The cerebral angiome: High resolution MicroCT imaging of the whole brain cerebrovasculature in female and male mice.

The cerebrovascular system provides crucial functions that maintain metabolic and homeostatic states of the brain. Despite its integral role of supporting cerebral viability, the topological organization of these networks remains largely uncharacterized. This void in our knowledge surmises entirely from current technological limitations that prevent the capturing of data through the entire depth of the brain. We report high-resolution reconstruction and analysis of the complete vascular network of the entire brain at the capillary level in adult female and male mice using a vascular corrosion cast procedure. Vascular network analysis of the whole brain revealed sex-related differences of vessel hierarchy. In addition, region-specific network analysis demonstrated different patterns of angioarchitecture between brain subregions and sex. Furthermore, our group is the first to provide a three-dimensional analysis of the angioarchitecture and network organization in a single reconstructed tomographic data set that encompasses all hierarchy of vessels in the brain of the adult mouse.

Optical fiber nanoprobe preparation for near-field optical microscopy by chemical etching under surface tension and capillary action.

We propose a technique of chemical etching for fabrication of near perfect optical fiber nanoprobe (NNP). It uses photosensitive single mode optical fiber to etch in hydro fluoric (HF) acid solution. The difference in etching rate for cladding and photosensitive core in HF acid solution creates capillary ring along core-cladding boundary under a given condition. The capillary ring is filled with acid solution due to surface tension and capillary action. Finally it creates near perfect symmetric tip at the apex of the fiber as the height of the acid level in capillary ring decreases while width of the ring increases with continuous etching. Typical tip features are short taper length (approximately 4 microm), large cone angle (approximately 38 degrees ), and small probe tip dimension (<100 nm). A finite difference time domain (FDTD) analysis is also presented to compare near field optics of the NNP with conventional nanoprobe (CNP). The probe may be ideal for near field optical imaging and sensor applications.

Eastern Indian 3800-million-year-old crust and early mantle differentiation.

Samarium-neodymium data for nine granitic and tonalite gneisses occurring as remnants within the Singhbhum granite batholith in eastern India define an isochron of age 3775 +/- 89 x 10(6) years with an initial (143)Nd/(144)Nd ratio of 0.50798 +/- 0.00007. This age contrasts with the rubidium-strontium age of 3200 x 10(6) years for the same suite of rocks. On the basis of the new samarium-neodynium data, field data, and petrologic data, a scheme of evolution is proposed for the Archean crust in eastern India. The isotopic data provide evidence that parts of the earth's mantle were already differentiated with respect to the chondritic samarium-neodymium ratio 3800 x l0(6) years ago.

Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study.

Arsenic is a known global groundwater contaminant. The organochlorine insecticide endosulfan has gained significance as an environmental pollutant due to its widespread use in the control of many food- and non-food-crop-damaging insects. The adverse effects produced by arsenic or endosulfan alone in humans and animals are well documented, but very little is known about the consequences of their coexposure. We evaluated whether their simultaneous exposure can induce oxidative stress and affect antioxidative systems and certain membrane-bound enzymes in erythrocytes of broiler chickens. Day-old chicks were exposed to 3.7 ppm of arsenic via drinking water or 30 ppm of endosulfan-mixed feed or similarly coexposed to these in the same dose levels for 60 days. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum glucose, and levels of glutathione (GSH) and glycosylated hemoglobin (GHb) in blood. LPO was increased with all of the treatments. Catalase was decreased with endosulfan and the coexposure, but not with arsenic, whereas GSH was decreased with arsenic and endosulfan, but not with the coexposure. All of the treatments increased SOD and GPx activities. GST activity was increased only in the coexposed birds. None of the treatments affected the activities of total ATPase and Mg2+-ATPase. Na+-K+-ATPase activity was decreased in the endosulfan-treated and the coexposed birds. All three exposures increased erythrocyte AChE activity. Endosulfan increased the serum glucose level and arsenic and endosulfan increased GHb levels, but these were not altered in the coexposed birds. Erythrocyte protein content was insignificantly decreased with these treatments. Overall, the effects of coexposure were not appreciably different from either of the agents, except on AChE, GSH, and glucose. The results do not reflect any specific type of interaction between these agents in chicken erythrocytes, but they do indicate that the coexposure induces a low level of oxidative stress, which is comparable to that induced by arsenic or endosulfan.

