Sleepy Consensus in the Known Participation Model

We study sleepy consensus in the known participation model, where replicas are aware of the minimum number of awake honest replicas. Compared to prior works that almost all assume the unknown participation model, we provide a fine-grained treatment of sleepy consensus in the known participation model and show some interesting results. First, we present a synchronous atomic broadcast protocol with $5\Delta+2\delta$ expected latency and $2\Delta+2\delta$ best-case latency, where $\Delta$ is the bound on network delay and $\delta$ is the actual network delay. In contrast, the best-known result in the unknown participation model (MMR, CCS 2023) achieves $14\Delta$ latency, more than twice the latency of our protocol. Second, in the partially synchronous network (the value of $\Delta$ is unknown), we show that without changing the conventional $n \geq 3f+1$ assumption, one can only obtain a secure sleepy consensus by making the stable storage assumption (where replicas need to store intermediate consensus parameters in stable storage). Finally, still in the partially synchronous network but not assuming stable storage, we prove the bounds on $n \geq 3f+2s+1$ without the global awake time (GAT) assumption (all honest replicas become awake after GAT) and $n \geq 3f+s+1$ with the GAT assumption, where $s$ is the maximum number of honest replicas that may become asleep simultaneously. Using these bounds, we transform HotStuff (PODC 2019) into a sleepy consensus protocol via a timeoutQC mechanism and a low-cost recovery protocol

Morphoproteomic Evidence of Constitutively Activated and Overexpressed mTOR Pathway in Cervical Squamous Carcinoma and High Grade Squamous Intraepithelial Lesions

Human papilloma virus (HPV) infection of the uterine cervix is linked to the pathogenesis of cervical cancer. Preclinical in vitro and in vivo studies using HPV-containing human cervical carcinoma cell lines have shown that the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor, erlotinib, can induce growth delay of xenografts. Activation of Akt and mTOR are also observed in cervical squamous cell carcinoma and, the expression of phosphorylated mTOR was reported to serve as a marker to predict response to chemotherapy and survival of cervical cancer patients. Therefore, we investigated: a) the expression level of EGFR in cervical squamous cell carcinoma (SCC) and high-grade squamous intraepithelial lesions (HSIL) versus non-neoplastic cervical squamous epithelium; b) the state of activation of the mTOR pathway in these same tissues; and c) any impact of these signal transduction molecules on cell cycle. Formalin-fixed paraffin-embedded tissue microarray blocks containing 20 samples each of normal cervix, HSIL and invasive SCC, derived from a total of 60 cases of cervical biopsies and cervical conizations were examined. Immunohistochemistry was utilized to detect the following antigens: EGFR; mTOR pathway markers, phosphorylated (p)-mTOR (Ser2448) and p-p70S6K (Thr389); and cell cycle associated proteins, Ki-67 and S phase kinase-associated protein (Skp)2. Protein compartmentalization and expression were quantified in regard to proportion (0-100%) and intensity (0-3+). Mitotic index (MI) was also assessed. An expression index (EI) for pmTOR, p-p70S6K and EGFR, respectively was calculated by taking the product of intensity score and proportion of positively staining cells. We found that plasmalemmal EGFR expression was limited to the basal/parabasal cells (2-3+, EI = 67) in normal cervical epithelium (NL), but was diffusely positive in all HSIL (EI = 237) and SCC (EI 226). The pattern of cytoplasmic p-mTOR and nuclear p-p70S6K expression was similar to that of EGFR; all showed a significantly increased EI in HSIL/SCC versus NL (p<0.02). Nuclear translocation of p-mTOR was observed in all SCC lesions (EI = 202) and was significantly increased versus both HSIL (EI = 89) and NL (EI = 54) with p<0.015 and p<0.0001, respectively. Concomitant increases in MI and proportion of nuclear Ki-67 and Skp2 expression were noted in HSIL and SCC. In conclusion, morphoproteomic analysis reveals constitutive activation and overexpression of the mTOR pathway in HSIL and SCC as evidenced by: increased nuclear translocation of pmTOR and p-p70S6K, phosphorylated at putative sites of activation, Ser2448 and Thr389, respectively; correlative overexpression of the upstream signal transducer, EGFR, and increases in cell cycle correlates, Skp2 and mitotic indices. These results suggest that the mTOR pathway plays a key role in cervical carcinogenesis and targeted therapies may be developed for SCC as well as its precursor lesion, HSIL

Electronic Nose Feature Extraction Methods: A Review

Many research groups in academia and industry are focusing on the performance improvement of electronic nose (E-nose) systems mainly involving three optimizations, which are sensitive material selection and sensor array optimization, enhanced feature extraction methods and pattern recognition method selection. For a specific application, the feature extraction method is a basic part of these three optimizations and a key point in E-nose system performance improvement. The aim of a feature extraction method is to extract robust information from the sensor response with less redundancy to ensure the effectiveness of the subsequent pattern recognition algorithm. Many kinds of feature extraction methods have been used in E-nose applications, such as extraction from the original response curves, curve fitting parameters, transform domains, phase space (PS) and dynamic moments (DM), parallel factor analysis (PARAFAC), energy vector (EV), power density spectrum (PSD), window time slicing (WTS) and moving window time slicing (MWTS), moving window function capture (MWFC), etc. The object of this review is to provide a summary of the various feature extraction methods used in E-noses in recent years, as well as to give some suggestions and new inspiration to propose more effective feature extraction methods for the development of E-nose technology

