Quantum Information Scrambling in Non-Markovian Open Quantum System.

In this paper, we investigate the dynamics of a spin chain whose two end spins interact with two independent non-Markovian baths by using the non-Markovian quantum state diffusion (QSD) equation approach. Specifically, two issues about information scrambling in an open quantum system are addressed. The first issue is that tripartite mutual information (TMI) can quantify information scrambling properly via its negative value in a closed system, whether it is still suitable to indicate information scrambling in an open quantum system. We find that negative TMI is not a suitable quantifier of information scrambling in an open quantum system in some cases, while negative tripartite logarithmic negativity (TLN) is an appropriate one. The second one is that up to now almost all information scrambling in open quantum systems reported were focus on a Markovian environment, while the effect of a non-Markovian environment on information scrambling is still elusive. Our results show that the memory effect of an environment will be beneficial to information scrambling. Moreover, it is found that the environment is generally detrimental for information scrambling in the long-term, while in some cases it will be helpful for information scrambling in the short-term.

Relaxin mitigates microvascular damage and inflammation following cardiac ischemia-reperfusion.

Microvascular obstruction (MVO) and leakage (MVL) forms a pivotal part of microvascular damage following cardiac ischemia-reperfusion (IR). We tested the effect of relaxin therapy on MVO and MVL in mice following cardiac IR injury including severity of MVO and MVL, opening capillaries, infarct size, regional inflammation, cardiac function and remodelling, and permeability of cultured endothelial monolayer. Compared to vehicle group, relaxin treatment (50 µg/kg) reduced no-reflow area by 38% and the content of Evans blue as a permeability tracer by 56% in jeopardized myocardium (both P < 0.05), effects associated with increased opening capillaries. Relaxin also decreased leukocyte density, gene expression of cytokines, and mitigated IR-induced decrease in protein content of VE-cadherin and relaxin receptor. Infarct size was comparable between the two groups. At 2 weeks post-IR, relaxin treatment partially preserved cardiac contractile function and limited chamber dilatation versus untreated controls by echocardiography. Endothelial cell permeability assay demonstrated that relaxin attenuated leakage induced by hypoxia-reoxygenation, H2O2, or cytokines, action that was independent of nitric oxide but associated with the preservation of VE-cadherin. In conclusion, relaxin therapy attenuates IR-induced MVO and MVL and endothelial leakage. This protection was associated with reduced regional inflammatory responses and consequently led to alleviated adverse cardiac remodeling.

Microvascular leakage in acute myocardial infarction: characterization by histology, biochemistry, and magnetic resonance imaging.

Cardiac microvascular obstruction (MVO) after ischemia-reperfusion (I/R) has been well studied, but microvascular leakage (MVL) remains largely unexplored. We characterized MVL in the mouse I/R model by histology, biochemistry, and cardiac magnetic resonance (CMR) imaging. I/R was induced surgically in mice. MVL was determined by administrating the microvascular permeability tracer Evans blue (EB) and/or gadolinium-diethylenetriaminepentaacetic acid contrast. The size of MVL, infarction, and MVO in the heart was quantified histologically. Myocardial EB was extracted and quantified chromatographically. Serial CMR images were acquired from euthanized mice to determine late gadolinium enhancement (LGE) for comparison with MVL quantified by histology. I/R resulted in MVL with its severity dependent on the ischemic duration and reaching its maximum at 24-48 h after reperfusion. The size of MVL correlated with the degree of left ventricular dilatation and reduction in ejection fraction. Within the risk zone, the area of MVL (75 ± 2%) was greater than that of infarct (47 ± 4%, P < 0.01) or MVO (36 ± 4%, P < 0.01). Contour analysis of paired CMR-LGE by CMR and histological MVL images revealed a high degree of spatial colocalization (r = 0.959, P < 0.0001). These data indicate that microvascular barrier function is damaged after I/R leading to MVL. Histological and biochemical means are able to characterize MVL by size and severity while CMR-LGE is a potential diagnostic tool for MVL. The size of ischemic myocardium exhibiting MVL was greater than that of infarction and MVO, implying a role of MVL in postinfarct pathophysiology.NEW & NOTEWORTHY We characterized, for the first time, the features of microvascular leakage (MVL) as a consequence of reperfused myocardial infarction. The size of ischemic myocardium exhibiting MVL was significantly greater than that of infarction or no reflow. We made a proof-of-concept finding on the diagnostic potential of MVL by cardiac magnetic resonance imaging.