The interferon-stimulated genes: targets of direct signaling by interferons, double-stranded RNA, and viruses.

The interferon system plays a profound role in determining the outcome of viral infection in mammals. Viruses induce the synthesis of interferon, which, in turn, blocks virus replication by inducing the expression of antiviral proteins encoded by interferon-stimulated genes. It is not widely appreciated that without the participation of interferon, many of the same genes can also be induced by a variety of virus-related agents, such as double-stranded RNA and viral proteins. In this chapter, we discuss different signaling pathways, activated by these agents, that lead to the induction of partially overlapping sets of genes, including the interferon-stimulated genes. We also review the biochemical and cellular properties of the protein products of a selected number of these genes including ISG56, ISG54, and ISG15.

DNA mismatch repair detected in human cell extracts.

A system to study mismatch repair in vitro in HeLa cell extracts was developed. Preformed heteroduplex plasmid DNA containing two single base pair mismatches within the SupF gene of Escherichia coli was used as a substrate in a mismatch repair assay. Repair of one or both of the mismatches to the wild-type sequence was measured by transformation of a lac(Am) E. coli strain in which the presence of an active supF gene could be scored. The E. coli strain used was constructed to carry mutations in genes associated with mismatch repair and recombination (mutH, mutU, and recA) so that the processing of the heteroduplex DNA by the bacterium was minimal. Extract reactions were carried out by the incubation of the heteroduplex plasmid DNA in the HeLa cell extracts to which ATP, creatine phosphate, creatine kinase, deoxynucleotides, and a magnesium-containing buffer were added. Under these conditions about 1% of the mismatches were repaired. In the absence of added energy sources or deoxynucleotides, the activity in the extracts was significantly reduced. The addition of either aphidicolin or dideoxynucleotides reduced the mismatch repair activity, but only aphidicolin was effective in blocking DNA polymerization in the extracts. It is concluded that mismatch repair in these extracts is an energy-requiring process that is dependent on an adequate deoxynucleotide concentration. The results also indicate that the process is associated with some type of DNA polymerization, but the different effects of aphidicolin and dideoxynucleotides suggest that the mismatch repair activity in the extracts cannot simply be accounted for by random nick-translation activity alone.

Cytogenetic effects of a mixture of selected metals following subchronic exposure through drinking water in male rats.

The current study examines the genotoxic effects of subchronic exposure via drinking water to a mixture of eight metals (arsenic, cadmium, lead, mercury, chromium, nickel, manganese and iron) found as contaminants of water sources in different parts of India and its possible association with oxidative stress. Male rats were exposed to the mixture at 0, 1, 10 and 100 times the mode concentration of each metal daily for 90 days. Another dose group at concentration equivalent to maximum permissible limit (MPL) for each metal and a reference group given ip cyclophosphamide were incorporated. The mixture at 100x level significantly increased chromosomal aberrations and micronuclei induction (2.4 folds) in bone marrow cells and reduced the ratio of polychromatic to normochromatic erythrocytes by 25%. The mixture significantly increased sister chromatid exchange in bone marrow (1.67 and 2.3 folds) and spleen (1.57 and 1.98 folds) cells with both 10x and 100x doses. Cyclophosphamide was more potent than the mixture in causing cytogenetic damage in these parameters. In rat spleen, the mixture at 10x and 100x doses caused dose-dependent increase in lipid peroxidation (25.95 and 52.71%) and decrease in the activities of superoxide dismutase (20.36 and 40.62%), catalase (18.24 and 35.50%), glutathione peroxidase (22.33 and 36.12%) and glutathione reductase (19.22 and 31.35%) and in the level of GSH (19.76 and 35.15%). The results suggest that the mixture induced genotoxicity in rat bone marrow and spleen cells at concentrations relatively higher than that found in groundwater sources and the genotoxic effect could relate to induction of oxidative stress. However, observations with lower doses indicate that additive or synergistic interactions following exposure to metal components at MPL levels or at mode concentrations of contemporary groundwater levels in India may not result in clastogenicity in male rats.

Effects of oxidizing and reducing agents on ovine pulmonary artery responses to nitric oxide donors, sodium nitroprusside and 3-morpholino-sydnonimine.

