Synthesis and utilization of polyol-modified high specific surface area Ca(OH)2: an investigation.

Calcium hydroxide (Ca(OH)2) finds widespread use in the petrochemical industry, particularly in flue gas desulfurization applications. However, its conventional usage is limited by its inherently low specific surface area, hampering its efficiency. To address this limitation, this study aims to develop a simple and industrially scalable preparation process for Ca(OH)2 with a high specific surface area, thereby enhancing its effectiveness in various applications. This study aimed to develop a preparation process for making Ca(OH)2 with a high specific surface area, suitable for industry and easy to make. Ca(OH)2 with a specific surface area of 41.555 m2/g was successfully synthesized by incorporating polyols during lime digestion. The prepared high specific surface area Ca(OH)2 is more than five times the specific surface area of ordinary Ca(OH)2. Incorporation of polyols within the lime digestion process induces a reduction in both Ca(OH)2 grain size and particle dimensions, concurrently amplifying the specific surface area and optimizing mass transfer efficiency. Specifically, the desulfurization breakthrough time for Ca(OH)2 subject to a 15% triethanolamine modification was notably extended to 879 s, surpassing the desulfurization breakthrough time of unaltered Ca(OH)2 by more than tenfold. Moreover, the modified Ca(OH)2 exhibited remarkable efficacy in neutralizing acidic wastewater. A new approach for the preparation of high-performance Ca(OH)2 is proposed in this study, which could facilitate the industrial production of Ca(OH)2 with high specific surface area.

Association of genetic variations in FoxP3 gene with Graves' disease in a Southwest Chinese Han population.

BACKGROUND: Graves' disease (GD) is a T cell-mediated organ-specific autoimmune disease. Forkhead box P3 (FoxP3) is an excellent marker for the induction and development of regulatory T cells (Tregs). Recent studies showed that single-nucleotide polymorphisms (SNPs) in the FoxP3 gene were associated with the increased susceptibility to several autoimmune diseases. In the present study, we investigated the association of FoxP3 gene polymorphisms with GD in a Southwest Chinese Han population. METHODS: A two-stage case-control study was performed in 890 healthy controls (male, 282; female, 608) and 503 patients with GD (male, 138; female, 365). Four SNPs (rs3761548, rs3761549, rs3761547, and rs2280883) were genotyped by the polymerase chain reaction-restriction fragment length polymorphism assay. The χ2 test was used to compare the genotype distributions and allele frequencies between GD patients and healthy controls. RESULTS: In the first stage, the significantly increased frequencies of the A allele (p = .031, odds ratio [OR] = 1.635) and AA genotype (p = .023, OR = 3.257), together with a significantly decreased frequency of the C allele (p = .031, OR = 0.611) of FoxP3/rs3761548 were found in female patients with GD. None of the other FoxP3 SNPs was associated with GD susceptibility. Subsequent validation and combination of data confirmed the association between FoxP3/rs3761548 and the female patients with GD (A allele: p < .001, OR = 1.672; AA genotype: p = .005, OR = 2.488; CC genotype: p = .001, OR = 0.622; C allele: p < .001, OR = 0.615, respectively). CONCLUSION: Our findings suggest that FoxP3/rs3761548 is significantly associated with female GD patients in a Southwest Chinese Han population.

Knockdown of PROM2 Enhances Paclitaxel Sensitivity in Endometrial Cancer Cells by Regulating the AKT/FOXO1 Pathway.

BACKGROUND: Endometrial cancer is a very common and highly lethal reproductive malignant tumour in women. Paclitaxel (PTX) is a usual drug utilized in chemotherapy for endometrial cancer. It has been uncovered that PROM2 participates in the progression of various cancers through playing a promoter. However, the regulatory function of PROM2 in PTX treatment for endometrial cancer remains unclear. METHODS: The cell viability (IC50) was examined through CCK8 assay. The mRNA and protein expressions of genes were measured through RT-qPCR and western blot. The proliferation was evaluated through colony formation and EdU assays. The cell apoptosis was assessed through flow cytometry. RESULTS: In this work, through bioinformatic analysis on online websites, it is found that the up-regulated expression of PROM2 existed in endometrial cancer. In addition, the survival probability of UCEC patients with high PROM2 expression was worse. This study adopted PTX treatment for obtaining the PTX-resistant cells (HEC-1A/PTX and KLE/PTX). Furthermore, suppression of PROM2 enhanced PTX sensitivity through decreasing IC50 and proliferation in endometrial cancer. Additionally, knockdown of PROM2 facilitated cell apoptosis in HEC-1A/PTX and KLE/PTX cells. Next, we found that silencing of PROM2 retards the AKT/FOXO1 pathway. At last, rescue assays reversed the strengthened PTX sensitivity mediated by PROM2 inhibition after SC79 treatment (AKT activator). CONCLUSION: Knockdown of PROM2 enhanced PTX sensitivity in endometrial cancer through modulating the AKT/FOXO1 pathway. This study hinted that PROM2 may be a useful therapeutic target for PTX treatment in endometrial cancer.

