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Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Shenzhen University Science & Engineering is the property of Editorial Department of Journal of Shenzhen University Science & Engineering and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Atomic & Molecular Physics (1000-0364) is the property of Journal of Atomic & Molecular Physics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In this paper, based on mass action kinetics and Michaelis-Menten equation, we built a theoretical model to study the activation of metastatic carcinogenic pathways induced by abnormal accumulation of insulin. Theoretical model considers that insulin regulates the AKT-MDM2-P53-PTEN signaling pathway by activating the PI3 K-AKT-mTOR signaling pathway, and the abnormal accumulation of insulin induces the activation of the JAK2/STAT5 metastatic carcinogenic pathway. We found that tyrosine phosphorylated STAT5 monomers are rapidly converted to STAT5 dimers during the signal transduction process of the JAK2/STAT5 pathway. As the abnormal accumulation of insulin increases, the expression levels of phosphorylated STAT5 dimers and tyrosine phosphorylated STAT5 dimers further increase. This indicates that abnormal insulin accumulation induces activation of the JAK2/STAT5 metastatic oncogenic pathway. Abnormal accumulation of insulin directly increases the expression of JAK2, which leads to an abnormal increase in the expression of AKT. It results in disorders of cellular glycogen metabolism. In the same time, the tumor suppressor effect of P53 protein reduces, promoting the occurrence and development of cancer. We also found, under the action of JAK2/STAT5 metastatic oncogenic signaling pathway, the tumor suppressor effect of miR-378 is significantly weakened, which also indicates the complexity of metastatic cancer. By analyzing the sensitivity of each parameter in the model, the sensitivity of the JAK2/STAT5 signaling pathway to the creation of carcinogenic microenvironment is determined. The theoretical results are consistent with the experiment, and can provide a reference for the design of treatment plans to inhibit metastatic cancer. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill kinetics and Michaelis - Menten equation, we built a theoretical model to study the influence of time delay and noise on Notch signal path dynamics. We found that in the time delay of Herl and Her7 gene transcription regulates the dynamics of the Notch signaling pathway to a large extent. Due to the time delay regulation, the Notch system dynamics undergoes Hopf bifurcation. The steady state is transformed into a periodic evolution characteristic. By investigating the noise effect of the Notch signal path, we also found that the periodic oscillation dynamics of the Notch system changes due to the disturbance of the noise. Under the condition of low noise amplitude, the altered periodic rhythm in the Notch signaling pathway can be balanced and restored by time delay, which shows that the time delay of Herl and Her7 transcription promotes the periodic oscillation of the Notch signaling pathway. In a strong noise environment, it is difficult for the time delay to regulate the change of Notch signal, and its signal path dynamics is largely affected by noise. The theoretical results are consistent with the experimental ones, and further reveal a regulatory mechanism of time delay and noise on the dynamics of the Notch signaling pathway, which can provide a theoretical basis for the design of pathway treatments to prevent various diseases and cancers caused by Notch dysfunction. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill dynamics and Michaelis-Menten equation, we built a theoretical model to study the mechanism of Hepatitis B virus (HBx) promoting the development of hepatocellular carcinoma (HCC) through interaction with CREB (cAMP-response element binding protein).The theoretical model takes the HBx-CPAP (centrosome P4.1 associated protein)-AKT (protein kinase B)-GSK3 (Glycogen Synthase Kinase3)-P53 pathway into consideration. We found that with the increase of CREB concentration (CREB concentration=0.01-0.05), HBx has amplification effect, which leads to the significant decrease of tumor suppressor function of P53. The overexpression of inflammatory factor (NF-κB) creates an inflammatory microenvironment. CREB also regulates the secondary growth of AKT and affects cell glycogen metabolism. These factors contribute to the occurrence and development of HCC. Our theoretical results are consistent with the experimental observations, and provide a fundamental understanding of the HBx promoting the development of HCC through interaction with CREB. The results provide a theoretical basis for designing treatment plans that blocks the transition of hepatitis to HCC. