gebhart/patrepeval huggingface dataset:
Synergistic effect of cytokines EPO, IL-3 and SCF on the proliferation, differentiation and apoptosis of erythroid progenitor cells. (2007)

Erythroblasts were obtained from murine spleen. After cultured for 12 hr, the cells were divided into four groups with the use of the following cytokines in culture: EPO, EPO+SCF, EPO+IL-3, and EPO+IL-3+SCF. Cell proliferation assay was done. Apoptosis rates were obtained by using a flow cytometer. Mitochondrial membrane potential (MMP) was assessed in flow cytometry (FCM) by labeling with rhodamine 123. Mitochondrial enzyme activity (MEA) was evaluated with MTT colorimetric assay. The cells were labeled with Fluo-3/Am Ester and Ca(2+) concentration was measured. The expression of Bax mRNA and Bcl-2 mRNA was analyzed by RT-PCR. At same time, the expression of Bax and Bcl-2 was analyzed by western blotting. Our results showed that IL-3 and SCF have synergistic effects with EPO on the proliferation, differentiation and apoptosis of erythroid progenitors.
A Topology Control Algorithm for Effective Power Efficiency and Throughput for Wireless Mesh Networks (2008)

Wireless mesh networks (WMNs) have become a better alternative for extending wireless Local Area Networks (WLANs) to provide network coverage up to the furthest of far flung rural areas. This has been implemented by using a meshed backbone network interconnecting the mesh access points (MAPs) that manages each of the WLANs. The routing algorithms use the mesh backbone to establish inter-WLAN routes which are subsequently used by the distantly distributed mesh clients to communicate in a multihop fashion. In this work, a fully scalable power-efficient localized distributed topology control algorithm is proposed to effectively construct such a meshed backbone network of access points. The performance of the algorithm is evaluated via several simulations carried out in the NS-2 simulation environment. The resultant network topology is shown to have (1) reduced average node degree which leads to reduced traffic interference, (2) increased throughput and (3)increased network lifetime.
Processor allocation in parallel battlefield simulation (1992)

Load balancing is a critical issue for exploiting the parallelism in any application and, particularly, in battlefield simulation where the computational load dynamically changes with both time and space. Domain decomposition is an effective means to balance the load distribution in battlefield simulation. However, finer domain decompositions that lead to better load balance incur heavier communication overhead. Earlier attempts in parallelizing battlefield sinlulation have traded load balance in favor of low con~-munication overhead. In this paper, we present three parallel battlefield simulators, implemented on Intel's iPSC/2 and BBN Butterfly GP-1OOO multicomputers, with finer domain decomposition and address the communication overhead problem by processor allocation strategies that suit the underlying architecture of the machine, On the shared-memory BBN Butterfly, the strategy leads to a new parallel battlefield simulation with dynamic load balancing. Execution times of these simulators are provided, which show that the communication overhead is tolerable.
A secure Email gateway (building an RCAS external interface) (2002)

Fielding secure computer systems requires tradeoffs between functionality, flexibility, and security to meet the users' needs. Multilevel secure (MLS) computer systems provide better control over classified information than traditional systems and allow users from a diverse population access to information they need while protecting sensitive data. Users want the functionality of non-MLS computer systems; graphical user interfaces, a rich assortment of software, and electronic connectivity with other systems. Compartmented mode workstations (CMW) can provide such an environment. An overview of secure system architectures and an example MLS network provide the framework for discussing the risks associated with interconnecting MLS systems and unclassified networks, and approaches for mitigating those risks. A secure Email gateway, using a high-assurance (AI) network component, provides the necessary safeguards for protecting the MLS network from external attacks.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
Matrix Ductility and Toughening of Epoxy Resins (1989)

