Endometrial stem cells alleviate cisplatin-induced ferroptosis of granulosa cells by regulating Nrf2 expression.

BACKGROUND: Premature ovarian failure (POF) caused by cisplatin is a severe and intractable sequela for young women with cancer who received chemotherapy. Cisplatin causes the dysfunction of granulosa cells and mainly leads to but is not limited to its apoptosis and autophagy. Ferroptosis has been also reported to participate, while little is known about it. Our previous experiment has demonstrated that endometrial stem cells (EnSCs) can repair cisplatin-injured granulosa cells. However, it is still unclear whether EnSCs can play a repair role by acting on ferroptosis. METHODS: Western blotting and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were applied to detect the expression levels of ferroptosis-related genes. CCK-8 and 5-Ethynyl-2'-deoxyuridine (EdU) assays were used to evaluate cell viability. Transmission electron microscopy (TEM) was performed to detect ferroptosis in morphology. And the extent of ferroptosis was assessed by ROS, GPx, GSSG and MDA indicators. In vivo, ovarian morphology was presented by HE staining and the protein expression in ovarian tissue was detected by immunohistochemistry. RESULTS: Our results showed that ferroptosis could occur in cisplatin-injured granulosa cells. Ferroptosis inhibitor ferrostatin-1 (Fer-1) and EnSCs partly restored cell viability and mitigated the damage of cisplatin to granulosa cells by inhibiting ferroptosis. Moreover, the repair potential of EnSCs can be markedly blocked by ML385. CONCLUSION: Our study demonstrated that cisplatin could induce ferroptosis in granulosa cells, while EnSCs could inhibit ferroptosis and thus exert repair effects on the cisplatin-induced injury model both in vivo and in vitro. Meanwhile, Nrf2 was validated to participate in this regulatory process and played an essential role.

Characterization of the prognostic, diagnostic, and immunological roles of DSCC1 and its genomic alteration and instability in human cancers.

DNA replication and sister chromatid cohesion 1 (DSCC1) exerts various functions including sister chromatid cohesion. DSCC1 overexpression plays an important role in cancer development, such as in colorectal, breast, and hepatocellular cancers. The specific role of DSCC1 in tumor progression remains largely unknown, necessitating a pan-cancer investigation to understand the potential function of DSCC1 in various cancers. In this study, we obtained data on physiological conditions, transcriptional expression, survival prognosis, genomic alteration, genomic instability, enriched pathways, immune infiltration, and immunotherapy from The Cancer Genome Atlas, The Genotype-Tissue Expression, cBioPortal, and other publicly available databases to systematically characterize the oncogenic and immunological roles of DSCC1 in 33 different cancers. We found that DSCC1 expression was upregulated at both mRNA and protein levels in various cancers. Additionally, DSCC1 expression was associated with higher tumor stage and grade in specific cancers. DSCC1 was a potential pan-cancer prognostic biomarker for its close association with patient prognosis and a diagnostic biomarker for its high predictive value in distinguishing tumor tissues from normal tissues. DSCC1 was universally amplified across different cancers and tightly associated with genomic instability. Moreover, DSCC1 had a close relationship with tumor immune cell infiltration; thus, it could be used as a potential biomarker for predicting the response and survival of patients with cancer who receive immune checkpoint blockade treatment. To sum up, our study revealed that DSCC1 is a promising target for tumor therapy.

Validity of the Chinese version of the weekly calendar planning activity (WCPA) on assessing executive function in adults with stroke.

The weekly calendar planning activity (WCPA) is a performance-based assessment of executive function (EF) via a cognitively-based instrumental activity of daily life (C-IADL). This study aimed to examine the validity of the Chinese version of the WCPA in adults with stroke and to explore the characteristics of cognitive strategy use among the population. Fifty-eight hospitalized patients with stroke aged 26-82 years and 53 controls completed the WCPA, two neuropsychological tests and instrumental activity of daily life (IADL) scale. Participants with stroke were subdivided into a stroke cognitive impaired group (Stroke-CI) and a general stroke group (Stroke-NCI) based on the Montreal Cognitive Assessment. Results showed that the WCPA was able to discriminate between Stroke-CI with controls and the Stroke-NCI group with controls. We found significant limitations in stroke patients' ability to use strategies. Concurrent and ecological validities were demonstrated through correlations between the neuropsychological test scores, IADL and the WCPA performance. This study provides initial evidence for the validity of the Chinese version of the WCPA-10 for adults with stroke and suggests the need to use performance-based tests even in patients with normal cognitive screening test results. The WCPA could provide useful information for strategy-based interventions for adults with stroke.

