The dysfunction of CD8+ T cells triggered by endometriotic stromal cells promotes the immune survival of endometriosis.

Endometriosis is defined as an oestrogen-dependent and inflammatory gynaecological disease of which the pathogenesis remains unclear. This study aimed to investigate the cellular heterogeneity and reveal the effect of CD8+ T cells on the progress of endometriosis. Three ovarian endometriosis patients were collected, and single-cell RNA sequencing (scRNA-seq) progressed and delineated the cellular landscape of endometriosis containing five cell clusters. The endometrial cells (EMCs) were the major component, of which the mesenchymal cells were preponderant and characterized with increased inflammation and oestrogen synthesis in endometriosis. The proportion of T cells, mainly CD8+ T cells rather than CD4+, was reduced in endometriotic lesions, and the cytokines and cytotoxicity of ectopic T cells were depressed. CD8+ T cells depressed the proliferation of ESCs through inhibiting CDK1/CCNB1 pathway to arrest the cell cycle and triggered inflammation through activating STAT1 pathway. Correspondingly, the coculture with ESCs resulted in the dysfunction of CD8+ T cells through upregulating STAT1/PDCD1 pathway and glycolysis-promoted metabolism reprogramming. The endometriotic lesions were larger in nude mouse models with T-cell deficiency than the normal mouse models. The inhibition of T cells via CD90.2 or CD8A antibody increased the endometriotic lesions in mouse models, and the supplement of T cells to nude mouse models diminished the lesion sizes. In conclusion, this study revealed the global cellular variation of endometriosis among which the cellular count and physiology of EMCs and T cells were significantly changed. The depressed cytotoxicity and aberrant metabolism of CD8+ T cells were induced by ESCs with the activation of STAT1/PDCD1 pathway resulting in immune survival to promote endometriosis.

RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial-mesenchymal transition and proliferation in endometriosis.

Endometriosis is a benign gynaecological disease appearing with pelvic pain, rising dysmenorrhoea and infertility seriously impacting on 10% of reproductive-age females. This research attempts to demonstrate the function and molecular mechanism of RhoA/ROCK pathway on epithelial-mesenchymal transition (EMT) and proliferation in endometriosis. The expression of Rho family was abnormally changed in endometriotic lesions; in particular, RhoA and ROCK1/2 were significantly elevated. Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial-mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up-regulated the RhoA activity and expression of RhoA and ROCK1/2. RhoA overexpression reinforced the effect of oestrogen on promoting EMT and proliferation, and RhoA knockdown impaired the effect of oestrogen. oestrogen receptor α (ERα) was involved with the regulation of oestrogen on EMT and proliferation and up-regulated RhoA activity and expression of RhoA and ROCK1/2. The function of ERα was modulated by the change in RhoA expression. Furthermore, phosphorylated ERK that was enhanced by oestrogen and ERα promoted the protein expression of RhoA/ROCK pathway. Endometriosis mouse model revealed that oestrogen enhanced the size and weight of endometriotic lesions. The expression of RhoA and phosphorylated ERK in mouse endometriotic lesions was significantly elevated by oestrogen. We conclude that abnormal activated RhoA/ROCK pathway in endometriosis is responsible for the function of oestrogen/ERα/ERK signalling, which promoted EMT and proliferation and resulted in the development of endometriosis.

Establishment of an immortalized stromal cell line derived from human Endometriotic lesion.