Nitrovasodilators-sodium nitroprusside (SNP; 10(-9)-10(-4) M) and 3-morpholino-sydnonimine (SIN-1; 10(-9)-10(-4) M) produced concentration-dependent relaxation of the fourth generation sheep pulmonary artery, preconstricted with 5-hydroxytryptamine (1 microM). Oxidizing agents [oxidized glutathione (GSSG, 1 mM) and CuSO4 (5 and 20 microM)] and reducing agents [dithiothreitol (DTT, 0.1 mM), ascorbic acid (1 mM) and reduced glutathione (GSH, 1 mM)] caused opposite effects on nitric oxide (NO)-induced vasodilation in the artery. Ascorbic acid and GSH potentiated the NO responses, while GSSG and CuSO4 inhibited relaxation caused by the nitrovasodilators. DTT, however, reduced the relaxant potency and efficacy of SNP and SIN-1. Pretreatment of the pulmonary artery strips with DTT (0.1 mM) inhibited SNP (10 microM)-induced Na(+)-K(+)-ATPase activity, while ascorbic acid (1 mM) and GSH (1 mM) had no effect either on basal or SNP (10 microM)-stimulated 86Rb uptake, an index of Na(+)-K(+)-ATPase activity, in ovine pulmonary artery. The results suggest that reducing agents like ascorbic acid may have beneficial effect in improving the vascular function under oxidative stress.

Effect of fenvalerate, a pyrethroid insecticide on membrane fluidity.

Fenvalerate is a commonly used pyrethroid insecticide, used to control a wide range of pests. We have studied its interaction with the membrane using fluorescence polarization and differential scanning calorimetry (DSC) techniques. Fenvalerate was found to decrease the DPH fluorescence polarization value of synaptosomal and microsomal membrane, implicating that it makes the membrane more fluid. At different concentrations of fenvalerate, the activation energy of the probe molecule in the membrane also changes revealed from the change in slope of the Arrhenius plot. At higher concentrations the insecticide slowly saturates the membrane. The effects of fenvalerate on model membrane were also studied with liposomes reconstituted with dipalmitoylphosphatidylcholine (DPPC). Fenvalerate decreased the phase transition temperature (Tm) of DPPC by 1.5 C degrees at 40 microM concentration, but there was no effect on the cooperativity of the transition as interpreted from the DSC thermogram. From the change in the thermogram profile with fenvalerate it has been interpreted that it localizes in the acyl chain region of the lipid, possibly between C10 and C16 region and weakens the acyl chain packing. Fenvalerate was also found to interact with DPPC liposomes containing cholesterol to fluidize it.

Effects of calcium channel blocker, mibefradil, and potassium channel opener, pinacidil, on the contractile response of mid-pregnant goat myometrium.

The present study was undertaken to investigate the in vitro influence of mibefradil, a calcium channel blocker, and pinacidil, a potassium channel opener, on pregnant goat myometrial spontaneous rhythmic contractility and contractions induced with the agonist, oxytocin. Longitudinal strips from the distal region of uterus, collected from goats at midgestation, were mounted in an organ bath for recording isometric contractions. Mibefradil (10(-8)-10(-4) M) or pinacidil (10(-10)-10(-4) M), added cumulatively to the bath at an increment of 1 log unit, caused concentration-dependent inhibition of the spontaneous rhythmic contractions of isolated uterine strips. The rhythmic contraction was, respectively, abolished at 100 and 10 microM concentrations of mibefradil and pinacidil. In a concentration-dependent manner, mibefradil (1 and 10 microM) antagonized the contractions elicited with oxytocin (10(-5)-10(-2) IU). Pretreatment of uterine strips with glibenclamide (10 microM), a selective KATP channel blocker, caused a rightward shift of the concentration-response curve of pinacidil with a concomitant decrease in its pD2 value. Pinacidil (0.3, 1 and 3 microM), in a concentration-related manner, antagonized the oxytocin (10(-5)-10(-2) IU)-induced contractile response. The inhibition of spontaneous rhythmic contractions and antagonism of oxytocin-induced contraction by mibefradil in the pregnant goat myometrium may be related to the antagonism of voltage-dependent Ca2+ channels, while by pinacidil suggests that KATP channel could be a therapeutic target for tocolysis.

Effect of isoproturon pretreatment on the biochemical toxicodynamics of anilofos in male rats.

