西瓜TALE基因家族鉴定及表达分析

TALE基因家族在调控花器官发育、花分生组织形成、器官形态发生、果实发育、植物非生物胁迫响应及激素响应中发挥重要作用。利用生物信息学的方法鉴定了西瓜TALE基因家族成员,并分析了其基因结构、系统发育树、保守基序、顺式作用元件、组织特异性表达,以及低温胁迫和干旱胁迫后基因的表达情况,为西瓜TALE基因家族的功能研究和利用提供了理论依据。结果表明,西瓜TALE基因家族共包含19个成员。系统发育分析将ClTALE家族分为BEL1-like和KNOX两个亚家族,KNOX亚家族又可进一步划分为两个分支ClassⅠ和ClassⅡ。顺式作用元件分析表明,ClTALE基因的启动子中富含光、植物激素和非生物胁迫响应的顺式元件,其中光响应元件最多。西瓜组织特异性表达分析表明,ClBLH09在根中高表达,ClBLH01在卷须、雌花和雄花中高表达,因此西瓜TALE基因家族可能参与了西瓜的生长发育过程。低温胁迫(0、3、6、12、24、36和48 h)和干旱胁迫(0、1、2、3、4、5、6、7和8 d)不同时间后基因的表达分析表明,ClBLH08和ClKN02在低温胁迫下呈现上调趋势,ClBLH04和ClBLH05在干旱胁迫下呈上调的趋势,因此西瓜TALE基因家族可能在低温胁迫和干旱胁迫中发挥作用。

Value of N-Terminal Pro B-Type Natriuretic Peptide,High-Sensitivity C-Reactive Protein,and Homocysteine Levels in Predicting Cardiovascular Events in Chronic Heart Failure Patients After Discharge

Objective:To investigate the value of N-terminal pro B-type natriuretic peptide(NT-proBNP),high-sensitivity C-reactive protein(hs-CRP),and homocysteine(Hcy)levels in predicting cardiovascular events(CV)in patients with chronic heart failure(CHF).Methods:A total of 63 patients with CHF admitted to our hospital between June 2019 and July 2021 were selected.Their NT-proBNP,hs-CRP,and Hcy levels were detected at discharge,and a 12-month follow-up was done after their discharge to collect clinical data.The collected data were inclusive of data from 21 CHF patients with cardiovascular disease and 42 CHF patients without cardiovascular disease.The effect of NT-proBNP,hs-CRP,and Hcy levels on the occurrence of CV was analyzed.Results:The levels of NT-proBNP,hs-CRP,and Hcy in the group with cardiovascular disease were significantly higher than those in the group without cardiovascular disease(P<0.05);the levels of serum NT-proBNP,hs-CRP,and Hcy at discharge had certain value in predicting short-term CV in CHF patients(P<0.05).Conclusion:NT-proBNP,hs-CRP,and Hcy levels can be used to predict CV in CHF patients,thus having clinical application value.

A Tale of Two Continents-An Autobiography

On 14th September 2023,we were gathered in a Beijing conference hall to exchange views with the leaders of the Chinese Association for International Understanding.We had been introduced about the Association by researcher Zhang Yaowu during our field trips.However,when we met Ai Ping,I had no idea that we were talking with the author of"A Tale of Two Continents:An Autobiography".In receiving his signed book,I realized that the speaker was the current Vice-President of the Chinese Association for International Understanding and a Deputy Minister and an Ambassador Extraordinary and Plenipotentiary of China to Ethiopia.