FGF2 promotes the proliferation of injured granulosa cells in premature ovarian failure via Hippo-YAP signaling pathway.

Young women undergoing anticancer treatment are at risk of premature ovarian failure (POF). Endometrial-derived stem cells (EnSCs) have demonstrated significant therapeutic potential for treating ovarian insufficiency, although the underlying mechanisms remain to be fully understood. This study aims to further investigate the therapeutic effects of EnSCs, particularly through the paracrine action of fibroblast growth factor 2 (FGF2), on POF. The findings show that exogenous FGF2 enhances the survival of ovarian granulosa cells damaged by cisplatin. FGF2 stimulates the proliferation of these damaged cells by suppressing the Hippo signaling pathway and activating YAP expression. In vivo experiments also revealed that FGF2 treatment significantly improves ovarian reserve and endocrine function in mice with POF. These results suggest that FGF2 can boost the proliferative capacity of damaged ovarian granulosa cells through the Hippo-YAP signaling pathway, providing a theoretical foundation for using EnSCs and FGF2 in clinical treatments for POF.

FTO attenuates the cytotoxicity of cisplatin in KGN granulosa cell-like tumour cells by regulating the Hippo/YAP1 signalling pathway.

Premature ovarian failure (POF) is a devastating condition for women under 40 years old. Chemotherapy, especially the use of cisplatin, has been demonstrated to promote the apoptosis of granulosa cells in primary and secondary follicles, leading to POF. Our previous studies demonstrated that fat mass- and obesity-associated (FTO) plays an essential role in protecting granulosa cells from cisplatin-induced cytotoxicity. Various studies have suggested that the Hippo/YAP signalling pathway plays a significant role in regulating cell apoptosis and proliferation. Additionally, YAP1 is the main downstream target of the Hippo signalling pathway and is negatively regulated by the Hippo signalling pathway. However, whether the Hippo/YAP signalling pathway is involved in the protective effect of FTO on granulosa cells has not been determined. In this study, we found that after cisplatin treatment, the apoptosis of granulosa cells increased in a concentration-dependent manner, accompanied by the downregulation of FTO and YAP1. Furthermore, overexpression of FTO decreased cisplatin-induced granulosa cell apoptosis, inhibited the Hippo/YAP kinase cascade-induced phosphorylation of YAP1, and promoted the entry of YAP1 into the nucleus. The downstream targets of YAP1 (CTGF, CYR61, and ANKRD1) were also increased. Si-RNA-mediated downregulation of FTO promoted cisplatin-induced granulosa cell apoptosis, activated the Hippo/YAP kinase cascade, and inhibited the YAP1 entry into the nucleus. These effects were completely reversed by the small molecule inhibitor of YAP1-verteporfin (VP). Taken together, these data suggested that FTO-YAP1 plays a positive role in regulating the proliferation of injured granulosa cells induced by cisplatin.

Integrative bioinformatics analysis of WDHD1: a potential biomarker for pan-cancer prognosis, diagnosis, and immunotherapy.

