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Objectives: To compare the clinical characteristics and prognosis of women with clear cell versus high-grade serous ovarian carcinoma.Methods: Retrospective analysis of the clinical data of 50 cases patients with ovarian clear cell carcinoma (OCCC) and 103 cases with high-grade serous ovarian carcinoma (HGSOC), who were initially treated and completed standardized therapy in Affiliated Hospital of Qingdao University from January 2013 to December 2017.Results: There were significant differences in age, gravidity (G > 1), chief complaint, with ovarian endometriosis, tumor diameter, unilateral or bilateral, cystic and solid tumor, CA125, HE4, CA199, lactate dehydrogenase (LDH), and FIGO stage between the two groups. The differences in the prognosis between OCCC patients and HGSOC patients with early stage (FIGO I-II) were not statistically significant. The 5-year overall survival and progression-free survival of OCCC patients were significantly worse than those of HGSOC patients with advanced stage (FIGO III-IV) (P < 0.05). FIGO stage and non-R0 resection were independent risk factors affecting the prognosis of patients with ovarian clear cell carcinoma, screening by Cox regression analysis. FIGO stage, the lowest value of CA125, and non-R0 resection were independent risk factors affecting the prognosis of patients with high-grade serous ovarian cancer.Conclusions: The clinical characteristics and prognosis of OCCC are different from those of HGSOC. OCCC patients have a significantly worse prognosis than those with HGSOC in the advanced stage (FIGO Ⅲ-Ⅳ). Satisfactory tumor resection is an essential factor related to the prognosis of patients with OCCC and HGSOC.

The blended wing body (BWB) aircraft as a novel aircraft configuration has a poor longitudinal static stability. A V-tail is installed on the BWB to improve the longitudinal static stability, which achieves the limited improvements. Therefore, the BWB is investigated to further improve the longitudinal static stability with experimental tests and numerical simulations in this paper. The variation with angle of attack (AOA) α of the pitching moment coefficient (Cm) is divided into three regions, i.e., the first AOA region with static stability, the AOA region with static instability, and the second AOA region with static stability. It is found that the position of the forebody vortex acting on the V-tail surface is closely related to the longitudinal static stability of the BWB aircraft. Through increasing the spanwise distance of the V-tail to change the position of the forebody vortex acting on the V-tail surface, the AOA region with static instability is decreased. The longitudinal static stability of the BWB aircraft is improved. The evolution of associated pressure distributions, flow separations and vortical structures is presented in detail.

Cervical cancer (CC) is the fourth most common cancers among women worldwide. T-box transcription factor 1 (TBX1), a member of the T-box family, has anti-tumor effects in some types of cancer, but its role in CC is yet unknown. The aim of this study is to investigate the functions and underlying mechanisms of TBX1 in CC. Online database UALCAN showed that TBX1 was down-regulated in CC tissues compared with normal tissues and patients with lower TBX1 expression level had a poor prognosis. TBX1 overexpression significantly decreased the proliferation, migration, and invasion of Hela and SiHa cells. Conversely, cell apoptosis and chemosensitivity to cisplatin were promoted in TBX1-overexpressing CC cells. Moreover, up-regulation of TBX1 inhibited both AKT and MAPK signaling pathways. Furthermore, dual luciferase report assay indicated that TBX1 could directly bind to miR-6727-5p. In addition, TBX1 expression was inhibited by miR-6727-5p mimic and up-regulated by miR-6727-5p inhibitor. Knockdown of TBX1 reversed the inhibitory effect of the miR-6727-5p inhibitor on CC cells. This study demonstrates that TBX1, a target gene of miR-6727-5p, acts as a tumor suppressor in CC, indicating that TBX1 may be a new target for CC therapy.