千穗谷TALE转录因子家族的生物信息学分析

TALE转录因子广泛存在于植物中,对植物的生长发育和对外界环境的响应发挥着重要作用。本研究在千穗谷(Amaranthus hypochondriacus)基因组中共鉴定出11个TALE基因。系统发育分析将千穗谷TALE家族蛋白分为BELL和KNOX两个亚家族,同一亚家族中的AhTALEs基因具有相似的基因结构,编码蛋白也具有类似的结构域。蛋白二级结构和三级结构分析都表明AhTALEs蛋白由螺旋-角-螺旋的结构构成。此外,对千穗谷与其他物种的TALE基因共线性关系、组织表达特性和AhTALEs基因启动子区的顺式作用元件分析发现,不同AhTALEs亚家族在各组织中的表达模式不同,并且发现启动子区包含大量非生物胁迫和激素响应元件,这为AhTALE家族的进化分析提供了依据。qRT-PCR分析发现AhTALEs基因在低温和干旱胁迫下的表达水平有不同程度的变化,表明AhTALEs基因能够响应低温和干旱胁迫应答。本研究为开展千穗谷中TALE转录因子在非生物胁迫中的生物学功能研究提供了重要参考。

Experimental study on the apoptosis of cervical cancer Hela cells induced by juglone through c-Jun N-terminal kinase/c-Jun pathway

Objective: To study the regulatory effect and molecular mechanism of juglone on apoptosis of cervical cancer Hela cells. Methods: Cervical cancer Hela cells were cultured and treated with different dosages of juglone (10, 20, and 40 pmol/L, respectively) and c-Jun N-terminal kinase (JNK) inhibitor SP600125 (10, 20, and 40 mu mol/L. respectively). Then cellular proliferative activity and the expression of JNK/c-Jun pathway molecule and apoptotic molecule in the cells were detected. Results: After 6, 12. 18 and 24 h of treatment, the value for proliferative activity of cells treated with juglone was significantly lower than that of control group (p<0.05), and the anti-proliferative effect was more significant as the treatment period and juglone dosage increased (P<0.05). The protein expressions of Box, CytC, Fas, FasL, Caspase-3, and p-c-Jun in cells treated with juglone were significantly higher than those of control group (P<0.05), and the protein expressions of Bax, CytC, Fas. FasL, Caspase-3, p-JNK and p-c-Jun increased more remarkably as the juglone dosage increased (P<0.05). In cells treated with 40 pmol/L juglone and SP600125, the protein expressions of Bax, CytC, Fas. Fast.. and Caspase-3 were significantly lower than those of cells treated with 40 pmol/L juglone (J<0.05), and the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 reduced more remarkably as the SP600125 dosage increased (P<0.05). Conclusion: Juglone can increase the expression of apoptotic molecules in mitochondrial pathway and death receptor pathway by activating JNK/c-Jun pathway, thus inducing apoptosis of cervical cancer cells.

Neutrophil-to-lymphocyte ratio compared to N-terminal pro-brain natriuretic peptide as a prognostic marker of adverse events in elderly patients with chronic heart failure

Background The neutrophil-to-lymphocyte （N/L） ratio has been associated with poor prognosis in patients with heart failure, but it has not been compared with N-terminal pro-brain natriuretic peptide （NT-proBNP） in elderly patients with chronic heart failure （CHF）. We sought to make this comparison. Methods A total of 1355 elderly patients with CHF were analyzed. A multivariate logistic regression model was used to analyze the variables associated with atrial fibrillation （AF）. Cox regression analysis was used to assess the multivariable rela- tionship between the N/L ratio, NT-proBNP level, and subsequent major cardiovascular events （MCE）. Results In the multiple logistic regression analysis, the N/L ratio was demonstrated as a risk factor for AF in elderly patients with CHF [odds ratio （OR）： 1.079, 95% confi- dence interval （CI）： 1.027-1.134, P = 0.003]. The median follow-up period was 18 months. In a multivariable model using tertiles of both variables, the highest tertile of the N/L ratio was significantly associated with MCE [hazard ratio （HR）： 1.407, 95% CI： 1.098-1.802, P = 0.007] compared with the lowest tertile. Similarly, the highest NT-proBNP tertile was also significantly associated with MCE （HR： 1.461, 95% CI： 1.104-1.934, P- 0.008）. Conclusions In elderly patients with CHF, the N/L ratio is one of the important risk factors for AF and it is an inexpensive and readily available marker with similar independent prognostic power to NT-proBNP. The risk of MCE increases 1.407-fold when the N/L ratio is elevated to the highest tertile.

Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats

Objective:To investigate the effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats.Methods:A total of 40 healthy male SD rats were randomly divided into the sham group(Croup A,n=10,saline 5 mL/d),ischemia-reperfusion group(Group B,n=10,saline S mL/d),atorvastatin group(Group C,n=10.atorvastatin 20 mg/kg·d),atorvastatin + N-amino-arginine group(Group D,n=10,atorvastatin 20 mg/kg·d + N-amino arginine 15 mg/kg).Myocardial ischemia-reperfusion rat model was eslablished after 3 days of gavage.N-amino arginine 15 mg/kg was given by tail vein injection 15 min before ischemia.After reperfusion,enzymology indicators such us creatine kinase(CK) and lactate dehydrogenase and the oxidative stress parameters such as nitric oxide(NO),malondialdehyde(MDA) and total superoxide dismutase(TSOD),and n-terminal pro-brain natriuretic peptide(NT-proBNP)expression was detected by immunohistochemistry.Results:LDH and CK levels of group A were significantly lower than the outer three groups,and group B was the highest.There was significant difference between group B and group C(P<0.05),and no significant difference between group B and group D(P>0.05).MDA levels in group B were significantly higher than the other three groups.The lowest was group A,followed by group C,the difference among groups was significantly(P<0.05).TSOD and NO levels in group B was the lowest,the level in group A was the highest,followed by group C,the difference among groups was significant(P<0.05).NT-proBNP level in group B was significantly higher than the other three groups,the lowest was group A,followed by group C,the difference among groups was significant(P<0.05).Conclusions:Atorvastatin has a protective effect on the myocardial injury in the myocardial ischemia and reperfusion rats.It can increase NO synthesis and decrease MDA content,increase serum TSOD activity and the oxidative stress effect,meanwhile protect myocardial cells and reduce myocardial injury.

Plasma N-terminal pro-brain natriuretic peptide levels in elderly patients with isolated diastolic dysfunction

Objective To investigate plasma N-terminal pro-brain natriuretic peptide (NT-BNP) levels and to assess their clinical significance in elderly patients with isolated diastolic dysfunction. Methods Plasma NT-BNP level were measured by electrochemiluminescence immunoassay in 34 symptomatic patients (Group 1), 34 asymptomatic patients (Group 2) with isolated diastolic dysfunction, and in 16 elderly healthy subjects (control group, Group 3), serving controls. Colored Doppler echocardiography was performed to evaluate the patients' cardiac structures and functions. Results The plasma NT-BNP level in Group 1 was significantly higher than those in Group 2 and Group 3 and increased with the severity of heart failure. There was no significant difference of plasma NT-BNP levels between Group 2 and Group 3 (p>0.05). A NT-BNP value of 102.75 pg/mL showed a sensitivity of 88.2%, a specificity of 87.5%, and an accuracy of 88.1% for diagnosing diastolic dysfunction. Patients with restrictive filling pattern on echocardiography had higher NT-BNP levels than those of impaired relaxation pattern (1961.2±304.9 versus 460.1±92.7pg/mL, p<0.001). Conclusion The elevation of plasma NT-BNP level in elderly patients with isolated diastolic dysfunction correlates with the severity of their diastolic abnormalities. The level of plasma NT-BNP has an important clinical value in the diagnosis of elderly patients with isolated diastolic dysfunction.