BACKGROUND: Although WD repeat and high-mobility group box DNA binding protein 1 (WDHD1) played an essential role in DNA replication, chromosome stability, and DNA damage repair, the panoramic picture of WDHD1 in human tumors remains unclear. Hence, this study aims to comprehensively characterize WDHD1 across 33 human cancers. METHODS: Based on publicly available databases such as TCGA, GTEx, and HPA, we used a bioinformatics approach to systematically explore the genomic features and biological functions of WDHD1 in pan-cancer. RESULTS: WDHD1 mRNA levels were significantly increased in more than 20 types of tumor tissues. Elevated WDHD1 expression was associated with significantly shorter overall survival (OS) in 10 tumors. Furthermore, in uterine corpus endometrial carcinoma (UCEC) and liver hepatocellular carcinoma (LIHC), WDHD1 expression was significantly associated with higher histological grades and pathological stages. In addition, WDHD1 had a high diagnostic value among 16 tumors (area under the ROC curve [AUC] > 0.9). Functional enrichment analyses suggested that WDHD1 probably participated in many oncogenic pathways such as E2F and MYC targets (false discovery rate [FDR] < 0.05), and it was involved in the processes of DNA replication and DNA damage repair (p.adjust < 0.05). WDHD1 expression also correlated with the half-maximal inhibitory concentrations (IC50) of rapamycin (4 out of 10 cancers) and paclitaxel (10 out of 10 cancers). Overall, WDHD1 was negatively associated with immune cell infiltration and might promote tumor immune escape. Our analysis of genomic alterations suggested that WDHD1 was altered in 1.5% of pan-cancer cohorts and the "mutation" was the predominant type of alteration. Finally, through correlation analysis, we found that WDHD1 might be closely associated with tumor heterogeneity, tumor stemness, mismatch repair (MMR), and RNA methylation modification, which were all processes associated with the tumor progression. CONCLUSIONS: Our pan-cancer analysis of WDHD1 provides valuable insights into the genomic characterization and biological functions of WDHD1 in human cancers and offers some theoretical support for the future use of WDHD1-targeted therapies, immunotherapies, and chemotherapeutic combinations for the management of tumors.

Fatty Acid Oxidation Mediated by Malonyl-CoA Decarboxylase Represses Renal Cell Carcinoma Progression.

Fatty acid metabolism reprogramming is a prominent feature of clear cell renal cell carcinoma (ccRCC). Increased lipid storage supports ccRCC progression, highlighting the importance of understanding the molecular mechanisms driving altered fatty acid synthesis in tumors. Here, we identified that malonyl-CoA decarboxylase (MLYCD), a key regulator of fatty acid anabolism, was downregulated in ccRCC, and low expression correlated with poor prognosis in patients. Restoring MLYCD expression in ccRCC cells decreased the content of malonyl CoA, which blocked de novo fatty acid synthesis and promoted fatty acid translocation into mitochondria for oxidation. Inhibition of lipid droplet accumulation induced by MLYCD-mediated fatty acid oxidation disrupted endoplasmic reticulum and mitochondrial homeostasis, increased reactive oxygen species levels, and induced ferroptosis. Moreover, overexpressing MLYCD reduced tumor growth and reversed resistance to sunitinib in vitro and in vivo. Mechanistically, HIF2α inhibited MLYCD translation by upregulating expression of eIF4G3 microexons. Together, this study demonstrates that fatty acid catabolism mediated by MLYCD disrupts lipid homeostasis to repress ccRCC progression. Activating MLYCD-mediated fatty acid metabolism could be a promising therapeutic strategy for treating ccRCC. SIGNIFICANCE: MLYCD deficiency facilitates fatty acid synthesis and lipid droplet accumulation to drive progression of renal cell carcinoma, indicating inducing MYLCD as a potential approach to reprogram fatty acid metabolism in kidney cancer.

Quality of sexual life and associated factors: a cross-sectional survey of Chinese breast cancer patients.

PURPOSE: This study aimed to explore Chinese breast cancer patients' quality of sexual life (QSL) and factors associated with QSL. METHODS: The questionnaires in this cross-sectional study include the general information questionnaire, cognition and assessment of sexual health questionnaire, Self-acceptance Questionnaire (SAQ), Medical Coping Modes Questionnaire (MCMQ), and Quality of Sexual Life Questionnaire (QSLQ); 201 breast cancer patients were required to complete the questionnaires assessing characteristic information, cognition and assessment of sexual health, QSL, self-acceptance, and coping style. Finally, hierarchical regression was used to analyze the factors associated with QSL in Chinese breast cancer patients. RESULTS: The mean age (at the time of the survey) of the breast cancer patients was 48.31±9.15. The mean score of the QSLQ (range 28-140) was 75.14±16.57. Hierarchical regression analysis showed that the associated factors of breast cancer patients' QSL included age (at the time of the survey), education level, type of surgery, cognition and assessment of sexual health, self-acceptance, and avoidance and acceptance-resignation coping styles, that independent variables explained 60.4% of the variance. CONCLUSION: The QSL among Chinese breast cancer patients needs to be improved. Our findings indicated that breast cancer patients with older age, lower education level, or modified radical mastectomy have poor QSL. Breast cancer patients learn correct information about sexual health, enhance self-acceptance, and reduce acceptance-resignation, and avoidance coping could be intervention strategies to improve their QSL.

