Saba R. Raza

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Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks (DSBs),(More)
Cellular senescence suppresses cancer by stably arresting the proliferation of damaged cells1. Paradoxically, senescent cells also secrete factors that alter tissue microenvironments2. The pathways regulating this secretion are unknown. We show that damaged human cells develop persistent chromatin lesions bearing hallmarks of DNA double-strand breaks(More)
The precursor form of the nerve growth factor (proNGF), forms a heterotrimeric complex with the receptors p75 and sortilin; this complex has been implicated in neuron cell death. However, it is not known whether proNGF and the receptors p75 and sortilin contribute to age- and disease-related neurodegeneration. Here we show that proNGF induces cell death in(More)
Several studies have sought to demonstrate that neurodegeneration during disease and in old age is associated with reduced neurotrophic support. Little positive evidence has been forthcoming, either in relation to the availability of neurotrophins or to expression and function of the relevant receptors. Recently, a novel way in which neurotrophins could(More)
VIP, which has been demonstrated to reduce or prevent oxidant injury in the lungs and other organs, is shown here to protect against excitotoxic injury of the lung and excitotoxic death of cortical neuronal cells in primary culture. Glutamate killing of neuron-like PC-12 cells, attributable to oxidant stress rather that to excitotoxicity, is also reduced or(More)
The excitatory amino acid glutamate serves important neurologic functions, but overactivation of its N-methyl-D-aspartate (NMDA) receptor is toxic to neurons (excitotoxicity). We report that NMDA receptor blocker MK-801 (dizocilpine maleate) attenuated oxidant injury induced by paraquat or by xanthine oxidase. We conclude that excitotoxicity may be a key(More)
(1) A beta peptides potentiate vasoconstriction, caused by norepinephrine, and possibly other endogenous vasoconstrictors. If this potentiation occurs in the cerebral circulation, close to sites of A beta deposition in AD brains, the enhanced vasoconstriction could result in neuronal ischemia and death. (2) By neutralizing this deleterious effect of A beta,(More)
In the version of this article initially published online and in print, the labelling of the radiation doses in Fig. 1a was reversed. The correct version of this figure is shown below. This error has been corrected in both the HTML and PDF versions of the article. In the version of this article initially published online and in print, the images in the left(More)
Oesophageal atresia/Tracheo-oesophageal fistula (OA/TOF) are common congenital malformations of the foregut in newborns. Until recently little was known about the pathogenesis of these anomalies. Adriamycin, a chemotherapy agent, has been found to cause birth defects in mice that resemble the OA/TOF anomalies providing an animal model to study the etiology(More)
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