Enhancement of humoral immune responses to HBsAg by heat shock protein gp96 and its N-terminal fragment in mice

AIM: Most studies on the immune effect of gp96 were focused on its enhancement of CTLs. It is interesting to know whether gp96 could influence the humoral immune response, and whether the recombinant N-terminal fragment of gp96 could substitute native gp96 to stimulate the immune system.METHODS: gp96 isolated from livers of normal mice and its N-terminal fragment (amino acid 22-355) expressed in E coli were used for immunization of BALb/c mice. Eight groups of mice received one of the following regiments subcutaneously in 100 μL phosphate buffered saline (PBS)at an interval of 3 wk. Group 1: PBS only; group 2:gp96 only; group 3: N-terminal fragment only; group 4: HBsAg only; group 5: HBsAg+gp96; group 6: HBsAg+N-terminalfragment; group 7: HBsAg+incomplete Freud's adjuvant; group 8: HBsAg+N-terminal fragment (95 ℃ heated for 30 min). Serum anti-HBsAg antibody levels were assayed by ELISA. CTL responses in splenocytes were analyzed by ELISPOT after the last vaccination.RESULTS: The average titer of serum anti-HBsAg antibodyin the mice immunized with HBsAg together with gp96 or its N-terminal fragment were much higher than those immunized with HBsAg alone detected by ELISA. The cellular immune response of the mice immunized with HBsAg together with gp96 or its N-terminal fragment was not different with those immunized with HBsAg alone measured by ELISPOT assay.CONCLUSION: gp96 or its N-terminal fragment greatly improved humoral immune response induced by HBsAg, but failed to enhance the CTL response, which demonstrated the potential of using gp96 or its N-terminal fragment as a possible adjuvant to augment humoral immune response against HBV infection.

c-Jun N-terminal kinase-mediated Rubicon expression enhances hepatocyte lipoapoptosis and promotes hepatocyte ballooning

AIM: To clarify the relationship between autophagy and lipotoxicity-induced apoptosis, which is termed "lipoapoptosis," in non-alcoholic steatohepatitis. METHODS: Male C57BL/6J mice were fed a high-fat diet(HFD) for 12 wk, after which the liver histology and expression of proteins such as p62 or LC3 were evaluated. Alpha mouse liver 12(AML12) cells treated with palmitate(PA) were used as an in vitro model. RESULTS: LC3-Ⅱ, p62, and Run domain Beclin-1 interacting and cysteine-rich containing(Rubicon) proteins increased in both the HFD mice and in AML12 cells in response to PA treatment. Rubicon expression was decreased upon c-Jun N-terminal kinase(JNK) inhibition at both the m RNA and the protein level in AML12 cells. Rubicon knockdown in AML12 cells with PA decreased the protein levels of both LC3-Ⅱ and p62. Rubicon expression peaked at 4 h of PA treatment in AML12, and then decreased. Treatment with caspase-9 inhibitor ameliorated the decrease in Rubicon protein expression at 10 h of PA and resulted in enlarged AML12 cells under PA treatment. The enlargement of AML12 cells by PA with caspase-9 inhibition was canceled by Rubicon knockdown.CONCLUSION: The JNK-Rubicon axis enhanced lipoapoptosis, and caspase-9 inhibition and Rubicon had effects that were cytologically similar to hepatocyte ballooning. As ballooned hepatocytes secrete fibrogenic signals and thus might promote fibrosis in the liver, the inhibition of hepatocyte ballooning might provide antifibrosis in the NASH liver.

All-trans Retinoic Acid Diminishes Collagen Production in a Hepatic Stellate Cell Line via Suppression of Active Protein-1 and c-Jun N-terminal Kinase Signal

