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As one of the security issues, privacy protection (PP) has become a research hotspot. The paper studies the synchronization problem of stochastic networks based on PP. First, a synchronization standard for stochastic network with delay is given based on PP. Second, a finite‐time (FnT) synchronization criterion for stochastic network without delay is given based on PP. The PP function of continuous time‐varying function is designed to mask the real state of the controlled complex network before converging to the real value in FnT and infinite time. Finally, the effectiveness of the method discussed in this article was verified through simulation examples. [ABSTRACT FROM AUTHOR]

Recently, many studies show that long non-coding RNAs (lncRNAs) play important roles in cancer biology. Although its expression was reported dysregulated during tumorigenesis, the contributions of lncRNAs to hepatocellular carcinoma (HCC) are still largely unknown. In particular, the lncRNA CARLo-5 has a functional role in cell-cycle regulation in colon cancer, while the clinical significance and biological function of CARLo-5 in HCC remain unelucidated. In order to fill those study blanks, the expression level of CARLo-5 in human HCC specimens was tested, and its correlation with clinicopathologic features as well as the prognosis for patients with HCC was analyzed. Additionally, MTT, wound healing and transwell assays were employed to investigate the biological function of CARLo-5. The results showed that CARLo-5 levels were significantly overexpressed in HCC tissues compared to ANLT. Besides, high expression of CARLo-5 was associated with liver cirrhosis ( P = 0.001), tumor number ( P < 0.001), vascular invasion ( P = 0.001), capsular formation ( P = 0.014) and Edmondson-Steiner grade ( P < 0.001), which proved that CARLo-5 was an independent risk factor for overall survival and disease-free survival. In addition, in highly metastatic HCC cell lines (HCCLM3 and MHCC97-L), CARLo-5 was up-regulated, but in lowly metastatic HCC cell lines (HepG2, SNU387), it showed down-regulated. Besides, by using gain and loss of function experiments in HCC cell lines (HCCLM3 and HepG2), the results showed that CARLo-5 overexpression significantly enhanced cell proliferation, migration and invasion in vitro. Our study also revealed that CARLo-5 was prominently up-regulated in HCC specimens and its high expression was associated with poor prognosis of HCC patients. Totally, those findings together indicate that CARLo-5 promotes proliferation and metastasis of HCC and potentially emerged as a novel therapeutic target. [ABSTRACT FROM AUTHOR]

This paper considers the first order consensus problem of multi-agent systems. A new kind of distributed control protocol is constructed for achieving distributed consensus. Based on linear matrix inequalities and the Lyapunov function method, the sufficient conditions for the achievement of the distributed consensus are obtained. Illustrative examples are provided to show the effectiveness of this method. [ABSTRACT FROM AUTHOR]

This paper discusses some basic dynamical properties of the chaotic finance system with parameter switching perturbation, and investigates chaos projective synchronization of the chaotic finance system with the time-varying delayed feedback controller, which are not fully considered in the existing research. Different from the previous methods, in this paper, the delayed feedback controller is not only time-varying, but also the time-varying delay is adaptive. Finally, an illustrate example is provided to show the effectiveness of this method. [ABSTRACT FROM AUTHOR]

This paper investigates the problem of two kinds of function projective synchronization of financial chaotic system with definite integration scaling function, which are not fully considered in the existing research. Different from the previous methods, in this paper, the following two questions are investigated: (1) two kinds of the definite integration scaling function projective synchronization are given; (2) the upper and lower limit of the definite integral scaling function are the bound dynamical systems. Finally, illustrative example is provided to show the effectiveness of this method. [ABSTRACT FROM AUTHOR]

Abstract: This paper investigates adaptive synchronization for dynamical networks of neutral type with time-delay. In comparison with those of the existing synchronization of dynamical networks of neutral type with time-delay, we assume that the given neutral type expression can be linear function, nonlinear function, or even any elementary transformation. Based on the Lyapunov stability theorem, the adaptive control law is derived to make the state of two dynamical networks of neutral type synchronized. Some numerical are also given to show the effectiveness of the proposed method. [Copyright &y& Elsevier]