Background Ovarian cancer is the fifth most common cause of cancer-related deaths and accounts for 3% of cancer cases occurring in women. Therefore, determining the underlying genes that can promote ovarian cancer progression is of great urgency. It has been reported that RHPN2 promotes tumour progression in various types of cancer, but its role in ovarian cancer pathogenesis remains unknown. Materials and Methods In this study, bioinformatic datasets were used to predict the expression of RHPN2 in clinical samples and determine the relationship between RHPN2 and the prognosis of ovarian cancer patients. Clinical samples were used to verify the prediction. RHPN2-targeting shRNA was used to investigate the effect of RHPN2 on ovarian cancer cells, and following RHPN2 knockdown, the proliferative and migratory capacities of ovarian cancer cells were tested. To determine the downstream signalling target of RHPN2, a luciferase reporter assay was conducted, and an animal experiment was carried out to confirm the effect of RHPN2 in vivo. Results The public datasets indicated that ovarian cancer tissues showed significantly higher RHPN2 expression than para-cancer normal tissues, and poor prognosis was observed in patients with higher RHPN2 expression, which was further confirmed in clinical samples. After RHPN2 was knocked down, the proliferation and migration of ovarian cancer cells were significantly impaired; a luciferase reporter assay indicated that the STAT3 signalling pathway was the most highly affected, and RHPN2 downregulation inhibited STAT3 nuclear translocation. STAT3 inhibitors partially rescued the tumour-promoting effect induced by RHPN2 overexpression, which was further confirmed by animal experiments. Conclusion Collectively, our results indicate that RHPN2 promotes malignant behaviours in ovarian cancer by activating STAT3 signalling.

Cervical cancer is one of the most prevalent gynecological malignancies. Although the functions of long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) and c-Myc in tumorigenesis have been acknowledged, the roles of c-Myc and lncRNA-PVT1 in the proliferation of cervical cancer are still unclear. Our study is designed to demonstrate the regulatory network involving c-Myc and lncRNA-PVT1 in cervical cancer. Quantitative real-time PCR and western blot assays were performed in our research to estimate the expression levels of RNA and proteins. CCK8 assays were applied to demonstrate the viability of HeLa and SiHa cells. Immunofluorescence assay was then used to investigate the co-localization of lncRNA-PVT1 and miR-486-3p. Binding of c-Myc to the promoter region of PVT1 was identified by ChIP-assay. Functionally, upregulation of lncRNA-PVT1 enhanced the proliferation and viability of cervical cancer cells. Mechanistically, lncRNA-PVT1 sponged miR-486-3p and released its repression of extracellular matrix protein 1. Besides, c-Myc functioned as an activator of lncRNA-PVT1 and upregulated its expression by binding to the promoter of PVT1 in cervical cancer cells. lncRNA-PVT1 was upregulated by c-Myc and thus enhanced the proliferation of cervical cancer cells by sponging miR-486-3p.

Five-aminolaevulinic acid photodynamic therapy (ALA-PDT) was used to treat 79 cervical intraepithelial neoplasia 2 (CIN 2) patients who desired preservation of fertility ,between Oct 2018 and Dec 2020. Three months after treatment, among the 65 patients who returned for follow-up, full recovery and improvement rates were 43/65 and 16/65, respectively, resulting in a total response rate of 90.77%. This suggests that ALA-PDT is worthy of clinical application, even as monotherapy. The result of immune testing also indicated significant promotion of CD4+T expression during the recovery process, highlighting the importance of immune responses in different prognoses.

The pattern of asymmetric vortices over a blunt-nose slender body is manageable and highly dependent on the location of artificial microperturbation (AMP) on the nose at a high angle of attack (AoA). A particle is introduced and attached to the nose surface to examine the mechanism of asymmetric flow induced by AMP at high AoA ( α = 50°). Wind tunnel experiments and numerical simulations were conducted to investigate the mechanism of asymmetric flow generated over the blunt-nose slender body. Perturbation flow (PF), which is separated from the AMP surface, divides the shear layer separating from the nose of the slender body into two parts (long and short). The shear layer separating is shown as separation line. The long part on the opposite side with AMP rolls up a vortex earlier than the short one on the same side with AMP. Moreover, the vortex from the long part exhibits higher vorticity than that from the short one. The differences in the two parts result in asymmetric vortices over the blunt-nose body at high AoA. The PF develops into the opposite side with AMP, thereby increasing the asymmetry of flow. The associated flow separation and evolution of streamlines are discussed in detail.

The cell-mediated protective and pathogenic immune responses to SARS-CoV-2 infection remain largely unknown. Here, we identified 76 distinct cell subsets in the PBMC samples that were associated with various clinical presentations of COVID-19 using scRNA-seq technology coupled with a deep and comprehensive analysis of unique cell surface markers and differentially expressed genes. Notable cell subsets include (NCAM1hiCD160+)NK and (TRAV1-2+CD8+)MAIT cells increased in the asymptomatic subjects, (LAG3+CD160+CD8+)NKT cells increased in the symptomatic patients, (CD68-CSF1R-IL1BhiCD14+)classical monocytes associated with age and disease severity, (CD33-HLA-DMA-CD14+)classical monocytes and (CLEC10A-S100A9lo)pDC associated with the viral persistence, neutrophils and (CD68-CSF1R-IL1BhiCD14+ )classical monocytes dramatically increased in a fatal patient, whereas (LAG3+CD160+CD8+)NKT and (FOXP3+IL2RA+IL7R+CD4+)Treg cells markedly increased in a patient with humoral immunodeficiency. The GO and KEGG analyses identified enriched pathways related to immune responses, inflammation, apoptosis and other processes. These findings may enhance our understanding of the immunopathogenesis of COVID-19 and help develop novel strategies against SARS-CoV-2 infection. Funding Information: This study is supported in part by the Department of Science and Technology of Shaanxi Province (Grant No. 2020ZDXM2-SF-02) (CZ and BS) and the operational funds from The First Affiliated Hospital of Xi’an Jiaotong University (CZ and BS). Declaration of Interests: The authors declare that they have no competing financial interests.

