Isoimperatorin Inhibits Angiogenesis by Suppressing VEGFR2 Signaling Pathway.

PURPOSE: Angiogenesis involves in many pathological processes, including tumor metastasis, diabetic retinopathy, and rheumatoid arthritis. Therefore, identifying therapeutic drugs that target angiogenesis may be a promising strategy for disease treatment. Isoimperatorin is a furanocoumarin with anti-inflammatory and anti-microbial effects. However, the impacts of isoimperatorin on angiogenesis and its underlying mechanisms remain unclear. This study aimed to verify its effects on vascular endothelial growth factor (VEGF)-induced endothelial angiogenesis. METHODS: We employed various assays including 5-ethynyl-2'-deoxyuridine incorporation assay, transwell migration assay, wound healing assay, tube formation assay, and Western blot to evaluate the effects of isoimperatorin on angiogenesis in vitro. Additionally, we utilized Western blot and immunofluorescence analysis to examine the activation of vascular endothelial growth factor receptor (VEGFR) 2 and its downstream signaling pathways following isoimperatorin treatment. To further validate the anti-angiogenic effects of isoimperatorin in vivo, we conducted a matrigel plug assay and established an orthotopic tumor model. RESULTS: We demonstrated that pretreatment with isoimperatorin inhibited VEGF-induced endothelial cell proliferation, migration, and tube formation. Isoimperatorin also suppressed angiogenesis in vivo in a matrigel plug assay and in an orthotopic tumor model. Our results revealed that isoimperatorin exhibited anti-angiogenic effects via inhibiting VEGFR2 and its downstream signaling pathways activation. CONCLUSIONS: Our study showed that isoimperatorin suppressed angiogenesis by targeting the VEGFR2 signaling pathway and could be a potential therapeutic agent for targeting angiogenesis.

A Parameter Estimation of Photovoltaic Models Using a Boosting Flower Pollination Algorithm.

An accurate and reliable estimation of photovoltaic models holds immense significance within the realm of energy systems. In pursuit of this objective, a Boosting Flower Pollination Algorithm (BFPA) was introduced to facilitate the robust identification of photovoltaic model parameters and enhance the conversion efficiency of solar energy into electrical energy. The incorporation of a Gaussian distribution within the BFPA serves the dual purpose of conserving computational resources and ensuring solution stability. A population clustering strategy is implemented to steer individuals in the direction of favorable population evolution. Moreover, adaptive boundary handling strategies are deployed to mitigate the adverse effects of multiple individuals clustering near problem boundaries. To demonstrate the reliability and effectiveness of the BFPA, it is initially employed to extract unknown parameters from well-established single-diode, double-diode, and photovoltaic module models. In rigorous benchmarking against eight control methods, statistical tests affirm the substantial superiority of the BFPA over these controls. Furthermore, the BFPA successfully extracts model parameters from three distinct commercial photovoltaic cells operating under varying temperatures and light irradiances. A meticulous statistical analysis of the data underscores a high degree of consistency between simulated data generated by the BFPA and observed data. These successful outcomes underscore the potential of the BFPA as a promising approach in the field of photovoltaic modeling, offering substantial enhancements in both accuracy and reliability.

Vinexin ß deficiency exacerbates diet-induced obesity, hepatosteatosis, insulin resistance and endoplasmic reticulum stress in mice.

Vinexin ß is a member of an adaptor protein family. Previous research has elucidated its role in cell adhesion and growth factor signaling. Recently, several studies demonstrated its role in metabolic abnormality, such as obesity and atherosclerosis. In this study, we found that vinexin ß-knockout (KO) mice were more obese and gained more obvious visceral fat accumulation than their wildtype (WT) littermates fed with high fat diet (HFD). KO mice also showed more severe hepatosteatosis when compared with the WT control, which was in line with the significant increase of key serum lipids in KO mice. Furthermore, we confirmed the inhibited Akt signaling and exacerbated insulin resistance which resulted in high fasting blood glucose in KO mice. The endoplasmic reticulum stress response was found obviously activated which may mediate the metabolic changes in KO mice. Our studies indicated that vinexin ß deficiency promotes the diet-induced metabolic disorders.

Association of Egg Consumption with Risk of All-Cause and Cardiovascular Disease Mortality: A Systematic Review and Dose-Response Meta-Analysis of Observational Studies.