Background and Aims: Lenvatinib is a first‐line drug commonly used in the treatment of advanced hepatocellular carcinoma (HCC). However, its clinical efficacy is very limited due to drug resistance. Therefore, there is a great need to explore its combination with other agents to achieve better therapeutic effects. Metformin has been demonstrated to show an anti‐cancer effect. This study aimed to investigate the combined effect of lenvatinib with metformin in HCC cells both in vitro and in vivo and elucidate the possible molecular mechanisms. Methods: Flow cytometry, colony formation, CCK‐8 and transwell assays were used to study the effect of Lenvatinib–Metformin combination on the malignant behaviour of HCC cells in vitro. Constructing an animal model of tumour‐bearing to study the effect of combined drugs on HCC in vivo. Western blot experiments were performed to assess the relationship between AKT and FOXO3 and the cellular translocation of FOXO3. Results: Our results suggested that Lenvatinib and Metformin synergistically inhibited HCC growth and motility. Mechanistically, the combination of Lenvatinib and Metformin synergistically suppressed the activation of the AKT signalling pathway, which in turn reduced the phosphorylation level of downstream effector FOXO3 and induced its nuclear aggregation. In vivo studies further confirmed the synergistic suppression of lenvatinib with metformin in HCC growth. Conclusion: The Lenvatinib–Metformin combination may provide a potential therapeutic strategy to improve the prognosis of HCC patients. [ABSTRACT FROM AUTHOR]

This paper investigates the bounded scaling function projective synchronization of uncertain chaotic systems using adaptive finite-time control. Based on finite-time control and inequality principle, the new adaptive finite-time controller is designed to achieve two chaotic systems scaling function projective synchronized, and uncertain parameters of chaotic systems are also identified. Moreover, in comparison with those of the existing scaling function synchronization, the given scaling function can be more complex bounded functions. Some numerical are also given to show the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

In this paper, the impulsive synchronization problem of Lü chaotic systems is investigated by using a novel hybrid controller. The proposed hybrid controller is composed of a single controller and impulsive controller. Using the impulsive theory and the novel hybrid controller, some sufficient conditions are derived for the synchronization of Lü chaotic systems. Numerical simulation example is provided to verify the effectiveness of the proposed approach. The simulation results show that the proposed control scheme has a fast convergence rate compared with the conventional single controller method and impulsive controller method. [ABSTRACT FROM AUTHOR]

As the COVID-19 outbreak has an impact on the global economy, there will be interest in how China's financial markets function during the outbreak. To investigate the path of risk contagion in China's financial sub-markets before and after the COVID-19 outbreak, we divided the 2016–2021 period into two phases. Based on the time of the COVID-19 outbreak, we divided the new stage of economic development into pre-epidemic and post-epidemic stages and employed the DCC-GARCH model to investigate the dynamic correlation coefficients among the financial sub-markets in China. Furthermore, we employed complex network theory and the minimum tree model to describe the risk contagion path between two-stage Chinese financial submarkets. Finally, we provided pertinent recommendations for investors and policymakers and conducted a brief discussion based on the findings of the research. [ABSTRACT FROM AUTHOR]

