Muon disrupts AKT hydrogen bond network in cancer

A cancer microenvironment generates strong hydrogen bond network system by the positive feedback loops supporting cancer complexity and robustness. Such network functions through the AKT locus generating high entropic energy supporting cancer metastatic robustness. Charged lepton particle muon follows the rule of Bragg effect during a collision with hydrogen network in cancer cells. Muon beam dismantles hydrogen bond network in cancer by the muon-catalyzed fusion, leading to apoptosis of cancer cells. Muon induces cumulative energy appearance on the hydrogen bond network in a cancer cell with its fast decay to an electron and two neutrinos. Thus, muon beam, muonic atom, muon neutrino shower, and electrons simultaneously cause fast neutralization of the AKT hydrogen bond network by the conversion of hydrogen into deuterium or helium, inactivating the hydrogen bond networks and inducing failure of cancer complexity and robustness with the disappearance of a malignant phenotype.     

Critical Evaluation of Branch Polarity and Apical Dominance as Dictators of Colony Astogeny in a Branching Coral

The high morphological resemblance between branching corals and trees, can lead to comparative studies on pattern formation traits, best exemplified in plants and in some cnidarians. Here, 81 branches of similar size of the hermatypic coral Stylophora pistillata were lopped of three different genets, their skeletons marked with alizarin red-S, and divided haphazardly into three morphometric treatment groups: (I) upright position; (II) horizontal position, intact tip; and (III) horizontal position, cut tip. After 1 y of in-situ growth, the 45 surviving ramets were brought to the laboratory, their tissues removed and their architectures analyzed by 22 morphological parameters (MPs). We found that within 1 y, isolated branches developed into small coral colonies by growing new branches from all branch termini, in all directions. No architectural dissimilarity was assigned among the three studied genets of treatment I colonies. However, a major architectural disparity between treatment I colonies and colonies of treatments II and III was documented as the development of mirror structures from both sides of treatments II and III settings as compared to tip-borne architectures in treatment I colonies. We did not observe apical dominance since fragments grew equally from all branch sides without documented dominant polarity along branch axis. In treatment II colonies, no MP for new branches originating either from tips or from branch bases differed significantly. In treatment III colonies, growth from the cut tip areas was significantly lower compared to the base, again, suggesting lack of apical dominance in this species. Changes in branch polarity revealed genet associated plasticity, which in one of the studied genets, led to enhanced growth. Different genets exhibited canalization flexibility of growth patterns towards either lateral growth, or branch axis extension (skeletal weight and not porosity was measured). This study revealed that colony astogeny in S. pistillata is a regulated process expressed through programmed events and not directly related to simple energy trade-off principles or to environmental conditions, and that branch polarity and apical dominance do not dictate colony astogeny. Therefore, plasticity and astogenic disparities encompass a diversity of genetic (fixed and flexible) induced responses.     

AKT as locus of cancer angiogenic robustness and fragility

Angiogenesis get full robustness in metastatic cancer, relapsed leukemia or lymphoma when complex positive feedback loop signaling systems become integrative. A cancer hypoxic microenvironment generates positive loops inducing formation of the vascular functional shunts. AKT is an upstream angiogenic locus of integrative robustness and fragility activated by the positive loops. AKT controls two downstream nodes the mTOR and NOS in nodal organization of the signaling genes. AKT phosphorylation is regulated by a balance of an oxidant/antioxidant. Targeting AKT locus represents new principle to control integrative angiogenic robustness by the locus chemotherapy. J. Cell. Physiol. 228: 21–24, 2013. © 2012 Wiley Periodicals, Inc.     

Quality of micropropagated plants—Vitrification

Summary Vitrification-Hyperhydrous shoot development, effects the survival and quality of several micropropagated plants ex-vitro. The leaves which are the immediate organ to be affected, exhibit abnormal morphology and physiology. Leaf malfunction is apparently a stress response to very rich media and high relative humidity. The understanding of the underlying mechanism of vitrification and its control in vitro can contribute to a more efficient micropropagation. Vitrification was found to be associated with elevated ethylene production which was related to hypolignification and poor cell wall development. Liquid and low agar media induced callose formation along with reduced and disoriented cellulose biosynthesis, manifested also in non-functioning guard cells. Malfunctioning stomata, in addition to defective cuticle contributed to increased transpiration and desiccation of in vitro formed leaves. The activity of various enzymes, associated with cell wall synthesis, was low and total proteins in normal leaves was higher than in vitreous ones. Various measures were found to reduce vitrification; lowered matrix and water potential in the medium, reduction in RH, low NH ₄ ⁺ , changes in Ca⁺⁺ levels and the removal of ethylene. These measures improved leaf morphogenesis, survival and the quality of several micropropagated plant species. Presented in the Session-in-Depth Transition of Plants From Culture to Establishment In Vivo,“ at the 41st Annual Meeting of the Tissue Culture Association, Houston, Texas, June 10–13, 1990.     

Lysosome activates AKT inducing cancer and metastasis

Hyperactivated lysosome causes cancer and induces metastasis or cancer relapse. Such activation occurs during excessive, intense, and protracted oxidative burst in the lysosome. The burst induces the formation of the constitutively active (permanently active) AKT locus generating cancer complexity and robustness. Such condition has the tendency to persist by stabilized intense signaling inducing upregulation of cell function and metabolic setup at the higher level. Most intense activator of the lysosome is the fungus Aspergillus fumigatus, which activates the AKT, a critical element in lysosome control, inducing cancer development, metastatic progression, or cancer relapse. Targeting the AKT active site of hydrogen network, by redox balance change or hydrogen balance change or muon-catalyzed fusion or laser-induced fusion with anti- A. fumigatus medication converts active AKT locus into inactive element, inducing disappearance of malignant phenotype.     

In vitro corm production in the saffron crocus (Crocus sativus L.)

Means to increase the reproductive capacity of Crocus sativus L., in vitro, are described. Cytokinins and auxin were found to be essential for development of bud explants. Ethylene and ethaphon pretreatments inhibited leaf development but induced corm production. Microsurgery of the apical bud combined with ethylene pretreatment increased both sprouting and corm production.     

DNA Methylation Mediates Persistent Epileptiform Activity In Vitro and In Vivo

Epilepsy is a chronic brain disorder involving recurring seizures often precipitated by an earlier neuronal insult. The mechanisms that link the transient neuronal insult to the lasting state of epilepsy are unknown. Here we tested the possible role of DNA methylation in mediating long-term induction of epileptiform activity by transient kainic acid exposure using in vitro and in vivo rodent models. We analyzed changes in the gria2 gene, which encodes for the GluA2 subunit of the ionotropic glutamate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptor and is well documented to play a role in epilepsy. We show that kainic acid exposure for two hours to mouse hippocampal slices triggers methylation of a 5’ regulatory region of the gria2 gene. Increase in methylation persists one week after removal of the drug, with concurrent suppression of gria2 mRNA expression levels. The degree of kainic acid-induced hypermethylation of gria2 5’ region varies between individual slices and correlates with the changes in excitability induced by kainic acid. In a rat in vivo model of post kainic acid-induced epilepsy, we show similar hypermethylation of the 5’ region of gria2. Inter-individual variations in gria2 methylation, correlate with the frequency and intensity of seizures among epileptic rats. Luciferase reporter assays support a regulatory role for methylation of gria2 5’ region. Inhibition of DNA methylation by RG108 blocked kainic acid-induced hypermethylation of gria2 5’ region in hippocampal slice cultures and bursting activity. Our results suggest that DNA methylation of such genes as gria2 mediates persistent epileptiform activity and inter-individual differences in the epileptic response to neuronal insult and that pharmacological agents that block DNA methylation inhibit epileptiform activity raising the prospect of DNA methylation inhibitors in epilepsy therapeutics.