BACKGROUND: Endometriosis is a benign gynecological disease with obviously feature of estrogen-dependence and inflammatory response. The applications of primary endometriotic stromal cells in research of endometriosis are restricted for short life span, dedifferentiation of hormone and cytokine responsiveness. The objective of this study was to establish and characterize immortalized human endometriotic stromal cells (ihESCs). METHODS: The endometriotic samples were from a patient with ovarian endometriosis and the primary endometriotic stromal cells were isolated from the endometriotic tissues. The primary cells were infected by lentivirus to establish telomerase reverse transcriptase (hTERT)-induced immortalized cells. Quantification of mRNA and proteins was examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western Blot. CCK-8 assay and EdU labeling assay were assigned to assess the growth of ihESCs. Karyotype assay was performed to detect the chromosomes of ihESCs. Colony formation assay and nude mouse tumorigenicity assay were used to evaluate colony-formation and tumorigenesis abilities. RESULTS: ihESCs continuously overexpressed hTERT via infection of lentivirus and significant extended the life span reaching 31 passages. The morphology, proliferation and karyotype of ihESCs remained unchanged. The expression of epithelial-mesenchymal transition (EMT) markers, estrogen-metabolizing proteins and estrogen/progesterone receptors (ERs and PRs) were unaltered. Furthermore, the treatment of estrogen increased the proliferation and EMT of ihESCs. Lipopolysaccharides (LPS) and IL-1ß remarkably induced inflammatory response. The clonogenesis ability of ihESCs was consistent with primary cells, which were much lower than Ishikawa cells. In addition, nude mouse tumorigenicity assay demonstrated that ihESCs were unable to trigger tumor formation. CONCLUSION: This study established and characterized an immortalized endometriotic stromal cell line that exhibited longer life span and kept the cellular morphology and physiological function as the primary cells. The immortalized cells remained normal feedback to estrogen and inflammatory response. Moreover, the immortalized cells were not available with tumorigenic ability. Therefore, ihESCs would be serviceable as in vitro cell tool to investigate the pathogenesis of endometriosis.

Rare earth elements induced electronic engineering in Rh cluster toward efficient alkaline hydrogen evolution reaction.

The unique electronic and crystal structures of rare earth metals (RE) offer promising opportunities for enhancing the hydrogen evolution reaction (HER) properties of materials. In this work, a series of RE (Sm, Nd, Pr and Ho)-doped Rh@NSPC (NSPC stands for N, S co-doped porous carbon nanosheets) with sizes less than 2 nm are prepared, utilizing a simple, rapid and solvent-free joule-heat pyrolysis method for the first time. The optimized Sm-Rh@NSPC achieves HER performance. The high-catalytic performance and stability of Sm-Rh@NSPC are attributed to the synergistic electronic interactions between Sm and Rh clusters, leading to an increase in the electron cloud density of Rh, which promotes the adsorption of H+, the dissociation of Rh-H bonds and the release of H2. Notably, the overpotential of the Sm-Rh@NSPC catalyst is a mere 18.1 mV at current density of 10 mAcm-2, with a Tafel slope of only 15.2 mV dec-1. Furthermore, it exhibits stable operation in a 1.0 M KOH electrolyte at 10 mA cm-2 for more than 100 h. This study provides new insights into the synthesis of composite RE hybrid cluster nanocatalysts and their RE-enhanced electrocatalytic performance. It also introduces fresh perspectives for the development of efficient electrocatalysts.

[Relationship between perceptions of safety climate at workplace and depressive disorders in manufacturing workers].

OBJECTIVE: To investigate the risk factors for depressive disorders in manufacturing workers and to provide a basis for developing health promotion measures at workplace. METHODS: A questionnaire survey was performed in 8085 front-line production workers from 33 manufacturing enterprises in Nanhai District of Foshan, Guangdong Province, China. The questionnaire contained a survey of demographic characteristics, the Safety Climate Scale, the Center for Epidemiological Studies Depression Scale, etc. The multilevel logistic regression analysis was applied to investigate the risk factors for depressive disorders in workers. RESULTS: A total of 6260 workers completed the survey; their mean age was 31.1 ± 8.6 years, and 53.2% of them were males. The multilevel logistic regression analysis showed that after adjustment for sociodemographic factors such as age, sex, and martial status, more depressive disorders were reported in the enterprises with higher score of "production safety training" than in those with lower score (OR = 1.46, 95%CI = 1.07 ∼ 1.97); fewer depressive disorders were reported in the enterprises with higher score of "colleagues concerned about production safety" than in those with lower score (OR = 0.08, 95%CI = 0.03 ∼ 0.26); the relationships of "safety warnings and precautions" and "managers concerned about production safety" with workers' depressive disorders were not statistically significant (OR = 0.78, 95%CI = 0.48 ∼ 1.28; OR = 1.08, 95%CI = 0.68 ∼ 1.72). CONCLUSION: Depressive disorders in manufacturing workers are related to the safety climate at workplace, which indicates that a good safety climate at workplace should be created to prevent and control depressive disorders in workers.