Since the speed that the $p$ th moment of an output signal norm tends to 0 can be used to measure the quality of the output signal, the stability of the $p$ th moment of complex networks has been widely concerned. This article studies fixed-time synchronization in the $p$ th moment for time-varying delay stochastic multilayer networks, where fixed-time synchronization of multilayer networks is realized by using nonlinear feedback or delay feedback, and the concrete expression of fixed settling time is evaluated. Compared with some existing fixed-time control methods, the optimal combination relationship between the exponential power of fixed-time controllers and the $p$ th moment is given, and the designed controllers are continuous function. Finally, the effectiveness of the method is verified by numerical simulations. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to evaluate the potential utility of [68Ga]Ga-FAPI-04 PET/CT for diagnosing primary and metastatic lesions in patients with liver cancer, as well as to compare it with contrast-enhanced CT (CE-CT), liver MRI, and [18F]-FDG PET/CT. Methods: We performed a single-center post hoc retrospective analysis of data obtained from a prospective parent study (NCT04416165). This study included 34 patients diagnosed with or suspected hepatic lesions who underwent concomitant [68Ga]Ga-FAPI-04 and [18F]-FDG/CT scans. Moreover, these patients underwent liver MRI (n = 34) and CE-CT (n = 25). Histopathologic (n = 62) or radiographic follow-up (n = 128) served as the reference standard for the final diagnosis. Results: Among the 34 patients, 20, 12, and 2 patients presented with hepatocellular carcinomas, intrahepatic cholangiocarcinomas, and benign hepatic nodules, respectively. The sensitivities of CE-CT, MRI, [68Ga]Ga-FAPI-04, and [18F]-FDG/CT for detecting primary liver tumors were 96%, 100%, 96%, and 65%, respectively. Regarding the diagnosis of all intrahepatic lesions, the per-lesion detection rate of [68Ga]Ga-FAPI-04 PET/CT was slightly lower than that of MRI (85% vs. 100%, P = 0.34) and significantly higher than that of [18F]-FDG PET/CT (85% vs. 52%, P < 0.001). Regarding the diagnosis of all malignant lesions (including extrahepatic disease), the tumor detection rate of [68Ga]Ga-FAPI-04 PET/CT was 87.4%, which was significantly higher than that of [18F]-FDG PET/CT (65.0%, P < 0.001). Conclusions: Our findings indicate that the sensitivity of [68Ga]Ga-FAPI-04 PET/CT to correctly identify primary liver tumors and metastatic lesions is equivalent to that of CE-CT and liver MRI. Moreover, [68Ga]Ga-FAPI-04 PET/CT is better at identifying liver lesions than [18F]-FDG PET/CT, and its use may improve tumor staging, recurrence detection, and implementation of necessary treatment modifications. [ABSTRACT FROM AUTHOR]

Purpose: We evaluated the potential usefulness of [68Ga]Ga-DOTA-FAPI-04 positron emission tomography/computed tomography (PET/CT) for the diagnosis of primary and metastatic lesions in various types of cancer, compared with [18F] FDG PET/CT. Methods: A total of 75 patients with various types of cancer underwent contemporaneous [68Ga]Ga-DOTA-FAPI-04 and [18F] FDG PET/CT either for an initial assessment or for recurrence detection. Tumour uptake was quantified by the maximum standard uptake value (SUVmax). The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy of [18F] FDG and [68Ga]Ga-DOTA-FAPI-04 PET/CT were calculated and compared to evaluate the diagnostic efficacy. Results: The study cohort consisted of 75 patients (47 males and 28 females; median age, 61.5 years; age range, 32–85 years). Fifty-four patients with 12 different tumour entities underwent paired [68Ga]Ga-DOTA-FAPI-04 and [18F] FDG PET/CT for initial assessment, while the other 21 patients underwent paired scans for recurrence detection. [68Ga]Ga-DOTA-FAPI-04 PET/CT was able to clearly identify 12 types of malignant tumours with favourable tumour-to-background contrast, which resulted in a higher detection rate of primary tumours than did [18F] FDG PET/CT (98.2% vs. 82.1%, P = 0.021). Meanwhile, [68Ga]Ga-DOTA-FAPI-04 PET/CT showed a better sensitivity than [18F] FDG PET/CT in the detection of lymph nodes (86.4% vs. 45.5%, P = 0.004) and bone and visceral metastases (83.8% vs. 59.5%, P = 0.004). Conclusion: [68Ga]Ga-DOTA-FAPI-04 PET/CT showed a superior diagnostic efficacy than [18F] FDG PET/CT for the diagnosis of primary and metastatic lesions in patients with various types of cancer, especially in identifying liver metastases, peritoneal carcinomatosis, and brain tumours. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) has emerged as one of the most common malignancies worldwide. It is associated with a high mortality rate, as evident from its increasing incidence and extremely poor prognosis. The deubiquitinating enzyme 26S proteasome non-ATPase regulatory subunit 14 (PSMD14) has been reported to act as an oncogene in several human cancers. The present study aimed to reveal the functional significance of PSMD14 in HCC progression and the underlying mechanisms. We found that PSMD14 was significantly upregulated in HCC tissues. Overexpression of PSMD14 correlated with vascular invasion, tumor number, tumor recurrence, and poor tumor-free and overall survival of patients with HCC. Knockdown and overexpression experiments demonstrated that PSMD14 promoted proliferation, migration, and invasion in HCC cells in vitro, and facilitated tumor growth and metastasis in vivo. Mechanistically, we identified PSMD14 as a novel post-translational regulator of GRB2. PSMD14 inhibits degradation of GRB2 via deubiquitinating this oncoprotein in HCC cells. Furthermore, pharmacological inhibition of PSMD14 with O-phenanthroline (OPA) suppressed the malignant behavior of HCC cells in vitro and in vivo. In conclusion, our findings suggest that PSMD14 could serve as a novel promising therapeutic candidate for HCC. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is associated with high metastatic potential and high mortality. Accumulating evidence has demonstrated that speckle-type POZ protein (SPOP) is a key adaptor molecule of ubiquitination. However, the molecular mechanism of SPOP-mediated ubiquitination in HCC metastasis remains obscure. In the present study, our results indicated that SPOP expression was significantly downregulated in HCC and was associated with tumor size, differentiation and metastasis. Cox regression model showed that low SPOP expression was a risk factor related to the prognosis of HCC patients. Loss- and gain-of-function assays demonstrated that SPOP inhibited HCC cell migration and invasion in vitro . Mechanisitically, co-immunoprecipitation and ubiquitination assays revealed that SPOP recognized and bound SENP7 and promoted its degradation via ubiquitin-dependent proteolysis. Analysis of immunohistochemistry showed that vimentin expression was correlated negatively with SPOP and positively with SENP7. These results implied that increased degradation of SENP7 by overexpression of SPOP decreased vimentin levels, which in turn attenuated HCC cell metastasis. Moreover, in vivo assays showed that SPOP overexpression also significantly suppressed liver and lung metastases. In summary, SPOP inhibits HCC cell metastasis via ubiquitin-dependent SENP7 proteolysis and may thus serve as a new opinion for the prevention of HCC metastasis. [ABSTRACT FROM AUTHOR]

