Ischemic stroke has a high incidence,mortality and morbidity.It was demonstrated that higher white blood cell and neutrophil counts were correlated with larger infarct volume and increased stroke severity in patients with acute ischemic stroke.Recently,neutrophil/lymphocyte ratio (NLR) was shown to be correlated with risk of ischemic stroke and outcome in patients with acute ischemic stroke.This article reviews the predictive roles of NLR in ischemic stroke.

Objective:To examine the multiple mediating effects of cognitive fusion and network communication in the relationship between interpersonal relationship and mobile phone addiction tendency in college students.Methods:Questionnaire survey was conducted among 708 college students in a medical school using the mobile addiction tendency scale, E-communication inventory, Interpersonal relationship assessment scale and cognitive fusion questionnaire.SPSS 17.0 software was used for descriptive statistics and correlation analysis.Structural equation model was built with AMOS 21.0.The non parametric percentile bootstrap method with variance correction was used to test the significance of mediating effect.Results:(1) The sample mobile phone dependence detection rate was 13.56%.(2)There were statistical differences in conversation scores((3.49±1.85), (2.51±1.64)), making friends ((4.53±1.83), (3.21±1.72)), getting along with opposite gender((2.70±1.55), (2.01±1.60)), dealing with people disturbance(2.02(1.00, 3.00), 1.46(0.00, 2.00))between different mobile phone addiction tendency( t/ Z=2.752-5.072, P<0.05). There were statistical differences in cognitive fusion ((40.60±7.55), (33.91±7.95)) between different mobile phone addiction tendency( t/ Z=5.385, P<0.05). There were statistical differences in negative results of network communication((28.60±6.77), (23.31±7.03)), social perception of network communication((32.36±6.68), (29.17±7.82)), self exposure and emotional experience of network((23.36±6.61), (18.18±6.30)), cognition of network communication((28.19±6.85), (22.75±6.76)), entertainment of network ((6.74±1.81), (6.00±1.67)) between different mobile phone addiction tendency( t/ Z=2.647~5.195, P<0.05). (3) There was a statistically significant positive correlation between interpersonal relationship, mobile phone addiction tendency, cognitive fusion, and E-communication inventory scores ( r=0.226-0.423, P<0.01). (4) Multi-mediating model analysis showed that interpersonal relationship could affect mobile phone addiction tendency through cognitive fusion and network communication not only in a parallel way but also in a chain way.The direct effect from interpersonal relationship to mobile phone addiction tendency was 0.20, and the total indirect effect from interpersonal disturbance to mobile phone addiction tendency through cognitive fusion and network communication was 0.18.And the effects of cognitive fusion, network communication, and the chain mediating accounted for 50.0%, 33.3%, and 16.7% of the total indirect effect respectively.The 95% CI of the Bootstrap output were (0.04-0.19), (0.02-0.14)and(0.01-0.05). Conclusions:College students' interpersonal disturbances affect mobile phone addiction tendency through multiple mediations of cognitive fusion and online communication.

Anlotinib has strong antiangiogenic effects and leads to vessel normalization.However,the"window period"characteristic in regulating vessel normalization by anlotinib cannot fully explain the long-term survival benefits achieved through combining it with other drugs.In this study,through RNA sequencing(RNA-seq)and label-free quantitative proteomics analysis,we discovered that anlotinib regulated the expression of components of the extracellular matrix(ECM),leading to a significant reduction in ECM stiffness.Our bioinformatic analysis revealed a potential positive relationship between the ECM pathway and gefitinib resistance,poor treatment outcomes for programmed death 1(PD-1)targeting,and unfavourable prognosis following chemotherapy in lung cancer patients.We administered anlotinib in combination with these antitumour drugs and visualized their distribution using fluorescent labelling in various tumour types.Notably,our results demonstrated that anlotinib prolonged the retention time and distribution of antitumour drugs at the tumour site.Moreover,the combination therapy induced notable loosening of the tumour tissue structure.This reduction was associated with decreased interstitial fluid pressure and tumour solid pressure.Additionally,we observed that anlotinib effectively suppressed the Ras homologue family member A(RhoA)/Rho-associated protein kinase(ROCK)signalling pathway.These findings suggest that,in addition to its antiangiogenic and vessel normalization effects,anlotinib can increase the distribution and retention of antitumour drugs in tumours by modulating ECM expression and physical properties through the RhoA/ROCK signalling pathway.These valuable insights contribute to the development of combination therapies aimed at improving tumour targeting in cancer treatment.