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill dynamics and Michaelis-Menten equation, we built a theoretical model tostudy the physical mechanism of VPRBP protein and Abl kinase inducing and inhibiting prostate cancer. We found that DNA damage quickly activates ATM and activates the up-regulation of p53. The subsequent damage of DNA damage will be largely inhibited by the up-regulation of p53 expression. VPRBP protein up-regulates MDM2, which makes the expression level of p53 abnormal. Thus, it is impossible to normalize the occurrence and development of prostate cancer. By investigating the role of Abl in the progression of prostate cancer, We also found that Ab1 down-regulates the expression level of AKT. Due to the inhibitory effect of Ab1 on AKT, which inhibits the expression level of MDM2 in the AKT signaling pathway, thereby stabilizing the expression of p53. This indicates that the deficient Ab1 can weaken the degree of inhibition of AKT. It not only makes cell metabolism disorder, but also promotes the abnormal expression level of p53 in the normal cycle and weakens the tumor suppression induced by DNA damage, and thus promotes the occurrence and development of prostate cancer. Based on the model in this paper, it can be predicted that VPRBP and Abl as regulators that induce and inhibit prostate cancer are more sensitive to existing and potential anti-cancer treatments. VPRBP and Abl, acting as a time delay effect in the process of inducing and inhibiting prostate cancer, can result in the increased accumulation of p53 and PTEN in the signal pathway and the decrease of AKT, as well as the Plk1 phase shift of periodic oscillations. It can be used to predict the cell cycle process aimed at blocking prostate cancer cells potential therapeutic effect. The results of this paper reveal a regulatory mechanism of VPRBP protein and Abl in the process of inducing and inhibiting prostate cancer. The theoretical results are consistent with experiments and can provide a theoretical basis for the design of treatment plans that block prostate cancer. [ABSTRACT FROM AUTHOR]

Based on Hill kinetics and Michaelis - Menten function, we investigate Nogo - Band JCAD inducing activation of hepatocellular carcinoma(HCC) gene. The theoretical model considers : (1) Nogo - B promotes the degradation of oxidized low density lipoprotein (ox LDL) by interacting with Autophagy - related 5 gene (ATG5), and the degraded oxLDL(DoxLDL) enhances the Yes - associated protein (YAP) activity in Hippo signaling pathway, which activates the expression of oncogenes(connective tissue growth factor (CTGF)) by promoting the production of a large amount of Lysopho - sphatidic acid (LPA); (2) JCAD interacts with large tumor suppressor homolog 2 (LATS2) to regulate phosphorylation of YAP. Dephosphorylated YAP activates tumor - related proliferation factors in the Hippo signaling pathway, in turn upregulating activation of YAP to promote HCC cell proliferation. We found that ox LDL degrades in a short time. The degradation of oxLD L promotes LPA largely, and then promotes the activation of YAP in Hippo signaling pathway. During this process, DoxLDL will quickly activate a large number of inactivated cascade path signals ( ( Lysophosphatidylcholine ( LPC), auto- taxin( ATX), LPA, etc. ), which activate expression of HCC gene. By analyzing the temporal evolutions of the levels of Nogo - B, it can be found that Nogo - Band ATG5 forms a complex NA. The ATG5 amplifies the signal of Nogo - B expression. It makes Nogo - B - enhanced activation expression, which promotes LPA production and activates YAP. A pulsed signal driven by the CEBPJ3 will also enhance the transcriptional activation of Nogo - B. The YAP and CTGF showed a steady state with the change of Nogo - B. This indicates further that oxLDL degradation induced by up - regulation of Nogo - B expression activates the stable oxLDL - Nogo - B - YAP - CTGF pathway. Hippo signaling is highly activated after ectopic Nogo - B expression. By analyzing the regulatory effects with the JACD and kinase LATS2, we found that JACD inhibits YAP phosphorylation, which greatly increases the expression level of CTGF. It is opposite to the effect of JCAD regulation, LATS2 promotes YAP phosphorylation, and then decreases the expression of CTGF and other proliferation factors. Our theoretical results are consistent with the experimental observations, and provide a fundamental understanding of the Non - alcoholic steatohepatitis ( NASH) inducing HCC [ABSTRACT FROM AUTHOR]

To observe the apoptosis rate of peripheral blood macrophages and the polarization level of macrophages M1/M2 in patients with normal coronary artery and patients with different types of coronary heart disease, and explore their significance. Methods Patients with stable angina (SA group), patients with unstable angina (UA group), patients with acute myocardial infarction (AMI group) and subjects with normal coronary artery (control group) were included, 40 cases for each group. General clinical data of all research subjects were collected, including gender, age, height, weight, body mass index (BMI), and alanine aminotransferase (ALT), serum creatinine (Scr), creatine kinase isoenzyme (CKMB), high-sensitivity troponin I (hs-TnI) within 48 hours after enrollment, and ejection fraction (EF) value from cardiac color Doppler ultrasound before discharge. Peripheral blood samples were collected from patients within 48 h after enrollment, and macrophages were isolated and cultured. Apoptosis rate of macrophages, proportion and ratio of M1 and M2 macrophages were detected, and the relationship between them and different types of coronary heart disease were analyzed. Logistic regression was used to analyze the effects of macrophage apoptosis rate and M1/M2 ratio on coronary heart disease and UA. Receiver operating characteristic (ROC) curve was used to analyze the apoptosis rate of macrophages, M1/M2 ratio and the predictive value of their combined application on coronary heart disease and UA. Results There were no significant differences in gender, age, height, body mass, BMI, ALT and Scr between the 4 groups. Compared with the control group, the SA group