Background Ovarian cancer is the fifth most common cause of cancer-related deaths and accounts for 3% of cancer cases occurring in women. Therefore, determining the underlying genes that can promote ovarian cancer progression is of great urgency. It has been reported that RHPN2 promotes tumour progression in various types of cancer, but its role in ovarian cancer pathogenesis remains unknown. Materials and Methods In this study, bioinformatic datasets were used to predict the expression of RHPN2 in clinical samples and determine the relationship between RHPN2 and the prognosis of ovarian cancer patients. Clinical samples were used to verify the prediction. RHPN2-targeting shRNA was used to investigate the effect of RHPN2 on ovarian cancer cells, and following RHPN2 knockdown, the proliferative and migratory capacities of ovarian cancer cells were tested. To determine the downstream signalling target of RHPN2, a luciferase reporter assay was conducted, and an animal experiment was carried out to confirm the effect of RHPN2 in vivo. Results The public datasets indicated that ovarian cancer tissues showed significantly higher RHPN2 expression than para-cancer normal tissues, and poor prognosis was observed in patients with higher RHPN2 expression, which was further confirmed in clinical samples. After RHPN2 was knocked down, the proliferation and migration of ovarian cancer cells were significantly impaired; a luciferase reporter assay indicated that the STAT3 signalling pathway was the most highly affected, and RHPN2 downregulation inhibited STAT3 nuclear translocation. STAT3 inhibitors partially rescued the tumour-promoting effect induced by RHPN2 overexpression, which was further confirmed by animal experiments. Conclusion Collectively, our results indicate that RHPN2 promotes malignant behaviours in ovarian cancer by activating STAT3 signalling.

BACKGROUND Dialysis frequency and dose are controversial prognostic factors of hemodialysis morbidity and mortality. The aim of this study was to find out the effect of frequency and dosage of dialysis on mortality and survival in a group of Chinese hemodialysis patients. MATERIAL AND METHODS In total, 183 patients seen from February 2008 to January 2018, who were on maintenance hemodialysis for at least 3 months, were included in the study cohort. An anonymized database of age, gender, diabetic status, comorbidities, date of initiation of dialysis, hematological characters, biochemical variables, and status of survived or died was established from DICOM (Digital Imaging and Communications in Medicine) files of patients. Kaplan-Meier and Cox-proportional hazard model was used for calculation of survival over time at 95% confidence level. RESULTS Overall, the 10-year survival rate was 27%. Kaplan-Meier analysis showed patient survival as 94% at one-year, 59% at 5-years, and 27% at 10-years. Hemoglobin, serum albumin, calcium, potassium, phosphorous, calcium-phosphorous-products, and hemodialysis frequency and the dose had a significant effect on survival. Cox regression proportional hazard model showed that patients with serum albumin level of >4 g/dL were better associated with survival. Patients who underwent twice-weekly hemodialysis had 4.26 times less chance of survival as compared to patients with thrice-weekly hemodialysis. A higher dialysis dose of >1.2 spKt/V offered better survival as compared to a lower dose of