Following acute and chronic liver injury,hepatic stellate cells (HSCs) become activated to undergo a phenotypic transformation into myofibroblast-like cells and lose their retinol content,but the mechanisms of retinoid loss and its potential roles in HSCs activation and liver fibrosis are not understood.The influence of retinoids on HSCs and hepatic fibrosis remains controversial.The purpose of this study was to evaluate the effects of all-trans retinoid acid (ATRA) on cell proliferation,mRNA expression of collagen genes [procollagen α1 (Ⅰ),procollagen α1 (Ⅲ)],profibrogenic genes (TGF-β 1,CTGF,MMP-2,TIMP-1,TIMP-2,PAI-1),fibrolytic genes (MMP-3,MMP-13) and the upstream element (JNK and AP-1) in the rat hepatic stellate cell line (CFSC-2G).Cell proliferation was evaluated by measuring BrdU incorporation.The mRNA expression levels of collagen genes [procollagen α1 (Ⅰ),procollagen α1 (Ⅲ)],profibrogenic genes (TGF-β 1,CTGF,MMP-2,TIMP-1,TIMP-2,PAI-1),and fibrolytic genes (MMP-3,MMP-13) were quantitatively detected by using real-time PCR.The mRNA expression of JNK and AP-1 was quantified by RT-PCR.The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen α1 (Ⅰ),procollagen α1 (Ⅲ)] and profibrogenic genes (TGF-β 1,CTGF,MMP-2,TIMP-1,TIMP-2,PAI-1),and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1.These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal,then decrease the mRNAs expression of profibrogenic genes (TGF-β 1,CTGF,MMP-2,TIMP-1,TIMP-2,PAI-1),and significantly induce the mRNA expression of MMP-3 and MMP-13.

Signal Transduction Pathways Mediated by Secreted and Non-Secreted Forms of Intact Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3) and Its 1-97 N-Terminal Fragment in PC-3 Human Prostate Cancer Cells

Our previous results indicated that both the secreted and the intracellular form of full length and 1-97 N-terminal fragment of IGFBP-3 induce apoptosis in PC-3 human prostate cancer cells in an IGF-dependent and independent manner. This study was undertaken to delineate possible down-stream signaling pathways that are involved in this process. Intact IGFBP-3 and its N-terminal 1-97 fragments with or without a signal propeptide were fused to YFP and expressed in PC-3 human prostate cancer cells. In some cases, the putative IGF-binding site was presented in full length IGFBP-3 and its N-terminal fragment was also mutated. Extent of apoptosis was quantified using FACS. Up-regulation of total Stat-1 and activation of phospho-Stat-1 were shown by western blot. TGF-β signal was measured by luciferase reporter assay. Results from inhibitor studies indicated that both the Caspase 8 and caspase 9 pathways are involved in IGFBP-3 (non-secreted form) which induced apoptosis in PC-3 cells. Exogenous addition of IGFBP-3 to PC-3 cells increased Stat-1 protein expression/tyrosine phosphorylation. Interestingly, results also showed that knockdown of Stat-1 by siRNA potentiated the IGFBP-3 induced apoptosis in PC-3 cells. In addition, both full-length IGFBP-3 and its 1-97 Nterminal fragments inhibited TGF-β signaling in these cells. This is the first report that compares the signal transduction pathways involved in apoptotic pathways mediated by IGFBP-3 in PC-3 human prostate cancer cells. Non-secreted form of full length IGFBP-3 and its N-terminal fragments induced apoptosis in PC-3 cells via activation of caspase 8 and caspase 9. Although, only non-secreted form of IGFBP-3 is involved in inducing apoptosis in PC-3 cells via caspase 8 and caspase 9 activation pathways but both secreted and non-secreted forms of IGFBP-3 are involved in modulating Stat-1 and TGF-β pathways to induce apoptotic actions in PC-3 cells. Non-secreted intact IGFBP-3 and its N-terminal fragments induced apoptosis in PC-3 cells via activation of caspase 8 and caspase 9 pathways. Modulation in STAT-1 and TGF-β pathways may also be important for IGFBP-3 induced apoptosis in PC-3 cells in general. These studies clearly demonstrate that secreted and non-secreted FL and 1-97 N-terminal fragments induce apoptosis in PC-3 cells by regulating different mechanistic pathways.