A Network Pharmacology Study on the Cervix Prescription for Treatment of Cervical Cancer.

Purpose: Based on the method of network pharmacology to explore the mechanism of the cervical prescription (CP) in the treatment of cervical cancer (CC). Methods: We obtained the active ingredients and potential targets in the CP from the literature and the systematic pharmacological analysis platform of traditional Chinese medicine (BATMAN-TCM); the database was used to search for targets related to cervical cancer and to map CP and targets; the core targets were screened, and the protein-protein interaction network (PPI) was constructed using the TCM compound-target network and STRING database. Gene ontology (GO) and Kyoto Gene and Genome Encyclopedia (KEGG) pathway enrichment analysis of overlapping targets were performed using DAVID 6.8 online tool. Results: The CP contains 2 active ingredients, corresponding to 301 nonreactive targets; 10 GO biological process related items and 73 signal pathways were obtained. Cell experiments confirmed that the medicated serum of CP could effectively inhibit the proliferation and invasion ability of Hela cells. Conclusion: This study provides valuable information for TCM researchers and clinicians to better understand the main therapeutic targets and therapeutic roles of herbal decoctions in clinical settings. The results of our study preliminarily clarified that the cervical prescription has an inhibitory effect on cervical cancer cells.

TKTL1 participated in malignant progression of cervical cancer cells via regulating AKT signal mediated PFKFB3 and thus regulating glycolysis.

BACKGROUND: Cervical cancer (CC) is the second most common cancer among women with high morbidity and mortality. TKTL1 is a key protein in glucose metabolism in cancer cells and controls the pentose phosphate pathway (PPP). In this paper, we aim to explore whether TKTL1 can participate in the malignant process of CC cells through glucose metabolism. METHODS: The expression and activity of TKTL1 in CC cell lines were detected by RT-qPCR and Western blot. Cell transfection was conducted to interfere the expression of TKTL1 in SiHa cells, with efficiency detected by RT-qPCR and Western blot. Cell proliferation was then measured by CCK-8 kits. Wound Healing and Transwell experiments were performed to respectively detect the levels of cell migration and invasion, and western blot was used to detect the expressions of migration-related proteins. Tunel and Western blot were used to detect the apoptosis and apoptosis-related proteins. Glucose uptake, lactate production, and ATP production were measured by corresponding commercial kits. Next, the expression of p-Akt, AKT, p-MTOR, mTOR, HK2 and PFKFB3 was detected by Western blot. The mechanism was further investigated by interfering the expression of HK2 and PFKFB3 and adding AKT agonist SC79. At the animal level, the tumor bearing mouse model of CC was constructed, and the weight, volume and pathological morphology of the tumor tissue were detected to verify the cell experiment. RESULTS: TKTL1 expression was increased in CC cells. Interference of TKTL1 expression can inhibit TKTL1 enzyme activity, proliferation, invasion and migration of CC cells, and simultaneously suppress the generation of glycolysis. In addition, the results showed that TKTL1 activated PFKFB3 through AKT rather than HK2 signaling and is involved in glycolysis, cell invasion, migration, and apoptosis of CC cells. In animal level, inhibition of TKTL1 also contributed to decreased tumor volume of CC tumor bearing mice and improved histopathological status. CONCLUSION: TKTL1 participated in malignant progression of CC cells via regulating AKT signal-mediated HK2 and PFKFB3 and thus regulating glucose metabolism.

Qiu's Neiyi Recipe Regulates the Inflammatory Action of Adenomyosis in Mice via the MAPK Signaling Pathway.

