Growth prediction of Microcystis aeruginosa based on a secondary decomposition integration model.

Microcystis aeruginosa is the dominant species in the blooms of eutrophic lakes such as Taihu Lake in China. Chlorophyll-a is one of the most common indicators to characterize its biomass. The nonlinearity and unsteadiness of the chlorophyll-a sequence decrease the prediction accuracy. In this paper, a secondary decomposition prediction method based on the integration of wavelet decomposition, variational modal decomposition, and gated recurrent unit (WD-VMD-GRU) is proposed. First, the original sequence is decomposed once using wavelet decomposition (WD). Then, the components with higher sample entropy values are decomposed using variational modal decomposition (VMD). Finally, each component is predicted using a gated recurrent unit (GRU), and the final prediction results are obtained by reconstructing each component result. The decomposition effect is ranked as VMD > WD > CEEMDAN > EMD. The WD-VMD-GRU model has a significant advantage compared to the basic model, with an increase of over 6.5% in R2. The secondary decomposition reduces the difficulty of predicting GRU components and has better prediction performance. The RMSE, MAE, and R2 were 1.752, 1.450, 0.969 at 2-day prediction, and 3.169, 2.711, 0.908 at 6-day prediction. Therefore, the WD-VMD-GRU model is superior in accuracy to other methods and can provide a scientific basis for the growth prediction research of M. aeruginosa.

An outbreak of epidemic keratoconjunctivitis caused by human adenovirus type 8 in primary school, southwest China.

BACKGROUND: Two outbreaks of epidemic keratoconjunctivitis (EKC) occurred successively with an interval of 5 days in two primary boarding schools in Weixi Lisu Autonomous County, Diqing, and Tibetan Autonomous Prefecture, Yunnan. The aims of this study were to determine the intensity and characteristics of the outbreaks, as well as the clinical manifestations in the patients, the risk factors for infection and the pathogen responsible for the two outbreaks. METHODS: An outbreak investigation was conducted in two primary schools, and a case-control study including patients from the Weixi County Ethnic Primary School was performed. Relevant specimens were collected according to the case definition, and next-generation sequencing was employed to identify the pathogen. An epidemiological investigation method was used to analyse the related epidemiological characteristics, such as risk factors. The phylogenetic tree was constructed by MEGA 7.0. RESULTS: A total of 331 acute conjunctivitis cases, including probable cases of EKC, were reported in the two schools, and the attack rates were 30.59% (171/559, 95%CI: 26.76-34.42) and 20.41% (160/784, 95%CI: 17.58-23.24), respectively. Cases occurred in all grades and classes in both schools, and only one staff member in each school presented illness. The epidemics lasted for 54 days and 45 days, respectively. The patients had typical manifestations of EKC, such as acute onset, follicular hyperplasia, pseudomembrane formation, preauricular lymphadenopathy, corneal involvement and blurred vision, and a relatively long disease course (average 9.40 days, longest 23 days and shortest 7 days). The risk factor for infection was close contact with a patient or personal items contaminated by a patient. The pathogen responsible for the outbreaks was HAdV-8. The virus was highly similar to the 2016 HAdV-8 strain from Tibet, China. CONCLUSIONS: This study strongly suggests that HAdV-8 could lead to serious consequences. This is the second report of a HAdV-8-associated EKC outbreak in mainland China. Tibetan HAdV-8 might be circulating in southwest China; therefore, it is necessary to monitor the pathogens causing acute conjunctivitis in this area.

Radiomics-based fertility-sparing treatment in endometrial carcinoma: a review.

In recent years, with the increasing incidence of endometrial carcinoma in women of child-bearing age, to decision of whether to preserve patients' fertility during treatment has become increasingly complex, presenting a formidable challenge for both physicians and patients. Non-fertility-sparing treatment can remove lesions more thoroughly than fertility-sparing treatment. However, patients will permanently lose their fertility. In contrast, fertility-sparing treatment can treat tumors without impairing fertility, but the risk of disease progression is high as compared with non-fertility-sparing treatment. Therefore, it is extremely important to accurately identify patients who are suitable for fertility-sparing treatments. The evaluation of prognostic factors, including myometrial invasion, the presence of lymph node metastases, and histopathological type, is vital for determining whether a patient can receive fertility-sparing treatment. As a non-invasive and quantitative approach, radiomics has the potential to assist radiologists and other clinicians in determining more precise judgments with regard to the above factors by extracting imaging features and establishing predictive models. In this review, we summarized currently available fertility-sparing strategies and reviewed the performance of radiomics in predicting risk factors associated with fertility-sparing treatment. This review aims to assist clinicians in identifying patients suitable for fertility-sparing treatment more accurately and comprehensively and informs more appropriate and rigorous treatment decisions for endometrial cancer patients of child-bearing age.Critical relevance statement: Radiomics is a promising tool that may assist clinicians identify risk factors about fertility-sparing more accurately and comprehensively.