S-adenosyl-methionine decreases ethanol-induced apoptosis in primary hepatocyte cultures by a c-Jun N-terminal kinase activity-independent mechanism

AIM： To determine the role of c-Jun N-terminal kinase （JNK） activity in ethanol-induced apoptosis and the modulation of this signaling cascade by S-Adenosylmethionine （AdoMet）. METHODS： Primary hepatocyte cultures were pretreated with 100 IJmol/L SP600125, a selective JNK inhibitor, 1 mL/L DMSO or 4 mmol/L AdoMet and then exposed to 100 mmo/L ethanol. Hepatocyte apoptosis was determined by the TUNEL and DNA ladder assays. JNK activity and its inhibition by SP600125 and AdoMet were determined by Western blot analysis of c-jun phosphorylation and Bid fragmentation. SP600125 and AdoMet effects on the apoptotic signaling pathway were determined by Western blot analysis of cytochrome c release and pro-caspase 3 fragmentation. The AdoMet effect on glutathione levels was measured by EIIman＇s method and reactive oxygen species （ROS） generation by cell cytometry. RESULTS： The exposure of hepatocytes to ethanol induced JNK activation, c-jun phosphorylation, Bid fragmentation, cytochrome c release and pro-caspase 3 cleavage; these effects were diminished by SP600125, and caused a significant decrease in ethanol-induced apoptosis （P〈 0.05）. AdoMet exerted an antioxidant effect maintaining glutathione levels and decreasing ROS generation, without a significant effect on JNK activity, and prevented cytochrome c release and pro-caspase 3 cleavage.CONCLUSION： The JNK signaling cascade is a key component of the proapoptotic signaling pathway induced by ethanol. JNK activation may be independent from ROS generation, since AdoMet which exerted antioxidant properties did not have a significant effect on JNK activity. JNK pathway modulator agents and AdoMet may be components of promising therapies for alcoholic liver disease （ALD） treatment.

N-terminal pro-brain natriuretic peptide but not high-sensitivity C-reactive protein is related to severity of coronary artery stenosis in patients with acute coronary syndrome

Objective Biochemical indicators such as N-terminal pro-brain type natriuretic peptide（NT pro-BNP）and high-sensitivity Creactive protein（hsCRP）predict mortality in acute coronary syndrome（ACS）.However,little is known about the relationship of these factors with severity of coronary artery stenosis in patients with.Methods Three hundred and thirty-one subjects including 246 unstable angina pectoris patients and 85 myocardial infarction patients were recruited and classified into two groups：single-vessel disease group（1-vessel disease,n=93）and multiple-vessel disease group（≥2-vessels disease,n=238）according to selective coronary angiography.Plasma levels of NT pro-BNP and hsCRP were measured and severity of coronary stenosis was determined by Gensini score.Results NT pro-BNP but not hsCRP level was higher in patients with myocardial infarction than in patients with unstable angina pectoris.The patients with multiple-vessel disease had significantly higher NT pro-BNP level but not hsCRP compared with those with single-vessel disease.NT pro-BNP levels increased significantly as left ventricle（LV）function decreased,and only NT proBNP but not hsCRP level was related to Gensini score of severity of coronary stenosis in ACS.Conclusion NT proBNP but not hsCRP level is related to severity of coronary artery stenosis in patients in ACS.

c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells

AIM:To investigate the roles of c-Jun N-terminal kinase (JNK) signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS:Human gastric cancer cell lines (SGC-7901) were treated with vitamin E succinate (VES) at 5,10,20 mg/L. Succinic acid and vitamin E were used as vehicle controls and condition medium only as an untreated (UT) control. Apoptosis was observed by 4′,6-diamidine-2′-phenylindole dihydrochloride (DAPI) staining for morphological changes and by DNA fragmentation for biochemical alterations. Western blot analysis was applied to measure the expression of JNK and phosphorylated JNK.After the cells were transiently transfected with dominant negative mutant of JNK (DN- JNK) followed by treatment of VES,the expression of JNK and c-Jun protein was determined. RESULTS:The apoptotic changes were observed after VES treatment by DNA fragmentation.DNA ladder in the 20 mg/L VES group was more clearly seen than that in 10 mg/L VES group and was not detected following treatment of UT control,succinate and vitamin E.VES at 5,10 and 20 mg/L increased the expression of p-JNK by 2.5-,2.8- and 4.2- fold,respectively.VES induced the phosphorylation of JNK beginning at 1.5 h and produced a sustained increase for 24 h with the peak level at 12 h.Transient transfection of DN-JNK blocked VES-triggered apoptosis by 52%.DN-JNK significantly increased the level of JNK,while decreasing the expression of VES-induced c-Jun protein. CONCLUSION:VES-induced apoptosis in human gastric cancer SGC-7901 cells involves JNK signaling pathway via c-Jun and its downstream transcription factor.