Inhibition of the Renin-Angiotensin System Post Myocardial Infarction Prevents Inflammation-Associated Acute Cardiac Rupture.

PURPOSE: Inhibition of the renin-angiotensin system (RAS) is beneficial in patient management after myocardial infarction (MI). However, whether RAS inhibition also provides cardiac protection in the acute phase of MI is unclear. METHODS: Male 129sv mice underwent coronary artery occlusion to induce MI, followed by treatment with losartan (L, 20 and 60 mg/kg), perindopril (P, 2 and 6 mg/kg), amlodipine (20 mg/kg as a BP-lowering agent) or vehicle as control. Drug effects on hemodynamics were examined. Effects of treatments on incidence of cardiac rupture, haematological profile, monocyte and neutrophil population in the spleen and the heart, cardiac leukocyte density, expression of inflammatory genes and activity of MMPs were studied after MI. RESULTS: Incidence of cardiac rupture within 2 weeks was significantly and similarly reduced by both losartan (L) and perindopril (P) in a dose-dependent manner [75% (27/36) in vehicle, 40-45% in low-dose (L 10/22, P 8/20) and 16-20% (L 5/32, P 4/20) in high-dose groups, all P < 0.05]. This action was independent of their BP-lowering action, as amlodipine reduced BP to a similar degree without effect on rupture (70%, 21/30). Compared to the control group, high dose losartan and perindopril decreased counts of white blood cells, neutrophils and lymphocytes (all P < 0.05), and inhibited splenic monocyte and neutrophil release into the circulation. Consequently, monocyte, neutrophil and leukocyte infiltration, inflammatory gene expressions (IL-1ß, IL-6, MMP9, MCP-1, TNF-α and TGFß1) and activity of MMP2 and MMP9 in the infarct tissue were attenuated by losartan and/or perindopril treatment (all P < 0.05). CONCLUSIONS: RAS inhibition by losartan or perindopril prevented cardiac rupture at the acute phase of MI through blockade of splenic release of monocytes and neutrophils and consequently attenuation of systemic and regional inflammatory responses.

MicroRNA-138 negatively regulates non-small cell lung cancer cells through the interaction with cyclin D3.

Previous studies demonstrate that microRNA-138 (miR-138) is critical in non-small cell lung cancer (NSCLC) regulation. We further explored the molecular mechanism of miR-138 in NSCLC. Lentivirus was used to upregulate miR-138 in NSCLC cell lines H460 and SPC-A1 cells. Previously known effects of miR-138 upregulation on NSCLC, proliferation, cell cycle division, and cisplatin sensitivity were examined in H460 and SPC-A1 cells. Moreover, previously unknown effect of miR-138 upregulation on NSCLC migration was also examined in H460 and SPC-A1 cells. A new miR-138 downstream target, cyclin D3 (CCND3), was assessed by dual-luciferase reporter assay and quantitative real-time PCR (qRT-PCR). CCND3 was then ectopically overexpressed in H460 and SPC-A1 cells. The effects of forced overexpression of CCND3 on miR-138-induced NSCLC regulations were further examined by proliferation, cell cycle, cisplatin sensitivity, and migration assays, respectively. Lentivirus-induced miR-138 upregulation inhibited NSCLC proliferation and cell cycle division, in line with previous findings. Moreover, we found that miR-138 upregulation had other anti-tumor effects, such as increasing cisplatin sensitivity and reducing cancer migration, in H460 and SPC-A1 cells. Luciferase assay and qRT-PCR showed that CCND3 was directly targeted by miR-138. Forced overexpression of CCND3 in H460 and SPC-A1 cells reversed the anti-tumor effects of miR-138 upregulation on cancer cell growth, cell cycle, cisplatin sensitivity, and migration. Our study revealed novel anti-cancer effects of miR-138 upregulation in NSCLC, as well as its new molecular target of CCND3.

Splenic release of platelets contributes to increased circulating platelet size and inflammation after myocardial infarction.

