Molecular Insights into the Role of Reactive Oxygen,Nitrogen and Sulphur Species in Conferring Salinity Stress Tolerance in Plants

Journal of Plant Growth Regulation - Salinity stress is the major abiotic stress that affects crop production and productivity as it has a multifarious negative effect on the growth and development...     

Establishment of a human fetal cardiac myocyte cell line

Summary Human cardiac myocytes undergo degeneration, cytolysis, and necrosis in a number of clinical disease conditions such as myocarditis, dilated cardiomyopathy, and during episodes of cardiac allograft rejection. The precise cellular, biochemical, and molecular mechanisms that lead to such abnormalities in myocytes have been difficult to investigate because at present it is not possible to obtain and maintain viable cell cultures of human adult cardiac myocytes in vitro. However, human fetal cardiac myocytes are relatively easy to maintain and culture in vitro, but their limited availability and growth, variability from one preparation to another, and varying degrees of contamination with endothelial and epithelial cell types have made it difficult to obtain reliable data on the effect of cardiotropic viruses and cardiotoxic drugs on such myocytes. These thoughts prompted us to attempt to derive a cell line of human cardiac origin. Highly enriched human fetal cardiac myocytes were transfected with the plasmids pSV2Neo and pRSVTAg and gave rise to a cell line (W1) which has been maintained in culture for 1 yr. Morphologic and phenotypic analyses of W1 cells by flow microfluorometry and immunoperoxidase techniques indicate that the W1 cell line shares many properties of human fetal cardiac myocytes, but appears not to react with specific antibodies known to react with markers unique to human endothelial, epithelial, skeletal muscle, and dendritic cells. These preliminary data suggest that the W1 cells may provide a unique source of an established cell line that shares many properties ascribed to human cardiac myocytes. This study was supported by grant 1RO1-25566-03 from the National Institutes of Health, Bethesda, MD, to A. Ahmed-Ansari and by a Grant-in-Aid from the American Heart Association, Georgia Affiliate, to Nicolas Neckelmann.     

Norditerpenoid alkaloids from the roots of Aconitum heterophyllum Wall with antibacterial activity

Two new aconitine-type norditerpenoid alkaloids 6-dehydroacetylsepaconitine (1) and 13-hydroxylappaconitine (2), along with three known norditerpenoid alkaloids lycoctonine, delphatine and lappaconitine were isolated from the roots of the Aconitum heterophyllum Wall. These compounds exhibited significant antibacterial activity. The structure of compound 1 and 2 were deduced on the basis of their spectral data.     

The hydration of chloroacetonitriles catalyzed by mono- and dinuclear Ru(II)- and Os(II)-arene complexes

The hydration of nitriles to the corresponding amides is an important reaction for both laboratory and industry purposes. The classical synthesis method requires harsh conditions, gives low yields, and is nonselective due to further hydrolysis of the amides into carboxylic acids. To obtain good yields and high selectivity, transition metal complexes have been utilized as catalysts for this transformation. Herein, a series of Ru(II)- and Os(II)-arene complexes--based on pyranone, thiopyranone, and pyridinone ligands--were assayed on the hydration of chloroacetonitriles. The influence of the substitution pattern of the ligand, and of the nuclearity and of the type of substrate on the yield, the selectivity, and the turnover numbers are discussed.     

Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging.

Skeletal muscle loss during aging leads to an increased risk of falls, fractures, and eventually loss of independence. Resistance exercise is a useful intervention to prevent sarcopenia; however, the muscle protein synthesis (MPS) response to resistance exercise is less in elderly compared with young subjects. On the other hand, essential amino acids (EAA) increase MPS equally in both young and old subjects when sufficient EAA is ingested. We hypothesized that EAA ingestion following a bout of resistance exercise would stimulate anabolic signaling and MPS similarly between young and old men. Each subject ingested 20 g of EAA 1 h following leg resistance exercise. Muscle biopsies were obtained before and 1, 3, and 6 h after exercise to measure the rate of MPS and signaling pathways that regulate translation initiation. MPS increased early in young (1-3 h postexercise) and later in old (3-6 h postexercise). At 1 h postexercise, ERK1/2 MNK1 phosphorylation increased and eIF2alpha phosphorylation decreased only in the young. mTOR signaling (mTOR, S6K1, 4E-BP1, eEF2) was similar between groups at all time points, but MNK1 phosphorylation was lower at 3 h and AMP-activated protein kinase-alpha (AMPKalpha) phosphorylation was higher in old 1-3 h postexercise. We conclude that the acute MPS response after resistance exercise and EAA ingestion is similar between young and old men; however, the response is delayed with aging. Unresponsive ERK1/2 signaling and AMPK activation in old muscle may be playing a role in the delayed activation of MPS. Notwithstanding, the combination of resistance exercise and EAA ingestion should be a useful strategy to combat sarcopenia.     

