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Introduction Nelarabine, a prodrug of arabinosylguanine has lineage-specific toxicity for T lymphoblasts and is used to treat refractory or relapsed T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma patients. The most commonly observed adverse effects associated with nelarabine are mainly hematological, i.e. neutropenia, anemia, and thrombocytopenia. Additionally, neurological, and gastrointestinal toxicities have been reported. Central nervous system neurotoxicity associated with nelarabine is very rare. Case description A 37-year-old man patient diagnosed with T-cell acute lymphoblastic leukemia had experienced generalized tonic-clonic seizure which lasted for a few seconds and upper extremity weakness after three weeks of the nelarabine infusion. Computed tomography and magnetic resonance imaging have shown periventricular and nucleus caudatus abnormalities. Radiological findings suggested toxic leukoencephalopathy and acute infarct of right nucleus caudatus. Management and outcome After high-dose steroids, intravenous immunoglobulin, and support treatment, his neurologic symptoms disappeared except for mild peroral numbness. However, radiological sequelae persisted despite clinical improvement. Conclusion Physicians involved in the care of these patients who use nelarabine should be aware of the fact that cerebral toxicity of the nelarabine may occur especially in the presence of predisposing factors. It is crucial to monitor closely those patients receiving nelarabine and also those who have additional predisposing factors for neurotoxicity.

WOS: 000361609000019 PubMed ID: 25180956 Objective The Notch pathway seems to function as an antiangiogenic factor, negatively regulating the sprouting effect of vascular endothelial growth factor (VEGF). This function is well defined in embryonic and tumor vasculature. However, little is known about its function in ischemia-induced angiogenesis. In the first part of this study, we investigated the role of Notch in reparative angiogenesis after ischemia. In the second part, we hypothesized that anti-Notch therapy will result in increased angiogenic sprouting. We analyzed the effect of Notch inhibition in the induction of angiogenic sprouting. Methods In the first part, we investigated the effect of ischemia on the Notch ligand delta-like ligand 4 (DLL4). Twenty rats were divided equally into 2 groups. In the surgery group, dorsal skin flap was used as model of ischemia. In the control group, no surgical procedure was performed. DLL4 and VEGF gene expressions were assessed. Immunohistochemical staining was used for detection of DLL4 in tissue materials. Plasma levels of VEGF and DLL4 were measured. In the second part, we investigated the effect of Notch inhibition using a gamma-secretase inhibitor (GSI) on inducing neoangiogenesis. Twenty rats were assigned to 2 equal groups. In all animals, dorsal skin flap was raised and sutured back into its bed. Animals in the GSI-treated group received GSI intravenously after surgery for 3 days. Saline was administered in the control group. Necrotic area measurements, microangiography, and histologic evaluations were performed to compare groups. Results In the first part, VEGF and DLL expressions increased in ischemic tissues (P < 0.01). Immunohistochemical analysis revealed that DLL4 expression was upregulated in capillary endothelial cells after ischemia. Plasma levels for VEGF and DLL4 were higher in the animals that underwent surgery (P < 0.01). In the second part, GSI treatment resulted in higher flap survival rates (P < 0.05). Microscopic analysis exhibited increase in the number of microvascular structures after GSI treatment (P < 0.05). Microangiographic evaluation showed that neovascularization increased in the GSI-applied flaps. Conclusions We present an evidence for the importance of the Notch pathway in the regulation of ischemia-induced angiogenesis. Notch inhibition promotes flap survival by creating a neovasculature that has an increase in vascular density.

Corrosion rate determination is often based on linear polarization (LPR) technique, carried out on small specimens in a controlled environment. The current is measured when the specimen is polarized away from its corrosion potential and the corrosion current gives the corrosion rate using Faraday's law. An important parameter in this calculation is the specimen area exposed. When testing rough, porous specimens such as thermally sprayed aluminum (TSA), the geometrical surface area does not represent the real surface area and hence the corrosion rate is not the actual corrosion rate. To measure the actual corrosion rate aluminum was thermally sprayed onto glass and the surface was characterized using a confocal microscope. These specimens were exposed to seawater at 25, 50 and 100°C, and the linear polarization resistance was determined using a potentiostat at room temperature. This was converted to a corrosion rate based on geometric and the actual surface area.

In the present investigation, the effect of maleic hydrazide (MH) has been studied on seed germination, mitosis, and pollen fertility of Trigonella foenum-graecum L. to test its cytotoxicity. Six different concentrations (0.01%, 0.02%, 0.03% 0.04%, 0.05%, and 0.06%) of maleic hydrazide (MH) were given at seed level. The abnormalities noticed were both physiological and clastogenic. Fragments, stickiness of chromosomes, univalents, multivalents, and anaphase bridges were the most frequent abnormalities. The decrease in seed germination and pollen fertility was found significant at 0.05 level. Mitotic index reduced gradually as the concentrations of Maleic Hydrazide increased and it was found significant at 0.01 and 0.05 levels.