Tuning oxygen release of sodium-ion layered oxide cathode through synergistic surface coating and doping.

Layered transition metal oxides have the greatest potential for commercial application as cathode materials for sodium-ion batteries. However, transition metal oxides inevitably undergo an irreversible oxygen loss process during cycling, which leads to structural changes in the material and ultimately to severe capacity degradation. In this work, using density function theory (DFT) calculations, the Ni-O bond is revealed to be the weakest of the M-O bonds, which may lead to structural failure. Herein, the synergistic surface CeO2 modification and the trace doping of Ce elements stimulate oxygen redox and improve its reversibility, thus improving the structural stability and electrochemical performance of the material. Theoretical calculations prove that Na0.67Mn0.7Ni0.2Co0.1O2 (MNC) obtains electrons from CeO2, avoiding destruction of the Ni-O bond by over-energy released during the charging process and inhibiting oxygen loss. The capacity retention was 77.37% for 200 cycles at 500 mA g-1, compared to 33.84% for the unmodified Na0.67Mn0.7Ni0.2Co0.1O2. Overall, the present work demonstrates that the synergistic effect of surface coating and doping is an effective strategy for realizing tuning oxygen release and high electrochemical performance.

Lipoxin A4 depresses inflammation and promotes autophagy via AhR/mTOR/AKT pathway to suppress endometriosis.

BACKGROUND: Endometriosis is a benign gynecological disease with the feature of estrogen dependence and inflammation. The function of autophagy and the correlation with inflammation were not yet revealed. METHODS: Autophagosomes were detected by transmission electron microscopy. Gene Expression Omnibus (GEO) database was referred to analyze the expression of autophagy-related genes. Quantification of mRNA and protein expression was examined by qRT-PCR and Western Blot. Immunohistochemistry was performed to explore the expression of proteins in tissues. The mouse model of endometriosis was performed to analyze the autophagic activity and effect of LXA4. RESULTS: The expression of autophagy-related genes in endometriotic lesions were unusually changed. The number of autophagosomes and LC3B-II expression was diminished, and p62 was increased in ectopic lesions from both patients and mice. Interleukin 1ß (IL1ß) attenuated the expression of LC3B and promoted the level p62. The autophagy activator MG-132 upregulated the expression of LC3B and reduced IL1ß, IL6, and p62. LXA4 reversed the inhibitory effect of IL1ß on the expression of LC3B and p62, and blocking the receptor of LXA4 AhR (aryl hydrocarbon receptor) resulted in the incapacitation of LXA4 to influence the effect of IL1ß. LXA4 depressed the phosphorylation of AKT and mTOR to against IL1ß, and blocking AhR negatively regulated the effect of LXA4 on AKT/mTOR pathway. LXA4 reduced the ectopic lesions and the expression of IL1ß and p62, but enhanced LC3B-II in endometriotic mouse models. CONCLUSION: In endometriosis, increased inflammation of ectopic lesions prominently depresses autophagy. LXA4 could regulate autophagy by suppressing inflammatory response through AhR/AKT/mTOR pathway.

[Associations of occupational safety atmosphere and behaviors with unintentional injuries].

OBJECTIVE: To evaluate the associations of perception of safety atmosphere at workplace, occupational safety attitude and behaviors with occupational unintentional injury among manufacturing workers. METHODS: A cross-sectional study was performed and a self-administered questionnaire was used to inquire socio-demographic characteristics, perceived safety atmosphere, occupational safety attitudes, occupational safety behaviors and occupational unintentional injuries among 10585 manufacturing workers selected from 46 enterprises in Guangdong. Structural equation modeling was applied to assess the relationship of the perception of safety atmosphere at workplace, occupational safety attitude, and occupational safety behaviors with occupational unintentional injury. RESULTS: Among 24 pathways supposed in structural equation model, 20 pathways (except for the attitude toward occupational safety, the attitude toward managers' support, the work posture and individual protection) were significantly related to the occupational unintentional injuries. The further analysis indicated that the perceived safety atmosphere might impact the occupational unintentional injuries by the attitude toward occupational safety and occupational safety behaviors. CONCLUSION: Workers' perception of safety atmosphere indirectly influenced on occupational unintentional injuries through occupational safety attitudes and occupational safety behaviors.