This paper is concerned with finite-time synchronization for a class of the complex dynamical network with non-derivative and derivative coupling. Different from the existing related results, a new finite-time synchronization theory is proposed to investigate finite-time synchronization of the complex dynamical network with non-derivative and derivative coupling, several new and effective criteria are derived to realize synchronization in finite time of the addressed complex dynamical network with non-derivative and derivative coupling. Finally, some numerical examples are provided to verify the theoretical results established in this paper. [ABSTRACT FROM AUTHOR]

L4949 --> Purpose: Hepaotocellular carcinoma (HCC) is one of the most lethal human malignancies. The majority of HCC patients are diagnosed at an advanced stage, leading to systemic therapy as the primary treatment. However, lack of efficacious approaches and resistance to cytotoxic chemotherapy result in low survival rate among these patients. Therefore, exploiting novel and efficacious therapies is impervious. This study aims to determine whether β‐Lapachone (β‐Lap) could be a potential chemotherapeutic agent for HCC. Experimental Design: We firstly analyzed the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1) and Catalase (CAT) in HCC patients using data from The Cancer Genome Atlas (TCGA), then examined their expression levels in our collected clinical patient samples and cell lines. Cell cytotoxicity and mechanism of of ß‐Lap were evaluated in wild type HCC cell line cells, stable NQO1 overexpression and knockout of SK‐HEP‐1 and PLC/PRF/5 cells, respectively. Preclinical therapeutic efficacious of ß‐Lap was finally validated in subcutaneous and orthotopic xenograft in vivo. Results: Concomitant high NQO1 and low CAT levels were observed in HCC patient samples, offering an ideal target for NQO1 bioactivatable drug β‐Lap. Treatment of β‐Lap hold great promise in NQO1‐selective killing of HCC cells, causing ROS accumulation and PARP1 hyperactivation, together with a greatly decrease of NAD+ and ATP levels and an increase of double‐strand break (DSB) lesions over time in vitro. Administration of β‐Lap in orthotopic xenograftin vivo, as well as subcutaneous, significantly inhibited tumor growth and prolonged mice survival. Conclusions: Our data suggest that NQO1 is an ideal potential biomarker and NQO1:CAT is a therapeutic window for NQO1 bioactivatable drugs in HCC and offers preclinical proof‐of‐concept for β‐Lap as a promising new chemotherapeutic agent for NQO1‐postive HCC patients regardless of oncogenic driver or passenger mutations. [ABSTRACT FROM AUTHOR]