Exosomal lncRNA CHL1-AS1 Derived from Peritoneal Macrophages Promotes the Progression of Endometriosis via the miR-610/MDM2 Axis.

BACKGROUND: Exosomes secreted by peritoneal macrophages (pMφ) are deeply involved in the development of endometriosis (EMs). Exosomes can mediate cell-to-cell communication by transferring biological molecules. This study aimed to explore the effect and mechanism of exosomal long non-coding RNA (lncRNA) CHL1-AS1 derived from pMφ on EMs. MATERIALS AND METHODS: Exosomes (exo) from pMφ were isolated, identified, and co-cultured with ectopic endometrial stromal cells (eESCs) to investigate the biological functions of pMφ-exo. qRT-PCR was used to detect the expression of lncRNA CHL1-AS1 in pMφ-exo from EMs and control patients and verify the transportation of lncRNA CHL1-AS1 from pMφ to eESCs. The effects of exosomal lncRNA CHL1-AS1 on eESC proliferation, migration, invasion, and apoptosis were also detected. The relationships among lncRNA CHL1-AS1, miR-610, and MDM2 (mouse double minute 2) were verified by dual-luciferase reporter assay. The in vivo experiments were conducted to verify the effects of exosomal lncRNA on EMs using a xenograft model of EMs. RESULTS: Exosomes from pMφ were successfully isolated. EMs-pMφ-exo promoted eESC proliferation, migration, and invasion and inhibited their apoptosis. lncRNA CHL1-AS1 was upregulated in EMs-pMφ-exo and transported from pMφ to eESCs via exosomes. lncRNA CHL1-AS1 was found to act as a competing endogenous RNA of miR­610 to promote the expression of MDM2. EMs-pMφ-exo shuttled lncRNA CHL1-AS1 to promote eESC proliferation, migration, and invasion and inhibit apoptosis by downregulating miR-610 and upregulating MDM2. Furthermore, exosomal lncRNA CHL1-AS1 promoted EMs lesions growth by increasing MDM2 in vivo. CONCLUSION: The results demonstrate that exosomal lncRNA CHL1-AS1 promotes the proliferation, migration, and invasion of eESCs and inhibits their apoptosis by downregulating miR-610 and upregulating MDM2, which might be a potential therapeutic target for EMs.

Parallel Loop Binding Compression Suture, a Modified Procedure for Pernicious Placenta Previa Complicated With Placenta Increta.

Objective: To evaluate the efficacy and safety of parallel loop binding compression suture of the lower uterus during cesarean section in pernicious placenta previa complicated with placenta increta. Methods: This retrospective study was performed in patients with pernicious placenta previa complicated with placenta increta or percreta between November 2014 and December 2020 at the Qilu Hospital of Shandong University. Patients underwent parallel loop binding compression suture surgery were defined as study group, and patients underwent traditional surgery with figure-of-eight sutures as the main hemostatic method were defined as control group. Postpartum hemorrhage was evaluated as the primary outcome. The secondary outcomes included age, gestational weeks, operative time, fetal childbirth time, prevention of hysterectomy, blood transfusion, duration of postoperative catheterization, duration of antibiotic treatment, and postoperative hospitalization (days). Additionally, neonatal outcomes were evaluated. Results: A total of 124 patients were enrolled in the study, including 38 patients receiving parallel loop binding compression suture surgery in the study group, and 86 patients in the control group. With parallel loop binding compression suture, the average operation time was significantly reduced (109.0 ± 33.5 vs. 134.4 ± 54.2 min, p = 0.00), and the volume of blood lost were also decreased (2152.6 ± 1169.4 vs. 2960.5 ± 1963.6 ml, p = 0.02), which correspondingly reduced RBC transfusion (7.2 ± 3.5 vs. 10.3 ± 8.7 units, p = 0.03) and FFP transfusion (552.6 ± 350.3 vs. 968.0 ± 799.8 ml, p = 0.00). The fetal childbirth time was extended (14.1 ± 5.6 vs. 11.0 ± 8.0 min, p = 0.03), however, there was no increase in NICU admission rates (36.9 vs. 34.9%, p = 0.83). Except for one premature infant (32 weeks) death in the control group, all infants at our hospital were safely discharged after treatment. Conclusion: Parallel loop binding compression suture is an effective, swift, practical, and safe method to reduce postpartum bleeding in women with pernicious placenta previa, complicated with placenta increta. Besides, it has no adverse effects on newborns.

