[en] BNL has always been a leader in the world of superconducting magnets, which are essential to the great modern accelerators such as the Relativistic Heavy Ion Collider at BNL, or the Large Hadron Collider at CERN, Switzerland. These magnets are made of material that, cooled to 4 Kelvins (K) (-452 Farenheit) become superconducting, that is, lose essentially all resistance to electricity. For the past decade, however, Lab researchers have been exploring the use of new materials that become superconducting at higher temperatures. These materials can operate at the relatively high temperature of 77 K (-351 F), allowing them to be cooled by cheap, plentiful liquid nitrogen, rather than helium, and can create very high magnetic fields. Now far in the lead of this area of research, BNL scientists are exploring avenues for high temperature superconducting magnets that are energy efficient and have magnetic fields that are a million times stronger than the Earth's. If successful, these new magnets could potentially revolutionize usage in future accelerators, play a key role in energy efficiency and storage, and make possible new applications such as muon colliders and MRI screening in remote areas.

[en] Chemicals are not single minded, yet in majority of cases biological activities are cumulate index of their physio-chemical nature. Taurine (2-amino ethane sulfonic acid) differs in its physical constituents to other neuro active amino acids in way of having 1.5 pka and 82 pkb showing more acidic and more basic than common neuro active amino acid like; aspartic acid, B Alanine and GABA. The intra molecular hydrogen bonding with lower proton affinity of the amino group in taurine than in GABA enables taurine ability to penetrate blood brain barrier, but at slower rate. Having sulphur, atom; adds addition value, as sulphur is necessary for sustaining the life processes. Sulphur containing amino acids (SAA) are not too many; generally SAA contains sulphur in their lower oxidation state (-2); for some reason sulphur in low oxidation state protects from oxygen toxicity and radiation damage. The composite effects of its distinct physical activities provided a label of meta-vitamin to indispensable amino acids with a wide spectrum of beneficial actions in diabetic to epilepsy, and from hypertension to ageing. It is well establish that high doses of ionized radiation leads to the enhanced leakage of taurine from the damage cells to extracellular fluid followed by increased urinary extraction. Radiation induced taurine depletion can itself have various harmful effects. Though taurine radio protective action mechanism is still incomplete but high level of taurine have been found in experimental studies with animals or in isolated cells exposed to high doses of ionization radiation. It is believe that taurine radio protective action is combination of multiple beneficial effects involving several action mechanism, during the exposure to ionizing radiation taurine may function as antioxidant, and in scavenging the harmful molecules, it is also possible that taurine may be helping to reduce the post traumatic inflammatory after radiation exposure or it may be participating to enhance the growth rate of leukocytes and leukocytes progenitor cells or it may be acting as antifibrogenic agent, Besides these; role of taurine as strong osmolyte is well established to add further taurine depilation due to rough therapy of cancer patient can be checked with taurine supplementation which has shown greater survival possibilities. Taurine has been shown to function as good antidote against several different toxic substances and has effective role in prophylaxis of fibrosis in patients exposed to high level of ionizing radiation. (author)

[en] We review the progress on LHC IR upgrades made by the US-LARP collaboration since the last CARE meeting in November 2004. We introduce a new optics design with doublet focusing, and discuss energy deposition calculations with an open mid-plane dipole. We present the results of a beam-beam experiment at RHIC. This experiment was the first phase of a planned test of the wire compensation principle at RHIC

[en] This paper presents a new approach for developing and demonstrating high field magnet technology based on a magnet and test facility developed specifically for it. The traditional approach for carrying out high field magnet R&D has been building a new magnet to demonstrate a new design, new material or new technology. However, building a high field magnet is time consuming and expensive. To overcome this limitation, Brookhaven National Laboratory (BNL) built and successfully tested a 10 T Nb₃Sn dipole DCC017 with large enough open or clear space (31 mm wide and 338 mm high) so that a pair of racetrack coils could be inserted into this opening without disassembling the magnet. The motivation be-hind this design was to facilitate a magnet R&D program where the new coils (with a large range in width and height accommodated) would reside in a high field region in direct contact with the existing coils (just as other magnet coils) and thus become an integral part of the magnet. We summarize the approach, the magnet, the test facility, past experiences, current and future test plans and planned up-grade. Here, the magnet facility is now available to service the needs of the wider community for testing cable and insert coils in a back-ground field of up to 10 T.

[en] As part of the LHC Accelerator Research Program (LARP) to build a high performance quadrupole magnet with Nb₃Sn conductor, a pair of 3.6 m-long Nb₃Sn racetrack coils has been made at Brookhaven National Laboratory (BNL) and installed in two shell-type support structures built by Lawrence Berkeley National Laboratory (LBL). These magnet assemblies have been tested at 4.5 K at BNL to gauge the effect of extended length and prestress on the mechanical performance of the long structure compared to earlier short models. This paper presents the results of quench testing and compares the overall performance of the two versions of the support structure. We also summarize the shell strain measurements and discuss the variation of quench current with ramp rate.

