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States in 26Na were populated in the (d, pγ) reaction, induced by bombarding deuterium target nuclei with an intense reaccelerated beam of 25Na ions from the ISAC2 accelerator at TRIUMF. Gamma-rays were recorded in coincidence with protons and used to extract differential cross sections for 21 states up to the neutron decay threshold of 5 MeV. Results for levels below 3 MeV are discussed in detail and compared with shell model calculations and with previous work. The angular distributions of decay gamma-rays were measured for individual states and are compared to theoretically calculated distributions, highlighting some issues for future work. [ABSTRACT FROM AUTHOR]

Mitochondrial diseases are not uncommon, and may result from mutations in both nuclear and mitochondrial DNA (mtDNA). At present, only palliative therapies are available for these disorders, and interest in the development of efficient treatment protocols is high. Here, we demonstrate that in cells heteroplasmic for the T8993G mutation, which is a cause for the NARP and MILS syndromes, infection with an adenovirus, which encodes the mitochondrially targeted R.XmaI restriction endonuclease, leads to selective destruction of mutant mtDNA. This destruction proceeds in a time- and dose-dependent manner and results in cells with significantly increased rates of oxygen consumption and ATP production. The delivery of R.XmaI to mitochondria is accompanied by improvement in the ability to utilize galactose as the sole carbon source, which is a surrogate indicator of the proficiency of oxidative phosphorylation. Concurrently, the rate of lactic acid production by these cells, which is a marker of mitochondrial dysfunction, decreases. We further demonstrate that levels of phosphorylated P53 and γH2ax proteins, markers of nuclear DNA damage, do not change in response to infection with recombinant adenovirus indicating the absence of nuclear DNA damage and the relative safety of the technique. Finally, some advantages and limitations of the proposed approach are discussed.Gene Therapy (2008) 15, 516–523; doi:10.1038/gt.2008.11; published online 7 February 2008 [ABSTRACT FROM AUTHOR]

This study was designed to test the hypothesis that poly(ADP-ribose) polymerase (PARP) plays a role in the repair of damage to mitochondrial DNA (mtDNA). A rat insulinoma cell line was transfected with a PARP antisense vector that was under the control of a dexamethasone promoter. Transfected cells were selected for stable integration of the antisense vector. Several cell lines containing the antisense vector were isolated. For these studies, one of these lines (clone 5) was chosen for further evaluation. When cells were treated with dexamethasone for 72 h, PARP activity was diminished by 60%. Western blot analysis revealed a concomitant reduction in PARP protein. When clone 5 cells were exposed to the simple methylating agent methylnitrosourea (MNU) without previous treatment with dexamethasone, repair of lesions in mtDNA was found to be similar to that seen in wild-type cells or in wild-type cells treated with dexamethasone. However, when clone 5 cells were pretreated with dexamethasone for 72 h, repair of MNU-induced damage was significantly inhibited. To ascertain whether the PARP activity that was inhibited by the antisense treatment was the same as that found in the nucleus, repair studies were performed on fibroblasts derived from PARP knockout mice and their normal wild-type controls. Attenuated repair was also seen in the cells in which the gene for PARP was inactivated. These are the first studies to demonstrate that PARP can facilitate the repair of simple alkylation damage to mtDNA. [ABSTRACT FROM AUTHOR]

The mass spectra of a series of ortho, meta and para substituted isopropyl benzene derivatives have been determined where the second substituent is COOH, C(O)NH2, C(O)C6H5, C(Ph)(=NPh) or CH(Ph)(NHPh). Two bis-isopropylbenzophenones have also been studied. The spectra are characterized by prominent ortho effects which distinguish the ortho derivatives from the meta and para. [ABSTRACT FROM AUTHOR]

Net photosynthesis and leaf resistance's in turgid sorghum leaves were compared with those of intact leaves which underwent relatively slow loss of water, and with excised leaves which lost water rapidly. Reduced net photosynthesis in intact leaves can largely be accounted for by stomatal closure; this is not so for excised leaves. Stomata of excised leaves both started and completed closure at much lower leaf water contents than those of attached leaves. [ABSTRACT FROM AUTHOR]

A linear approximation procedure has been applied to the derivation of shading coefficients for minor lobe control from symmetrical, but possibly irregularly shaped, transducer arrays, for which the relationship between the coefficients and output pressure is linear. Examples are included for the traditional problems of finding optimum coefficients for uniform and low minor lobe response from planar arrays, including one of a ''honeycomb'' array on a hexagonal grid, which could not be handled by analytical methods employed hitherto. Subject Classification: [43]85.40; [43]30.85; [43]20.55; [43]85.84. [ABSTRACT FROM AUTHOR]

Exposure of whole sorghum plants to cold (5° C) or hot (30° C) nights, or exposure of shoots only to a range of low night temperatures (5-15° C) reduced both the rate and extent of stomatal opening during the succeeding day. Photosynthesis was correspondingly reduced. The reduction in the rate of stomatal opening could be attributed to a development of water deficits in the leaves. [ABSTRACT FROM AUTHOR]