Apoptotic effect of selenium mushroom extract from Qinba on multiple myeloma cells.

Qinba selenium mushroom is a mushroom belonging to the Basidiomycetes family, which is believed to have anti- oxidant, anti-tumoral and anti-mutagenic activities. However, the efficacy of Qinba selenium mushroom against multiple myeloma has not been confirmed. The present study aimed to investigate the apoptotic effect of FA-2-b-ß, the selenium mushroom extract from Qinba on multiple myeloma (MM) cells. The MM RPMI-8226 cells were treated with FA-2-b-ß at different concentrations and time points. MM RPMI-8226 cell proliferation and apoptosis were detected by the Cell Counting Kit-8 (CCK-8) assay and Annexin V/propidium iodide (PI) assay, RT-QPCR and western blotting analyses were performed to determine the proteins and pathways involved. The results of the present study demonstrated that FA-2-b-ß has high anti-proliferative activities and strong pro-apoptotic effects on MM RPMI-8226 cells, and its pharmacological effects on proliferation changes occurred in a dose- and time-dependent manner. In addition, we found that FA-2-b-ß was able to induce cell apoptosis and promote cell cycle arrest at G0/G1 phase. In summary, the results illustrate the involvement of FA-2-b-ß in mediating G0/G1 cell cycle arrest and apoptosis in MM RPMI-8226 cells, which suggested that FA-2-b-ß might have therapeutic potential against multiple myeloma as an effective compound, and may provide useful information for the development of a novel therapeutic target in this area.

Comprehensive bioinformatics analysis reveals the prognostic value, predictive value, and immunological roles of ANLN in human cancers.

Anillin (ANLN) is a unique scaffolding, actin-binding protein, which is essential for the integrity and ingression of the cleavage furrow. It is mainly involved in the cytokinesis process, while its role in various tumors has not been fully addressed and remains largely elusive. To provide a thorough perspective of ANLN's roles among diverse malignancies, we conducted a comprehensive, pan-cancer analysis about ANLN, including but not limited to gene expression levels, prognostic value, biological functions, interacting proteins, immune-related analysis, and predictive value. As a result, when compared to normal tissues, ANLN expression is elevated in most cancers, and its expression also differs in different immune subtypes and molecular subtypes in diverse cancers. In addition, in 17 types of cancer, ANLN expression is increased in early tumor stages, and higher ANLN expression predicts worse survival outcomes in more than ten cancers. Furthermore, ANLN shows close correlations with the infiltration levels of most immune cells, and enrichment analysis using ANLN co-expressed genes reveals that ANLN plays essential roles in cell cycle, mitosis, cellular senescence, and p53 signaling pathways. In the final, ANLN exhibits high accuracy in predicting many cancers, and subsequent multivariate analysis suggests ANLN could be an independent prognostic factor in specific cancer types. Taken together, ANLN is proved to be a novel and promising biomarker for its excellent predictive utility, promising prognostic value, and potential immunological roles in pan-cancer. Targeting ANLN might be an attractive approach to tumor treatment.

Integrated Bioinformatics Analysis of Serine Racemase as an Independent Prognostic Biomarker in Endometrial Cancer.

Endometrial cancer (EC) kills about 76,000 women worldwide, with the highest incidence in industrialized countries. Because of the rise in disease mortality and new diagnoses, EC is now a top priority for women's health. Serine racemase (SRR) is thought to play a role in the central nervous system, but its role in cancers, particularly in EC, is largely unknown. The current study starts with a pan-cancer examination of SRR's expression and prognostic value before delving into SRR's potential cancer-suppressing effect in patients with EC. SRR may affect the endometrial tumor immune microenvironment, according to subsequent immune-related analysis. SRR expression is also linked to several genes involved in specific pathways such as ferroptosis, N6-methyladenosine methylation, and DNA damage repair. Finally, we used the expression, correlation, and survival analyses to investigate the upstream potential regulatory non-coding RNAs of SRR. Overall, our findings highlight the prognostic significance of SRR in patients with EC, and we can formulate a reasonable hypothesis that SRR influences metabolism and obstructs key carcinogenic processes in EC.