LRP6 is involved in the proliferation, migration and invasion of trophoblast cells via miR­346.

Low­density lipoprotein receptor­related protein 6 (LRP6) promotes metastasis in numerous types of cancer; however, its role in trophoblast cells has been less frequently reported. In the present study, the effects of up­ and downregulation of LRP6 on trophoblast cells were investigated accordingly. The study aimed to develop a therapeutic target for gestational choriocarcinoma. The expression levels of LRP6 in pre­eclampsia (PE) tissues, trophoblast cell lines and gestational choriocarcinoma cells were determined using reverse transcription­quantitative polymerase chain reaction (RT­qPCR) assay. Double­luciferase reporter analysis was conducted to detect the regulatory gene of LRP6. Furthermore, the proliferative, migratory and invasive abilities of trophoblasts and gestational choriocarcinoma cells were determined by CCK­8, wound healing, and Transwell assays, respectively. The expression levels of the genes and proteins of interest [matrix metalloproteinase (MMP)­2, MMP­9, tissue inhibitor of metalloproteinase­1 (TIMP­1), and TIMP­2] associated with tumor cell invasion were measured by performing RT­qPCR and western blotting, respectively. The National Center for Biotechnology Information database revealed that LRP6 was relatively highly expressed in placental tissues, but was poorly expressed in PE tissues and trophoblast cell lines. The upregulation of LRP6 not only increased the activity, migration and invasion of trophoblast cells, but it also promoted the expression of MMP­2 and MMP­9, whereas it inhibited the expression levels of TIMP­1 and TIMP­2. Such results followed the opposite trend to those of downregulation of LRP6 in gestational choriocarcinoma cells. Moreover, LRP6 was predicted to be the target gene for microRNA (miR)­346, which was highly expressed in PE tissues and trophoblast cell lines. The present study also revealed that LRP6 could reverse the effects of miR­346 on the proliferation, migration and invasion of trophoblast cells. Therefore, considered collectively, the results of the present study have demonstrated that LRP6 is involved in the proliferation, migration and invasion of trophoblast cells via miR­346, and that LRP6 may serve as a potential target in cancer treatment.

Cervical Cancer Cells-Secreted Exosomal microRNA-221-3p Promotes Invasion, Migration and Angiogenesis of Microvascular Endothelial Cells in Cervical Cancer by Down-Regulating MAPK10 Expression.

PURPOSE: Cervical cancer (CC) is recognized as a common cancer with a high risk worldwide. Exosomal microRNAs (miRNAs) have received attention for their increasing potentials in CC therapy. In this study, we identify the involvement of miR-221-3p in CC progression by affecting angiogenesis of microvascular endothelial cells (MVECs). METHODS: Microarray-based gene expression profiling was conducted to retrieve the differentially expressed genes in CC. The expression patterns of miR-221-3p were measured by RT-qPCR, while Western blot analysis and RT-qPCR were performed to determine the expression of MAPK10 in the CC tissues and cells, followed by verification of the interaction between miR-221-3p and MAPK10 using dual luciferase reporter gene assay. Then the effects of miR-221-3p and MAPK10 on cell activities were assessed through gain- and loss-of-function experiments in CC. Subsequently, the impact of exosomal miR-221-3p on MVEC proliferation, migration, invasion and angiogenesis was examined after exosomal isolation from CC cells and co-cultured with MVECs. RESULTS: Gene expression profile showed that MAPK10 might participate in CC with a low expression. Moreover, miR-221-3p was highly expressed and MAPK10 was poorly expressed in CC tissues and cells. It was observed that miR-221-3p targeted MAPK10. Depletion of miR-221-3p blocked the cell proliferation, invasion and migration in CC by up-regulating MAPK10. Moreover, CC cells-derived exosomes carrying miR-221-3p accelerated MVEC proliferation, invasion, migration and angiogenesis in CC by regulating MAPK10. CONCLUSION: CC cells-derived exosomes harboring miR-221-3p enhanced MVEC angiogenesis in CC by decreasing MAPK10.