BACKGROUND: The management of adenomyosis is challenging and limiting. Qiu's Neiyi recipe (Qiu) is a traditional Chinese medicine (TCM) prescription clinically used for endometriosis treatment in China, but the effect and mechanism of Qiu on adenomyosis are undefined. METHODS: An experimental adenomyosis model was induced in female neonatal ICR mice administrated with tamoxifen. The adenomyosis mice were divided into five groups: high-, middle-, and low-Qiu's group, danazol group, and model group. The mice just administrated with the solvent only (no tamoxifen or drugs) were served as the control group. After 28 days of administration, the body, uterine, spleen, and thymus weights of all mice were examined. Then, the myometrial infiltration and the expression of inflammatory factors were detected by histology examination, ELISA, and qRT-PCR in the uterus. In addition, the MAPK/ERK signaling pathway-related protein expression in adenomyosis mice was detected by immunohistochemical (IHC) staining, qRT-PCR, and western blotting. RESULTS: In experimental adenomyosis mice, Qiu treatment improved the symptoms of adenomyosis by reducing the myometrial infiltration and increasing the index of spleen and thymus. The elevated levels of IL-1ß, IL-6, and TNF-α in serum and uterus tissues of adenomyosis model mice were also decreased after Qiu treatment. The improvement of Qiu on the adenomyosis was achieved by inhibiting the activated MAPK/ERK signaling pathway, including reducing the mRNA and protein expressions of p-ERK/ERK, p-JNK/JNK, and p-p38/p38 in the uterus tissues. CONCLUSION: Qiu alleviated the inflammatory reaction and uterus histological changes in mice with adenomyosis, and the potential mechanism is through the inhibition of the MAPK/ERK signaling pathway. Qiu may be a promising treatment for adenomyosis.

Research on Radiosensitivity of the Protein Kinase B Signaling Pathway in Cervical Cancer.

The main characteristics of cervical cancer are abnormal and uncontrolled cell proliferation, and it regulates cell growth, differentiation, and cell death through genetic and epigenetic changes. This paper mainly discusses the radiosensitivity of the cervical cancer protein kinase B signaling pathway and discusses the specific mechanisms that affect the occurrence and development of cervical cancer. In addition, this paper studies the effect of transient transfection knocking down the expression of TRIP4 in cervical cancer cells on the expression of key proteins in related signaling pathways and explores the mechanism of its specific effects and finds the mechanism of TRIP4's effect on cervical cancer radiosensitivity. The findings of this study show for the first time that knocking down TRIP4 inhibits cell viability by inhibiting the P13K/AKT and MAPK/ERK pathways, and this corresponds to the first part of the experimental results, which show that knocking down TRIP4 inhibits colony formation and increases apoptosis in HeLa and SiHa cells. Moreover, simultaneous inhibition of TRIP4 and hTERT proteins can increase the radiosensitivity of cervical cancer cells. These findings indicate that the inhibition of TRIP4 may be a new type of treatment that selectively targets the P13K/AKT and MAPK/ERK pathways and hTERT pathways in cervical cancer cells and provides a therapeutic option for the treatment of cervical cancer.

PIF1 Affects the Proliferation and Apoptosis of Cervical Cancer Cells by Influencing TERT.

INTRODUCTION: Cervical cancer is a common malignancy in female and it is a serious disease threatening women's lives. We aimed to explore whether PIF1 helicase expression could affect cell proliferation and apoptosis, and whether its mechanisms were related to the expression and activity of TERT. METHODS: Western blot analysis was used to detect the expressions of PIF1 and TERT in End1/E6E7, Hela, SiHa, Ca-Ski and C-33A cells and apoptosis-related proteins (Bax, Bcl-2 and Caspase-3). RT-qPCR and Western blot analysis determined the expressions of PIF1 and TERT after transfection. After transfection or cycloastragenol (CAG) treatment, the proliferation, apoptosis, cell cycle and telomerase TERT activity were analyzed by CCK-8 assay, flow cytometry analysis and ELISA assay. Co-immunoprecipitation assay was used to verify the interactions between PIF1 and TERT. RESULTS: The expressions of PIF1 and TERT in End1/E6E7, Hela, SiHa, Ca-Ski and C-33A cells were increased. As PIF1 and TERT expressions in C-33A cells showed the minimum increase, C-33A cells were chosen for the next study. PIF1 interference inhibited the proliferation, decreased the ratio of G2/M phase and promoted apoptosis of transfected cells, and PIF1 interference promoted the expressions of Bax and Caspase-3 and suppressed the Bcl-2 expression. Furthermore, PIF1 interference down-regulated the telomerase activity. The effect of PIF1 overexpression was opposite to that of PIF1 interference. Co-immunoprecipitation assay demonstrated that PIF1 could combine with TERT. CAG treatment effectively reversed the effect of PIF1 interference on proliferation, cycle and apoptosis of C-33A cells transfected with shRNA-PIF1. Moreover, CAG treatment increased the expressions of PIF1 and TERT. DISCUSSION: PIF1 helicase could promote the proliferation and suppress the apoptosis of cervical cancer cells by down-regulating the activity of telomerase TERT.