Epoxy resins can be modified by a number of reagents to produce solids that possess a variety of mechanical properties. Some of these reagents lead to the formation of two-phase structures that are much tougher than single-phase epoxies. Toughness depends largely on the physical and geometric properties of the separated phase. However, the properties of the rigid epoxy matrix are equally important, because the plastic processes responsible for toughening take place within the matrix. The ductility of epoxies can be varied in several ways. Some of them and the consequences for fracture resistance are considered in this chapter.
p53 gene therapy in a rat model of hepatocellular carcinoma: intra-arterial delivery of a recombinant adenovirus. (1998)

p53 tumor suppressor gene therapy has been proposed for cancers characterized by inactivation of p53 function, and successful therapy will require efficient strategies for gene delivery. To maximize transgene expression in tumors, a clinical strategy has been proposed to treat neoplasms in the liver via hepatic artery administration of a recombinant adenovirus encoding wild-type p53 (rAd-p53). We have developed a syngeneic rat model using a p53mut hepatocellular carcinoma cell line (McA-RH7777) that results in multifocal liver tumor nodules to provide experimental support for this strategy. Treatment of McA-RH7777 cells with rAd-p53 in vitro resulted in efficient transgene expression, growth suppression, and apoptosis. Intrahepatic artery dosing with rAd-p53 or an adenovirus encoding beta-galactosidase (rAd-betagal) increased transgene expression in tumor tissue and decreased systemic exposure when compared with i.v. dosing. Daily hepatic artery dosing of rAd-p53 suppressed tumor growth when compared with untreated rats or animals treated with rAd-betagal. These data demonstrate the potential for arterial gene delivery to tumors using recombinant adenoviruses, and support continued investigation of rAd-p53 gene therapy for liver malignancies.
An efficient method for loading indium-111 into liposomes using acetylacetone. (1982)

The efficient loading of high levels of In-111 into the inner aqueous compartment of liposomes can be achieved using a water-soluble lipophilic chelate, acetylacetone. The loading method involves the incubation of the acetylacetone-In-111 complex with liposomes entrapping 1mM nitrilotriacetic acid. The loading process is carried out in isotonic saline, 10 mM Tris-HCI, pH 7.6, at room temperature. Results indicate that In-111 ions are concentrated in the internal aqueous compartment of liposomes by acetylacetone, which mediates the transport of In-111 ions across the outermost lipid bilayer of liposomes, permitting subsequent transfer to the encapsulated nitrilotriacetic acid. As much as 90% of the acetylacetone-chelated In-111 becomes internalized in the aqueous compartment of liposomes and bound by entrapped nitrilotriacetic acid. Using liposomes made from bovine brain shingomyelin/cholesterol, our results indicate that the loaded liposomes retain the entrapped internally bound In-111 even after incubation with serum at 37 degrees C for 24 hr.
Molecular basis of cellular response to cisplatin chemotherapy in non-small cell lung cancer (Review) (2004)

Cisplatin is one of the most potent anticancer agents, displaying significant clinical activity against a variety of solid tumors. For more than two decades, the most effective systemic chemotherapy for non-small cell lung cancer (NSCLC), the leading cause of cancer morbidity and mortality among men and women in the western world, was cisplatin-based combination treatment. Unfortunately, the outcome of cisplatin therapy on NSCLC seems to have reached a plateau. Therefore, the biological mechanisms of cisplatin action need to be understood in order to overcome the treatment plateau on NSCLC. Moreover, the development of resistance is a hurdle in the use of this drug. The molecular mechanisms that underlie this chemoresistance are largely unknown. Possible mechanisms of acquired resistance to cisplatin include reduced intracellular accumulation of cisplatin, enhanced drug inactivation by metallothionine and glutathione, increased repair activity of DNA damage, and altered expression of oncogenes and regulatory proteins. In addition, it is generally accepted that cytotoxicity of cisplatin is mediated through induction of apoptosis and arrest of cell cycle resulting from its interaction with DNA, such as the formation of cisplatin-DNA adducts, which activates multiple signaling pathways, including those involving p53, Bcl-2 family, caspases, cyclins, CDKs, pRb, PKC, MAPK and PI3K/Akt. Increased expression of anti-apoptotic genes and mutations in the intrinsic apoptotic pathway may contribute to the inability of cells to detect DNA damage or to induce apoptosis. Towards an understanding of the molecular basis of the cellular response to cisplatin-based chemotherapy in NSCLC, in this review we provide some insights into the pathways involved in cisplatin damage from entering the cells to execution of apoptosis or survival of NSCLC cells. We believe that as more and more molecular mechanisms of response to cisplatin-based therapy are unraveled, this knowledge should provide a basis for further studies to improve our understanding of molecular events associated with lung NSCLC as well as to devise novel and effective therapeutic approaches to overcome the treatment plateau or reverse drug resistance in this disease.
Interrelations of Oxygen Concentration, Fish Density, and Performance of Atlantic Salmon in an Ozonated Water Reuse System (1988)