Multifunctional Carbon Modification Enhancement for Vanadium-Based Phosphates as an Advanced Cathode of Zinc-Ion Batteries.

In recent years, rechargeable aqueous zinc-ion batteries (ZIBs) have shown extraordinary potential due to their safety, nontoxicity, sustainable zinc resources, and low price. However, the lack of suitable cathode materials hinders the development of ZIBs. Recently, layered phosphates have been widely used as cathode materials. As one typical phosphate cathode, vanadium oxyphosphate (VOPO4) has inherently low electronic conductivity and structural dissolution in electrochemical reactions, limiting its development. To solve these problems, VOPO4/C is prepared by combining multifunctional carbon material with a VOPO4 interlayer and an external surface, which not only improves the electronic conductivity of the composite material but also effectively inhibits the dissolution of VOPO4 in the electrolyte. As a result, the prepared VOPO4/C could deliver a reversible capacity of 140 mA h g-1 at a current density of 100 mA g-1. Furthermore, the rate performance of the VOPO4/C composite has also been improved significantly. In the process of charging and discharging, zinc ions in the composite show perfect intercalate and deintercalate performance.

Surgical treatment for primary mitral valve tumor: a 25-year single-center experience.

OBJECTIVE: Primary mitral valve (MV) tumor is a rare lesion, and to date, there have been few larger surgical series of MV tumors. We retrospectively analyzed 11 cases of primary MV tumors regarding clinical and pathological features, surgical procedure and long-term outcomes. METHODS: From November 1983 to December 2008, we operated on 11 patients (age 36.3 ± 17.7 years, weight 55.4 ± 11.2 kg) with primary MV tumors. Symptoms were cardiac in 8 cases (72.7%) and neurologic in 3 (26.3%). Surgical procedures included en bloc excision and MV repair in 8 cases and tumor resection and MV replacement in 3. No radiotherapy or chemotherapy was given to patients with malignant tumors. RESULTS: Pathological diagnosis was papillary fibroelastoma in 3 cases, myxoma in 3, lymphangioma in 1, lipoma in 1, hemangioma in 1 and sarcoma in 2. No early deaths or complications occurred. Late death occurred in 2 patients with sarcoma 1 year postoperatively. At the latest follow-up, with a maximum of 25 years (mean 10.6 ± 8.8), the 9 survivors were in New York Heart Association functional class I with normal MV function and no echocardiographic evidence of local recurrence. CONCLUSIONS: The majority of primary MV tumors are benign. They can cause cardiac or neurologic symptoms and should be excised as soon as a diagnosis is made. For benign tumors, valve-sparing resection and valve repair are often possible with excellent long-term outcomes. The prognosis of malignant MV tumors is poor.

Systematic Review and Bioinformatic Analysis of microRNA Expression in Autism Spectrum Disorder Identifies Pathways Associated With Cancer, Metabolism, Cell Signaling, and Cell Adhesion.