Acute myocardial infarction (AMI) is characterized by a rapid increase in circulating platelet size but the mechanism for this is unclear. Large platelets are hyperactive and associated with adverse clinical outcomes. We determined mean platelet volume (MPV) and platelet-monocyte conjugation (PMC) using blood samples from patients, and blood and the spleen from mice with AMI. We further measured changes in platelet size, PMC, cardiac and splenic contents of platelets and leucocyte infiltration into the mouse heart. In AMI patients, circulating MPV and PMC increased at 1-3 h post-MI and MPV returned to reference levels within 24 h after admission. In mice with MI, increases in platelet size and PMC became evident within 12 h and were sustained up to 72 h. Splenic platelets are bigger than circulating platelets in normal or infarct mice. At 24 h post-MI, splenic platelet storage was halved whereas cardiac platelets increased by 4-fold. Splenectomy attenuated all changes observed in the blood, reduced leucocyte and platelet accumulation in the infarct myocardium, limited infarct size and alleviated cardiac dilatation and dysfunction. AMI-induced elevated circulating levels of adenosine diphosphate and catecholamines in both human and the mouse, which may trigger splenic platelet release. Pharmacological inhibition of angiotensin-converting enzyme, ß1-adrenergic receptor or platelet P2Y12 receptor reduced platelet abundance in the murine infarct myocardium albeit having diverse effects on platelet size and PMC. In conclusion, AMI evokes release of splenic platelets, which contributes to the increase in platelet size and PMC and facilitates myocardial accumulation of platelets and leucocytes, thereby promoting post-infarct inflammation.

The destruction box is involved in the degradation of the NTE family proteins by the proteasome.

Neuropathy target esterase (NTE) and NTE-related esterase (NRE) are endoplasmic reticulum (ER) membrane-anchored proteins belonging to the NTE protein family. NTE and NRE are degraded by macroautophagy and by the ubiquitin-proteasome pathway. However, the regulation of NTE and NRE by proteasome has not been well understood. Western blotting showed that the deletion of the regulatory region of NTE and NRE led to protein accumulation compared with that of the corresponding wild-type proteins. Further, deletion and site-directed mutagenesis experiments demonstrated that the destruction (D) box was required for the proteasomal degradation of NTE and NRE. However, unlike the deletion of the regulatory region, the deletion of the D box did not affect the subcellular localisation of NTE or NRE or disrupt the ER. Moreover, the deletion of the D box or the regulatory region of NTE has similar inhibitory effects on cell growth, which are greater than those produced by the full-length NTE. Here, for the first time, we show that the D box is involved in the regulation of NTE family proteins by the proteasome but not in their subcellular localisation. In addition, these results suggest that the NTE overexpression-mediated inhibition of cell growth is related to active protein levels but not to its ER disruption effect.

Spontaneous ventricular tachyarrhythmias in ß2-adrenoceptor transgenic mice in relation to cardiac interstitial fibrosis.

Myocardial fibrosis is regarded as a pivotal proarrhythmic substrate, but there have been no comprehensive studies showing a correlation between the severity of fibrosis and ventricular tachyarrhythmias (VTAs). Our purpose was to document this relationship in a transgenic (TG) strain of mice with fibrotic cardiomyopathy. TG mice with cardiac overexpression of ß2-adrenoceptors (ß2-AR mice) and non-TG (NTG) littermates were studied at 4-12 mo of age. VTA was quantified by ECG telemetry. The effect of pharmacological blockade of ß2-ARs on VTA was examined. Myocardial collagen content was determined by hydroxyproline assay. NTG and TG mice displayed circadian variation in heart rate, which was higher in TG mice than in NTG mice (P <0.05). Frequent spontaneous ventricular ectopic beats (VEBs) and ventricular tachycardia (VT) were prominent in TG mice but not present in NTG mice. The frequency of VEB and VT episodes in TG mice increased with age (P < 0.01). Ventricular collagen content was greater in TG mice than in NTG mice (P <0.001) and correlated with age (r = 0.71, P < 0.01). The number of VEBs or VT episodes correlated with age (r = 0.83 and r = 0.73) and the content of total or cross-linked collagen (r = 0.62∼0.66, all P <0.01). While having no effect in younger ß2-TG mice, ß2-AR blockade reduced the frequency of VTA in old ß2-TG mice with more severe fibrosis. In conclusion, ß2-TG mice exhibit interstitial fibrosis and spontaneous onset of VTA, becoming more severe with aging. The extent of cardiac fibrosis is a major determinant for both the frequency of VTA and proarrhythmic action of ß2-AR activation.