BACKGROUND: Recent studies have reported conflicting associations between egg consumption and the risk of all-cause or cardiovascular disease (CVD) mortality, including ischemic heart disease (IHD) mortality and stroke mortality. With accumulating evidence, up-to-date evidence about the association should be synthesized. OBJECTIVES: We aimed to assess the association of the risk of all-cause and CVD mortality with egg consumption. METHODS: We searched the PubMed, Embase, and Web of Science databases through 3 November, 2021 for observational studies conducted in participants ≥18 y of age and which provided ORs, RRs, or HRs and 95% CIs for ≥3 egg consumption categories or for increased intake of egg addressing the associations of interest. A random-effects model was used to pool the reported risk estimates. Restricted cubic splines were used to examine the dose-response association. RESULTS: Twenty-four articles with 48 reports (25 for all-cause mortality, 11 for CVD mortality, 6 for IHD mortality, and 6 for stroke mortality) involving 11,890,695 participants were included. Intake of each 1-egg/d increment was associated with increased risk of all-cause mortality (RR: 1.06; 95% CI: 1.02, 1.10; P = 0.008), but the association was restricted to women, Americans, and studies with adjustments for hyperlipidemia. Egg consumption was linearly associated with CVD mortality only in participants >60 y of age, Americans, studies with follow-up duration ≥15 y, and studies with adjustments for hyperlipidemia (P ≤ 0.018). No significant association was found between egg consumption and IHD or stroke mortality (P ≥ 0.080). CONCLUSIONS: Egg consumption was linearly associated with a modestly increased risk of all-cause mortality and, in older participants, Americans, and studies with longer follow-up or adjustments for hyperlipidemia, CVD mortality. These findings suggest that it may be prudent to avoid high egg consumption.

Identification of a Novel Antisepsis Pathway: Sectm1a Enhances Macrophage Phagocytosis of Bacteria through Activating GITR.

The inability to effectively control invading bacteria or other pathogens is a major cause of multiple organ dysfunction and death in sepsis. As the first-line defense of the immune system, macrophages play a crucial role in the removal of pathogens during sepsis. In this study, we define secreted and transmembrane 1A (Sectm1a) as a novel ligand of glucocorticoid-induced TNFR (GITR) that greatly boosts macrophage phagocytosis and bactericidal capacity. Using a global Sectm1a knockout (KO) mouse model, we observed that Sectm1a deficiency significantly suppressed phagocytosis and bactericidal activity in both recruited macrophages and tissue-resident macrophages, which consequently aggravated bacterial burden in the blood and multiple organs and further increased systemic inflammation, leading to multiple organ injury and increased mortality during polymicrobial sepsis. By contrast, treatment of septic mice with recombinant Sectm1a protein (rSectm1a) not only promoted macrophage phagocytosis and bactericidal activity but also significantly improved survival outcome. Mechanistically, we identified that Sectm1a could bind to GITR in the surface of macrophages and thereby activate its downstream PI3K-Akt pathway. Accordingly, rSectm1a-mediated phagocytosis and bacterial killing were abolished in macrophages by either KO of GITR or pharmacological inhibition of the PI3K-Akt pathway. In addition, rSectm1a-induced therapeutic effects on sepsis injury were negated in GITR KO mice. Taken together, these results uncover that Sectm1a may represent a novel target for drug development to control bacterial dissemination during sepsis or other infectious diseases.

Neobaicalein Inhibits Th17 Cell Differentiation Resulting in Recovery of Th17/Treg Ratio through Blocking STAT3 Signaling Activation.