Hsa_circ_103973 Acts as a Sponge of miR-335 to Promote Cervical Cancer Progression.

BACKGROUND: Cervical cancer (CC) ranks as the second most common malignancy in women, accounting for more two 2 million deaths every year in the world. Recently, circular RNAs (circRNAs) have been reported to regulate the progression of multiple human tumors; however, whether it involves in CC remains largely elusive. MATERIALS AND METHODS: Two GEO circRNA expression profiles (GSE102686, GSE113696) were downloaded to analyze the differentially expressed circRNAs using bioinformatics methods. Expression of circ_103973, miR-335 and PPP6C in CC tissues and cell lines were examined by qRT-PCR. Cell apoptosis was assessed with PI/Annexin-V double staining followed by the analysis of flow cytometry. Cell proliferation was evaluated by MTT and colony formation assays. Interaction between circ_103973 and miR-335, as well as miR-335 and PPP6C, were verified by dual-luciferase reporter assay. RESULTS: Circ_103973 was found to be highly expressed in both GSE102686 and GSE113696 datasets as well as in CC tissue samples and cell lines. Higher levels of circ_103973 were correlated to a worse outcome of CC patients. Knockdown of circ_103973 significantly promoted CC cell apoptosis and inhibited CC cell proliferation in vitro. Mechanistically, we demonstrated that circ_103973 served as a sponge of miR-335, which directly targeted PPP6C in CC cells. miR-335 was found to be decreased in CC, while PPP6C was found to be increased in CC. Moreover, anti-miR-335 could reverse the inhibitory effects of circ_103973 knockdown on CC cell proliferation, and this phenomenon could be blocked by si-PPP6C. CONCLUSION: Circ_103973 promoted CC cell proliferation in vitro by physically binding miR-335, which further targeted and regulated PPP6C.

Long non-coding RNA activated by transforming growth factor-ß promotes proliferation and invasion of cervical cancer cells by regulating the miR-144/ITGA6 axis.

NEW FINDINGS: What is the central question of this study? This study was designed to investigate the molecular mechanism and biological roles of long non-coding RNA activated by transforming growth factor-ß (lncRNA ATB) in the progression of cervical cancer. What is the main finding and its importance? Our study provided new insight into the cross-talk between lncRNA ATB, miR-144 and ITGA6, shedding light on the therapy for cervical cancer. ABSTRACT: The present study was designed to investigate the molecular mechanism and biological roles of long non-coding RNA activated by transforming growth factor-ß (lncRNA ATB) in the progression of cervical cancer. The expression levels of lncRNA ATB, miR-144 and integrin α6 (ITGA6) were detected in human cervical cancer cell lines using quantitative real-time PCR and western blotting. Cell viability was quantified by MTT assay at 12, 24, 36, 48 and 72 h after transfection, and cell invasion was determined by the Transwell migration assay. The association among lncRNA ATB, miR-144 and ITGA6 was disclosed by a dual-luciferase reporter assay. We found that lncRNA ATB was highly expressed in human cervical cancer cell lines. Further investigation indicated that lncRNA ATB functioned as a competitive endogenous RNA (ceRNA) for miR-144 to promote cervical cancer cell proliferation and invasion. We demonstrated that ITGA6 was a direct target of miR-144, and lncRNA ATB facilitated the proliferation and invasion of cervical cancer cells via the miR-144/ITGA5 axis. In conclusion, the lncRNA ATB/miR-144/ITGA6 axis might be a promising therapeutic target for cervical cancer.

