Strong Analytic Controllability for Hydrogen Control Systems

The realization and representation of so(4,2) associated with the hydrogen atom Hamiltonian are derived. By choosing operators from the realization of so(4,2) as interacting Hamiltonians, a hydrogen atom control system is constructed, and it is proved that this control system is strongly analytically controllable based on a time-dependent strong analytic controllability theorem.Comment: 6 pages; corrected typo; added equations in section III for representation states of so(4,2). accepted by CDC 200

Analytic Controllability of Time-Dependent Quantum Control Systems

The question of controllability is investigated for a quantum control system in which the Hamiltonian operator components carry explicit time dependence which is not under the control of an external agent. We consider the general situation in which the state moves in an infinite-dimensional Hilbert space, a drift term is present, and the operators driving the state evolution may be unbounded. However, considerations are restricted by the assumption that there exists an analytic domain, dense in the state space, on which solutions of the controlled Schrodinger equation may be expressed globally in exponential form. The issue of controllability then naturally focuses on the ability to steer the quantum state on a finite-dimensional submanifold of the unit sphere in Hilbert space -- and thus on analytic controllability. A relatively straightforward strategy allows the extension of Lie-algebraic conditions for strong analytic controllability derived earlier for the simpler, time-independent system in which the drift Hamiltonian and the interaction Hamiltonia have no intrinsic time dependence. Enlarging the state space by one dimension corresponding to the time variable, we construct an augmented control system that can be treated as time-independent. Methods developed by Kunita can then be implemented to establish controllability conditions for the one-dimension-reduced system defined by the original time-dependent Schrodinger control problem. The applicability of the resulting theorem is illustrated with selected examples.Comment: 13 page

B801: Performance Evaluations of Potato Clones and Varieties in the Northeastern States 1983

Cooperative potato clone and variety trials were conducted at 23 locations to determine field, storage, and processing behavior of selected clones and varieties grown under soil, climatic, and cultural management common to the potato growing areas of 13 cooperating states and the Province of New Brunswick, Canada. These tests are all contributions to Regional Project NE107 entitled, Breeding and Evaluation of New Potato Clones for the Northeast. The primary objective of this project is to determine clone stability over a wide range of soil, climate, and cultural conditions.https://digitalcommons.library.umaine.edu/aes_bulletin/1119/thumbnail.jp

Studies on the mechanism of the hepatitis B virus X protein (pX)-mediated hepatocarcinogenesis

The Hepatitis B Virus (HBV) X protein (pX), required for the viral life cycle, is implicated in HBV-mediated hepatocarcinogenesis by an unknown mechanism. pX is a multifunctional protein, with activities affecting transcription, cell growth, and apoptosis. pX activates transcription by two mechanisms: via direct interaction with the basal transcriptional apparatus and cellular bZip transcription factors, and via activation of cytoplasmic signaling pathways. To understand the mechanism by which pX transforms hepatocytes, conditional, tetracycline-controlled mouse hepatocyte AML 12 cell lines were constructed which express HBV pX, via the tetracycline-controlled expression system. One such cell line (3pX-1) displays characteristics of adult hepatocytes and pX-dependent oncogenic transformation. Another clonal cell line (4pX-1) is a de-differentiated hepatocyte cell line, which lacks pX-dependent transformation. Comparative analyses of this cellular model system were applied to investigate the early signaling events activated by pX, while the hepatocytes are becoming transformed. The following pX-dependent differences are observed between the pX-transforming (3pX-1) and non-transforming (4pX-1) cell lines: (1) Differential immediate early gene (IEG) expression: Selective Activating Transcription Factor 3 (ATF3) messenger Ribonucleic Acid (mRNA) induction and prolonged c-fos expression in 3pX-1 cells. (2) Differential mitogenic pathway activation: Sustained activation of the Ras-Raf-MAPK pathway and transient activation of the c-Jun N-terminal Kinase (JNK) pathway in 3pX-1 cells. The inverse is observed with the non-transforming 4pX-1 cell line. (3) Differential phosphorylation of endogenous CREB and c-Jun: prolonged phosphorylation of cAMP Response Element Binding Protein (CREB) in 3pX-1 cells and prolonged phosphorylation of c-Jun in 4pX-1 cells. To demonstrate the functional significance of the mitogenic pathway activation by pX, a variant of pX tagged with Nuclear Localization Sequence (pX-NLS) was used to construct conditional cell lines, via the Tet-off system. These cell lines display markedly reduced pX-dependent hepatocyte transformation and minimal mitogenic pathway activation. Taken together, these results support the significance of the mitogenic pathway activation by pX in hepatocyte transformation