Effectiveness of combining plasma exchange with plasma perfusion in acute fatty liver of pregnancy: a retrospective analysis.

BACKGROUND/AIMS: Acute fatty liver of pregnancy (AFLP) is a severe liver failure condition that has limited therapeutic approaches. We aimed to evaluate the efficacy of combining plasma exchange (PE) and plasma perfusion (PP) with conventional therapy for the treatment of AFLP using a retrospective analysis. METHODS: Among 22 patients with AFLP, 16 cases were treated with conventional treatment (CT group), while the other 6 cases were treated with PE and PP in addition to conventional therapy (CT+PE+PP group). Treatment efficacy was based primarily on survival and secondarily on liver and kidney functions 2 weeks after treatment. Adverse effects were also assessed at the same time point. RESULTS: In the CT+PE+PP group, 5 (83.3%) patients improved, while 1 (16.7%) patient died of multiple organ dysfunction syndrome. In the CT group, 3 (18.75%) patients improved, while 13 (81.2%) patients died of complications. Liver and kidney functions and survival were significantly improved in the CT+PE+PP group (p < 0.05) compared to the CT group. CONCLUSIONS: Timely application of PE and PP in the early phase of AFLP may be a promising treatment to halt or reverse the progression of AFLP.

Expression of turtle riboflavin-binding protein represses mitochondrial electron transport gene expression and promotes flowering in Arabidopsis.

BACKGROUND: Recently we showed that de novo expression of a turtle riboflavin-binding protein (RfBP) in transgenic Arabidopsis increased H2O2 concentrations inside leaf cells, enhanced the expression of floral regulatory gene FD and floral meristem identity gene AP1 at the shoot apex, and induced early flowering. Here we report that RfBP-induced H2O2 presumably results from electron leakage at the mitochondrial electron transport chain (METC) and this source of H2O2 contributes to the early flowering phenotype. RESULTS: While enhanced expression of FD and AP1 at the shoot apex was correlated with early flowering, the foliar expression of 13 of 19 METC genes was repressed in RfBP-expressing (RfBP+) plants. Inside RfBP+ leaf cells, cytosolic H2O2 concentrations were increased possibly through electron leakage because similar responses were also induced by a known inducer of electron leakage from METC. Early flowering no longer occurred when the repression on METC genes was eliminated by RfBP gene silencing, which restored RfBP+ to wild type in levels of FD and AP1 expression, H2O2, and flavins. Flowering was delayed by the external riboflavin application, which brought gene expression and flavins back to the steady-state levels but only caused 55% reduction of H2O2 concentrations in RfBP+ plants. RfBP-repressed METC gene expression remedied the cytosolic H2O2 diminution by genetic disruption of transcription factor NFXLl and compensated for compromises in FD and AP1 expression and flowering time. By contrast, RfBP resembled a peroxisomal catalase mutation, which augments the cytosolic H2O2, to enhance FD and AP1 expression and induce early flowering. CONCLUSIONS: RfBP-repressed METC gene expression potentially causes electron leakage as one of cellular sources for the generation of H2O2 with the promoting effect on flowering. The repressive effect on METC gene expression is not the only way by which RfBP induces H2O2 and currently unappreciated factors may also function under RfBP+ background.

Clinical analysis of 12 cases of ovarian neuroendocrine carcinoma.

BACKGROUND: Neuroendocrine neoplasms of the female genital tract are rare. AIM: To enhance our clinical understanding of neuroendocrine carcinoma (NEC) of the ovary. METHODS: A retrospective review was conducted on 12 patients diagnosed with NEC of the ovary, analyzing clinicopathological characteristics, treatment modalities, and survival status. RESULTS: The median age at diagnosis was 34.5 years (range: 20 to 62 years). Among the 12 cases, 9 were small cell carcinoma of the ovary and 3 were large cell NEC. Five cases were stage I tumors, one case was stage IV, and six cases were stage III. Eleven patients underwent surgery as part of their treatment. All patients received adjuvant chemotherapy. Among the 12 patients, one patient received radiotherapy, and one patient with a BRCA2 mutation was administered PARP inhibitor maintenance after chemotherapy. The median progression-free survival was 13 months, and the median overall survival was 19.5 months. Four cases remained disease-free, while eight cases experienced tumor recurrence, including three cases that resulted in death due to disease recurrence. CONCLUSION: NEC of the ovary is a rare condition that is more common in women of childbearing age and is associated with aggressive behavior and poor clinical outcomes. Surgical resection remains the mainstay of treatment, with some patients benefiting from adjuvant chemoradiation therapy.