Background: Previous studies have identified differentially expressed microRNAs in autism spectrum disorder (ASD), however, results are discrepant. We aimed to systematically review this topic and perform bioinformatic analysis to identify genes and pathways associated with ASD miRNAs. Methods: Following the Preferred Reporting Items for Systematic reviews and Meta-Analyses, we searched the Web of Science, PubMed, Embase, Scopus, and OVID databases to identify all studies comparing microRNA expressions between ASD persons and non-ASD controls on May 11, 2020. We obtained ASD miRNA targets validated by experimental assays from miRTarBase and performed pathway enrichment analysis using Metascape and DIANA-miRPath v3. 0. Results: Thirty-four studies were included in the systematic review. Among 285 altered miRNAs reported in these studies, 15 were consistently upregulated, 14 were consistently downregulated, and 39 were inconsistently dysregulated. The most frequently altered miRNAs including miR-23a-3p, miR-106b-5p, miR-146a-5p, miR-7-5p, miR-27a-3p, miR-181b-5p, miR-486-3p, and miR-451a. Subgroup analysis of tissues showed that miR-146a-5p, miR-155-5p, miR-1277-3p, miR-21-3p, miR-106b-5p, and miR-451a were consistently upregulated in brain tissues, while miR-4742-3p was consistently downregulated; miR-23b-3p, miR-483-5p, and miR-23a-3p were consistently upregulated in blood samples, while miR-15a-5p, miR-193a-5p, miR-20a-5p, miR-574-3p, miR-92a-3p, miR-3135a, and miR-103a-3p were consistently downregulated; miR-7-5p was consistently upregulated in saliva, miR-23a-3p and miR-32-5p were consistently downregulated. The altered ASD miRNAs identified in at least two independent studies were validated to target many autism risk genes. TNRC6B, PTEN, AGO1, SKI, and SMAD4 were the most frequent targets, and miR-92a-3p had the most target autism risk genes. Pathway enrichment analysis showed that ASD miRNAs are significantly involved in pathways associated with cancer, metabolism (notably Steroid biosynthesis, Fatty acid metabolism, Fatty acid biosynthesis, Lysine degradation, Biotin metabolism), cell cycle, cell signaling (especially Hippo, FoxO, TGF-beta, p53, Thyroid hormone, and Estrogen signaling pathway), adherens junction, extracellular matrix-receptor interaction, and Prion diseases. Conclusions: Altered miRNAs in ASD target autism risk genes and are involved in various ASD-related pathways, some of which are understudied and require further investigation.

Foreign investors and stock price crash risk: Evidence from China.

This study examines whether and how foreign investors affect firm-specific crash risk. Based on China's stock market, we show that foreign investors significantly increase stock price crash risk and the positive association is more pronounced in firms with high levels of information asymmetry or efficient internal control. We address endogeneity issue using a quasi-natural experiment, namely, the revision of Foreign Investment Industrial Guidance Catalog in 2011, and results still hold. Overall, this study provides policy implications on the effect of foreign investor in emerging capital markets.

Establishment and characterization of immortalized human eutopic endometrial stromal cells.

PROBLEM: The application of primary eutopic endometrial cells from endometriosis patients in research is restricted for short life span, dedifferentiation of hormone responsiveness. METHOD OF STUDY: Human telomerase reverse transcriptase (hTERT)-induced immortalized cells (iheESCs) were infected by lentivirus. mRNA level was examined by qRT-PCR, and protein expression was quantified by Western blot. CCK-8 and EdU assay were assigned to assess the proliferation. The migration and invasion of cells were assessed by transwell assay. Clone formation assay and nude mouse tumorigenicity assay were used to evaluate colony-formation and tumorigenesis abilities. RESULTS: hTERT mRNA and protein were significantly expressed higher in iheESCs compared to primary cells. iheESCs grew without morphological change for 42 passages which is much longer than 18 passages of primary cells. There was no obvious difference between primary cells and iheESCs in growth, mobility, and chromosome karyotype. Furthermore, the expression of epithelial-mesenchymal transition (EMT) markers and estrogen/progesterone receptors remained unchanged. The decidualization of iheESCs could be induced by progesterone and cAMP. Estrogen increased the proliferation and mobility of iheESCs, and lipopolysaccharides (LPS) induced the IL-1ß and IL-6 promoting inflammatory response. The colony-forming ability of iheESCs, like primary cells, was lower than Ishikawa cells. In addition, tumorigenicity assay indicated that iheESCs were unable to trigger tumor formation in BALB/c nude mouse. CONCLUSIONS: This study established and characterized iheESCs that kept the cellular physiology of primary cells and were not available with tumorigenic ability. Thus, iheESCs would be useful as in vitro cell model to investigate pathogenesis of endometriosis.

[Clinical analysis of unroofed coronary sinus syndrome with atrioventricular canal defect].