Long Noncoding RNA FOXD2-AS1 Promotes the Malignancy of Cervical Cancer by Sponging MicroRNA-760 and Upregulating Hepatoma-Derived Growth Factor.

Although the functions of long noncoding RNA (lncRNA) called FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) have been well studied in multiple human cancer types, its expression status and detailed roles in cervical cancer remain unknown and merit investigation. This study was aimed at assessing FOXD2-AS1 expression in cervical cancer and at determining its effects on the aggressive behavior of cervical cancer in vitro and in vivo. Expression of FOXD2-AS1 in cervical cancer tissues and cell lines was determined via reverse-transcription quantitative PCR. The effects of FOXD2-AS1 on cervical cancer cells were examined by a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow-cytometric analysis, migration and invasion assays, and an in vivo tumorigenicity assay. FOXD2-AS1 was found to be significantly upregulated in cervical cancer tissues and cell lines. High FOXD2-AS1 expression was notably linked with the Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and depth of cervical invasion in patients with cervical cancer. Kaplan-Meier survival analysis revealed significantly shorter overall survival of patients when the tumor expression of FOXD2-AS1 was higher in comparison with those in patients with lower FOXD2-AS1 expression. In vitro functional assays revealed that downregulation of FOXD2-AS1 led to suppression of proliferation, migration, and invasiveness as well as to the induction of apoptosis of cervical cancer cells. In addition, FOXD2-AS1 silencing hindered tumor growth in vivo. Mechanism investigation revealed that FOXD2-AS1 functioned as a molecular sponge of microRNA-760 (miR-760). Furthermore, hepatoma-derived growth factor (HDGF) was validated as a direct target gene of miR-760 in cervical cancer cells. Moreover, an miR-760 knockdown reversed the effects of FOXD2-AS1 silencing on cervical cancer cells. FOXD2-AS1 possesses significant oncogenic activity in cervical cancer progression; this activity is mediated by sponging of miR-760 with consequent upregulation of HDGF. The FOXD2-AS1-miR-760-HDGF axis might harbor promising targets for novel treatment strategies of cervical cancer.

Effectiveness of two different acupuncture strategies in patients with vulvodynia: Study protocol for a pilot pragmatic controlled trial.

BACKGROUND: Vulvodynia, or vulvar pain, is a common condition in women; however, there are few evidence-based clinical trials evaluating nonpharmacological therapies for this condition. Acupuncture is one complementary and integrative medicine therapy used by some patients with vulvodynia. This study evaluates two different acupuncture strategies for the treatment of vulvodynia and aims to evaluate whether either of the acupuncture protocols reduces vulvar pain, pain duration or pain with intercourse. The study also examines how long the effect of acupuncture lasts in women with vulvodynia. METHODS/DESIGN: The study is designed as a randomized controlled trial, focused on two acupuncture protocols. Fifty-one patients who have had vulvodynia for more than 3 months will be recruited. Among them, 34 patients will be randomized into Groups 1a and 1b; those who are unwilling to receive acupuncture will be recruited into the standard care group (Group 2). Patients in Group 1a will have acupuncture focused on the points in the pudendal nerve distribution area, while patients in Group 1b will receive acupuncture focused on traditional (distal) meridian points. Patients in Group 2 will receive routine conventional treatments, such as using pain medications, local injections and physical therapies or other nonsurgical procedures. Acupuncture will last 45 min per session, once or twice a week for 6 weeks. The primary outcome measurement will be objective pain intensity, using the cotton swab test. The secondary outcome measurement will be subjective patient self-reported pain intensity, which will be conducted before cotton swab test. Pain intensities will be measured by an 11-point Numeric Pain Rating Scale. Pain duration and pain score during intercourse are recorded. Local muscle tension, tenderness and trigger points (Ashi points) are also recorded. All measurements will be recorded at baseline (before the treatment), at the end of each week during treatment and at the end of the 6 weeks. Follow-up will be done 6 weeks following the last treatment. DISCUSSION: Results of this trial will provide preliminary data on whether acupuncture provides better outcomes than nonacupuncture treatments, i.e., standard care, and whether acupuncture focused on the points in pudendal nerve distribution, near the pain area, has better results than traditional acupuncture focused on distal meridian points for vulvodynia. TRIAL REGISTRATION: Clinicaltrials.gov: NCT03481621. Register: March 29, 2018.