LncRNA GAS5 restrains ISO-induced cardiac fibrosis by modulating mir-217 regulation of SIRT1.

Considering the effect of SIRT1 on improving myocardial fibrosis and GAS5 inhibiting occurrence and development of myocardial fibrosis at the cellular level, the aim of the present study was to investigate whether LncRNA GAS5 could attenuate cardiac fibrosis through regulating mir-217/SIRT1, and whether the NLRP3 inflammasome activation was involved in this process. Isoprenaline (ISO) was given subcutaneously to the male C57BL/6 mice to induce myocardial fibrosis and the AAV9 vectors were randomly injected into the left ventricle of each mouse to overexpress GAS5. Primary myocardial fibroblasts (MCFs) derived from neonatal C57BL/6 mice and TGF-ß1 were used to induce fibrosis. And the GAS5 overexpressed MCFs were treated with mir-217 mimics and mir-217 inhibitor respectively. Then the assays of expression levels of NLRP3, Caspase-1, IL-1ß and SIRT1 were conducted. The findings indicated that the overexpression of GAS5 reduced the expression levels of collagen, NLRP3, Capase-1, IL-1ß and SIRT1 in ISO treated mice and TGF-ß1 treated MCFs. However, this effect was significantly weakened after mir-217 overexpression, but was further enhanced after knockdown of mir-217. mir-217 down-regulates the expression of SIRT1, leading to increased activation of the NLRP3 inflammasome and subsequent pyroptosis. LncRNA GAS5 alleviates cardiac fibrosis induced via regulating mir-217/SIRT1 pathway.

[Influence of EphA2 siRNA transfection on the biological behavior of human ovarian carcinoma cell].

OBJECTIVE: To explore EphA2 siRNA transfection and its influence on the biological behavior of human ovarian carcinoma cells. METHODS: One pairs of siRNA was synthesized and transfected into the human ovarian carcinoma cell line SKOV3. Observation of the transfection efficiency through the fluorescence inverted microscope was followed by the evaluation of expression of EphA2 protein using Western blot. The effects of EphA2 siRNA on proliferation of SKOV3 cells were observed by drawing cell growth curves and measuring cloning efficiency, and the adhesion and invasion of SKOV3 were detected by cell adhesion assay and Matrigel-boyden chamber method respectively. RESULTS: After successful transfection, a large number of fluorescent particles were observed under the fluorescence inverted microscope. The expression of EphA2 protein was obviously suppressed by EphA2 siRNA (P < 0.05). The cell proliferation, adhesiveness and invasiveness were significantly inhibited (P < 0.05). However, no changes in colony-forming efficiency were observed (P > 0.05). CONCLUSION: Down-regulation of EphA2 gene by EphA2 siRNA in SKOV3 cell line showed retardation of cell growth, proliferation and partial reversion of the malignant phenotype, including the ability of adhesion and invasion. EphA2 may be a new and potent target of gene therapy in ovarian carcinoma.

Role of dopamine D2 receptors in ischemia/reperfusion induced apoptosis of cultured neonatal rat cardiomyocytes.

BACKGROUND: Myocardial ischemia/reperfusion injury is the major cause of morbidity and mortality for cardiovascular diseases. Dopamine D2 receptors are expressed in cardiac tissues. However, the roles of dopamine D2 receptors in myocardial ischemia/reperfusion injury and cardiomyocyte apoptosis are unclear. Here we investigated the effects of both dopamine D2 receptors agonist (bromocriptine) and antagonist (haloperidol) on apoptosis of cultured neonatal rat ventricular myocytes induced by ischemia/reperfusion injury. METHODS: Myocardial ischemia/reperfusion injury was simulated by incubating primarily cultured neonatal rat cardiomyocytes in ischemic (hypoxic) buffer solution for 2 h. Thereafter, these cells were incubated for 24 h in normal culture medium. RESULTS: Treatment of the cardiomyocytes with 10 µM bromocriptine significantly decreased lactate dehydrogenase activity, increased superoxide dismutase activity, and decreased malondialdehyde content in the culture medium. Bromocriptine significantly inhibited the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischemia/reperfusion injury. Bromocriptine also down-regulated the expression of caspase-3 and -9, Fas and Fas ligand, and up-regulated Bcl-2 expression. In contrast, haloperidol (10 µM) had no significant effects on the apoptosis of cultured cardiomyocytes under the aforementioned conditions. CONCLUSIONS: These data suggest that activation of dopamine D2 receptors can inhibit apoptosis of cardiomyocytes encountered during ischemia/reperfusion damage through various pathways.

