Objective To evaluate the effects of malignant ascites on the morphological characteristics and the proliferation and migration abilities of the tumor cell and ovarian cancer cell lines(SKOV3)in the ovarian cancerous ascites.Methods Tumor cells extracted from the ovarian cancerous ascites were cultured in vitro with DMEM high glucose culture medium,and ovarian cancer cell lines( SKOV3) were cultured in DMEM high glucose and DMEM high glucose with different proportion of malignant ascites.The morphological characteristics of the cells were observed by optical microscope and electron microscope respectively.Cell proliferation ability was de-tected by CCK kit;The effect of SKOV3 on the migration of ovarian cancer cell lines was measured by scratch test.Results The morphological characteristics of tumor cells and ovarian cancer cell lines( SKOV3) in ovarian cancer ascites were significantly different.The proliferation ability of tumor cells was decreased without the asci-tes.The proliferation and migration abilities of SKOV3 cultured in mixed culture medium were significantly im-proved compared with the cells cultured in high glucose medium.Conclusion The change of tumor cell morphol-ogy in ascites benefits its abilities of proliferation and migration.The malignant ascites promote the abilities of pro-liferation and migration of ovarian cancer cell line(SKOV3).

Electroencephalography (EEG), as a convenient and non-invasive technique, is highly sensitive to brain function abnormalities and has been widely applied in the diagnosis and treatment of epilepsy and other neurological diseases (applied research in stroke field has a history of decades). In recent years, with the deepening of related research and rapid development of artificial intelligence technology, EEG has shown new potential in early diagnosis, disease monitoring and prognosis assessment of stroke. This review discusses the recent advance in EEG in evaluating the diagnosis, therapeutic efficacy, and prognoses of stroke in the last 5 years, so as to provide references for improving the diagnosies, treatments and prognoses of stroke patients.

Objective:To investigate the characteristics of transcranial sonography (TCS) in patients with restless legs syndrome (RLS), and analyze the correlations of scores of RLS Self-rating Severity Scale by International Restless Leg Syndrome Study Group (IRLS) and TCS parameters with clinical data of these patients.Methods:Twenty-one patients with RLS admitted to the Sleep Disorder Clinic of our hospital from September 2020 to January 2021 were selected as RLS group, and 23 healthy controls at the same time period were recruited as control group. IRLS was used to evaluate the severity of patients in the RLS group, and the 14-item Hamilton anxiety rating scale (HAMA-14) and 24-item Hamilton depression rating scale (HAMD-24) were used to evaluate the anxiety and depression of subjects from the 2 groups. Pittsburgh Sleep Quality Scale (PSQI), Insomnia Severity Index (ISI) and Epworth Sleepiness Scale (ESS) were used to evaluate the sleep quality of subjects from the 2 groups. TCS was used to examine the occurrence of hypoechoic substantia nigra and raphe nucleus rupture and the width of the third ventricle in the two groups. The clinical data and TCS parameters of patients in the 2 groups were compared, and the correlations of IRLS scores and TCS parameters with clinical features of patients in the RLS group were analyzed.Results:As compared with those in the control group, the HAMA-14, HAMD-24, ISI and PSQI scores in the RLS group were statistically higher ( P<0.05). As compared with the control group, RLS group had significantly higher proportion of patients with hypoechoic substantia nigra or raphe nucleus rupture ( P<0.05). In RLS patients, the IRLS scores were positively correlated with HAMA-14, HAMD-24, and ISI scores ( P<0.05); ESS scores were negatively correlated with hypoechoic substantia nigra and width of the third ventricle ( rs=-2.005, P=0.045; r=-0.477, P=0.029); width of the third ventricle was negatively correlated with gender (male) and years of education ( rs=-0.592, P=0.005; r=-0.627, P=0.002), and positively correlated with age and course of the disease ( r=0.756, P<0.001; r=0.167, P=0.047). Conclusions:Patients with RLS are prone to anxiety, depression and sleep disorders; their TCS shows hypoechoic substantia nigra and raphe nucleus rupture. RLS severity may affect HAMA-14, HAMD-24, and ISI scores. Gender, age, years of education, course of disease, and ESS scores of RLS patients may affect TCS related parameters.

Objective:To evaluate the effects of bosutinib on acute lung injury in mice with endotoxemia.Methods:Sixty clean-grade healthy male C57BL/6 mice, aged 8-12 weeks, weighing 20-25 g, were divided into 4 groups ( n=15 each) using a random number table method: control group (group C), bosutinib group (group B), endotoxemia group (group lipopolysaccharide [LPS]) and bosutinib plus endotoxemia group (group B+ LPS). Septic acute lung injury model was developed by intraperitoneal injection of LPS.Bosutinib 5 mg/kg was injected via the tail vein at 0.5 h before establishing the model in group B+ LPS and at the corresponding time point in group B. At 24 h after developing the model, the mice were sacrificed for microscopic examination of the pathological results of lung tissues which were scored for calculation of the lung coefficient (LI) and wet/dry lung weight (W/D) ratio, and for determination of the content of Evans blue in lung tissues (by Evans blue staining), expression of vascular endothelial cadherin (VE-cadherin), vascular cell adhesion molecule 1 (VCAM-1), phosphorylated nuclear transcription factor κB p65 (p-NF-κB p65), phosphorylated nuclear factor κB inhibitory protein α (pIκB-α) (by Western blot) and expression of interleukin-1beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) mRNA (using real-time polymerase chain reaction). Results:Compared with group C, the LI, W/D ratio, Evans blue content in lung tissues and lung injury score were significantly increased, and the expression of IL-1β mRNA, TNF-α mRNA, IL-6 mRNA, VCAM-1, p-NF-κB p65 and pIKB-α was up-regulated, and the expression of VE-cadherin was down-regulated in group LPS ( P<0.05), and no significant change was found in the parameters mentioned above in group B ( P>0.05). Compared with group B, the LI, W/D ratio, Evans blue content in lung tissues and lung injury score were significantly decreased, and the expression of IL-1β mRNA, TNF-α mRNA, IL-6 mRNA, VCAM-1, p-NF-κB p65 and pIKB-α was down-regulated, and the expression of VE-cadherin was up-regulated in group LPS ( P<0.05). Conclusions:Bosutinib can ameliorate the acute lung injury in mice with endotoxemia.