FGF2 Is Protective Towards Cisplatin-Induced KGN Cell Toxicity by Promoting FTO Expression and Autophagy.

It is widely known that chemotherapy-induced apoptosis of granulosa was the main reason for premature ovarian failure (POF). In addition, accumulating evidence has demonstrated that autophagy was involved in it. Studies before have reported that fibroblast growth factor-2 (FGF2) could attenuate cell death via regulating autophagy. In our previous study, FGF2 could decrease granulosa cell apoptosis in cisplatin-induced POF mice. Furthermore, obesity-associated protein [fat mass and obesity-associated protein (FTO)], which decreased significantly in POF mice, could inhibit cell apoptosis via activating autophagy. Moreover, downregulation of FTO could decrease the expression of paracrine factor FGF2. However, the relationship between FTO and FGF2 in granulosa cell autophagy is still unknown. In the present study, Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2-deoxyuridine (EdU) assays showed that exogenous addition of FGF2 could promote cisplatin-induced injured granulosa cell proliferation. Western blotting indicated that FGF2 could inhibit apoptosis of injured granulosa cells via autophagy. Inhibition of autophagy by chemicals suppressed the effect of FGF2 and promoted injured cell apoptosis. In addition, the expression of FTO was decreased in injured cells, and FGF2 addition could reverse it. Overexpression of FTO reduced injured cell apoptosis via activating the autophagy process. Our findings indicated that FGF2 activates autophagy by regulating the expression of FTO, thereby reducing the apoptosis of the injured cells.

A Metabolism-Related Gene Landscape Predicts Prostate Cancer Recurrence and Treatment Response.

Background: Prostate cancer (PCa) is the most common malignant tumor in men. Although clinical treatments of PCa have made great progress in recent decades, once tolerance to treatments occurs, the disease progresses rapidly after recurrence. PCa exhibits a unique metabolic rewriting that changes from initial neoplasia to advanced neoplasia. However, systematic and comprehensive studies on the relationship of changes in the metabolic landscape of PCa with tumor recurrence and treatment response are lacking. We aimed to construct a metabolism-related gene landscape that predicts PCa recurrence and treatment response. Methods: In the present study, we used differentially expressed gene analysis, protein-protein interaction (PPI) networks, univariate and multivariate Cox regression, and least absolute shrinkage and selection operator (LASSO) regression to construct and verify a metabolism-related risk model (MRM) to predict the disease-free survival (DFS) and response to treatment for PCa patients. Results: The MRM predicted patient survival more accurately than the current clinical prognostic indicators. By using two independent PCa datasets (International Cancer Genome Consortium (ICGC) PCa and Taylor) and actual patients to test the model, we also confirmed that the metabolism-related risk score (MRS) was strongly related to PCa progression. Notably, patients in different MRS subgroups had significant differences in metabolic activity, mutant landscape, immune microenvironment, and drug sensitivity. Patients in the high-MRS group were more sensitive to immunotherapy and endocrine therapy, while patients in the low-MRS group were more sensitive to chemotherapy. Conclusions: We developed an MRM, which might act as a clinical feature to more accurately assess prognosis and guide the selection of appropriate treatment for PCa patients. It is promising for further application in clinical practice.

FTO protects human granulosa cells from chemotherapy-induced cytotoxicity.

BACKGROUND: Premature ovarian failure (POF) is a serious problem for young women who receive chemotherapy, and its pathophysiological basis is the dysfunction of granulosa cells. According to previous reports, menstrual-derived stem cells (MenSCs) can restore ovarian function and folliculogenesis in mice with chemotherapy-induced POF. Fat mass- and obesity-associated (FTO) was reported to be associated with oocyte development and maturation. FTO was decreased in POF and may be a biomarker for the occurrence of POF. Knockdown of FTO in granulosa cells promoted cell apoptosis and inhibited proliferation. But the relationship between FTO and ovarian repair was still unclear. This study was aimed at investigating the FTO expression level and the role of FTO in the MenSCs recovering the function of injured granulosa cells. METHOD: First, cisplatin was used to establish a granulosa cell injury model. Then, the MenSCs and injured granulosa cell coculture model and POF mouse model were established in this study to explore the role of FTO. Furthermore, gain- and loss-of-function studies, small interfering RNA transfection, and meclofenamic acid (MA), a highly selective inhibitor of FTO, studies were also conducted to clarify the regulatory mechanism of FTO in granulosa cells. RESULTS: MenSCs coculture could improve the function of injured granulosa cells by increasing the expression of FTO. MenSCs transplantation restored the expression of FTO in the ovaries of POF mice. Overexpression of FTO restored the injured cell proliferation and decreased apoptosis by regulating the expression of BNIP3. Down-regulation of FTO got the opposite results. CONCLUSIONS: In the treatment of MenSCs, FTO has a protective effect, which could improve the viability of granulosa cells after cisplatin treatment by decreasing the expression of BNIP3. Meanwhile, FTO may provide new insight into therapeutic targets for the chemotherapy-induced POF.