Huangqin is the dried root of Scutellaria baicalensis Georgi, which has been widely utilized for heat-clearing (Qingre) and dewetting (Zaoshi), heat-killed (Xiehuo) and detoxifying (Jiedu) in the concept of Traditional Chinese Medicine and is used for treating inflammation and cancer in clinical formulas. Neobaicalein (NEO) is of flavonoid isolated from Huangqin and has been reported to possess prominent anti-inflammatory effects in published work. Th17/Treg balance shift to Th17 cells is an essential reason for autoimmune inflammatory diseases. However, the role NEO plays in Th17 and Treg and the underlying mechanism has not been elucidated yet. Network pharmacology-based study revealed that NEO predominantly regulated IL-17 signaling pathway. Moreover, our result shown that NEO (3-30 µmol/L) down-regulated Th17 differentiation and cellular supernatant and intracellular IL-17A level and tumor necrosis factor α production in a concentration-dependent manner. The further mechanism research revealed that NEO also specifically inhibited phosphorylation of STAT3(Tyr725) and STAT4 (Y693) without influence on activation of STAT5 and STAT6 in splenocytes. Immunofluorescence results illuminated that NEO effectively blocked STAT3 translocated into nucleus. Interestingly, NEO at appreciated dose could only inhibit Th17 cell differentiation and have no effect on Treg differentiation. The present study revealed that NEO effectively inhibited Th17 cell differentiation through specifically blocking the activation of STAT3 signaling without inactivation of STAT5 and STAT6. Additional inhibitory effect on activation of STAT4 by NEO also suggested the potential for antagonism against Th1 differentiation. All work suggested that NEO may be a potential candidate for immunoregulation and treating autoimmune inflammatory diseases through inhibiting immune cell viability and T cell differentiation.

Clinical characteristics and survival outcomes of malignant struma ovarii confined to the ovary.

BACKGROUND: Malignant struma ovarii (MSO) is a unique type of ovarian malignancy that data on the survival outcome is limited and management strategy remains controversial due to its extreme rarity. METHODS: To investigate the clinical characteristics and treatment options in patients with MSO confined to the ovary, while also evaluating the recurrent-free survival (RFS) and overall survival (OS) rate in this population, a retrospective study was conducted. One hundred twenty-five cases of MSO confined to the ovary were enrolled and their clinical characteristics, treatment strategies, and results of follow-up were analyzed. OS and RFS were assessed by Kaplan-Meier analyses and Cox regression models. RESULTS: The most common pathological subtype in this cohort was papillary carcinoma (44.8%). Other reported subtypes, in order of prevalence, were follicular variant of papillary carcinoma, follicular carcinoma, and mixed follicular-papillary carcinoma. Surgical treatment options varied in this cohort that 8.0% of the patients received ovarian cystectomy, 33.6% underwent unilateral salpingo-oophorectomy (USO), 5.6% received bilateral salpingo-oophorectomy (BSO), 21.6% received total abdominal hysterectomy with BSO (TAH/BSO), and 17.6% were treated with debulking surgery; 20.0% of them received radioiodine therapy (RAI). Twenty-seven patients experienced recurrence with a median RFS of 14.0 years (95% confidence interval [CI], 9.5-18.5). The 5-year and 10-year recurrent rate were 27.1, 35.2%, respectively. Eight patients died during follow-up, with five attributed to MSO; the 5-year, 10-year, and 20-year OS rate was 95.3, 88.7 and 88.7%, respectively. However, the univariate and multivariate Cox regression showed no potential risk factor for RFS and OS. CONCLUSION: Patients with MSO confined to the ovary had an excellent survival outcome, despite varied treatment strategies, and the recurrent rate was relatively high. We recommend USO as the preferred surgical option in this population since more aggressive surgery does not improve outcomes and the benefits of RAI are uncertain.

Clinical characteristics and management of Turner patients with a small supernumerary marker chromosome.

OBJECTIVE: To summarize the clinical characteristics of Turner syndrome (TS) with a small supernumerary marker chromosome (sSMC) and discuss the clinical significance and management of TS patients with sSMC. METHODS: A retrospective analysis was conducted on the clinical data of 244 patients with disorders of sexual development admitted to Peking Union Medical College Hospital from February 1984 to July 2020. RESULTS: Among the 244 patients with a disorder of sexual development, 69 cases of TS were identified in which 13 patients had sSMC. Their ages ranged from 3 to 28 years old with an average of 14.31 ± 6.40 years. All 13 sSMC-positive patients had typical clinical manifestations of TS except ambiguous genitalia in four cases. SRY gene testing was performed in 11sSMC-positive patients and 10 patients were positive for SRY and one was negative. Among the 10 SRY-positive patients, two cases had hirsutism and clitoral enlargement and two cases had clitoral enlargement only. Nine sSMC and SRY-positive patients underwent gonadectomy and one had left gonadal gonadoblastoma with seminoma in situ and right gonadal seminoma in situ. CONCLUSIONS: Although the sSMC positive detection rate in DSD patients is uncommon (5.33% in our sample), the positive SRY detection rate in sSMC-positive TS patients was extremely high in our TS patients. And TS patients with sSMC and SRY positive had a significantly increased risk of gonadal germ cell tumors. Routine SRY screening should be performed in TS patients with sSMC, and a gonadectomy should be performed in TS patients with sSMC and SRY positive to prevent the occurrence of tumors.