Abstract In a 16-week study, we stocked duplicate groups of 3.3-g Atlantic salmon (Salmo salar) in 25-fish increments (25 to 100 fish/6.5-L jar) and in 250-fish increments (250 to 1,000 fish/144-L trough), in an ozonated, 100% closed water reuse system, to examine changes in fish performance in response to rearing at different densities and loadings within the system. Maximum rearing density (kg!m3) reached 219 in jars and 125 in troughs. Maximum loading (ratio of fish weight to water flow) reached 0.45 kg/(L/min) in jars, and 0.79 kg/(L/min) in troughs. A rise in water temperature from 18.9 to 21°C during weeks 11 and 12 was accompanied by a drop in effluent dissolved oxygen (DO), followed by an increase in mortality and a decline in biweekly weight gain. Later declines in water temperature to 18.4°C, and reductions in biomass, were followed by reduced mortality and increased weight gain. In both jars and troughs, mortality increased when dissolved oxygen dropped to 6.5 mg/L or lower, water temperature reached 19.6°C, and biomass reached 50–75 kg/m3, or 0.1–0.2 kg/(L/min) flow. Changes in DO, weight gain, and mortality per unit change in density (kg biomass/m3), were lower in jars than in troughs, but changes in these responses in terms of flow (kg/[L/min]) were lower in troughs. Results of this study suggest that, for optimum growth, survival, and feed conversion of Atlantic salmon in an ozonated water reuse system, dissolved oxygen should be at least 6.5 mg/L. Maintenance of an acceptable level of oxygen should minimize detrimental effects offish density or elevated water temperature.
Rapid, single-step purification of restriction endonucleases on Cibacron Blue F3GA-agarose (1978)

After sonication and high-speed centrifugation, crude extracts of B. amyloliquefaciens, P. alcalifaciens, X. holicola, and B. globiggi were adsorbed on the dye Cibacron blue F3GA convalently cross-linked to agarose. The restriction endonucleases BamHI, PalI, XhoI, and BglI together with BglII were isolated by elution of the dye column with linear gradients to 0.5 M NaCl. The enzymes so purified were free of contaminating nucleic acids and other nucleases and were sufficiently concentrated for direct, specific DNA hydrolysis.
Monocyte chemotactic protein-2, monocyte chemotactic protein-3, and fibroblast-induced cytokine. Three new chemokines induce chemotaxis and activation of basophils. (1994)