The interaction between iNKT cells and B cells.

Invariant natural killer T cells (iNKTs) bridge the innate immunity with the adaptive immunity and their interaction with B cells has been extensively studied. Here, we give a complete overview of these two cells, from their mechanism of interaction to clinical prospects and existing problems. In our introduction, we describe the relationship between iNKTs and B cells and explore the current research hotspots and future directions. We begin with how B cells interact and benefit from the innate and adaptive help of iNKTs. Next, we describe the multiple roles of these cells in infections, autoimmunity, and cancers. Lastly, we look into the potential immunotherapies that can be based on iNKTs and the possible treatments for infectious, autoimmune, and other diseases.

NGF Signaling Interacts With the Hippo/YAP Pathway to Regulate Cervical Cancer Progression.

Nerve growth factor (NGF) is increasingly implicated in cervical cancer progression, but its mechanism in cervical cancer is unclear. Here, studies demonstrate that NGF inhibits the Hippo signaling pathway and activates Yes-associated protein (YAP) to induce cervical cancer cell proliferation and migration. Our results suggested that stimulation of NGF promoted cell growth and migration and activated YAP in HeLa and C-33A cell lines. The expression of YAP target genes (CTGF and ANKRD1) was upregulated after NGF treatment. The NGF inhibitor Ro 08-2750 and siRNA-mediated NGF receptor gene silencing suppressed HeLa and C-33A cells proliferation and migration, activated large suppressor kinase 1 (LATS1) kinase activity, and suppressed YAP function. In addition, the expression of YAP target genes (CTGF and ANKRD1) was suppressed by Ro 08-2750 treatment in HeLa and C-33A cells. Interestingly, proliferation was significantly higher in NGF-treated cells than in control cells, and this effect was completely reversed by the YAP small molecule inhibitor-verteporfin. Furthermore, the mouse xenograft model shows that NGF regulates YAP oncogenic activity in vivo. Mechanistically, NGF stimulation inactivates LATS1 and activates YAP, and NGF inhibition was found to induce large suppressor kinase 1 (LATS1) phosphorylation. Taken together, these data provide the first direct evidence of crosstalk between the NGF signaling and Hippo cancer pathways, an interaction that affects cervical cancer progression. Our study indicates that combined targeting of the NGF signaling and the Hippo pathway represents a novel therapeutic strategy for treatment of cervical cancer.

Body Composition and Metabolic Improvement in Patients Followed Up by a Multidisciplinary Team for Obesity in China.

BACKGROUND: This study evaluated the effectiveness of the multidisciplinary team (including a specialist, a dietitian, a physical exercise trainer, a surgeon for bariatric surgery, an acupuncturist, and several health educators) for obesity management and the body composition change and improvements in metabolic biomarkers during a 2-year follow-up. MATERIALS AND METHODS: A total of 119 patients participated in the multidisciplinary team for obesity. Patients were followed up at 3 months, 6 months, 1 year, 18 months, and 2 years after their first visit. Individuals were divided into the high-protein diet (HPD) and standard-protein diet (SPD) group according to their results on a diet questionnaire that they filled out during follow-up. RESULTS: After 1.2 years, the mean body weight of the participants dropped from 89.7 kg to 80.9 kg (p < 0.001). The body adiposity index was reduced from 33.9 to 32.0 (p < 0.001), while the fat-free mass index from 17.0 to 15.2 (p = 0.043). Fasting glucose and HbA1c were also lower after treatment (p = 0.002 and 0.038 for FPG and HbA1c, respectively). Fasting insulin and HOMA-IR were reduced (p = 0.002 and <0.001 for fasting insulin and HOMA-IR, respectively). HDL-c increased along with weight loss (1.06 mmol/L vs. 1.19 mmol/L, p < 0.001), and transaminase levels significantly dropped (p = 0.001 and 0.021 for ALT and AST, respectively). During treatment, mean protein intake was 29.9% in the HPD group and 19.5% in the SPD group (p < 0.001). Weight loss, reduction of visceral fat area, maintenance of lean body mass, body adiposity index, and fat-free mass index showed no statistical significance between the HPD and SPD groups, as well as glucose metabolic variables. CONCLUSIONS: A multidisciplinary team for obesity management could significantly reduce body weight and improve metabolic indicators, including HDL-c, transaminase, and insulin resistance. A high-protein diet does not produce better weight control or body composition compared with a standard calorie-restricted diet.