Anilofos and isoproturon are important herbicides of organophosphorus and substituted phenylurea groups, respectively. Isoproturon is an inducer of hepatic drug-metabolizing enzymes. Animals and humans have the potential to be exposed to the mixture of these intentionally introduced environmental xenobiotics, but toxicological interactions between these herbicides are not known. Effects of isoproturon pretreatment (675 mg/kg/day for 3 consecutive days) on the toxic actions of anilofos administered orally as a single dose (850 mg/kg) were evaluated by determining some biochemical attributes in blood (erythrocyte/plasma), brain and liver of rats. Anilofos or isoproturon alone or in combination failed to produce any noticeable signs of cholinergic hyperactivity and behavioural alterations. Isoproturon did not potentiate the anticholinesterase action of anilofos in blood and liver. Inhibition of brain acetylcholinesterase was significantly protected. No significant alteration in anilofos-mediated production of lipid peroxidation was observed in erythrocyte and brain of isoproturon-pretreated rats, but it was significantly increased in liver. Anilofos did not affect GSH and GST. The isoproturon-mediated increase in GSH levels of brain (threefold) and liver (3.6-fold) was also not affected following combined administration. GST activity was increased in liver of rats given isoproturon alone (fourfold) or in combination with anilofos (2.8-fold). Activities of total ATPase, Mg2+-ATPase and Na+-K+-ATPase were not affected in rats given either anilofos alone or herbicides in sequence. With these treatments, there were no alterations in the protein content of plasma, brain and liver. Overall findings of the study indicate that isoproturon pretreatment does not alter the toxicity of anilofos, the GSH-GST metabolic pathway may not have a significant implication in the detoxification of anilofos and the production of a reactive oxygen species may be a factor in mediating anilofos toxicity.

Influence of malathion pretreatment on the toxicity of anilofos in male rats: a biochemical interaction study.

Toxicity of organophosphates stems mainly from the accumulation of acetylcholine due to inhibition of acetylcholinesterase (AChE). The consequences of excess acetylcholine depend on the events initiated by the interaction of acetylcholine with cholinergic receptors. Lipid peroxidation (LPO) induced by organophosphates also seems to be mediated via cholinergic receptors. Anilofos is a widely used thionoorganophosphate herbicide, while malathion is a thionoorganophosphate insecticide. Thionoorganophosphates undergo mixed function oxidase (MFO)-catalyzed bioactivation to oxons and can induce cholinergic crisis in mammals. Thus, factors (e.g. exposure to certain xenobiotics) which alter the MFO activity, can be assumed to affect the toxicity of these organophosphates. It was investigated in rats if malathion as an inhibitor of MFO can alter the toxicity of anilofos, examining certain biochemical traits in blood, brain and liver. Malathion or anilofos and their combination did not produce any obvious signs of toxicity. Malathion did not alter the anticholinesterase action of anilofos in blood, brain and liver. LPO was increased in erythrocytes, brain and liver with anilofos or malathion and their combination. Production of lipid peroxide in brain of malathion-pretreated rats given anilofos was significantly greater than in rats given anilofos alone. Malathion decreased glutathione (GSH) contents of liver and blood. Glutathione-S-transferase (GST) activity was decreased in the liver with malathion and its combination with anilofos. Total adenosine triphosphatase (ATPase) activity was not affected. Activities of Mg(2+)-ATPase and Na(+)-K(+)-ATPase were increased in the liver and erythrocytes, respectively, with the pesticide combination. Protein level in plasma was decreased with malathion and its combination with anilofos, but only with the combination in the liver. Results of the study indicate that malathion pretreament may not essentially alter the anticholinesterase action of anilofos, but may enhance anilofos-mediated oxidative damage to rat brain.

Kinetics of induction and decay of error-prone DNA repair activity in Escherichia coli after treatment with nalidixic acid.

Inducible error-prone DNA repair activity was detected by infecting nalidixic acid-pretreated E. coli cells with UV-irradiated phage phi X174. Induction and decay kinetics of reactivation very much resembled that of mutagenesis of the UV-damaged phage. Repair as well as mutagenic activity increased for about 30 min. The maximal error-prone repair capacity, which was induced in the cell during the 30 min nalidixic acid treatment, rapidly died out during subsequent cell growth in absence of nalidixic acid. Induction of this repair mode was not observed in a recA- mutant. In the presence of nalidixic acid plus rifampicin both repair and mutagenic effects were abolished.