Hepatitis B Virus X Protein Activates the p38 Mitogen-Activated Protein Kinase Pathway in Dedifferentiated Hepatocytes

Hepatitis B virus X protein (pX) is implicated in hepatocarcinogenesis by an unknown mechanism. Employing a cellular model linked to pX-mediated transformation, we investigated the role of the previously reported Stat3 activation by pX in hepatocyte transformation. Our model is composed of a differentiated hepatocyte (AML12) 3pX-1 cell line that undergoes pX-dependent transformation and a dedifferentiated hepatocyte (AML12) 4pX-1 cell line that does not exhibit transformation by pX. We report that pX-dependent Stat3 activation occurs only in non-pX-transforming 4pX-1 cells and conclude that Stat3 activation is not linked to pX-mediated transformation. Maximum Stat3 transactivation requires Ser727 phosphorylation, mediated by mitogenic pathway activation. Employing dominant negative mutants and inhibitors of mitogenic pathways, we demonstrate that maximum, pX-dependent Stat3 transactivation is inhibited by the p38 mitogen-activated protein kinase (MAPK)-specific inhibitor SB 203580. Using transient-transreporter and in vitro kinase assays, we demonstrate for the first time that pX activates the p38 MAPK pathway only in 4pX-1 cells. pX-mediated Stat3 and p38 MAPK activation is Ca(2+) and c-Src dependent, in agreement with the established cellular action of pX. Importantly, pX-dependent activation of p38 MAPK inactivates Cdc25C by phosphorylation of Ser216, thus initiating activation of the G(2)/M checkpoint, resulting in 4pX-1 cell growth retardation. Interestingly, pX expression in the less differentiated hepatocyte 4pX-1 cells activates signaling pathways known to be active in regenerating hepatocytes. These results suggest that pX expression in the infected liver effects distinct mitogenic pathway activation in less differentiated versus differentiated hepatocytes

Strong Analytic Controllability for Hydrogen Control Systems

The realization and representation of so(4,2) associated with the hydrogen atom Hamiltonian are derived. By choosing operators from the realization of so(4,2) as interacting Hamiltonians, a hydrogen atom control system is constructed, and it is proved that this control system is strongly analytically controllable based on a time-dependent strong analytic controllability theorem

Development of a Novel System To Study Hepatitis Delta Virus Genome Replication

Hepatitis delta virus (HDV) genome replication requires the virus-encoded small delta protein (δAg). During replication, nucleotide sequence changes accumulate on the HDV RNA, leading to the translation of δAg species that are nonfunctional or even inhibitory. A replication system was devised where all δAg was conditionally provided from a separate and unchanging source. A line of human embryonic kidney cells was stably transfected with a single copy of cDNA encoding small δAg, with expression under tetracycline (TET) control. Next, HDV genome replication was initiated in these cells by transfection with a mutated RNA unable to express δAg. Thus, replication of this RNA was under control of the TET-inducible δAg. In the absence of TET, there was sufficient δAg to allow a low level of HDV replication that could be maintained for at least 1 year. When TET was added, both δAg and genomic RNA increased dramatically within 2 days. With clones of such cells, designated 293-HDV, the burst of HDV RNA replication interfered with cell cycling. Within 2 days, there was a fivefold enhancement of G(1)/G(0) cells relative to both S and G(2)/M cells, and by 6 days, there was extensive cell detachment and death. These findings and those of other studies that are under way demonstrate the potential applications of this experimental system