Urticaria - some observations

Urticaria has been known from antiquity. The disorder was known to the Arabs as essera and it has found a place in the writings of Cesius (circa 30 BC–45 AD). Although the condition was recognised as an entity, its cause was a mystery to the physicians of those times. It was initially thought to be a manifestation of idiosyncrasy and later believed to be a form of neuroses. However, now the pathophysiological basis of urticaria is well understood. The development of antihistamine group of drugs, paved the way for the management of urticaria

Entanglement and spin squeezing in the three-qubit transverse Ising model

We study entanglement and spin squeezing in the ground state of three qubits interacting via the transverse Ising model. We give analytical results for the entanglement and spin squeezing, and a quantitative relation between the concurrence, quantifying the entanglement of two spins, and the spin squeezing parameter, measuring the degree of squeezing. Finally, by appropriately choosing the exchange interaction and strengths of the transverse field, we propose a scheme for generating entangled W state from an unentangled initial state with all spins down.Comment: Four pages and two figure

Spin squeezing and pairwise entanglement for symmetric multiqubit states

We show that spin squeezing implies pairwise entanglement for arbitrary symmetric multiqubit states. If the squeezing parameter is less than or equal to 1, we demonstrate a quantitative relation between the squeezing parameter and the concurrence for the even and odd states. We prove that the even states generated from the initial state with all qubits being spin down, via the one-axis twisting Hamiltonian, are spin squeezed if and only if they are pairwise entangled. For the states generated via the one-axis twisting Hamiltonian with an external transverse field for any number of qubits greater than 1 or via the two-axis counter-twisting Hamiltonian for any even number of qubits, the numerical results suggest that such states are spin squeezed if and only if they are pairwise entangled.Comment: 6 pages. Version 3: Small corrections were mad

Luminescence of ZnS Nanoparticles in Organic Phase And Effect Of Doping

Abstract- The present work provides a potentially efficient and a simple chemical route for the synthesis of ZnS & Zn(1-x)MnxS nanocrystals in organic phase at ambient room temperature. The nanostructures of the prepared undoped ZnS and Mn 2+ doped ZnS:Mn nanoparticles have been analysed using UV-Vis spectrophotometer and Fourier Transform Infrared studies have been studied. There is a wavelength shift in the emission of manganese doped samples. The size and shape of the synthesized nanoparticles have been studied using the Transmission Electron Microscope. Chemical manipulation towards both size and shape tunable preparation is achieved successfully. Index Terms- Quantum confinement; absorption; emission; Doping; Capping agent; organic phase. 1

Diethylcarbamazine in allergic rhinitis (a double-blind study)

Diethyl carbamazine (DEC) essentially an antifilarial drug has been shown to be useful in allergic rhinitis in a double blind study

Hypoxia modulates the expression of leucine zipper-positive MYPT1 and its interaction with protein kinase G and Rho kinases in pulmonary arterial smooth muscle cells

We have shown previously that acute hypoxia downregulates protein kinase G (PKG) expression and activity in ovine fetal pulmonary vessels and pulmonary arterial smooth muscle cells (SMC). Here, we report that acute hypoxia also reduces the expression of leucinezipper-positive MYPT1 (LZ+MYPT1), a subunit of myosin light chain (MLC) phosphatase, in ovine fetal pulmonary arterial SMC. We found that in hypoxia, there is greater interaction between LZ+ MYPT1 and RhoA and Rho kinase 1 (ROCK1)/Rho kinase 2 (ROCK2) and decreased interaction between LZ+ MYPT1 and PKG, resulting in increased MLC20 phosphorylation, a higher pMLC20/MLC20 ratio and SMC contraction. In normoxic SMC PKG overexpression, LZ+ MYPT1 expression is upregulated while PKG knockdown had an opposite effect. LZ+ MYPT1 overexpression enhanced the interaction between PKG and LZ+ MYPT1. Overexpression of a mutant LZ- MYPT1 isoform in SMC mimicked the effects of acute hypoxia and decreased pMLC20/MLC20 ratio. Collectively, our data suggest that hypoxia downregulates LZ+ MYPT1 expression by suppressing PKG levels, reduces the interaction of LZ+ MYPT1 with PKG and promotes LZ+ MYPT1 interaction with RhoA or ROCK1/ROCK2, thereby promoting pulmonary arterial SMC contraction

The Fission Yeast Pre-mRNA-processing Factor 18 (prp18(+)) Has Intron-specific Splicing Functions with Links to G(1)-S Cell Cycle Progression

The fission yeast genome, which contains numerous short introns, is an apt model for studies on fungal splicing mechanisms and splicing by intron definition. Here we perform a domain analysis of the evolutionarily conserved Schizosaccharomyces pombe pre-mRNA-processing factor, SpPrp18. Our mutational and biophysical analyses of the C-terminal alpha-helical bundle reveal critical roles for the conserved region as well as helix five. We generate a novel conditional missense mutant, spprp18-5. To assess the role of SpPrp18, we performed global splicing analyses on cells depleted of prp18(+) and the conditional spprp18-5 mutant, which show widespread but intron-specific defects. In the absence of functional SpPrp18, primer extension analyses on a tfIId(+) intron 1-containing minitranscript show accumulated pre-mRNA, whereas the lariat intron-exon 2 splicing intermediate was undetectable. These phenotypes also occurred in cells lacking both SpPrp18 and SpDbr1 (lariat debranching enzyme), a genetic background suitable for detection of lariat RNAs. These data indicate a major precatalytic splicing arrest that is corroborated by the genetic interaction between spprp18-5 and spprp2-1, a mutant in the early acting U2AF59 protein. Interestingly, SpPrp18 depletion caused cell cycle arrest before S phase. The compromised splicing of transcripts coding for G(1)-S regulators, such as Res2, a transcription factor, and Skp1, a regulated proteolysis factor, are shown. The cumulative effects of SpPrp18-dependent intron splicing partly explain the G1 arrest upon the loss of SpPrp18. Our study using conditional depletion of spprp18(+) and the spprp18-5 mutant uncovers an intron-specific splicing function and early spliceosomal interactions and suggests links with cell cycle progression