[Expression and prognostic significance of EphA2 and EphrinA-1 in ovarian serous carcinomas].

OBJECTIVE: To investigate the expression and prognostic significance of EphA2 and EphrinA-1 in ovarian serous carcinomas. METHODS: Ninety five tumors from the patients with ovarian serous carcinomas and 2 ovarian cancer cell lines were recruited. The expressions of EphA2 and EphrinA-1 were examined by means of immunohistochemistry. The relationships among protein expression and clinicopathological features, survival of patients were analyzed. The mRNA and protein expressions of EphA2 and EphrinA-1 in ovarian cancer cell lines were measured with semiquantitative polymerase chain reaction and western blotting. RESULTS: The protein expressions of EphA2 and EphrinA-1 in tumor were 92.6% (88/95)and 97.9% (93/95) respectively, while were 40%(8/20) and 30% (6/20) in adjacent ovarian tissue (P = 0.000). EphA2 immunohistochemical staining could be observed in both tumour and vascular endothelial cells, and EphrinA-1 mainly localized in the tumor cells. The expression of EphA2 was significantly associated with the expression of EphrinA-1 (r = 0.98, P = 0.02). There was no significant correlation between the expressions of EphA2/EphrinA-1 and age, FIGO stage, residual tumour size and histological grade. High levels of both EphA2 and EphrinA-1 protein expression were significantly associated with a shorter overall survival in multivariate analysis (P < 0.05). High levels of EphA2 and EphrinA-1 mRNA and protein were detected in OVCAR3 and SKOV3 cell lines. CONCLUSION: There are over-expression of EphA2 and EphrinA-1 in ovarian serous carcinomas and ovarian cancer cell lines. Tumours with higher expression levels of both EphA2 and EphrinA-1 significantly associated with poorer clinical outcome.

A retrospective study of azithromycin and ceftizoxime for the management of children with Mycoplasma pneumoniae pneumonia.

ABSTRACT: The aim of this study was to compare the clinical efficacy of azithromycin and ceftizoxime (AC) and erythromycin and amoxicillin/sulbactam (EAS) in the treatment of children with Mycoplasma pneumoniae pneumonia (MPP).In this retrospective study, a total of 92 eligible children with MPP were included, and they were divided into a treatment group (n = 46) and a control group (n = 46). All patients were treated with intravenous ambroxol, and nebulized inhalation of budesonide and terbutaline. In addition, patients in the treatment group received AC. Patients in the control group underwent EAS. All patients in both groups were treated for a total of 10 days. Outcomes consist of erythrocyte sedimentation rate, C-reactive protein, serum lactate dehydrogenase, and interleukin 6, fever clearance time, time of cough disappearance, time of rale disappearance, time of signs disappeared by X-ray, and adverse events. All outcomes were measured after 10-day treatment.After treatment, patients who received AC exerted better improvements in erythrocyte sedimentation rate (P < .01), C-reactive protein (P < .01), serum lactate dehydrogenase (P < .01), interleukin 6 (P < .01), fever clearance time (P < .01), time of cough disappearance (P < .01), time of rale disappearance (P < .01), and time of signs disappeared by X-ray (P < .01), than those in patients who received EAS. In addition, there were not significant differences in adverse events between 2 groups.The results of this study showed that AC may benefit more than EAS for the children with MPP.

[Effect of glucagon-like peptide-1 on hypoxia-reoxygenation induced injury in neonatal rat cardiomyocytes].

OBJECTIVE: To observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes. METHODS: Cultured neonatal rat cardiomyocytes were randomly divided into seven groups: normal control group, H/R group, GLP-1 + H/R group, GLP-1 + H/R + UO126 group, GLP-1 + H/R + LY294002 group, H/R + UO126 group, H/R + LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected. RESULTS: Compared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspase-3 activity were all significantly increased in H/R group (all P < 0.01). However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [the activity of LDH (128.47 +/- 7.96) U/L vs. (223.96 +/- 22.10) U/L, P < 0.01, and cardiomyocyte apoptosis rate (2.84 +/- 2.56)% vs. (12.58 +/- 6.69)%, P < 0.01, and Caspase-3 activity (36,809 +/- 4750) RLU vs. (57,602 +/- 9161) RLU, P < 0.01], while LY294002 (PI3K inhibitor) and UO126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury. CONCLUSIONS: GLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.