Effects of Dexmedetomidine as an Analgesic Adjuvant for Surgery of Femur Fracture: A Systematic Review and Meta-Analysis.

Patients who undergo surgery of femur fracture suffer the excruciating pain. Dexmedetomidine (DEX) is a unique α2-adrenergic receptor agonist with sedative and analgesic properties, whose efficacy and safety are still unclear for surgery of femur fracture. Randomized controlled trials comparing the effects of addition of DEX to general or local anesthesia in surgery of femur fracture were searched from MEDLINE, EMBASE, and the Cochrane Library database. Patients who received DEX infusion had a significant longer time to rescue analgesia compared with those without DEX coadministration. DEX treatment seemed to reduce the visual analog score; however, the significance did not reach any statistical difference. DEX as an analgesic adjuvant did not reduce the onset of sensory block time, shorten the time to achieve maximum sensory block level, and provide a longer duration of sensory block. The difference in mean sedation scores between 2 groups was not statistically significant. As for adverse effects, DEX therapy significantly increased the rate of hypotension. In conclusion, dexmedetomidine as a local anesthetic adjuvant in femur fracture surgery had a longer duration of rescue analgesia. However, the incidence of hypotension was markedly increased in these patients. It was worth noting that the evidence was of low to moderate quality.

Association of a unicornuate uterus with adverse obstetric outcomes: A retrospective cohort study.

OBJECTIVE: To estimate the association of unicornuate uterus (UU) with adverse obstetric outcomes. METHODS: Using data from 26 737 singleton childbirths from a tertiary hospital from 1999 to 2019, we identified 44 births from women with a UU. A total of 367 births from women with a normal uterus were randomly selected as controls. The outcome measures were preterm birth (PTB), breech presentation, and cesarean delivery. The subdivisions of PTB and indications for cesarean delivery were described. RESULTS: The presence of UU was associated with an increased risk of PTB (adjusted risk ratio [aRR], 2.3; 95% confidence interval [CI], 1.1-4.9), breech presentation (aRR, 6.2; 95% CI, 2.9-13.2), and cesarean delivery (aRR, 2.1; 95% CI, 1.8-2.7). For women with a UU, most PTBs (7/9) were moderate to late PTBs, and approximately half of the PTBs (4/9) were iatrogenic due to preeclampsia (PE). Breech presentation, PE, and prior surgery for rudimentary horn resection were UU-related indications for cesarean delivery. CONCLUSIONS: Women with a UU have a higher risk of PTB, breech presentation, and cesarean delivery. Understanding of the subdivisions of PTBs and indications for cesarean delivery might help clinicians when counseling women with pregnancy complicated by a UU.

MicroRNA-223 is essential for maintaining functional ß-cell mass during diabetes through inhibiting both FOXO1 and SOX6 pathways.

The initiation and development of diabetes are mainly ascribed to the loss of functional ß-cells. Therapies designed to regenerate ß-cells provide great potential for controlling glucose levels and thereby preventing the devastating complications associated with diabetes. This requires detailed knowledge of the molecular events and underlying mechanisms in this disorder. Here, we report that expression of microRNA-223 (miR-223) is up-regulated in islets from diabetic mice and humans, as well as in murine Min6 ß-cells exposed to tumor necrosis factor α (TNFα) or high glucose. Interestingly, miR-223 knockout (KO) mice exhibit impaired glucose tolerance and insulin resistance. Further analysis reveals that miR-223 deficiency dramatically suppresses ß-cell proliferation and insulin secretion. Mechanistically, using luciferase reporter gene assays, histological analysis, and immunoblotting, we demonstrate that miR-223 inhibits both forkhead box O1 (FOXO1) and SRY-box 6 (SOX6) signaling, a unique bipartite mechanism that modulates expression of several ß-cell markers (pancreatic and duodenal homeobox 1 (PDX1), NK6 homeobox 1 (NKX6.1), and urocortin 3 (UCN3)) and cell cycle-related genes (cyclin D1, cyclin E1, and cyclin-dependent kinase inhibitor P27 (P27)). Importantly, miR-223 overexpression in ß-cells could promote ß-cell proliferation and improve ß-cell function. Taken together, our results suggest that miR-223 is a critical factor for maintaining functional ß-cell mass and adaptation during metabolic stress.