Neurotoxicity of isoproturon, a substituted phenylurea herbicide, in mice.

Effects of single oral administration of isoproturon (0.5, 1.0 and 2.0 g/kg) on CNS of male mice were studied. At higher doses, spontaneous motor activity (SMA) and forced locomotor activity (FLA) were reduced. Reduction of SMA and FLA was lesser than the reference drug-chlorpromazine hydrochloride (Ch. HCl; 15 mg/kg). Isoproturon, at all doses, potentiated both pentobarbital and barbital-induced sleeping time. At higher doses, potentiation of pentobarbital-induced hypnosis was comparable to Ch.HCl but isoproturon was more effective in inducing hypnosis with barbital. Isoproturon could not protect mice against amphetamine-induced aggregation toxicity. Isoproturon exhibited anticonvulsant activity against both supramaximal electroshock seizures and pentylenetetrazol-induced convulsions. It had no anticonvulsant activity against strychnine but only caused delay in onset of and protection from mortality. At higher doses, anticonvulsant action of isoproturon was comparable to diphenylhydantoin (50 mg/kg) and phenobarbital sodium (100 mg/kg). The study reveals that isoproturon has distinct inhibitory effect on central motor performance and sedative action on CNS. And also it has anticonvulsive and protective actions.

Subacute toxicity of anilofos, a new organophosphorus herbicide, in male rats: effect on some physical attributes and acetylcholinesterase activity.

In acute toxicity study, rats showed dose-dependent signs of cholinergic hyperactivity and behavioural alterations. Maximum intensity of symptoms was not associated with mortality. Oral LD50 was 1681 mg/kg. In subacute toxicity study, rats were orally administered 50, 100 or 200 mg/kg of anilofos once daily for 28 days. Signs and symptoms were observed mainly with 200mg/kg. At this dose, anilofos induced hypothermia and progressive weight loss. None of the anilofos-treated rats died. Weight of brain, lung, testis was not altered, while of liver, heart, spleen and kidney increased. Anilofos inhibited cholinesterase (ChE) activities of erythrocyte (41-67%), plasma (36%), blood (37-64%), brain (63-73%) and liver (28-48%). Total protein was decreased in plasma and liver. Results indicate moderate toxic potential of anilofos in mammals, substantial contribution of CNS-mediated effects in causing anilofos toxicity and no direct relationship between hypothermia and level of ChE inhibition.

Fetotoxic and teratogenic potential of substituted phenylurea herbicide, isoproturon, in rats.

Effect of isoproturon (0.225, 0.45 and 0.90 g/kg/day) administered (po) from day 6 through 15 of gestation was studied on pregnant rats and their offsprings. There were no distinct clinical signs other than dose-related depression and drowsiness of pregnant rats. None of the animals died due to toxicity of isoproturon. At higher doses, decreased maternal body weight was observed during the advanced stage of pregnancy. The litter size, fetal weight and crown-rump and transumbilical lengths were decreased. There was increase in fetal resorption frequency and the number of fetuses with stunted growth. The compound had no effect on fetal sex ratio. No major visceral and skeletal malformations were observed. The study indicates fetotoxic potential of the compound.

Subacute toxicity of anilofos, a new organophosphorus herbicide in male rats: effect on lipid peroxidation and ATPase activity.

Effects of anilofos on lipid peroxidation--an index of oxidative stress, ATPase activity--an integral part of active transport mechanisms for cations, GSH level and GST activity were evaluated in blood (erythrocyte/plasma), brain and liver of male rats after daily oral exposure to 50, 100 or 200 mg/kg for 28 days. None of the doses increased lipid peroxidation. The lowest dose, rather, produced marginally significant decrease in peroxidation in liver. Different doses of anilofos decreased GSH content and activities of GST and ATPases. Inhibition of total ATPase (34-44%) and Na+-K+-ATPase (45-52%) activities was maximum in liver, while that of Mg2+-ATPase (46-56%) was more in erythrocyte. Results indicate that anilofos may not cause oxidative damage to cell membrane in repeatedly exposed animals and may cause neuronal/cellular dysfunction by affecting ionic transport across cell membrane.

Effect of isoproturon on male reproductive system: clinical, histological and histoenzyonological studies in rats.