Aim Pre-eclampsia (PE) is a pregnancy complication characterized by new onset maternal hypertension and proteinuria. Its underlying mechanisms are unclear. This study investigated the relationship between progesterone and endoplasmic reticulum stress (ERS) associated apoptosis induced by interleukin (IL)-1β via the glucose regulated protein 78 (GRP78)/protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C/EBP-homologous protein (CHOP) pathway in BeWo cells. Methods Venous blood and placental tissues were collected from PE patients, normal pregnancy and preterm delivery cases, respectively. Progesterone serum levels were detected by enzyme-linked immunosorbent assay and ERS-related protein expression in placentas was examined by immunohistochemistry, reverse transcriptase-polymerase chain reaction and Western blot. BeWo cells were stimulated by IL-1β to induce ERS associated apoptosis in vitro. The apoptotic rate was measured by flow cytometry. The mechanism of progesterone acting on IL-1β induced ERS associated apoptosis was investigated by reverse transcriptase-polymerase chain reaction, Western blot and PERK small interfering RNA, with RU486 used as a receptor inhibitor. Results PE patients exhibited decreased serum levels of progesterone and activated ERS and increased ERS-related protein expression. IL-1β could induce ERS and associated cell apoptosis by activating the GRP78/PERK/CHOP signal pathway, which could be inhibited by progesterone. PERK could be upregulated and phosphorylation activated in ERS. The protective effects of progesterone could be attenuated by RU486. Conclusion IL-1β could induce ERS associated cell apoptosis by activating the GRP78/PERK/CHOP signal pathway in BeWo cells and may play an important role in PE occurrence. Progesterone levels were decreased in patients with PE and seemed to have a protective effect by inhibiting ERS associated cell apoptosis.

The repeatable and determinate pattern of asymmetric vortices at a regular state can be obtained by manually setting an artificial micro-perturbation (AMP) on the nose tip of a pointed-nosed slender body at a high angle of attack (AoA). Wind tunnel experiments and numerical simulations were conducted to investigate the predominant role of AMP in an asymmetric flow at α = 50°. The bi-stable asymmetric flow structures are presented when AMP rotates around the body axis. Thus, the corresponding side force acting on the slender body is shown as a square wave with two periods. The shear layer separation is presented as the separation lines to investigate the bi-stable asymmetry induced by the AMP. Results show that the AMP restricts the flow separation on the same side of the model with itself when it is located at windward. The separation location on the same side of the AMP moves to the leeward of the model (or the separation angle on the same side of the AMP increases); hence, the vortex rolls up from this side later than the other side. When the AMP is located at leeward of the slender body, it promotes the separation of flow on the same side of the model with itself. Thus, the separation location on the same side of the AMP moves to the windward of the model (or the separation angle on the same side of the AMP decreases) and the vortex rolls up from this side earlier the other side.

The long non-coding RNA (lncRNA) XLOC_006390 is increased in various human cancer tissues and it plays important roles in cell growth and migration. However, the role of lncRNA XLOC_006390 in the progression and metastasis of cervical cancer has not been evaluated and remains unclear. In the present study, we hypothesized that lncRNA XLOC_006390 is also increased in cervical cancer, and upregulation of lncRNA XLOC_006390 contributes to cervical cancer metastasis. The expression of lncRNA XLOC_006390 in cervical cancer tissues and cell lines was analyzed using quantitative reverse-transcription-polymerase chain reaction (qRT-PCR). RNA interference approach and an overexpression system were used to investigate the cellular functions of XLOC_006390 and SET domain containing 8 (SET8). Cell Counting Kit-8 (CCK-8) assay was performed to detect cell proliferation. Cell migration and invasion abilities were evaluated by Transwell assays. Western blotting and immunofluorescence were performed to detect SET8 protein expression. The results revealed that XLOC_006390 was increased in cervical cancer tissues. Patients with high XLOC_006390 expression were associated with FIGO stages III and IV (P=0.0170), lymphatic metastasis (P=0.0078) and distant metastasis (P=0.0025). Furthermore, SET8 was also increased in cervical cancer tissues and its expression was positively associated with XLOC_006390, and XLOC_006390 regulated SET8 expression. In addition, knockdown or overexpression of XLOC_006390 and SET8 expression suppressed or promoted cervical cancer cell proliferation, migration and invasion in vitro, respectively. In conclusion, our data suggest that lncRNA XLOC_006390 promotes cervical cancer cell growth and metastasis through the regulation of SET8, at least partly, which indicate the critical roles of XLOC_006390 and SET8 in cervical cancer progression and metastasis.