The Integrity of the HMR complex is necessary for centromeric binding and reproductive isolation in Drosophila

Postzygotic isolation by genomic conflict is a major cause for the formation of species. Despite its importance, the molecular mechanisms that result in the lethality of interspecies hybrids are still largely unclear. The genus Drosophila, which contains over 1600 different species, is one of the best characterized model systems to study these questions. We showed in the past that the expression levels of the two hybrid incompatibility factors Hmr and Lhr diverged in the two closely related Drosophila species, D. melanogaster and D. simulans, resulting in an increased level of both proteins in interspecies hybrids. The overexpression of the two proteins also leads to mitotic defects, a misregulation in the expression of transposable elements and decreased fertility in pure species. In this work, we describe a distinct six subunit protein complex containing HMR and LHR and analyse the effect of Hmr mutations on complex integrity and function. Our experiments suggest that HMR needs to bring together components of centromeric and pericentromeric chromatin to fulfil its physiological function and to cause hybrid male lethality.     

Novel mutations of MYO15A associated with profound deafness in consanguineous families and moderately severe hearing loss in a patient with Smith-Magenis syndrome

Mutations in myosin XVA are responsible for the shaker 2 ( sh2) phenotype in mice and nonsyndromic autosomal recessive profound hearing loss DFNB3 on chromosome 17p11.2. We have ascertained seven families with profound congenital hearing loss from Pakistan and India with evidence of linkage to DFNB3 at 17p11.2. We report three novel homozygous mutations in MYO15A segregating in three of these families. In addition, one hemizygous missense mutation of MYO15A was found in one of eight Smith-Magenis syndrome (del(17)p11.2) patients from North America who had moderately severe sensorineural hearing loss.     

Comparative Evaluation of Trace Metal Distribution and Correlation in Human Malignant and Benign Breast Tissues

Selected trace metals were analyzed in human malignant and nonmalignant (benign) breast tissue samples by the flame atomic absorption spectrophotometric method. In malignant tissues, dominant mean concentrations were revealed by Na, K, Ca, Mg, Fe, Zn, and Al at 927, 552, 231, 61.7, 36.5, 18.3, and 8.94 microg/g, respectively, while the mean metal levels in benign tissues were 903, 435, 183, 63.3, 24.7, 14.5, and 10.1 microg/g, respectively. Average concentrations of Cd, Co, Cr, Cu, Fe, Mn, K, Ca, and Zn were noted to be significantly higher in the malignant tissues compared with the benign tissues. Significantly strong correlations (r > 0.50) in malignant tissues were observed between Mn and Co, Mn and Cd, Cd and Cr, Fe and Mn, Cd and Co, Fe and Co, Mg and Pb, Cd and Fe, Mg and Ni, Pb and Ni, Ni and Sr, and Fe and Pb, whereas, Cd and Co, Cd and Mn, Co and Mg, Co and Mn, Cu and Mn, Co and Ni, Mg and Ni, Cd and Cu, Cd and Ni, Ca and Mg, Mn and Pb, Cu and Ni, Fe and Ni, Cd and Mg, Co and Cu, Cr and Na, and Cd and Cr revealed strong and significant relationships in benign tissues at p < 0.001. Principal component analysis of the metals data yielded six principal components for malignant tissues and five principal components for benign tissues, with considerably different loadings, duly supported by cluster analysis. The study revealed a considerably different pattern of distribution and mutual correlations of trace metals in the breast tissues of benign and cancerous patients.     

The quality of chimpanzee T-cell activation and simian immunodeficiency virus/human immunodeficiency virus susceptibility achieved via antibody-mediated T-cell receptor/CD3 stimulation is a function of the anti-CD3 antibody isotype

While human immunodeficiency virus type 1 (HIV-1) infection is associated with hyperimmune activation and systemic depletion of CD4⁺ T cells, simian immunodeficiency virus (SIV) infection in sooty mangabeys or chimpanzees does not exhibit these hallmarks. Control of immune activation is thought to be one of the major components that govern species-dependent differences in the disease pathogenesis. A previous study introduced the idea that the resistance of chimpanzees to SIVcpz infection-induced hyperimmune activation could be the result of the expression of select sialic acid-recognizing immunoglobulin (Ig)-like lectin (Siglec) superfamily members by chimpanzee T cells. Siglecs, which are absent on human T cells, were thought to control levels of T-cell activation in chimpanzees and were thus suggested as a cause for the pathogenic differences in the course of SIVcpz or HIV-1 infection. As in human models of T-cell activation, stimulation had been attempted using an anti-CD3 monoclonal antibody (MAb) (UCHT1; isotype IgG1), but despite efficient binding, UCHT1 failed to activate chimpanzee T cells, an activation block that could be partially overcome by MAb-induced Siglec-5 internalization. We herein demonstrate that anti-CD3 MAb-mediated chimpanzee T-cell activation is a function of the anti-CD3 MAb isotype and is not governed by Siglec expression. While IgG1 anti-CD3 MAbs fail to stimulate chimpanzee T cells, IgG2a anti-CD3 MAbs activate chimpanzee T cells in the absence of Siglec manipulations. Our results thus imply that prior to studying possible differences between human and chimpanzee T-cell activation, a relevant model of chimpanzee T cell activation needs to be established.