c-Jun N-terminal kinase is required for thermotherapyinduced apoptosis in human gastric cancer cells

AIM:To investigate the role of c-Jun N-terminal kinase(JNK) in thermotherapy-induced apoptosis in human gastric cancer SGC-7901 cells.METHODS:Human gastric cancer SGC-7901 cells were cultured in vitro.Following thermotherapy at 43 ℃ for 0,0.5,1,2 or 3 h,the cells were cultured for a further 24 h with or without the JNK specific inhibitor,SP600125 for 2 h.Apoptosis was evaluated by immunohistochemistry [terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)] and flow cytometry(Annexin vs propidium iodide).Cell proliferation was determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide.The production of p-JNK,Bcl-2,Bax and caspase-3 proteins was evaluated by Western blotting.The expression of JNK at mRNA level was determined by reverse transcription polymerase chain reaction.RESULTS:The proliferation of gastric carcinoma SGC-7901 cells was significantly inhibited following thermotherapy,and was 32.7%,30.6%,43.8% and 52.9% at 0.5,1,2 and 3 h post-thermotherapy,respectively.Flow cytometry analysis revealed an increased population of SGC790l cells in G0/G1 phase,but a reduced population in S phase following thermotherapy for 1 or 2 h,compared to untreated cells(P < 0.05).The increased number of SGC-790l cells in G0/G1 phase was consistent with induced apoptosis(flow cytometry) following thermotherapy for 0.5,1,2 or 3 h,compared to the untreated group(46.5% ± 0.23%,39.9% ± 0.53%,56.6% ± 0.35% and 50.4% ± 0.29% vs 7.3% ± 0.10%,P < 0.01),respectively.This was supported by the TUNEL assay(48.2% ± 0.4%,40.1% ± 0.2%,61.2% ± 0.29% and 52.0% ± 0.42% vs 12.2% ± 0.22%,P < 0.01) respectively.More importantly,the expression of p-JNK protein and JNK mRNA levels were significantly higher at 0.5 h than at 0 h post-treatment(P < 0.01),and peaked at 2 h.A similar pattern was detected for Bax and caspase-3 proteins.Bcl-2 increased at 0.5 h,peaked at 1 h,and then decreased.Furthermore,the JNK specific inhibitor,SP600125,suppressed p-JNK,Bax and caspase-3 at the protein level in SGC790l cells following thermotherapy,compared to mock-inhibitor treatment,which was in line with the decreased rate of apoptosis.The expression of Bcl-2 was consistent with thermotherapy alone.CONCLUSION:Thermotherapy induced apoptosis in gastric cancer cells by promoting p-JNK at the mRNA and protein levels,and up-regulated the expression of Bax and caspase-3 proteins.Bcl-2 may play a protective role during thermotherapy.Activation of JNK via the Bax-caspase-3 pathway may be important in thermotherapy-induced apoptosis in gastric cancer cells.