Epithelial ovarian cancer (EOC) is the most frequent cause of cancer‑associated mortality among all types of gynecological cancer. The high recurrence rate and the poor 5‑year survival rate indicate that more effective therapeutic strategies are required. The aim of the present study was to investigate the role and potential mechanisms of songorine in treating EOC. EOC cells were cultured with different concentrations of songorine, following which MTT and flow cytometric analyses were conducted to measure cell viability and apoptosis. Wound healing and Transwell assays were used to detect cell migration and invasion abilities. Furthermore, associated molecules in the glycogen synthase kinase (GSK)‑3β/β‑catenin and B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X (Bax) signaling pathways were semi‑quantified by western blotting. Finally, tumor size measurements, pathological observations, western blot analysis and toxicological evaluations were performed in SKOV‑3 tumor‑bearing BALB/c nude mice to investigate the efficacy and safety of songorine. As expected, songorine inhibited EOC cell survival, invasion and migration, promoted EOC cell apoptosis and suppressed mammalian EOC tumorigenic behavior. In particular, GSK3β inhibitor treatment restored the songorine‑induced regulation of the GSK3β/β‑catenin signaling pathway. Furthermore, in the in vitro and in vivo experiments, songorine consistently downregulated the expression of N‑cadherin, vimentin, matrix metalloproteinase (MMP)‑2, MMP‑9, phosphorylated‑GSK3β, β‑catenin and Bcl‑2, and upregulated the expression of E‑cadherin, cleaved caspase‑3, cleaved caspase‑9 and Bax. In conclusion, songorine exerted its anticancer effect through the GSK3β/β‑catenin and Bcl‑2/Bax signaling pathways. These results highlight the potential use of songorine as a novel therapeutic agent for EOC.

Non-premixed pelletization was proposed in low-cost coal-biomass pellet production for Circulating Fluidized Bed combustors. A novel non-premixed pelletization structure C-B-C (coal-biomass-coal) was proposed according to simulation results. Comprehensive study on the combustion behaviour of non-premixed coal-biomass pellet with such structure was carried out at heating rate over 200 ℃/s in a concentrating photothermal reactor. The result showed that the addition of biomass in non-premixed coal-biomass pellet could promote the combustion process but also cause slagging. The addition of biomass significantly increased the reaction index of the whole combustion process while the activation energies during devolatilization to ignition decreased linearly from 47.44 kJ/mol to 23.18 kJ/mol. Biomass promoted CO generation, increased NO emission (due to higher N content and lower chamber temperature) and decreased SO2 emission, during the combustion of non-premixed coal-biomass pellets. The feasibility of coal-biomass non-premixed pelletization method was verified.

Three-dimensional numerical simulations are carried out to study the hydrodynamic performance and flow features of a bio-inspired underwater propulsor. The propulsor is constituted by a passive pitching panel. The leading edge of the panel is prescribed under a periodic heaving motion while the panel pitches passively due to the employing of a stiffness-lumped torsional spring at the leading edge. Effects of the torsional spring stiffness have been put emphases on. A real-time tunable stiffness strategy is presented and employed in the study. We first study the passive pitching effects on the hydrodynamics and flow features of the panel using a series of constant stiffness and then we study the tunable stiffness effects using cosinusoidal curve based waveforms, in which the effects of phase difference ( φ ) between the stiffness profile and the oscillation motion and as well as the effects of stiffness fluctuation amplitude ( G k ) are investigated, respectively. The stiffness profile beneficial for propulsion efficiency is further applied to cases with different oscillation amplitudes. A high-fidelity immersed boundary method based direct numerical simulation (DNS) solver is employed to acquire the fluid dynamics and to simulate the flow. The panel passive pitching motion is solved by coupling the DNS flow solver and the Euler rigid body dynamic equation. Results show that for the constant stiffness cases, the panel generates sinusoidal-like pitching motion, and in certain stiffness range, flexibility could benefit efficiency while holding some extent of stiffness could enhance the thrust. For the tunable stiffness cases, it is found that both the mean thrust and propulsive efficiency improved when the stiffness change is in-phase with the heaving motion ( φ = 0 ° ). The largest mean thrust is found at φ = 120 ° . The wake profile shows that in the constant stiffness cases and φ = 120 ° case, the panel in each cycle generates a pair of elongated and twisted vortex tubes, the vortex tubes in each pair interconnected with each other and induces unprofitable interactions. While in the φ = 0 ° case the panel generates a pair of round and closed vortex loops in each cycle and the vortex loops separated directly after they have been detached from the panel and thus avoided the unprofitable vortex interactions. The stiffness fluctuation amplitude ( G k ) effects study (all employing the in-phase stiffness profile) shows that all the three tested cases ( G k = 0 . 25 G 0 , 0 . 5 G 0 , 0 . 75 G 0 ) acquired thrust and efficiency enhancement while the G k = 0 . 5 G 0 case acquired the largest efficiency benefit and the G k = 0 . 75 G 0 case had the largest thrust. Wake profiles show entire vortex loops may not be formed when G k is small while larger G k may affect the arrangement of the vortex loops thus may generate unprofitable vortex interactions. The results of cases with motions with variable oscillating amplitudes ( A ∗ ) show employing the real-time altering stiffness profile ( φ = 0 ° , G k = 0 . 5 G 0 ) improves the propulsion performance in a certain range of A ∗ ( 0 . 4 ≤ A ∗ ≤ 0 . 8 ). Results from this paper demonstrated the potential of using real-time tunable stiffness in the design of passive pitching propulsors of underwater vehicles that pursue higher performance.