microRNA-210/ Long non-coding RNA MEG3 axis inhibits trophoblast cell migration and invasion by suppressing EMT process.

INTRODUCTION: Pre-eclampsia is characterized by insufficient spiral artery remodeling, and trophoblast dysfunction plays an important role in this process. Noncoding RNAs (microRNAs (miRNAs) and long noncoding RNAs (LncRNAs) are included) can regulate trophoblasts. MicroRNA-210 (miR-210) can decrease trophoblast cell migration and invasion and may act as a biomarker for preeclampsia. LncRNA maternally expressed gene 3 (MEG3) plays a positive role in pre-eclampsia, and MEG3 can be a downstream target of miR-210 in human umbilical vein endothelial cells (HUVEC). However, the effect of miR-210 on MEG3 and the mechanism of action of the miR-210/MEG3 axis in trophoblasts remain unclear. METHOD: The localization of miR-210 and MEG3 in the human placenta in early pregnancy was determined by in situ hybridization. Then, HTR8/SVneo cells were used to investigated the effect of miR-210 on MEG3 expression and biological activity of trophoblasts in the migration and invasion assays. Gain- and loss-of-function experiments were performed to determine the mechanism of action of miR-210 and MEG3 in Epithelial-mesenchymal transition (EMT) of HTR8/SVneo cells. RESULTS: The qRT-PCR and western blotting results demonstrated that the upregulation of miR-210 decreases MEG3, N-cadherin and Vimentin expression and increases E-cadherin expression to inhibit EMT in HTR-8/SVneo cells. Inhibition of the expression of miR-210 results in the opposite effects. Gain- and loss-of-function assay indicated that miR-210 can impair the EMT, migration, and invasion of HTR8/SVneo cells by regulating the expression of MEG3. DISSCUSSION: MiR-210 may be a negative regulator of trophoblast EMT that acts by suppressing MEG3 expression.

How to restore medical services in the ophthalmic department in the post-pandemic period of COVID-19.

Currently, the epidemics situation of COVID-19 is still grim. As a high-risk department, it is necessary to take corresponding prevention and control measures in the ophthalmology department. To guide the ophthalmology department of medical institutions to recover from the post-pandemic period of COVID-19, we designed relevant prevention and control strategies formulated by the National Health Committee, combined with our practical work of hospital pandemic management. The prevention and control strategies contained ward settings, channel design, allocation of protective equipment, screening of hospitalized patients, supervision-guided improvement, ward disinfection, the management of patients and escorts. There are 64 doctors and nurses who had standardized training during the post-pandemic period in the ophthalmology department. A total of 185 patients were admitted to the ophthalmology department of our institution, and 107 operations were successfully performed during that period. We made a follow-up visit two weeks after discharge to ask whether the patients had fever and/or other symptoms and whether he had been diagnosed with a COVID-19 case. Ultimately the ophthalmic ward was free of infection with the novel coronavirus. These showed that our prevention strategies were effective for ophthalmology department to defending COVID-19 in the process of recovering medical services.

Medical waste management practice during the 2019-2020 novel coronavirus pandemic: Experience in a general hospital.

It is currently a critical period for the prevention and control of the COVID-19 pandemic. Since the medical waste disposal could be an important way to control the source of infection, standardization, and strict implementation of the management of COVID-19 related medical waste should be with careful consideration to reduce the risk of epidemic within hospitals. This study illustrates the practice of medical waste disposal responding to the 2019-2020 novel coronavirus pandemic.