Tumor susceptibility gene 101 ameliorates endotoxin-induced cardiac dysfunction by enhancing Parkin-mediated mitophagy.

Cardiac mitochondrial damage and subsequent inflammation are hallmarks of endotoxin-induced myocardial depression. Activation of the Parkin/PTEN-induced kinase 1 (PINK1) pathway has been shown to promote autophagy of damaged mitochondria (mitophagy) and to protect from endotoxin-induced cardiac dysfunction. Tumor susceptibility gene 101 (TSG101) is a key member of the endosomal recycling complexes required for transport, which may affect autophagic flux. In this study, we investigated whether TSG101 regulates mitophagy and influences the outcomes of endotoxin-induced myocardial dysfunction. TSG101 transgenic and knockdown mice underwent endotoxin/lipopolysaccharide treatment (10 µg/g) and were assessed for survival, cardiac function, systemic/local inflammation, and activity of mitophagy mediators in the heart. Upon endotoxin challenge and compared with WT mice, TSG101 transgenic mice exhibited increased survival, preserved cardiac contractile function, reduced inflammation, and enhanced mitophagy activation in the heart. By contrast, TSG101 knockdown mice displayed opposite phenotypes during endotoxemia. Mechanistically, both coimmunoprecipitation assays and coimmunofluorescence staining revealed that TSG101 directly binds to Parkin in the cytosol of myocytes and facilitates translocation of Parkin from the cytosol to the mitochondria. Our results indicate that TSG101 elevation could protect against endotoxin-triggered myocardial injury by promoting Parkin-induced mitophagy.

Mediating K+/H+ Transport on Organelle Membranes to Selectively Eradicate Cancer Stem Cells with a Small Molecule.

Molecules that are capable of disrupting cellular ion homeostasis offer unique opportunities to treat cancer. However, previously reported synthetic ion transporters showed limited value, as promiscuous ionic disruption caused toxicity to both healthy cells and cancer cells indiscriminately. Here we report a simple yet efficient synthetic K+ transporter that takes advantage of the endogenous subcellular pH gradient and membrane potential to site-selectively mediate K+/H+ transport on the mitochondrial and lysosomal membranes in living cells. Consequent mitochondrial and lysosomal damages enhanced cytotoxicity to chemo-resistant ovarian cancer stem cells (CSCs) via apoptosis induction and autophagy suppression with remarkable selectivity (up to 47-fold). The eradication of CSCs blunted tumor formation in mice. We believe this strategy can be exploited in the structural design and applications of next-generation synthetic cation transporters for the treatment of cancer and other diseases related to dysfunctional K+ channels.

Hippo pathway cooperates with ChREBP to regulate hepatic glucose utilization.

Hippo pathway plays a crucial role as a regulator of organ size and tumorigenesis that negatively regulates cell growth and survival. Recently lots of evidences show that Hippo pathway plays a crucial role in glucose metabolic metabolism to regulate energy status with cell growth. However, the detailed mechanism is still unclear. Here we report that Yes-associated protein (YAP), the terminal effector of Hippo pathway, interacts with carbohydrate response element binding protein (ChREBP) in the nucleus of the hepatocytes thereby promoting glycolysis and lipogenesis. A high carbohydrate (HCHO) diet could inactivate the Hippo pathway and encourage the combination of YAP and ChREBP, leading to glucose-induced hepatocyte glycolysis and lipogenesis through up-regulation of target genes such as L-PK and ACC in mice. Conversely, inhibition of YAP activity by phosphorylation or downregulation antagonized glycolysis and lipogenesis in mice fed with HCHO diet. These results suggest that YAP is a nuclear co-factor of ChREBP and that the Hippo pathway negatively affects hepatocyte glycolysis by inhibiting the function of YAP-ChREBP.

Tsg101 positively regulates physiologic-like cardiac hypertrophy through FIP3-mediated endosomal recycling of IGF-1R.