从“意境”到“译境”:基于翻译美学视域下的中译英歌词研究——以“Fairy Tale”为例

随着文化全球化的深入发展,中译英歌词翻译已经成为跨文化交流的一个重要领域。歌词翻译中如何协调“意境”(原歌曲传达的情感与美感)与“译境”(源语言与目标语言之间的差异)的平衡,依然是一个充满挑战与争议的问题。文章回顾了翻译美学的发展,强调其在跨文化交流中的作用,通过分析“Fairy Tale”的翻译实践,展示了如何在不同的美学层面上实现文化适应和情感表达。研究结果强调了翻译作为一种文化表达方式的重要性,提出将翻译美学应用于实际翻译工作中,以促进跨文化交流和理解。

RimJ-Catalyzed Sequence-Specific Protein N-Terminal Acetylation in <i>Escherichia coli</i>

In order to establish the sequence dependence of RimJ-mediated protein N-terminal acetylation in E. coli, the Z-domain variants differing by the second or third amino acid residue were expressed and analyzed by mass spectrometry. Only subsequent to the initiating methionine residue cleavage, the RimJ-catalyzed N-terminal acetylation mainly occurred at the N-terminal serine and threonine residues and was significantly enhanced by hydrophobic or negatively charged residues in the penultimate position.

c-Jun N-terminal kinase 3 deficiency protects axotomized retinal ganglion cells via affecting mitochondria involved apoptosis pathway

AIM: To illustrate the isoform-specific role and mechanism of c-Jun N-terminal kinases(JNKs) in mouse optic nerve axotomy induced neurotrauma. METHODS: We firstly investigated the expression of JNK1, JNK2, and JNK3 in the retinal ganglion cells(RGCs) by double-immunofluorescent staining. Then we created optic nerve axotomy model in wild type as well as JNK1, JNK2, JNK3, isoform specific gene deficiency mice. With that, we checked the protein expression profile of JNKs and its active form, and quantified the survival RGCs number by immunofluorescence staining. We further explored the molecules underlying isoform specific protective effect by real-time polymerase chain reaction(PCR) and Western blotting assay. RESULTS: We found that all the three isoforms of JNKs were expressed in the RGCs. Deficiency of JNK3, but not JNK1 or JNK2, significantly alleviated optic nerve axotomyinduced RGCs apoptosis. We further established that expression of Noxa, a pro-apoptotic member of BH3 family, was significantly suppressed only in JNK3 gene deficiency mice. But tumor necrosis factor receptor 1(TNFR1) and Fas, two key modulators of death receptor mediated apoptosis pathway, did not display obvious change in the expression. CONCLUSION: It is suggested that mitochondria mediated apoptosis, but not death receptor mediated apoptosis got involved in the JNK3 gene deficiency induced RGCs protection. Our study provides a novel insight into the isoform-specific role of JNKs in neurotrauma and indicates some cues for its therapeutics.

Elevated plasma levels of N-terminal pro-brain natriuretic peptide in patients with chronic hepatitis C during interferon-based antiviral therapy

AIM: To investigate plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), an established marker of cardiac function, in patients with chronic hepatitis C during interferon-based antiviral therapy. METHODS: Using a sandwich immunoassay, plasma levels of NT-proBNP were determined in 48 patients with chronic hepatitis C at baseline, wk 24 and 48 during antiviral therapy and at wk 72 during follow-up.RESULTS: Plasma NT-proBNP concentrations were significantly increased (P < 0.05) at wk 24, 48 and 72 compared to the baseline values. NT-proBNP concentrations at baseline and wk 24 were closely correlated (r = 0.8; P < 0.001). At wk 24, 7 (14.6%) patients had NT-proBNP concentrations above 200 ng/L compared to 1 (2%) patient at baseline (P = 0.059). Six of these 7 patients had been treated with high-dose IFN-α induction therapy. In multiple regression analysis, NT-proBNP was not related to other clinical parameters, biochemical parameters of liver disease or virus load and response to therapy.CONCLUSION: Elevated levels of NT-proBNP during and after interferon-based antiviral therapy of chronic hepatitis C may indicate the presence of cardiac dysfunction, which may contribute to the clinical symptoms observed in patients during therapy. Plasma levels of NT-proBNP may be used as a diagnostic tool and for guiding therapy in patients during interferon-based antiviral therapy.