[en] Prophylactic agents acutely administered in response to anticholinesterases intoxication can prevent toxic symptoms, including fasciculations, seizures, convulsions and death. However, anticholinesterases also have long-term unknown pathophysiological effects, making rational prophylaxis/treatment problematic. Increasing evidence suggests that in addition to excessive cholinergic stimulation, organophosphate compounds such as diisopropylphosphorofluoridate (DFP) induce activation of glutamatergic neurons, generation of reactive oxygen (ROS) and nitrogen species (RNS), leading to neurodegeneration. The present study investigated multiple affectors of DFP exposure critical to cerebral oxidative damage and whether antioxidants and NMDA receptor antagonist memantine provide neuroprotection by preventing DFP-induced biochemical and morphometric changes in rat brain. Rats treated acutely with DFP (1.25 mg/kg, s.c.) developed onset of toxicity signs within 7-15 min that progressed to maximal severity of seizures and fasciculations within 60 min. At this time point, DFP caused significant (p < 0.01) increases in biomarkers of ROS (F₂-isoprostanes, F₂-IsoPs; and F₄-neuroprostanes, F₄-NeuroPs), RNS (citrulline), and declines in high-energy phosphates (HEP) in rat cerebrum. At the same time, quantitative morphometric analysis of pyramidal neurons of the hippocampal CA1 region revealed significant (p < 0.01) reductions in dendritic lengths and spine density. When rats were pretreated with the antioxidants N-tert-butyl-α-phenylnitrone (PBN, 200 mg/kg, i.p.), or vitamin E (100 mg/kg, i.p./day for 3 days), or memantine (18 mg/kg, i.p.), significant attenuations in DFP-induced increases in F₂-IsoPs, F₄-NeuroPs, citrulline, and depletion of HEP were noted. Furthermore, attenuation in oxidative damage following antioxidants or memantine pretreatment was accompanied by rescue from dendritic degeneration of pyramidal neurons in the CA1 hippocampal area. These findings closely associated DFP-induced lipid peroxidation with dendritic degeneration of pyramidal neurons in the CA1 hippocampal area and point to possible interventions to limit oxidative injury and dendritic degeneration induced by anticholinesterase neurotoxicity.

[en] Carbamate insecticides mediate their neurotoxicity by acetylcholinesterase (AChE) inactivation. Male Sprague-Dawley rats acutely intoxicated with the carbamate insecticide carbofuran (1.5 mg/kg, sc) developed hypercholinergic signs within 5-7 min of exposure, with maximal severity characterized by seizures within 30-60 min, lasting for about 2 h. At the time of peak severity, compared with controls, AChE was maximally inhibited (by 82-90%), radical oxygen species (ROS) markers (F₂-isoprostanes, F₂-IsoPs; and F₄-neuroprostanes, F₄-NeuroPs) were elevated 2- to 3-fold, and the radical nitrogen species (RNS) marker citrulline was elevated 4- to 8-fold in discrete brain regions (cortex, amygdala, and hippocampus). In addition, levels of high-energy phosphates (HEPs) were significantly reduced (ATP, by 43-56%; and phosphocreatine, by 37-48%). Values of total adenine nucleotides and total creatine compounds declined markedly (by 41-56% and 35-45%, respectively), while energy charge potential remained unchanged. Quantitative morphometric analysis of pyramidal neurons of the hippocampal CA1 region revealed significant decreases in dendritic lengths (by 64%) and spine density (by 60%). Pretreatment with the N-methyl-D-aspartate (NMDA) receptor antagonist memantine (18 mg/kg, sc), in combination with atropine sulfate (16 mg/kg, sc), significantly attenuated carbofuran-induced changes in AChE activity and levels of F₂-IsoPs and F₄-NeuroPs, declines in HEPs, as well as the alterations in morphology of hippocampal neurons. MEM and ATS pretreatment also protected rats from carbofuran-induced hypercholinergic behavioral activity, including seizures. These findings support the involvement of ROS and RNS in seizure-induced neuronal injury and suggest that memantine by preventing carbofuran-induced neuronal hyperactivity blocks pathways associated with oxidative damage in neurons