OBJECTIVE: To analyze symptoms, associated anomalies, diagnostic approach, and surgical procedures in patients with unroofed coronary sinus syndrome and atrioventricular canal defect. METHODS: The clinical data of 20 patients with unroofed coronary sinus syndrome from September 1999 to October 2007 were reviewed retrospectively. There were 10 male and 10 female patients. The age ranged from 6 months to 38 years old, with a mean of (11.4 +/- 11.0) years old. The body weight ranged from 6.7 to 73.0 kg, with a mean of (28.4 +/- 21.3) kg. There were 18 cases of partial atrioventricular canal defect, 2 cases of complete atrioventricular canal defect, and 12 cases of common atrium. The initial diagnosis of unroofed coronary sinus syndrome was made by the surgeon at repair of a partial or complete atrioventricular canal defect in 20 patients. Complex unroofed coronary sinus with left superior vena cava (LSVC) directly draining into the left atrium was found in 11 cases, 1 case of LSVC was ligated, 10 cases were reconstructed the intraatrial baffle or the intracardiac tunnel to drain LSVC to right atrium. The other 9 patients with simple unroofed coronary sinus were repaired with other procedures. The associated cardiac lesions were corrected concomitantly. RESULTS: Death occurred in 1 patient with complex congenital cardiac disease due to pulmonary infection. In the 14 early survivors, who had been followed up from 4 months to 3 years, there was no death and severe complications. CONCLUSIONS: When associated with a partial or complete atrioventricular canal defect, LSVC and a common atrium, unroofed coronary sinus syndrome should be considered as a possible additional finding. Repair according to the type of unroofed coronary sinus syndrome is effective.

High expression of ZEB1 in endometriosis and its role in 17ß-estradiol-induced epithelial-mesenchymal transition.

Endometriosis is an estrogen-dependent disease associated with pain and infertility. The objective of this study was to determine the expression of ZEB1 in endometriosis and its role in 17ß-estradiol (E2)-induced epithelial-mesenchymal transition (EMT). 25 patients with endometriosis and 16 endometriosis-free patients were recruited for the study. Tissue expression of EMT makers was investigated by immunohistochemistry, then the expression of ZEB1 was quantified by qRT-PCR, immunohistochemistry, and western blot. The proliferation, DNA replication, and migration and invasion in ZEB1 knockdown Ishikawa cells were further respectively performed by MTS, Edu, wound healing and transwell assays. Luciferase assay was used to measure the ZEB1 promoter activity. Our results show that protein levels of E-cadherin and Keratin 18 decreased in endometriotic tissues. Meanwhile the expressions of ZEB1, Vimentin, and N-cadherin were significantly increased in endometriotic tissues. Down-regulation of ZEB1 inhibited Ishikawa cells proliferation, migration, invasion and EMT. E2 promoted the expression of ZEB1 through the ER genomic pathway, which contributed to the EMT process. The -1401 bp - -1901 bp region in the ZEB1 promoter was the main target of the E2 activity. The present results suggest that a high expression of ZEB1 plays an important role in the pathogenesis of endometriosis, and it may serve as a potential therapeutic target for endometriosis.

Lipoxin A4 Suppresses Estrogen-Induced Epithelial-Mesenchymal Transition via ALXR-Dependent Manner in Endometriosis.

OBJECTIVE: Epithelial-mesenchymal transition (EMT) is essential for embryogenesis, fibrosis, and tumor metastasis. Aberrant EMT phenomenon has been reported in endometriotic tissues of patients with endometriosis (EM). In this study, we further investigated the molecular mechanism of which lipoxin A4 (LXA4) suppresses estrogen (E2)-induced EMT in EM. STUDY DESIGN: The EMT markers were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot in eutopic endometrial epithelial cells (EECs) or investigated by immunohistochemistry and qRT-PCR in endometriotic lesion of EM mice. The invasion and migration under different treatments were assessed by transwell assays with or without Matrigel. The messenger RNA (mRNA) and activities of matrix metalloproteinase 2 (MMP-2) and MMP-9 were determined by qRT-PCR and gelatin zymography, respectively. Luciferase reporter assay was used to measure the activity of zinc finger E-box binding homeobox 1(ZEB1) promoter. The level of E2 in endometriotic tissues was assessed by enzyme-linked immunosorbent assay. RESULTS: In eutopic EECs, stimulatory effects of E2 on EMT progress, migration, and invasion were all diminished by LXA4. Lipoxin A4 reduced E2-induced ZEB1 promoter activity. Lipoxin A4 also attenuated the phosphorylation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase induced by E2. Co-incubation with Boc-2 rather than DMF antagonized the influence of LXA4. Animal experiments showed that LXA4 inhibited the EMT progress, MMP expression, and proteinase activities of endometriotic lesion in an LXA4 receptor (ALXR) manner, which suppressed the progression of EM. ZEB1 mRNA expression was upregulated and well correlated with E2 level in human endometrium. CONCLUSION: Lipoxin A4 suppresses E2-induced EMT via ALXR-dependent manner in eutopic EECs, which reveals a novel biological effect of LXA4 in EM.