Retinoid X receptor alpha (RXRα), a nuclear receptor of transcription factor, controls various physiological and pathological pathways including cellular growth, proliferation, differentiation, and apoptosis. Here, we report that RXRα is phosphorylated at its N-terminal A/B domain by cyclin-dependent kinase 1 (Cdk1) at the onset of mitosis, triggering its translocation to the centrosome, where phosphorylated-RXRα (p-RXRα) interacts with polo-like kinase 1 (PLK1) through its N-terminal A/B domain by a unique mechanism. The interaction promotes PLK1 activation, centrosome maturation, and mitotic progression. Levels of p-RXRα are abnormally elevated in cancer cell lines, during carcinogenesis in animals, and in clinical tumor tissues. An RXRα ligand XS060, which specifically inhibits p-RXRα/PLK1 interaction but not RXRα heterodimerization, promotes mitotic arrest and catastrophe in a tumor-specific manner. These findings unravel a transcription-independent action of RXRα at the centrosome during mitosis and identify p-RXRα as a tumor-specific vulnerability for developing mitotic drugs with improved therapeutic index. • Cdk1 phosphorylation of RXRα induces its translocation to centrosome during mitosis • Centrosomal RXRα modulates mitosis by interacting with PLK1 • Cdk1-phosphorylated RXRα confers tumor cells with vulnerability to RXRα inhibitors • An RXRα ligand promotes mitotic catastrophe by inhibiting p-RXRα/PLK1 interaction Xie and Zhou et al. report a transcription-independent function of RXRα. Upon phosphorylation by Cdk1 at the onset of mitosis, RXRα translocates to the centrosome, where it interacts with PLK1 to promote centrosome maturation and mitotic progression. The authors also identify Cdk1-phosphorylated RXRα as a tumor-specific vulnerability to an RXRα inhibitor. [ABSTRACT FROM AUTHOR]

Background: CDK5, an atypical member of the CDK family, play a significant role in the tumorigenesis of multiple organ, but CDK5 and its substrates in genesis and development of HCC is still unclear. Methods: Expression of CDK5 in HCC tumor and paired adjacent noncancerous tissues from 90 patients were measured by Western blotting, immunohistochemistry, and real-time PCR. The role of CDK5 in cell function and tumorigenesis was explored in HCC cell lines, ex vivo xenografts and diethylnitrosamine induced HCC model. Furthermore, comparative phosphoproteomic screening identified the oncoprotein TPX2 as a new substrate of CDK5. We also identified the effect of CDK5/P25 interaction blocker tamoxifen on HCC cell growth and migration. Results: CDK5 was increased in HCC tisues and the level of CDK5 was correlated with the severity of HCC based on patient recurrence and 5-year fatality rate. Exogenously expressed CDK5 but not kinase-dead CDK5 promoted proliferation, migration, and invasion of HCC cells. Functional ablation of CDK5 significantly inhibited the exacerbation of HCC cells. Xenograft implantation of HCC cells overexpressing CDK5 promoted tumorigenesis, and genetic knockdown of CDK5 reduced HCC growth and metastasis in vivo. More importantly, heterozygous knockout CDK5 (Cdk5+/−) attenuated HCC tumorigenesis induced by diethylnitrosamine. CDK5-mediated phosphorylation of TPX2 at serine 486 promoted its protein stability. TPX2 silence could restore HCC cell migration capability with overexpression CDK5. Treatment with tamoxifen inhibited cell growth and migration of HCC, demonstrating the role of active CDK5 in HCC. Conclusions: Our results suggest activation of CDK5 is associated with HCC tumorigenesis. CDK5-mediated phosphorylation and stabilization of TPX2 promotes hepatocellular proliferation and tumorigenicity. [ABSTRACT FROM AUTHOR]