Development of physiologic cardiac hypertrophy has primarily been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and subsequent activation of the protein kinase B (Akt) pathway. However, regulation of endosome-mediated recycling and degradation of IGF-1R during physiologic hypertrophy has not been investigated. In a physiologic hypertrophy model of treadmill-exercised mice, we observed that levels of tumor susceptibility gene 101 (Tsg101), a key member of the endosomal sorting complex required for transport, were dramatically elevated in the heart compared with sedentary controls. To determine the role of Tsg101 on physiologic hypertrophy, we generated a transgenic (TG) mouse model with cardiac-specific overexpression of Tsg101. These TG mice exhibited a physiologic-like cardiac hypertrophy phenotype at 8 wk evidenced by: 1) the absence of cardiac fibrosis, 2) significant improvement of cardiac function, and 3) increased total and plasma membrane levels of IGF-1R and increased phosphorylation of Akt. Mechanistically, we identified that Tsg101 interacted with family-interacting protein 3 (FIP3) and IGF-1R, thereby stabilizing FIP3 and enhancing recycling of IGF-1R. In vitro, adenovirus-mediated overexpression of Tsg101 in neonatal rat cardiomyocytes resulted in cell hypertrophy, which was blocked by addition of monensin, an inhibitor of endosome-mediated recycling, and by small interfering RNA-mediated knockdown (KD) of FIP3. Furthermore, cardiac-specific KD of Tsg101 showed a significant reduction in levels of endosomal recycling compartment members (Rab11a and FIP3), IGF-1R, and Akt phosphorylation. Most interestingly, Tsg101-KD mice failed to develop cardiac hypertrophy after intense treadmill training. Taken together, our data identify Tsg101 as a novel positive regulator of physiologic cardiac hypertrophy through facilitating the FIP3-mediated endosomal recycling of IGF-1R.-Essandoh, K., Deng, S., Wang, X., Jiang, M., Mu, X., Peng, J., Li, Y., Peng, T., Wagner, K.-U., Rubinstein, J., Fan, G.-C. Tsg101 positively regulates physiologic-like cardiac hypertrophy through FIP3-mediated endosomal recycling of IGF-1R.

Clinical characteristics, treatment and outcomes of adnexal torsion in pregnant women: a retrospective study.

BACKGROUND: Adnexal torsion during pregnancy is a gynecological emergency. Delayed diagnosis and treatment can cause ovarian necrosis and fetal loss. This study assessed the clinical characteristics, treatment and outcomes of adnexal torsion in pregnant women. METHODS: A retrospective study was conducted at a tertiary center between January 2008 and January 2018. Eighty-two pregnant women with surgically confirmed adnexal torsion were included. The clinical characteristics, ultrasound data, surgical interventions and pregnancy outcomes were analyzed. RESULTS: The median age of the patients was 28 (range, 18-38) years. The median gestational age was 11 (range, 6-31) weeks: 53 (64.6%) were in the first trimester, 21 (25.6%) were in the second trimester, and 8 (9.8%) were in the third trimester. The most common symptoms and signs were sudden pelvic pain (100%) and adnexal or pelvic masses (97.6%), followed by nausea and vomiting (61%). The Doppler blood flow signal disappeared in 62.5% of the patients. Sixty-three (76.8%) patients underwent laparoscopy, and 29 (24.2%) underwent laparotomy. The median gestational age in patients undergoing laparotomy was higher than that in those undergoing laparoscopy (26 weeks vs 10 weeks, p < 0.001). Fifty-three (64.6%) patients underwent conservative surgery, with 48 detorsions and cystectomies, 2 detorsions and cyst fenestrations, 1 detorsion only and 2 salpingectomies only. Twenty-nine (25.4%) patients underwent unilateral salpingo-oophorectomy. There were no cases of postoperative thrombosis, spontaneous abortion or recurrence during the same pregnancy. Seven patients underwent simultaneous artificial abortion. One patient experienced intrauterine fetal death, and 74 patients had live births. CONCLUSION: Surgical intervention was required as soon as possible. Laparoscopic conservative surgery is safe and may be appropriate to preserve ovarian function.

Cardioprotective effects of timosaponin B-II isolated from Anemarrhena rhizome in a zebrafish model.