Cytokine-dependent mediator release from basophils and mast cells may play an important role in the pathogenesis of allergic and inflammatory conditions. Many C-C chemokines have been found to activate basophils and mast cells. We investigated the effect of three newly identified C-C chemokines, monocyte chemotactic protein-2 and -3 (MCP-2, MCP-3) and fibroblast-induced cytokine (FIC) on basophils and mast cells. We found that all three cytokines induced histamine secretion from basophils in a dose-dependent manner. The secretion of histamine was a Ca(2+)-dependent process. MCP-3 was the most potent activator of basophils. MCP-3 and FIC activated basophils from all study subjects, whereas the histamine release by MCP-2 was donor-dependent. The histamine-releasing activity of MCP-2, MCP-3, and FIC was compared with that of MCP-1, RANTES, and macrophage inflammatory protein-1 alpha using basophils from 10 donors. MCP-1 was the most potent among all the C-C chemokines. However, MCP-3 was nearly as potent. MCP-2, MCP-3, and FIC induced significant chemotaxis of basophils. None of the cytokines activated mouse peritoneal mast cells. The synthesis of mRNA for MCP-3 was investigated by reverse-transcription PCR using allergen-stimulated PBMC and bronchoalveolar lavage cells. Both MNC and bronchoalveolar lavage cells expressed mRNA for MCP-3. The results of this study indicate that MCP-2, MCP-3, and FIC are novel histamine-releasing factors.
Potential Organ- or Tumor-Imaging Agents. 14. Myocardial Scanning Agents (1973)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTPotential Organ- or Tumor-Imaging Agents. 14. Myocardial Scanning AgentsR Counsell, Terry Yu, V Ranade, and A BuswinkCite this: J. Med. Chem. 1973, 16, 9, 1038–1040Publication Date (Print):September 1, 1973Publication History Published online14 August 2003Published inissue 1 September 1973https://pubs.acs.org/doi/10.1021/jm00267a601https://doi.org/10.1021/jm00267a601research-articleACS PublicationsRequest reuse permissionsArticle Views28Altmetric-Citations6LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
IoT device ﬁngerprinting with sequence-based features (2018)

Exponential growth of Internet of Things complicates the network management in terms of security and device troubleshooting due to the heterogeneity of IoT devices. In the absence of a proper device identification mechanism, network administrators are unable to limit unauthorized accesses, locate vulnerable/rogue devices or assess the security policies applicable to these devices. Hence identifying the devices connected to the network is essential as it provides important insights about the devices that enable proper application of security measures and improve the efficiency of device troubleshooting. Despite the fact that active device fingerprinting reveals in depth information about devices, passive device fingerprinting has gained focus as a consequence of the lack of cooperation of devices in active fingerprinting. We propose a passive, feature based device identification technique that extracts features from a sequence of packets during the initial startup of a device and then uses machine learning for classification. Proposed system improves the average device prediction F1-score up to 0.912 which is a 14% increase compared with the state-of-the-art technique. In addition, We have analyzed the impact of confidence threshold on device prediction accuracy when a previously unknown device is detected by the classifier. As future work we suggest a feature-based approach to detect anomalies in devices by comparing long-term device behaviors.
UML Activity Diagram-Based Automatic Test Case Generation For Java Programs (2007)

Journal Article UML Activity Diagram-Based Automatic Test Case Generation For Java Programs Get access Mingsong Chen, Mingsong Chen State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China Search for other works by this author on: Oxford Academic Google Scholar Xiaokang Qiu, Xiaokang Qiu State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China Search for other works by this author on: Oxford Academic Google Scholar Wei Xu, Wei Xu State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China Search for other works by this author on: Oxford Academic Google Scholar Linzhang Wang, Linzhang Wang State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China Search for other works by this author on: Oxford Academic Google Scholar Jianhua Zhao, Jianhua Zhao State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China Search for other works by this author on: Oxford Academic Google Scholar Xuandong Li Xuandong Li * State Key Laboratory of Novel Software Technology, Department of Computer Science and Technology, Nanjing University, Nanjing 210093, P.R.China *Corresponding author: lxd@nju.edu.cn Search for other works by this author on: Oxford Academic Google Scholar The Computer Journal, Volume 52, Issue 5, August 2009, Pages 545–556, https://doi.org/10.1093/comjnl/bxm057 Published: 25 August 2007 Article history Received: 24 September 2006 Revision received: 09 June 2007 Published: 25 August 2007
The modified structure of the lateral IGBT on the SOI wafer for improving the dynamic latch-up characteristics (1995)

The modified structure of the lateral IGBT(LIGBT) on an SOI wafer for improving the dynamic latch-up characteristics is presented together with its numerical simulations and experimental results. The modified LIGBT structure has a p/sup +/-emitter layer between the collector and gate regions. The current at which the latch-up occurs during the turn-off transient under an inductive load is estimated in comparison with that of the conventional LIGBT. The dynamic latch-up current at room temperature and 125/spl deg/C for the modified LIGBT were 350 A/cm/sup 2/ and 290 A/cm/sup 2/, respectively. These results indicate the improvement of about 3.5 times at room temperature and about 5.5 times at 125/spl deg/C compared with those for the conventional LIGBT. This remarkable improvement in the dynamic latch-up performance is accomplished at the expense of an increase of 0.8 V in the forward voltage drop.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
The PON1 gene and detoxication. (2000)