and the UA group, hs-TnI and CK-MB increased and EF decreased in the AMI group (P＜0.01). There were no significant differences in hs-TnI and CK-MB between the control group, the SA group and the UA group. There was no significant difference in EF between the UA group and the SA group, but which was lower than that of the control group (P＜ 0.01). The apoptosis rate of macrophages, the proportion of M1-type macrophages and the ratio of M1/M2 increased in the control group, the SA group, the UA group and the AMI group successively (P＜0.01). Logistic regression results showed that the increased M1/M2 ratio and apoptosis rate of macrophages were risk factors for coronary heart disease and UA. ROC analysis showed that the M1/M2 ratio and apoptosis rate of macrophages had certain diagnostic value for coronary heart disease, and the combined application had higher diagnostic value (AUC were 0.835, 0.898 and 0.926). The M1/M2 ratio and apoptosis rate had certain diagnostic value for UA, and the combined application had higher diagnostic value (AUC were 0.807, 0.796, 0.862). Conclusion The apoptosis rate of macrophages and M1/M2 ratio of macrophages are closely correlated with coronary heart disease and UA, and have certain predictive value. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill kinetics and Michaelis - Menten equation, we built a theoretical model to studyin the microenvironment of hepatocellular carcinoma( HCC), glycogen synthase kinase 3 (GSK3) - mediated insulin inhibition of glycogen metabolism, and P53 restores and regulates abnormal glycogen metabolism. We analyzed the influences of insulin activation of PI3K -AKT - mTOR signaling pathway on the circadian rhythm of GYS2 phosphorylation/dephosphorylation transition, and also investigated the restoration of circadian rhythm regulation of GYS2 phosphorylation/dephosphorylation transition by P53 through the AKT - MDM2 - P53 - PTEN signaling pathway. It was found that insulin activates and increases the expression level of AKT. As a result of the catalysis of AKT, GSK3 kinase is inhibited and weakened, which enhances the phosphorylation and inactivation of GYS2. In the case of l ow insulin concentration, the circadian rhythm of GYS2 dephosphorylation activation will be changed, which in tum changes the synthesis of GYS2 circadian rhythm. Under the condition of higher insulin concentration, the periodic oscillation of dephosphorylated GYS2 (dGYS2 ) over time will be greatly changed, and the synthesis of GYS2 circadian rhythm will be destroyed. Changing the expression level of P53, we found that P53 can significantly regulate and restore the abnormal circadian evolution of dGYS2 under conditions of lower and higher insulin concentrations. By the regulation of P53, the disordered dGYS evolves over time, with the increase or decrease of P53, the periodicity of the dGYS2 circadian rhythm is gradually restored. The theoretical results are consistent with the experiments. We further analyze the GSK3 - mediated insulin regulation mechanism of the circadian rhythm of GYS2 phosphorylation/dephosphorylation transition, and P53 s ability to regulate and restore abnormal GYS2 phosphorylation/dephosphorylation transition, which reveals a carcinogenic and anti-tumor mechanism of the occurrence and development of HCC. It can provide a theoretical basis for designing pathway treatment plan to block carcinogenic transformation. [ABSTRACT FROM AUTHOR]

In this paper, based on Hill dynamics and Michaelis - Menten equation, we built a theoretical model tostudy the physical mechanism of VPRBP protein and Ahl kinase inducing and inhibiting prostate cancer. We found that DNA damage quickly activates ATM and activates the up - regulation of p53. The subsequent damage of DNA damage will be largely inhibited by the up - regulation of p53 expression. VPRBP protein up - regulates MDM2, which makes the expression level of p53 abnormal. Thus, it is impossible to normalize the occurrence and development of prostate cancer. By investigating the role of Ahl in the progression of prostate cancer, We also found that Ahl down - regulates the expression level of AKT. Due to the inhibitory effect of Ahl on AKT, which inhibits the expression level of MDM2 in the AKT signaling pathway, thereby stabilizing the expression of p53. This indicates that the deficient Abl can weaken the degree of inhibition of AKT. It not only makes cell metabolism disorder, but also promotes the abnormal expression level of p53 in the normal cycle and weakens the tumor suppression induced by DNA damage, and thus promotes the occurrence and development of prostate cancer. Based on the model in this paper, it can be predicted that VPRBP and Abl as regulators that induce and inhibit prostate cancer are more sensitive to existing and potential anti - cancer treatments. VPRBP and Abl, acting as a time delay effect in the process of inducing and inhibiting prostate cancer, can result in the increased accumulation of p53 and PTEN in the signal pathway and the decrease of AKT, as well as the Plkl phase shift of periodic oscillations. It can be used to predict the cell cycle process aimed at blocking prostate cancer cells potential therapeutic effect. The results of this paper reveal a regulatory mechanism of VPRBP protein and Abl in the process of inducing and inhibiting prostate cancer. The theoretical results are consistent with experiments and can provide a theoretical basis for the design of treatment plans that block prostate cancer. [ABSTRACT FROM AUTHOR]