Isoproturon, a nonhalogenated substituted phenylurea herbicide, was evaluated for its cumulative toxic effects on testicular histomorphology., steroid hormone biosynthesis-related enzymes, spermatogenesis and sperm cells in adult albino rats. The compound, suspended in refined groundnut oil, was administered (po) to rats for 10 weeks @ 0,200, 400 and 800 mg/kg/day for 6 days/week. Isoproturon, at 800 mg/kg dose, decreased epididymal sperm count and percentage of motile sperms and increased the percentage of morphologically abnormal sperm cells. At the same dose, diameter of seminiferous tubules was reduced, number of tubules per microscopic field was increased and the percentage of tubules with evidence of spermatogenesis decreased. However, the percentage of damaged tubules was increased with 400 and 800 mg/kg doses. Histoenzymological observations revealed dose-related reduction in the activities of glucose-6-phosphate dehydrogenase and delta 5-3 beta-hydroxy steroid dehydrogenase. Activity of 17 beta-hydroxy steroid dehydrogenase was not affected appreciably. Overall findings suggest that isoproturon, at high dose, impairs androgen biosynthetic process, affects spermatogenesis and induces maturational anomalies of sperm cells in rat.

Subacute toxicity of urea herbicide, isoproturon, in male rats.

Isoproturon, a substituted phenylurea herbicide, was evaluated for its cumulative toxic effect on growth, organ weight and histomorphology of different organs in adult male rats. The compound (200, 400 and 800 mg/kg/day for 6 days/week), suspended in refined groundnut oil, was administered to rats p.o. for 7 and 10 weeks. There were no definite signs and symptoms of toxicity in treated rats but the herbicide significantly decreased the weekly body weight of rats at 800 mg/kg dose. Isoproturon, in all the three doses, increased the weight of liver in a dose-dependent manner. At 800 mg/kg dose, isoproturon increased the weight of kidney and heart, and decreased the weight of epididymis. Histopathological alterations in the organs were dose-dependent. Salient microscopic changes induced by isoproturon were hepatocellular degenerative changes and focal necrosis in liver, glomerular and tubular degeneration in kidney and haemosiderosis in spleen. Testis showed degeneration and desquamation of cells of germinal layers. Tubular lumens of testis and epididymis exhibited reduced number of spermatids and spermatozoa, respectively, indicating retardation of spermatogenesis.

Low-power inversion recovery MRI preserves brain tissue contrast for patients with Parkinson disease with deep brain stimulators.

BACKGROUND AND PURPOSE: Fast spin-echo short τ inversion recovery sequences have been very useful for MR imaging-guided deep brain stimulation procedures in Parkinson disease. However, high-quality fast spin-echo imaging deposits significant heat, exceeding FDA-approved limits when patients already have undergone deep brain stimulation and need a second one or a routine brain MR imaging for neurologic indications. We have developed a STIR sequence with an ultra-low specific absorption rate that meets hardware limitations and produces adequate tissue contrast in cortical and subcortical brain tissues for deep brain stimulation recipients. MATERIALS AND METHODS: Thirteen patients with medically refractory Parkinson disease who qualified for deep brain stimulation were imaged at 1.5T with a fast spin-echo short τ inversion recovery sequence modified to meet conditional MR imaging hardware and specific absorption rate restrictions. Tissue contrast-to-noise ratios and implant localization were objectively and subjectively compared by 2 neuroradiologists, and image quality for surgical planning was assessed by a neurosurgeon for high and low specific absorption rate images. RESULTS: The mean contrast-to-noise ratio for cerebral tissues without including the contrast-to-noise ratio for ventricular fluid was 35 and 31 for high and low specific absorption rate images. Subjective ratings for low specific absorption rate tissue contrast in 77% of patients were identical to (and in a few cases higher than) those of high specific absorption rate contrast, while the neurosurgical coordinates for fusing the stereotactic atlas with low specific absorption rate MR imaging were equivalent to those of the high specific absorption rate for 69% of patients. CONCLUSIONS: Patients with Parkinson disease who have already had a deep brain stimulation face a risk of neural injury if routine, high specific absorption rate MR imaging is performed. Our modified fast spin-echo short τ inversion recovery sequence conforms to very conservative radiofrequency safety limits, while it maintains high tissue contrast for presurgical planning, postsurgical assessment, and radiologic evaluations with greater confidence for radiofrequency safety.