ROOTING OF DATE PALM (PHOENIX DACTYLIFERA L.) OFFSHOOTS BY ISOPROTHIOLANE (IPT)

The experiment was conducted at Alhassa Oasis (25° 22′ N' latitude; 49°34′ E longitude) and altitude is 179 m a.s.l , Kingdom of Saudi Arabia. Treatments included the following Isoprothiolane (IPT) concentrations incorporated at the bottom of offshoot hole: control (without IPT), 25g, 50g, 75g, 100g, 200g and 500g / offshoot hole. The offshoots weight ranged between 25 – 30 kg. The IPT concentrations of 75 and 100 g/ offshoot hole seemed to be quite optimal for improving rooting of date palm offshoots. The best rooting percentage, length of root, root fresh and dry weights were obtained under 75 and 100 g/ offshoot whole IPT concentrations. Offshoots under the control and the lowest and highest IPT treatments reflected poor rooting ability. The chlorophyll content data although looked relatively similar between treatments, a slight edge of 75 and 100 g/ offshoot hole was noticeable. This relative edge might have played a significant role in the photosynthetic ability of offshoots. The efficiency of rooting of offshoots under both concentrations might have resulted from their edged photosynthetic ability

ROOTING OF DATE PALM (PHOENIX DACTYLIFERA L.) OFFSHOOTS BY ISOPROTHIOLANE (IPT)

The experiment was conducted at Alhassa Oasis (25° 22′ N' latitude; 49°34′ E longitude) and altitude is 179 m a.s.l , Kingdom of Saudi Arabia. Treatments included the following Isoprothiolane (IPT) concentrations incorporated at the bottom of offshoot hole: control (without IPT), 25g, 50g, 75g, 100g, 200g and 500g / offshoot hole. The offshoots weight ranged between 25 – 30 kg. The IPT concentrations of 75 and 100 g/ offshoot hole seemed to be quite optimal for improving rooting of date palm offshoots. The best rooting percentage, length of root, root fresh and dry weights were obtained under 75 and 100 g/ offshoot whole IPT concentrations. Offshoots under the control and the lowest and highest IPT treatments reflected poor rooting ability. The chlorophyll content data although looked relatively similar between treatments, a slight edge of 75 and 100 g/ offshoot hole was noticeable. This relative edge might have played a significant role in the photosynthetic ability of offshoots. The efficiency of rooting of offshoots under both concentrations might have resulted from their edged photosynthetic ability

Opposing Effects of Sirtuins on Neuronal Survival: SIRT1-Mediated Neuroprotection Is Independent of Its Deacetylase Activity

Background: Growing evidence suggests that sirtuins, a family of seven distinct NAD-dependent enzymes, are involved in the regulation of neuronal survival. Indeed, SIRT1 has been reported to protect against neuronal death, while SIRT2 promotes neurodegeneration. The effect of SIRTs 3–7 on the regulation of neuronal survival, if any, has yet to be reported. Methodology and Principal Findings: We examined the effect of expressing each of the seven SIRT proteins in healthy cerebellar granule neurons (CGNs) or in neurons induced to die by low potassium (LK) treatment. We report that SIRT1 protects neurons from LK-induced apoptosis, while SIRT2, SIRT3 and SIRT6 induce apoptosis in otherwise healthy neurons. SIRT5 is generally localized to both the nucleus and cytoplasm of CGNs and exerts a protective effect. In a subset of neurons, however, SIRT5 localizes to the mitochondria and in this case it promotes neuronal death. Interestingly, the protective effect of SIRT1 in neurons is not reduced by treatments with nicotinamide or sirtinol, two pharmacological inhibitors of SIRT1. Neuroprotection was also observed with two separate mutant forms of SIRT1, H363Y and H355A, both of which lack deacetylase activity. Furthermore, LK-induced neuronal death was not prevented by resveratrol, a pharmacological activator of SIRT1, at concentrations at which it activates SIRT1. We extended our analysis to HT-22 neuroblastoma cells which can be induced to die by homocysteic acid treatment. While the effects of most of the SIRT proteins were similar to that observed in CGNs, SIRT6 was modestly protective against homocysteic acid toxicity in HT-22 cells. SIRT5 was generally localized in th