[Clinical analysis of ten primary cardiac valve tumors].

OBJECTIVE: To investigate the clinical characteristics of primary valve tumors and the late surgical results of their resection. METHODS: We reviewed our clinical experience with the surgical treatment of ten primary valve tumors at Fuwai Hospital between November 1983 and November 2002. RESULTS: In this series, cardiac valve tumors constituted 2.65% (10/378) of all primary cardiac tumors, and the incidence of primary valve tumors was roughly one in 4000 cardiac operations. There were 5 male and 5 female patients aged 2 to 66 years (mean age, 30 years). The clinical presentations included exertional dyspnea in 7 patients, neurological symptoms in 2, and cyanosis at rest in 1 patient. The diagnosis was established by preoperative echocardiography in 8 patients, and in the other 2, it was confirmed by the findings at operation. All of the tumors were resected. Eight of the ten tumors were benign, and two were malignant. All patients survived the operation and recovered eventfully. Late outcomes were known for all patients. There were three late deaths. One patient with a benign tricuspid valve died 2 months postoperatively of an electrolyte disorder. The other 2 patients with a malignant mitral valve tumor died within 1 year postoperatively. The 7 survivors, all with a benign valve tumor, were followed up for an average of 5.7 years (range, 8 months to 19 years), and all were in functional Class I. Exercise tolerance improved to normal levels. The latest follow-up echocardiography showed no evidences of the local recurrence in any patients. CONCLUSION: Excellent early and late surgical results can be obtained in patients with benign valve tumors. The prognosis for the patients with a malignant valve tumor is poor.

[Some technical problems in setting up hospital PACS].

Having introduced PACS in brief, this paper presents some technical problems such as the selection of scale, function, database and monitor. And many solutions for these problems are given and compared with each other.

Acute and subchronic oral toxicity assessment of the herbal formula Kai-Xin-San.

ETHNOPHARMACOLOGICAL RELEVANCE: Kai-Xin-San (KXS) is a famous traditional Chinese medicine (TCM) formula. It has been used in the treatment of diseases including neurasthenia, Alzheimer's disease and neurosis. AIM OF THE STUDY: To provide information on the potential toxicity of KXS, we evaluated the acute and subchronic toxicity in rodents. MATERIALS AND METHODS: In acute study, a single administration of KXS was given orally to mice at doses ranging from 19.67 to 60.04 g/kg. In the sub-chronic oral toxicity study, KXS was administered to rats at 0, 1, 3 and 9 g/kg for 13 weeks. Moreover, 30 days of post treatment (withdrawal study) was conducted. Mortalities, clinical signs, body weight changes, food and water consumption, haematological and biochemical parameters, gross findings and organ weights were monitored during the study period. RESULTS: In the sub-chronic study in rats, daily oral administration of KXS at the dose of 9 g/kg/day result in significant increase in WBC, lymphocyte, alkaline phosphatase, blood sugar and significant decrease in bodyweight, serum Cre, CK and CHO at the last week of treatment. Recovery except for the body weight was observed after 30 days of post treatment. CONCLUSIONS: KXS is relatively safe for oral medication. The LD(50) of KXS was over 32.59 g/kg for mice. The no-observed-adverse-effect-level (NOAEL) was considered to be 19.67 g/kg/day for rats.