A Novel Feature Extraction Approach Using Window Function Capturing and QPSO-SVM for Enhancing Electronic Nose Performance

In this paper, a novel feature extraction approach which can be referred to as moving window function capturing (MWFC) has been proposed to analyze signals of an electronic nose (E-nose) used for detecting types of infectious pathogens in rat wounds. Meanwhile, a quantum-behaved particle swarm optimization (QPSO) algorithm is implemented in conjunction with support vector machine (SVM) for realizing a synchronization optimization of the sensor array and SVM model parameters. The results prove the efficacy of the proposed method for E-nose feature extraction, which can lead to a higher classification accuracy rate compared to other established techniques. Meanwhile it is interesting to note that different classification results can be obtained by changing the types, widths or positions of windows. By selecting the optimum window function for the sensor response, the performance of an E-nose can be enhanced

Overexpression of the peroxidase gene ZmPRX1 increases maize seedling drought tolerance by promoting root development and lignification

Drought is a main abiotic stress factor hindering plant growth, development, and crop productivity. Therefore, it is crucial to understand the mechanisms by which plants cope with drought stress. Here, the function of the maize peroxidase gene ZmPRX1 in drought stress tolerance was investigated by measurement of its expression in response to drought treatment both in a ZmPRX1 overexpression line and a mutant line. The higher root lignin accumulation and seedling survival rate of the overexpression line than that of the wild type or mutant support a role for ZmPRX1 in maize drought tolerance by regulating root development and lignification. Additionally, yeast one-hybrid, Dule luciferase and ChIP-qPCR assays showed that ZmPRX1 is negatively regulated by a nuclear-localized ZmWRKY86 transcription factor. The gene could potentially be used for breeding of drought-tolerant cultivars

Morphoproteomic analysis reveals an overexpressed and constitutively activated phospholipase D1-mTORC2 pathway in endometrial carcinoma

The mammalian target of rapamycin (mTOR) assembles into two distinct complexes: mTOR complex 1 (mTORC1) is predominantly cytoplasmic and highly responsive to rapamycin, whereas mTOR complex 2 (mTORC2) is both cytoplasmic and nuclear, and relatively resistant to rapamycin. mTORC1 and mTORC2 phosphorylatively regulate their respective downstream effectors p70S6K/4EBP1, and Akt. The resulting activated mTOR pathways stimulate protein synthesis, cellular proliferation, and cell survival. Moreover, phospholipase D (PLD) and its product, phosphatidic acid (PA) have been implicated as one of the upstream activators of mTOR signaling. In this study, we investigated the activation status as well as the subcellular distribution of mTOR, and its upstream regulators and downstream effectors in endometrial carcinomas (ECa) and non-neoplastic endometrial control tissue. Our data show that the mTORC2 activity is selectively elevated in endometrial cancers as evidenced by a predominant nuclear localization of the activated form of mTOR (p-mTOR at Ser2448) in malignant epithelium, accompanied by overexpression of nuclear p-Akt (Ser473), as well as overexpression of vascular endothelial growth factor (VEGF)-A isoform, the latter a resultant of target gene activation by mTORC2 signaling via hypoxia-inducible factor (HIF)-2alpha. In addition, expression of PLD1, one of the two major isoforms of PLD in human, is increased in tumor epithelium. In summary, we demonstrate that the PLD1/PA-mTORC2 signal pathway is overactivated in endometrial carcinomas. This suggests that the rapamycin-insensitive mTORC2 pathway plays a major role in endometrial tumorigenesis and that therapies designed to target the phospholipase D pathway and components of the mTORC2 pathway should be efficacious against ECa

Multicentric hepatic EBV-associated smooth muscle tumors in an AIDS patient: a case report, investigation of mTOR activation and review of the literature

Epstein-Barr virus (EBV) - associated smooth muscle tumors (EBV-SMT) are a rare, recently recognized distinct group of mesenchymal tumors that develop exclusively in patients with immunosuppression. It is believed that tumorigenesis is, at least in part, through the activation of the Akt/mammalian target of rapamycin (mTOR) signal pathway. We describe the clinicopathologic and immunohistochemical features of a multifocal hepatic EBV-SMT in a 34-year-old acquired immunodeficiency syndrome (AIDS) patient and investigate the activation status of the mTOR signal pathway in this tumor. In addition, we provide a review of the literature on the clinicopathologic findings of hepatic EBV-SMT in adult AIDS patients, and discuss their biologies and possible therapeutic strategies