Long intergenic non­protein coding RNA 00460 predicts a poor prognosis and promotes tumorigenesis of human osteosarcoma.

Osteosarcoma (OS) is the most common type of primary malignant bone tumor, which has a high incidence rate in children and adolescents. This research aims to reveal the role of long intergenic non­protein coding RNA 00460 (LINC00460) in OS by the loss­of­function experiment. LINC00460 is involved in the development of multiple types of tumor, but the role of LINC00460 in OS is unclear. To discover more effective molecular targets for the treatment of OS, the association between LINC00460 and OS prognosis was analyzed using the Gene Expression Profiling Interactive Analysis database. Additionally, small interfering RNA was used to knockdown LINC00460 gene expression in vitro to verify its biological effects on the viability, invasive and migratory potential of OS cells. LINC00460 knockdown significantly reduced the viability of OS cells and initiated cell cycle arrest within the G0/G1 phase through the decreased expression of cyclin D1 and CDK4/CDK6. In addition, LINC00460 knockdown promoted apoptosis of OS cells, and inhibited the migratory and invasive abilities of OS cells through the inhibition of the epithelial­mesenchymal transition pathway. In conclusion, the present study reported that LINC00460 may predict OS prognosis, and may serve an important role in mediating the viability, invasive and migratory potential of OS cells. Based on these findings, LINC00460 demonstrated promising potential as a future therapeutic target for OS treatment.

Comparison of the predictive performance of risk of malignancy indexes 1-4, HE4 and risk of malignancy algorithm in the triage of adnexal masses.

OBJECTIVES: For patients presenting with adnexal mass, it is important to correctly distinguish whether the mass is benign or malignant for the purpose of precise and timely referral and implication of correct line of management. The objective of this study was to evaluate the performance of Risk of malignancy Indexes (RMI) 1-4, Human Epididymis Protein 4 (HE4) and Risk of Malignancy Algorithm (ROMA) in differentiating the adnexal mass into benign and malignant. METHODS: A retrospective study using 155 patients diagnosed with adnexal mass between January 2014 to December 2014 in The First Affiliated Hospital of Zhengzhou University was conducted. The patient records were assessed for age, menopausal status, serum CA125 and HE4 levels, ultrasound characteristics of the pelvic mass and the final pathological diagnosis of the mass. RMI1, RMI2, RMI3, RMI4, ROMA were calculated for each patient and the sensitivity, specificity and the Receiver Operating Characteristics (ROC) curves were determined for each test to evaluate their performance. RESULTS: Among 155 patients with adnexal masses meeting inclusion criteria, 120 (77.4%) were benign, 8 (5.2%) borderline and 27 (17.4%) were malignant. RMI2 and RMI4 had the highest sensitivity (66.7%) while HE4 had the highest specificity (96.9%).Although ROMA had the highest area under the curve (AUC) of 0.886 it was not found to be statistically superior to the other tests. For epithelial ovarian cancers, ROMA (80%), HE4 (96.9%) and RMI 4 (0.868) had the highest sensitivity, specificity and AUC respectively however, the AUC characteristics were not statistically significant between any groups. Compared to the postmenopausal group (sensitivity 72.2-77.8%) all the tests showed lower sensitivity (42.9%) for the premenopausal group of patients. CONCLUSIONS: RMI 1-4, ROMA and HE4 were all found to be useful for differentiating benign/borderline adnexal masses from malignant ones for deciding optimal therapy, however no test was found to be significantly better than the other. None were able to differentiate between benign and borderline tumors. All of the tests demonstrated increased sensitivity when borderline tumors were considered low-risk, and when only epithelial ovarian cancers were considered.

Correction to: The Association Between Phosphorylated Neurofilament Heavy Chain (pNF-H) and Small Fiber Neuropathy (SFN) in Patients with Impaired Glucose Tolerance.

In the original article, there was some error in Table 2. The correct table is given below.