Timosaponin B-II (TB-II; (25S)-26-(ß-D-glucopyranosyloxy)-3ß-[(2-O-ß-D-glucopyranosyl-ß-D-galactopyranosyl) oxy]-5ß-furostan-22-ol is extracted from Anemarrhena. Its anti-inflammation, anti-oxidation, and anti-asthma properties have been widely explored. However, its effect on the heart has not been reported. In this study, we used zebrafish as a research model to determine the effects of TB-II on the heart and its toxic and anti-inflammatory effects. To explore the cause of cardioprotective effects of TB-II, we used transgenic zebrafish with macrophages and neutrophils labeled with fluorescent protein. We found for the first time that TB-II had a protective effect on the zebrafish heart. It did not affect the survival and hatching rates of zebrafish embryos, indicating its low toxicity. Results showed that TB-II may have cardioprotective effects, which might be related to its anti-inflammatory effects.

The clinical features and reproductive prognosis of ovarian neoplasms with hyperandrogenemia: a retrospective analysis of 33 cases.

The aim of this study is to review the natural course, clinical features, and reproductive prognosis of ovarian tumors associated with hyperandrogenemia. We retrospect 33 patients of ovarian tumors with hyperandrogenemia. Thirty cases (91%) were sex cord-stromal tumors. Sertoli-Leydig cell tumors, Leydig cell tumors, and steroid cell tumors were the most common types. It is not possible, to predict the pathological subtypes based on androgen levels alone. Most of these tumors were solid masses, with an average diameter of 3.9 cm. These tumors are soft or fragile, no clear boundary with normal tissue, thus excision is superior to exfoliation. The average disease course of the top three tumors was 32.6, 35.4, and 67.7 months, respectively. Among 11 married women with a desire to get pregnant, nine cases resumed menstrual periods after surgery and became pregnant naturally. Hyperandrogenemia might predict a better prognosis. The asynchronism of hyperandrogenemia and undetectable tumor may cause irreversible change and emotional depress, the methods of early diagnosis need further study.

Chiral Supersolid in Spin-Orbit-Coupled Bose Gases with Soft-Core Long-Range Interactions.

Chirality represents a kind of symmetry breaking characterized by the noncoincidence of an object with its mirror image and has been attracting intense attention in a broad range of scientific areas. The recent realization of spin-orbit coupling in ultracold atomic gases provides a new perspective to study quantum states with chirality. In this Letter, we demonstrate that the combined effects of spin-orbit coupling and interatomic soft-core long-range interaction can induce an exotic supersolid phase in which the chiral symmetry is broken with spontaneous emergence of circulating particle current. This implies that a finite angular momentum can be generated with neither rotation nor effective magnetic field. The direction of the angular momentum can be altered by adjusting the strength of spin-orbit coupling or interatomic interaction. The predicted chiral supersolid phase can be experimentally observed in Rydberg-dressed Bose-Einstein condensates with spin-orbit coupling.

[Change tendency during 30 years of infertility and endometriosis in Peking Union Medical College Hospital].

OBJECTIVE: To analyze the incidence of endometriosis in inpatients with infertility in Peking Union Medical College Hospital in 30 years. METHODS: The inpatients of Peking Union Medical College Hospital admitted between May 1983 and November 2013 was searched. The infertile patients receiving laparoscopy or laparotomy were included. The discharge diagnosis and the operation were summarized. The incidence of gynecologic diseases were demonstrated, such as endometriosis, pelvic adhesions, uterine fibroid, hydrosalpinx, ovarian benign tumor, and adenomyosis. The age was collected, and the change of age and the incidence of endometriosis was analyzed. RESULTS: The incidence of endometriosis in infertile female inpatients was 35.50% (95% CI: 34.50%-36.49%). The incidence showed relatively stable increasing tendency after 2004 (with P < 0.01). The age had increased significantly since 1996 (with P < 0.01); the average age was (29.76 ± 3.74) years old in 1996, and (32.85 ± 4.49) years old in 2013 (P < 0.01). The inpatients diagnosed with endometriosis had greater age, (32.67 ± 4.06) versus (32.04 ± 4.55) years old (P < 0.01); the incidence of endometriosis differed in different age group, the older group had higher incidence (χ² = 85.807, P < 0.01). CONCLUSIONS: Infertile female inpatients showed increasing incidence of endometriosis in recent years. Older infertile patients maybe have higher risk of endometriosis.