It has been assumed since its discovery that serum paraoxonase (PON1) plays a major role in the detoxication of specific organophosphorus compounds. It was also assumed that individuals with low PON1 activity would be more susceptible to paraoxon/parathion poisoning than individuals with higher PON1 activity. Evidence supporting this hypothesis was provided by injection of rabbit PON1 into rodents. Injected PON1 protected against paraoxon toxicity in rats and chlorpyrifos oxon toxicity in mice. The recent availability of PON1 knockout mice has provided an in vivo system with which one can more closely examine the role of PON1 in detoxication. PON1 knockout mice demonstrated dramatically increased sensitivity to chlorpyrifos oxon and diazoxon and moderately increased sensitivity to the respective parent compounds. The PON1 knockout mutation also resulted in the elimination of liver PON1 activity, accounting for the dramatic increase in sensitivity to chlorpyrifos oxon and diazoxon. Totally unexpected was our finding that the PON1 knockout mice were not more sensitive to paraoxon. This was particularly surprising in light of the earlier enzyme injection experiments. Differences in the relative catalytic efficiencies of rabbit vs. mouse PON1 for the specific oxon forms explain these observations. Mouse PON1 has good catalytic efficiency for the hydrolysis of diazoxon and chlorpyrifos oxon, but a poor efficiency for paraoxon hydrolysis relative to rabbit PON1. The human PON1Q192 isoform has a catalytic efficiency similar to that of mice, whereas the human PON1R192 isoform has a much better catalytic efficiency, predicting that individuals expressing high levels of the PONIR192 isoform may have increased resistance to paraoxon toxicity.
Conditional Ablation of Ezh2 in Murine Hearts Reveals Its Essential Roles in Endocardial Cushion Formation, Cardiomyocyte Proliferation and Survival (2012)

Ezh2 is a histone trimethyltransferase that silences genes mainly via catalyzing trimethylation of histone 3 lysine 27 (H3K27Me3). The role of Ezh2 as a regulator of gene silencing and cell proliferation in cancer development has been extensively investigated; however, its function in heart development during embryonic cardiogenesis has not been well studied. In the present study, we used a genetically modified mouse system in which Ezh2 was specifically ablated in the mouse heart. We identified a wide spectrum of cardiovascular malformations in the Ezh2 mutant mice, which collectively led to perinatal death. In the Ezh2 mutant heart, the endocardial cushions (ECs) were hypoplastic and the endothelial-to-mesenchymal transition (EMT) process was impaired. The hearts of Ezh2 mutant mice also exhibited decreased cardiomyocyte proliferation and increased apoptosis. We further identified that the Hey2 gene, which is important for cardiomyocyte proliferation and cardiac morphogenesis, is a downstream target of Ezh2. The regulation of Hey2 expression by Ezh2 may be independent of Notch signaling activity. Our work defines an indispensible role of the chromatin remodeling factor Ezh2 in normal cardiovascular development.
The Role of Glutamatergic Neurotransmission in the Pathophysiology of Alcoholism (1998)

Recent evidence suggests that ethanol abuse produces its diverse effects on the brain to a substantial degree by disrupting the function of the major excitatory neurotransmitter, glutamate. Ethanol, at concentrations associated with behavioral effects in humans, inhibits the N-methyl-D-aspartate (NMDA) receptor, which mediates the post-synaptic excitatory effects of glutamate. Tolerance to ethanol results in up-regulation of the NMDA receptor so that abrupt withdrawal produces a hyperexcitable state that leads to seizures, delerium tremens, and excitotoxic neuronal death. Ethanol's inhibition of the NMDA receptor in the fetal brain likely contributes to the CNS manifestations of fetal alcohol syndrome. Therapeutic strategies aimed at correcting glutamatergic dysregulation in alcoholism need to be explored.