Ppm In Brain Research Articles

Investigation of metabolite correlates of CEST in the human brain at 7 T.

Metabolite-weighted chemical exchange saturation transfer MRI can be used to indirectly image metabolites such as creatine and glutamate. This study aims to further explore the contrast of CEST at 2 ppm in the human brain at 7T and investigate the metabolite correlates of CEST at 2 ppm via correlations with magnetic resonance spectroscopy (MRS). Simulations were performed to establish the optimal acquisition parameters, such as total saturation time (tsat) and B1 root mean squared (B1rms) for CEST at 2 ppm in the human brain. Parameters were validated via in vitro phantom studies at 7T using concentrations, pH and temperature comparable to what is found in the human brain. Finally, 10 healthy volunteers were scanned at 7T for comparison with MRS. Our results show that the optimal parameters to acquire CEST at 2 ppm images are: B1rms = 2.14 μT & tsat = 1500 ms, respectively. Comparison with MRS showed no significant correlation between CEST at 2 ppm and total Creatine measured by MRS (R = 0.19; p-value = 0.273). However, a significant correlation was found between CEST at 2 ppm and Glu (R = 0.39; p-value = 0.033), indicating the broad Glutamate-weighted CEST as the main measurable contributor to CEST at 2 ppm. We identified and confirmed optimal CEST at 2 ppm sequence parameters and validated CEST at 2 ppm measurements in a controlled in vitro environment. Our findings suggest that glutamate is a substantial contributor to the CEST at 2 ppm contrast observed in the human brain, whereas the creatine contribution to CEST at 2 ppm in the brain did not show a measurable contribution.

Mercury and selenium levels, and selenium:mercury molar ratios of brain, muscle and other tissues in bluefish (Pomatomus saltatrix) from New Jersey, USA

A number of contaminants affect fish health, including mercury and selenium, and the selenium:mercury molar ratio. Recently the protective effects of selenium on methylmercury toxicity have been publicized, particularly for consumption of saltwater fish. Yet the relative ameliorating effects of selenium on toxicity within fish have not been examined, nor has the molar ratio in different tissues, (i.e. brain). We examined mercury and selenium levels in brain, kidney, liver, red and white muscle, and skin and scales in bluefish (Pomatomus saltatrix) (n=40) from New Jersey to determine whether there were toxic levels of either metal, and we computed the selenium:mercury molar ratios by tissues. Total mercury averaged 0.32±0.02ppm wet weight in edible muscle and 0.09±0.01ppm in brain. Selenium concentration averaged 0.37±0.03 in muscle and 0.36±0.03ppm in brain. There were significant differences in levels of mercury, selenium, and selenium:mercury molar ratios, among tissues. Mercury and selenium levels were correlated in kidney and skin/scales. Mercury levels were highest in kidney, intermediate in muscle and liver, and lowest in brain and skin/scales; selenium levels were also highest in kidney, intermediate in liver, and were an order of magnitude lower in the white muscle and brain. Mercury levels in muscle, kidney and skin/scales were positively correlated with fish size (length). Selenium levels in muscle, kidney and liver were positively correlated with fish length, but in brain; selenium levels were negatively correlated with fish length. The selenium:mercury molar ratio was negatively correlated with fish length for white muscle, liver, kidney, and brain, particularly for fish over 50cm in length, suggesting that older fish experience less protective advantages of selenium against mercury toxicity than smaller fish, and that consumers of bluefish similarly receive less advantage from eating larger fish.

Study the pathological and Residual Toxic effect of Malathion in Mice Nervous System

In present experiment , study was done on the pathological and residual effect of malathion in mice 50 white mice randomly divided into 3 group : 1st group including (20)mice was given single oral dose .1.5 ppm in drinking water 2nd group contain (20) mice given single dose 1.5 ppm malathion orally in drinking water and repeated the same dose at 2nd and 3rd week i.e (three repeated doses), the 3rd group (10) mice act as control group .The long of experiment was 60 days , the following parameter were done .
 1- Clinical Signs: treated group 1st and 2nd groups showed nausea and diarrhea
 2- Pathological changes : 1st and 2nd group showed lesion which were more significant in 2nd group .Pathological changes characterized by neuron necrosis , Brain odema , and mononuclear cell present with spinal cord damage .
 3- Residual investigation: which were more significant in 2nd group at 60 days of treatment, the Malathion residual reach 0.90 ppm in brain and spinal cord.