Orthotellurated derivatives of N,N-dimethylbenzylamine: crystal and molecular structures of [2-(dimethylaminomethyl)phenyl]tellurium(IV) tribromide and [2-(butyldichlorotelluro)benzyl]dimethylammonium chloride

The reaction of o-lithiobenzylamine with elemental tellurium followed by air oxidation furnished an ill defined 'tellurinic anhydride'. Halogenolysis reactions of this with bromine and sulphonyl chloride afforded the corresponding [2-(dimethylaminomethyl)phenyl]trihalogenotellurium(IV) derivatives. Reduction of the trihalides with excess of hydrazine hydrate gave novel [2-(dimethylaminomethyl)phenyl]halogenotellurium(II) derivatives. Metathesis of the chlorotellurium-(IV) and -(II) derivatives with sodium diethyldithiocarbamate resulted in the formation of dithiocarbamato derivatives. The crystal structure of [2-(dimethylaminomethyl)phenyl]tellurium(IV) tribromide is monoclinic, space group P21/n with a=9.226(6), b=15.439(8), c=9.618(5)Å. β=94.94(5)°, Z=4, and R=0.0419 for 938 observed reflections. The co-ordination about Te approximates to octahedral with a vacant equatorial site: two Br atoms axial, the third Br and the organic ligand equatorial [Te-Br(ax) 2.758(2) and 2.633(3), Te-Br(eq) 2.632(2), Te-C 2.12(1), and Te-N 2.42(1)Å]. The compound is essentially monomeric, with a weak association between Te and a neighbouring bromine atom [3.896(2)Å]. [2-(Butyldichlorotelluro)benzyl]dimethylammonium chloride is monoclinic, space group P21/n with a=14.278(12), b=8.349(5), c= 14.480(8)Å. β= 93.59(5)°, Z=4, and R=0.0288, for 2 245 observed reflections. The co-ordination about Te can also be considered as octahedral with a vacant equatorial site: two chlorines apical, and the chloride ion and two carbon atoms equatorial [Te-Cl 2.527(1) and 2.487(1), Te···Cl 3.337(2), Te-C 2.134(4) and 2.154(4)Å]. The quaternary nitrogen atom is twisted away from the tellurium atom, Te···N 4.380(4)Å, forming a hydrogen bond with a chloride ion

Epidemiology and genetics of dilated cardiomyopathy in the Indian context

Background: Dilated cardiomyopathy (DCM) still remains to be a poorly understood and less analyzed group of cardiac-muscle disorders when compared to hypertrophic cardiomyopathy (HCM). Also, the vast clinical heterogeneity among the patients has rendered the small and isolated kindred studies less informative on the genetics and epidemiology of DCM. Aim of the study: The study aimed at understanding the epidemiology and genetics of DCMs in the Indian context. Materials and methods/ Statistical analysis: One hundred seven DCM patients and 105 healthy individuals were included in the study for epidemiological and genetic risk factor identification and to fit the possible mode of inheritance. Single′s ascertainment methodology for segregation analysis and Penrose frequency estimates were followed to evaluate for the role of specific epidemiological factors in the disease etiology. Chi-square analysis was carried out to interpret the results statistically. Results and Conclusion: Our study suggests that epidemiological factors like gender, age at onset and vegetarian diet in conjunction with sarcomere gene mutations may play a role in the disease expression. Similarly, segregation analysis for the possible mode of inheritance showed a deviation from the autosomal dominant mode of inheritance, strengthening the underlying genetic heterogeneity of DCM

Epidemiology and genetics of dilated cardiomyopathy in the Indian context

Background: Dilated cardiomyopathy (DCM) still remains to be a poorly understood and less analyzed group of cardiac-muscle disorders when compared to hypertrophic cardiomyopathy (HCM). Also, the vast clinical heterogeneity among the patients has rendered the small and isolated kindred studies less informative on the genetics and epidemiology of DCM. Aim of the study: The study aimed at understanding the epidemiology and genetics of DCMs in the Indian context. Materials and methods/ Statistical analysis: One hundred seven DCM patients and 105 healthy individuals were included in the study for epidemiological and genetic risk factor identification and to fit the possible mode of inheritance. Single′s ascertainment methodology for segregation analysis and Penrose frequency estimates were followed to evaluate for the role of specific epidemiological factors in the disease etiology. Chi-square analysis was carried out to interpret the results statistically. Results and Conclusion: Our study suggests that epidemiological factors like gender, age at onset and vegetarian diet in conjunction with sarcomere gene mutations may play a role in the disease expression. Similarly, segregation analysis for the possible mode of inheritance showed a deviation from the autosomal dominant mode of inheritance, strengthening the underlying genetic heterogeneity of DCM

Experimental observation of the asymmetric instability of intermediate-reduced-volume vesicles in extensional flow

Vesicles provide an attractive model system to understand the deformation of living cells in response to mechanical forces. These simple, enclosed lipid bilayer membranes are suitable for complementary theoretical, numerical, and experimental analysis. A recent study [Narsimhan, Spann, Shaqfeh, J. Fluid Mech., 2014, 750, 144] predicted that intermediate-aspect-ratio vesicles extend asymmetrically in extensional flow. Upon infinitesimal perturbation to the vesicle shape, the vesicle stretches into an asymmetric dumbbell with a cylindrical thread separating the two ends. While the symmetric stretching of high-aspect-ratio vesicles in extensional flow has been observed and characterized [Kantsler, Segre, Steinberg, Phys. Rev. Lett., 2008, 101, 048101] as well as recapitulated in numerical simulations by Narsimhan et al., experimental observation of the asymmetric stretching has not been reported. In this work, we present results from microfluidic cross-slot experiments observing this instability, along with careful characterization of the flow field, vesicle shape, and vesicle bending modulus. The onset of this shape transition depends on two non-dimensional parameters: reduced volume (a measure of vesicle asphericity) and capillary number (ratio of viscous to bending forces). We observed that every intermediate-reduced-volume vesicle that extends forms a dumbbell shape that is indeed asymmetric. For the subset of the intermediate-reduced-volume regime we could capture experimentally, we present an experimental phase diagram for asymmetric vesicle stretching that is consistent with the predictions of Narsimhan et al

Activation of MEK-1 and SEK-1 by Tpl-2 proto-oncoprotein, a novel MAP kinase kinase kinase.

The Tpl-2 protein serine/threonine kinase was originally identified, in a C-terminally deleted form, as the product of an oncogene associated with the progression of Moloney murine leukemia virus-induced T cell lymphomas in rats. The kinase domain of Tpl-2 is homologous to the Saccharomyces cerevisiae gene product, STE11, which encodes a MAP kinase kinase kinase. This suggested that Tpl-2 might have a similar activity. Consistent with this hypothesis, immunoprecipitated Tpl-2 and Tpl-2deltaC (a C-terminally truncated mutant) phosphorylated and activated recombinant fusion proteins of the mammalian MAP kinase kinases, MEK-1 and SEK-1, in vitro. Furthermore, transfection of Tpl-2 into COS-1 cells or Jurkat T cells. markedly activated the MAP kinases, ERK-1 and SAP kinase (JNK), which are substrates for MEK-1 and SEK-1, respectively. Tpl-2, therefore, is a MAP kinase kinase kinase which can activate two MAP kinase pathways. After Raf and Mos, Tpl-2 is the third serine/threonine oncoprotein kinase that has been shown to function as a direct activator of MEK-1