregnancy loss (RPL), preeclampsia (PE), gestational diabetes mellitus (GDM), fetal growth restriction (FGR), repeated implantation failure (RIF), polycystic ovary syndrome (PCOS), and endometriosis. A pair of autonomous authors searched the literature in PUBMED, Web of Science, and Google Scholar databases from January 1, 1988 to October 1, 2021. PAI-1 4 G/5 G polymorphism plays a crucial part in the advancement of RPL via the change of metabolic, thrombotic, and immune issues. Moreover, PAI-1 may have a relationship with the occurrence and development of PE. In FGR, overexpression of PAI-1 leads to the excessive deposition of fibrin and diminished blood flow at the maternal-fetal interface, which affects the growth and development of the fetus. PAI-1 expression can be decreased by physical exercise and medical treatments, including metformin. In the future, extensive researches with rigorous inclusion standards involving diverse ethnic groups are needed to explore the functionality of PAI-1 in related gynecological and obstetrical diseases, and may be helpful to develop novel treatment methods to prevent or treat these diseases.