Objective To determine the effects of delayed umbilical cord clamping on the postpartum hemorrhage,instant and long-term newborn anemia,newborn jaundice.Methods In total,303 infants were selected during October 2016 to June 2017 in three hospitals in Beijing.They were randomly allocated into two groups receiving instant clamping of umbilical cord (less than 60s after delivery,n=158) and delayed clamping of umbilical cord(after cord pulsation ceased,n=145).Relevant indicators of maternal and neonatal outcomes are compared.Results There were significant differences between two groups in instant hemoglobin concentration and in 5～7 days (P＜0.05).There were no differences between two groups in transcutaneous bilirubin,the risk of anemia in three months,the risk of jaundice in 5～7 days and the need of blue-light therapy (P＞0.05).There were no differences between two groups of women in postpartum hemorrhage,the length of third stage of labor and the rate of breast feeding (P＞0.05).Conclusion Clamping the umbilical cord when cord pulsation has ceased does not have negative effects on delivery process and postpartum hemorrhage,but it increases the instant hemoglobin concentration and hemoglobin concentration after delivery in 5～7 days.Still it is unclear whether it will affect the risk of jaundice.

BACKGROUND:Cardiac hypertrophy is an adaptive response of the heart to physiological and pathological stimuli such as pressure overload.It is of compensatory significance in the early stage,but if the stimulation continues,it can cause cardiomyopathy leading to heart failure.MicroRNAs are involved in the regulation of cardiac hypertrophy.However,the role of miR-20a in pressure overload-induced cardiac hypertrophy has not been reported. OBJECTIVE:To investigate the role of miR-20a in pressure overload-induced cardiac hypertrophy and the underlying mechanisms. METHODS:Transverse aortic constriction was used to induce cardiac hypertrophy in vivo and angiotensin Ⅱ was used to induce H9c2 cell models of cardiac hypertrophy in vitro.MiR-20a was overexpressed in vivo by intramyocardial injection of miR-20a overexpressing adenovirus and in vitro by transfecting miR-20a mimic into H9c2 cells.Cardiac hypertrophy was assessed by measuring heart weight/body weight ratio,cell surface area,and myocardial fibrosis.The expression levels of atrial natriuretic peptide,brain natriuretic peptide,β-myosin heavy chain and miR-20a were detected by real-time fluorescence quantitative PCR.Mitochondrial fission was detected by MitoTracker.The downstream target genes of miR-20a were predicted by RNAhybrid software. RESULTS AND CONCLUSION:(1)The expression level of miR-20a was significantly decreased in both hypertrophic cardiomyocytes and hearts(P<0.05).(2)At the animal level,overexpression of miR-20a significantly inhibited transverse aortic constriction-induced cardiac hypertrophy,including decreasing the upregulated expression level of hypertrophic marker genes(P<0.05),reduced the enlarged heart volume,reducing the increased heart weight/body weight ratio(P<0.01),reducing the increased myocardial cross-sectional area(P<0.05),and attenuating fibrosis(P<0.01).(3)At the cellular level,overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced cardiomyocyte hypertrophy,including decreasing the upregulated expression levels of atrial natriuretic peptide(P<0.05),brain natriuretic peptide(P<0.01)and β-myosin heavy chain(P<0.05),reducing the increased protein/DNA ratio(P<0.01),and suppressing the increased cell surface area(P<0.05).(4)Overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced mitochondrial fission(P<0.05).(5)The results of RNAhybrid software analysis showed that miR-20a and the mRNA 3'untranslated region of cAMP-dependent protein kinase inhibitor alpha were well complementary and the predicted binding sites were highly conserved.(6)In conclusion,miR-20a is significantly down-regulated in pressure overload-induced cardiac hypertrophy.Overexpression of miR-20a inhibits cardiac hypertrophy at both the cellular level and animal level and attenuates angiotensin Ⅱ-induced mitochondrial fission.