Objective:To evaluate the effect of imatinib on the endotoxemia-induced acute lung injury in mice.Methods:Sixty SPF male, 8-12 weeks, C57BL/6 mice were randomly (random) divided into 4 groups ( n=15 each): control group (group C), imatinib group (groupⅠ), endotoxemia group (group LPS) and imatinib + endotoxemia group (group I+LPS). The endotoxemia model of acute lung injury was established. After 24 hours, the mice were sacrificed. The pathological changes of lung tissues were evaluated, the lung injury scores were calculated, and the wet/dry ratios of lung tissues were measured. ELISA was used to detect the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in serum. Detection kits were used to analyze the levels of malondialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and the ratio of reduced glutathione to oxidized glutathione (GSH/GSSG) in lung tissues; The expression levels of phosphorylated nuclear factor-kappa B (p-NF-κB), nuclear factor-erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in lung tissues were analyzed by western blotting. Results:Compared with the group C, the wet/dry (W/D) ratio of lungs [(3.47±0.41) vs. (5.58±0.47)], lung injury scores [(1.25±0.89) vs. (10.25±1.75)], and the levels of TNF-α and IL-6 in serum increased in the group LPS ( P<0.05). The levels of SOD, CAT, GSH and GSH/GSSG decreased, the level of MDA increased, and the expression of p-NF-κB, Nrf2 and HO-1 protein up-regulated ( P<0.05). Compared with the LPS group, the W/D ratio of lungs [(5.58±0.47) vs.(4.62±0.38)] and lung injury scores [(10.25±1.75) vs. (7.00±1.31)] in the I+LPS group decreased ( P<0.05), and the levels of TNF-α and IL-6 in the serum decreased ( P<0.05). In lung tissues, the levels of SOD, CAT, GSH and GSH/GSSG increased (all P<0.05), the level of MDA decreased (all P<0.05), the expression of p-NF-κB protein decreased, and the expression of Nrf2 and HO-1 protein increased ( P<0.05). Conclusions:Imatinib improves sepsis-induced acute lung injury in mice, and the mechanism of actions behind may be related to the inhibition of oxidative stress.

Objective:To evaluate the effects of heparin on focal adhesion kinase (FAK)/Ras homolog gene family member A (RhoA)/Rho-associated coiled-coil-containing protein kinase (ROCK) signaling pathways during acute lung injury (ALI) in septic mice.Methods:Thirty SPF healthy adult male C57BL/6J mice, aged 6-8 weeks, weighing 20-23 g, were assigned into 3 groups ( n=10 each) using a random number table method: control group (group C), ALI group, and heparin group (group H). Septic ALI model was prepared by intraperitoneal injection of lipopolysaccharide 15 mg/kg, while group C received the equal volume of normal saline. In group H, heparin sodium solution 10 U was injected via the tail vein at 30 min before developing the model. The equal volume of normal saline was injected in C and ALI groups. Venous blood samples were collected from the eyeballs under deep anesthesia at 24 h after lipopolysaccharide injection. The mice were subsequently sacrificed and lung tissues were obtained for determination of the serum concentrations of interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) (using enzyme-linked immunosorbent assay), wet/dry lung weight (W/D) ratio, expression of vascular endothelial adhesion factor 1 (VCAM-1) (by immunohistochemical staining) and expression of FAK, phosphorylated FAK (p-FAK), RhoA, GTP-bound RhoA (RhoA-GTP) and ROCK (by Western blot) and for examination of the pathological changes. The lung injury was assessed and scored. Results:Comparison with group C, the serum concentrations of IL-1β, IL-6 and TNF-α, W/D ratio and lung injury scores were significantly increased, and the expression of VCAM-1, p-FAK, RhoA-GTP and ROCK was up-regulated in ALI group ( P<0.05). Compared with ALI group, the serum concentrations of IL-1β, IL-6 and TNF-α, W/D ratio and lung injury scores were significantly decreased, and the expression of VCAM-1, p-FAK, RhoA-GTP and ROCK was down-regulated in H group ( P<0.05). Conclusions:The mechanism through which heparin mitigates ALI is associated with the inhibition of the FAK/RhoA/ROCK signaling pathway in septic mice.

Activation of the heart normally begins in the sinoatrial node (SAN). Electrical impulses spontaneously released by SAN pacemaker cells (SANPCs) trigger the contraction of the heart. However, the cellular nature of SANPCs remains controversial. Here, we report that SANPCs exhibit glutamatergic neuron-like properties. By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse, we found that SANPCs co-clustered with cortical neurons. Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system, expressing genes encoding glutamate synthesis pathway (Gls), ionotropic and metabotropic glutamate receptors (Grina, Gria3, Grm1 and Grm5), and glutamate transporters (Slc17a7). SANPCs highly expressed cell markers of glutamatergic neurons (Snap25 and Slc17a7), whereas Gad1, a marker of GABAergic neurons, was negative. Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca