Possibility of observing charged Higgs in the single top production via its τ\tau lepton decay at LHC

Single top quark production through weak interactions is considered to be an important source of charged Higgs in the Minimal Super Symmetric Standard Model. In the s-channel single top production having largest cross-section may appear as a propagator in the form of heavy resonance state decaying to a pair of top and bottom quark. The process under investigation is $pp \rightarrow H^{\pm}\rightarrow tb \rightarrow b\bar{b}W^{\pm} \rightarrow b\bar{b}\tau^{\pm} \nu_{\tau}$, where top quark exclusively decays into a pair of bottom quark and W boson while W boson subsequently decays to $\tau$ jet and neutrino. So the final state is characterized by the presence of two b jets, hadronic $\tau$ decay and missing transverse energy. Within the presence of QCD multijet and electroweak background events at LHC, it has been demonstrated that the charged Higgs signal observability is possible within the available MSSM parameter space (tan$\beta$, $m_{H^{\pm}})$ respecting all experimental and theoretical constraints. In order to show the observability potential of charged Higgs, the exclusion curves at 95$\%$ confidence level and 5$\sigma$ contours are plotted at different integrated luminosities with $\sqrt{s}=$14 TeV.Comment: arXiv admin note: substantial text overlap with arXiv:1711.0834

Development of Improved Methodologies Toward the Formation of C-C and C-N Bonds

Organometallic chemistry provides valuable tools for the formation of carbon-carbon and carbon-heteroatom bonds that would otherwise require multiple steps and resources to achieve through conventional methods. Studies toward the regioselective and stereoselective formation these types of bonds using different organometallic methods will be presented. Three focal areas have been studied: C-N bond formation, C-H borylation, and silylvinylation of alkynes. In Chapter 1, palladium-catalyzed amidation has been used to effectively form C-N bonds toward the synthesis of valuable imidazo[4,5-b]pyridines and imidazo[4,5-c]pyridines. The reaction conditions are tolerable for a variety of N-substituted-3-amino-2-chloropyridines. All current routes to expand the substrate scope in regards to substitution on the pyridine ring will be discussed. Chapter 2 will detail a new method for the synthesis of 3,3\u27-bis-arylated BINOL derivatives through an ortho C-H borylation of commercially available (R)-BINOL followed by an in situ Suzuki-Miyarua coupling. Conventionally, these compounds are made via time-consuming multi-step routes. Development of this new method, which takes a total time of 24 hours with only a single purification step, will be discussed in detail. In Chapter 3, ruthenium hydride-catalyzed silylvinylation of alkynes under an ethylene atmosphere has permitted the facile formation of highly functionalized diene systems. The synthesis of conjugated diene systems has been of great interest due to their prevalent appearance in naturally occurring compounds. Derivatizations of these novel diene systems will be presented, including a rare method for the trans-silylformylation of alkynes

Studies toward the total synthesis of eletefine

A method towards the total synthesis of eletefine is described. Two related convergent syntheses are explained which divide the molecule into two fragments. Improvements towards the synthesis of a bis-functionalized isoquinoline fragment are explained. Expansion on the knowledge and understanding of the isoquinoline system is also described. The synthesis illustrated entails a bromination of a triflate functionalized isoquinoline system and a regio-selective Sonogashira reaction. Suggestions towards the completion of the total synthesis are prescribed

A Deficit in Parvalbumin-Expressing Interneurons in the Hippocampus Leads to Physiological and Behavioral Phenotypes Relevant to Schizophrenia in a Genetic Mouse Model

Hippocampal GABAergic interneuron deficits are implicated in the pathophysiology of schizophrenia. Postmortem histological analyses show alteration in number and/or function of parvalbumin-expressing (PV+) GABAergic interneurons in the cerebral cortex of these patients. A parallel line of research using functional imaging of cerebral blood flow or volume has shown that hyperactivity of the hippocampus may contribute to psychotic symptoms as well as cognitive deficits in schizophrenia. It is not known if changes in GABA transmission, particularly in the number and function of PV+ interneurons, are causally related to hippocampal hyperactivity and expression of behavioral and cognitive abnormalities in schizophrenia. To help answer this question, we used genetic mouse models with deficits in cortical GABAergic interneuron development to test the hypothesis that a selective deficit in PV+ interneurons in the hippocampus can lead to schizophrenia relevant phenotypes such as hippocampal hyperactivity, dysregulation of the mesolimbic dopamine system, enhanced psychomotor responsiveness to amphetamine, and disruption of hippocampal dependent cognition. Here I describe my studies primarily on a mouse model with a deletion of the cell-cycle gene cyclin D2 (cD2 null). This mutation disrupts interneuron development in the medial ganglionic eminence (MGE), leading to a partial and selective deficit in PV+ interneurons in the neocortex and the hippocampus. I show that the cD2 null mouse shows regionally heterogeneous, persistent structural and functional deficit in PV+ interneurons, with a relatively larger and more functional deficit in the hippocampus. The GABAergic deficit in the hippocampus is associated with signs of disinhibition, such as increased cerebral blood volume as found by functional magnetic resonance imaging (fMRI).Upon establishing the evidence for hippocampal disinhibition in the cyclin D2 null mouse, I examined the relationship between this disinhibition and two areas of neural function know to be altered in psychosis and schizophrenia: Mesostriatal DA system function and hippocampus-mediated cognition. I found that the cD2 null mice showed increased dopamine population activity in the ventral tegmental area and enhanced psychomotor response to amphetamine. The latter was eliminated by a partial lesion of the ventral hippocampus, indicating hippocampal disinhibition as the driver of DA neuron dysregulation. In addition, cD2 null mice showed deficits in cognitive functions that recruit and depend on the hippocampus, such as the contextual and cued fear conditioning. Lastly, to test for a causal relationship between the PV+ interneuron deficit in the hippocampus, and the abnormalities in hippocampal metabolism, imaging phenotype, the mesolimbic dopamine dysfunction and contextual learning and memory, I examined the effects of replacing GABAergic interneurons to the hippocampus. I used transplantation of GABAergic interneuron precursors derived from the medial ganglionic eminence (MGE) into the adult hippocampus of cyclin D2 null mutants. MGE-derived progenitor cells developed into structurally and functionally mature PV+ and other GABAergic cells, and normalized hippocampal hypermetabolism. In addition, the MGE transplants normalized VTA dopamine cell activity, normalized amphetamine sensitivity and improved hippocampus-dependent learning and memory. Taken together, these studies establish the plausibility of a causal relationship between hippocampal PV+ interneuron pathology and psychosis-relevant pathophysiological and cognitive phenotypes. Moreover, they provide a rationale for limbic cortical GABAergic-interneuron-targeted treatment strategies in psychotic disorders