Co-combustion of biomass offers a great potential to reduce CO2 emissions but rarely mentioned co-combustion behavior of pelletized coal-biomass mixtures and inconclusive results based on single determinants formed obstacle for industrial application. In this study, ignition and flame characteristics, reaction and kinetic parameters and pollutant generation path were comprehensively investigated. Intrinsic combustion experiments were carried with the gas phase maintaining at room temperature in a concentrating photothermal reactor at heating rate over 200 °C/s. Same “homogeneous” ignition was evidenced while advanced devolatilization but more intense slagging behaviors were identified with the increase of biomass proportion. With the biomass proportion increased from 0% to 40%, the activation energies during devolatilization to ignition decreased non-linearly from 47.44 kJ/mol to 8.03 kJ/mol, indicating the existence of synergistic effect. CO exhibited relative high generation rates and the generation rate increased with the biomass content. Three fitted CO peaks were identified during co-combustion, which were contributed by devolatilization of coal and biomass, and combustion of char, respectively. First increased and then decreased NO emission with the increase of biomass proportion was evidenced for the higher N content in biomass but enhanced reduction by char and NH radicals with higher biomass proportion.

Control surface, which is often located in the trailing edge of wings, is important in the attitude control of an aircraft. However, the efficiency of the control surface declines severely under the high deflect angle of the control surface because of the flow separation. To improve the efficiency of control surface, this study discusses a novel flow control technique aimed at suppressing the flow separation by pulsed blowing at the leading edge of the control surface. Results indicated that flow separation over the control surface can be suppressed by pulsed blowing, and the maximum average pitching moment coefficient of the control surface can be increased by nearly 90% when average blowing momentum coefficient is 0.03 relative to that of without blowing. Moreover, the lift coefficient of the control surface can be 95% times higher than that of without blowing, and the drag coefficient of the control surface can be reduced by 43% compared with that of without blowing. Finally, this study shows that the average blowing momentum coefficient and non-dimensional frequency of pulsed blowing are two of the key parameters of the pulsed blowing control technique. Both experimental and numerical simulations are used in this study. The experiment is completed in D-4 wind tunnel of Beihang University under conditions of Re 0.8 × 10 6 .

A numerical investigation was conducted on an Unmanned Combat Air Vehicle (UCAV) model which is a moderately swept, tailless and flying wing configuration. A wind tunnel test was performed to validate the numerical results. Model forces and moments were measured using a six-component strain-gauged force balance. The computations were performed using a commercial Reynolds-Averaged Navier-Stokes (RANS) flow solver. The numerical results show that the lateral unstable of the model is caused by asymmetrical breakdown of the body vortex, and the flaps installed can induce earlier breakdown and intensity loss of the leeward vortex resulting in the enhancement of lateral stability.

Background Cervical intraepithelial neoplasia (CIN) may progress to cervical cancer if left untreated. The loop electrosurgical excision procedure (LEEP) of the transitional zone of the cervix is a standard form of treatment. However, human papillomavirus (HPV)-induced CIN may recur after LEEP. The purpose of this case report is to describe the successful use of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) as an adjunct to LEEP, in preventing the recurrence of CIN. Methods The effectiveness of this combined treatment was evaluated in six women. The diagnosis of HPV-induced CIN was determined using HPV DNA tests and liquid-based cervical cytology. Lesion removal was performed 3 h after application of ALA using a 635 nm light density of 80 mw/cm2. Results We treated 6 women aged 31–62 years who had persistent CIN following LEEP, with ALA-PDT (range, 4–7 treatments). Five of the 6 women were HPV negative on retesting 6–7 months after ALA-PDT. Most patients showed no signs of recurrence during the follow-up period. Conclusions Use of ALA-PDT following LEEP may prevent the recurrence of CIN. Monitoring HPV status by means of DNA testing and liquid-based cytology may be used as a standard for clinical diagnosis and treatment. Post-treatment care should be carefully considered because improper post-treatment care might directly lead to relapse.