[en] Exposure to excessive manganese (Mn) levels leads to neurotoxicity, referred to as manganism, which resembles Parkinson's disease (PD). Manganism is caused by neuronal injury in both cortical and subcortical regions, particularly in the basal ganglia. The basis for the selective neurotoxicity of Mn is not yet fully understood. However, several studies suggest that oxidative damage and inflammatory processes play prominent roles in the degeneration of dopamine-containing neurons. In the present study, we assessed the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates and associated neuronal dysfunctions both in vitro and in vivo. Results from our in vitro study showed a significant (p < 0.01) increase in biomarkers of oxidative damage, F₂-isoprostanes (F₂-IsoPs), as well as the depletion of ATP in primary rat cortical neurons following exposure to Mn (500 μM) for 2 h. These effects were protected when neurons were pretreated for 30 min with 100 of an antioxidant, the hydrophilic vitamin E analog, trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), or an anti-inflammatory agent, indomethacin. Results from our in vivo study confirmed a significant increase in F₂-IsoPs levels in conjunction with the progressive spine degeneration and dendritic damage of the striatal medium spiny neurons (MSNs) of mice exposed to Mn (100 mg/kg, s.c.) 24 h. Additionally, pretreatment with vitamin E (100 mg/kg, i.p.) or ibuprofen (140 μg/ml in the drinking water for two weeks) attenuated the Mn-induced increase in cerebral F₂-IsoPs? and protected the MSNs from dendritic atrophy and dendritic spine loss. Our findings suggest that the mediation of oxidative stress/mitochondrial dysfunction and the control of alterations in biomarkers of oxidative injury, neuroinflammation and synaptodendritic degeneration may provide an effective, multi-pronged therapeutic strategy for protecting dysfunctional dopaminergic transmission and slowing of the progression of Mn-induced neurodegenerative processes. -- Research highlights: ► Mn exposure leads to neurotoxicity in vitro and in vivo. ► Antioxidants and anti-inflammatory agents attenuate Mn-induced oxidative injury. ► These agents also protect the striatal neurons from dendritic atrophy and spine loss. ► These prophylactic strategies may be effective against Mn neurotoxicity.

[en] Glucose feeding can markedly exacerbate the toxicity of the anticholinesterase insecticide, parathion. We determined the effects of parathion on brain nitric oxide and its possible role in potentiation of toxicity by glucose feeding. Adult rats were given water or 15% glucose in water for 3 days and challenged with vehicle or parathion (18 mg/kg, s.c.) on day 4. Functional signs, plasma glucose and brain cholinesterase, citrulline (an indicator of nitric oxide production) and high-energy phosphates (HEPs) were measured 1-3 days after parathion. Glucose feeding exacerbated cholinergic toxicity. Parathion increased plasma glucose (15-33%) and decreased cortical cholinesterase activity (81-90%), with no significant differences between water and glucose treatment groups. In contrast, parathion increased brain regional citrulline (40-47%) and decreased HEPs (18-40%) in rats drinking water, with significantly greater changes in glucose-fed rats (248-363% increase and 31-61% decrease, respectively). We then studied the effects of inhibiting neuronal nitric oxide synthase (nNOS) by 7-nitroindazole (7NI, 30 mg/kg, i.p. x4) on parathion toxicity and its modulation by glucose feeding. Co-exposure to parathion and 7NI led to a marked increase in cholinergic signs of toxicity and lethality, regardless of glucose intake. Thus, glucose feeding enhanced the accumulation of brain nitric oxide following parathion exposure, but inhibition of nitric oxide synthesis was ineffective at counteracting increased parathion toxicity associated with glucose feeding. Evidence is therefore presented to suggest that nitric oxide may play both toxic and protective roles in cholinergic toxicity, and its precise contribution to modulation by glucose feeding requires further investigation

[en] Exposure to excessive manganese (Mn) levels results in neurotoxicity to the extrapyramidal system and the development of Parkinson's disease (PD)-like movement disorder, referred to as manganism. Although the mechanisms by which Mn induces neuronal damage are not well defined, its neurotoxicity appears to be regulated by a number of factors, including oxidative injury, mitochondrial dysfunction and neuroinflammation. To investigate the mechanisms underlying Mn neurotoxicity, we studied the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates (HEP), neuroinflammation mediators and associated neuronal dysfunctions both in vitro and in vivo. Primary cortical neuronal cultures showed concentration-dependent alterations in biomarkers of oxidative damage, F₂-isoprostanes (F₂-IsoPs) and mitochondrial dysfunction (ATP), as early as 2 h following Mn exposure. Treatment of neurons with 500 μM Mn also resulted in time-dependent increases in the levels of the inflammatory biomarker, prostaglandin E₂ (PGE₂). In vivo analyses corroborated these findings, establishing that either a single or three (100 mg/kg, s.c.) Mn injections (days 1, 4 and 7) induced significant increases in F₂-IsoPs and PGE₂ in adult mouse brain 24 h following the last injection. Quantitative morphometric analyses of Golgi-impregnated striatal sections from mice exposed to single or three Mn injections revealed progressive spine degeneration and dendritic damage of medium spiny neurons (MSNs). These findings suggest that oxidative stress, mitochondrial dysfunction and neuroinflammation are underlying mechanisms in Mn-induced neurodegeneration.