The long noncoding RNA plasmacytoma variant translocation 1 gene (LncRNA PVT1) has an important role in tumor occurrence and development, yet the role and underlying molecular mechanisms of this RNA in cervical cancer have not yet been elucidated. In the present study, three cervical cancer cell lines (HeLa, Ca Ski and SiHa) were used to verify how LncRNA PVT1 mediates cervical cancer development, and the H8 cell line was used as a control. A LncRNA PVT1 overexpression vector or small interfering RNAs targeting LncRNA PVT1 were transfected into cervical cancer cells to generate LncRNA PVT1 overexpression and silencing in these cells. LncRNA PVT1 overexpression accelerated the growth of cervical cancer cells by advancing the cell cycle and inhibiting cellular apoptosis; increases in Cyclin D1 (CCND1) mRNA and activated Bcl‑2 protein expression levels also supported this finding. Furthermore, NF‑κB activation and expression was increased by LncRNA PVT1 overexpression. In addition, NF‑κB activation or inhibition induced changes in cell viability, accompanied by changes in CCND1 and Bcl‑2 expression. Increases or decreases in microRNA‑16 (miR‑16) expression (using miR mimics and inhibitors) also corresponded to changes in LncRNA PVT1 expression, in vitro. miR‑16 mimics and inhibitor had opposite effects to those of NF‑κB activity, and miR‑16 was demonstrated to directly interact with the NF‑κB gene as measured using the dual‑luciferase assay. In summary, LncRNA PVT1 inhibits the effect of miR‑16, promoting the cell cycle and inhibiting cellular apoptosis of cervical cancer cells, potentially via the NF‑κB pathway. The data from the present study will contribute to the current knowledge surrounding the theoretical basis of cervical cancer and provide a new perspective for the treatment of cervical cancer.

Objective Cervical cancer is one of the most common malignant tumors. Our previous results showed that long non-coding RNA (lncRNA) XLOC_006390 plays an important role in cervical cancer. In this study, we have explored the mechanism of action of lncRNA XLOC_006390. Methods LncRNA XLOC_006390 was proposed to exercise its function as a competing endogenous RNA (ceRNA), and its potential targeted miRNAs was predicted through the database LncBase Predicted v.2. Two miRNAs, miR-331-3p, and miR-338-3p, were chosen for the study. Expression of miRNAs and lncRNA in cervical cancer cells and tissues was detected by reverse transcription polymerase chain reaction. To determine the correlation, silencing of XLOC_006390, over-expression of miR-331-3p, and miR-338-3p was performed in SiHa and Caski cell lines, respectively. Results Based on the interactive effect between miRNA and lncRNA, miR-331-3p and miR-338-3p were significantly downregulated in cervical cancer cells and tissues, and their expression levels were negatively related to that of lncRNA. Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006390 was knocked down. Further, XLOC_006390 was found to facilitate cervical cancer tumorigenesis and metastasis by downregulating miR-331-3p and miR-338-3p expression. Conclusion Taken together, our study demonstrated that XLOC_006390 may serve as a ceRNA and reversely regulates the expression of miR-331-3p and miR-338-3p, thus facilitating cervical cancer tumorigenesis and metastasis.

Background Cervical cancer is one of the malignant tumors which seriously threaten the women health worldwide. SPINT2 is an endogenous inhibitor of hepatocyte growth factor activator and down regulated or even silenced in many human malignant tumors. Objective This study was performed to explore the promoter methylation status of SPINT2 gene and the effect on its expression in cervical carcinoma. Methods HPV-positive and -negative cervical cancer cell lines, 50 cases of cervical carcinoma tissues, and 20 cases of normal cervical tissues were used for this study. The methylation status of promoter and the first exon of SPINT2 gene were analyzed. The expression of SPINT2 was analyzed by qRT-PCR. Results HPV E6/E7 infection affects SPINT2 methylation rate in cell lines. SPINT2 methylation rate of HT-3E6/E7 was 8.8%, while the methylation rate of SPINT2 in HT-3 was 0%. In cervical tissues, the methylation rate of SPINT2 in cervical cancers was 54%, while the methylation rate of SPINT2 in normal cervical samples was 25%. As for cervical cancers, the methylation rate of SPINT2 gene was higher in grade 3 than those of grade 2. Conclusions The expression of SPINT2 gene is regulated by its methylation status, and the methylation status of SPINT2 is altered by HPV infection. The aberrant methylation status of SPINT2 gene may play an important role in the development of cervical cancer.

Ovarian cancer is a highly metastatic malignancy and a leading cause of cancer-related death in postmenopausal women. Emodin is a natural anthraquinone isolated from several traditional Chinese medicines including Rhubarb and Polygonum cuspidatum. Recently, emodin was demonstrated to reduce the growth of human ovarian carcinoma cells. However, the mechanism remains unclear. In the present study, we identified that transforming growth factor (TGF)-β2 was significantly affected by emodin treatment in A2780 cells using microarray analysis. MicroRNA (miR)-199a was predicted as a potential miRNA targeting TGF-β2 by in silico prediction using TargetScan. The mRNA and protein levels of TGF-β2 were both significantly reduced by miR-199a. Spearman's correlation analysis revealed a significant correlation between the expression level of miR-199a and TGF-β2 in human ovarian cancer specimens. Silencing of miR-199a with miR-199a inhibitor significantly restored the reduction in TGF-β2 expression induced by emodin. Additionally, cell viability and colony formation of A2780 cells were markedly inhibited by emodin treatment, which was mediated by miR-199a. We analyzed the primary mature miR-199a-1 and miR-199a-2 transcripts in A2780 cells treated with emodin or dimethyl sulfoxide (DMSO) and found that only pri-miR-199a-1 was regulated by emodin. A conserved binding site of Forkhead box D3 (FOXD3) was identified within pri-miR‑199a-1. We further revealed that miR-199a expression was significantly regulated by FOXD3. Taken together, the present study demonstrated that emodin may directly promote FOXD3 expression and sequentially activates miR-199a, which in turn suppresses the expression of TGF-β2 to reduce cell viability and colony formation of A2780 cells.

To study the influence of hsa-miR-6727-5p on the proliferation, apoptosis, invasion and migration of Caski, Hela and SiHa cervical cancer cells.The CCK8 test, flow cytometry, Transwell and scratch healing experiments were used to measure the influence of hsa-miR-6727-5p on the proliferation, apoptosis, invasion and migration of Caski, Hela and SiHa cells.Compared with the negative control (empty vector) group, the hsa-miR-6727-5p expression in the cells transfected with hsa-miR-6727-5p mimics showed a significant increase (p0.01). CCK8 results showed that the hsa-miR-6727-5p overexpression enhanced significantly the proliferation of cervical cancer cells. Annexin V FITC/PI staining cell results showed that hsa-miR-6727-5p overexpression strongly inhibited the cervical cancer cells apoptosis. Transwell invasion in vitro test showed that hsamiR-6727-5p overexpression significantly enhanced the invasion ability of cervical cancer cells. The scratch healing test suggested that, compared with the control group, the migration ability of cells transfected with hsa-miR-6727-5p mimics in the experimental group was stronger.We confirmed at the cellular level that hsa-miR-6727-5p promoted the proliferation, invasion and migration of cervical cancer cells and inhibited the apoptosis through the overexpression or inhibition of hsa-miR-6727-5p. These results indicated that hsamiR-6727-5p played a role in promoting the cervical cancer.

Pre-eclampsia (PE) is a pregnancy complication characterized by new onset maternal hypertension and proteinuria. Its underlying mechanisms are unclear. This study investigated the relationship between progesterone and endoplasmic reticulum stress (ERS) associated apoptosis induced by interleukin (IL)-1β via the glucose regulated protein 78 (GRP78)/protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C/EBP-homologous protein (CHOP) pathway in BeWo cells.Venous blood and placental tissues were collected from PE patients, normal pregnancy and preterm delivery cases, respectively. Progesterone serum levels were detected by enzyme-linked immunosorbent assay and ERS-related protein expression in placentas was examined by immunohistochemistry, reverse transcriptase-polymerase chain reaction and Western blot. BeWo cells were stimulated by IL-1β to induce ERS associated apoptosis in vitro. The apoptotic rate was measured by flow cytometry. The mechanism of progesterone acting on IL-1β induced ERS associated apoptosis was investigated by reverse transcriptase-polymerase chain reaction, Western blot and PERK small interfering RNA, with RU486 used as a receptor inhibitor.PE patients exhibited decreased serum levels of progesterone and activated ERS and increased ERS-related protein expression. IL-1β could induce ERS and associated cell apoptosis by activating the GRP78/PERK/CHOP signal pathway, which could be inhibited by progesterone. PERK could be upregulated and phosphorylation activated in ERS. The protective effects of progesterone could be attenuated by RU486.IL-1β could induce ERS associated cell apoptosis by activating the GRP78/PERK/CHOP signal pathway in BeWo cells and may play an important role in PE occurrence. Progesterone levels were decreased in patients with PE and seemed to have a protective effect by inhibiting ERS associated cell apoptosis.